Myocardial Infarction (or Ml) strikes one and a half -million Americans every year.

Most of these patients

survive because they seek immediate treatment. But others ignore or fail to recognize the signs of an Ml.
And they delay treatment, which can lead to sudden death.
Today, this patient developed crushing, substernal chest pain that radiated down his left arm. Because he
has a history of coronary artery disease (or CAD), he took sublingual nitroglycerin as usual for an angina
attack. After he took it three times, his pain worsened, and he began sweating and vomiting. He realized his
condition was more serious than usual, and called for an ambulance.
This patient is one of the lucky ones. He recognized the signs of an Ml and received treatment even before
he reached the hospital. But he's not out of danger yet over the next few hours and days, he'll need rapid,
effective care to prevent potentially fatal complications.

But are you confident in your ability to manage his care? Do you know what causes an Ml and its signs and
symptoms? And can you intervene properly to relieve them?
To help you manage your patients successfully, this video will show what happens in the body before,
during, and after an MI. And it will highlight the effects of your interventions on your patients' survival.

Basically, an Ml is cardiac tissue death caused by reduced myocardial blood flow. In most patients, it results
from CAD, a condition that's brought about by atherosclerosis. In CAD, atherosclerotic plaque narrows the
lumen of a coronary artery, reducing the amount of blood and oxygen that reaches the heart's muscular wall
or myocardium. As plaque builds and the blood supply is cut off, tissue death, and Ml, may occur.
Normally, the coronary arteries surround the heart like a crown. The two main coronary arteries, the right and
left, originate from the ascending aorta, behind the aortic valve.

The right coronary artery has several branches:

 The conus artery,

 Sinoatrial (or SA) node artery,
 Atrioventricular (or AV) node artery,
 Posterior descending artery (or PDA),
 Marginal artery,
 Atrial artery and
 Ventricular artery

These arteries carry blood and oxygen to:

 The walls of the right atrium and ventricle,

 Parts of the interventricular septum, and
 Parts of the left ventricle's inferior and posterior walls

The left coronary artery has two main branches, including the:

 Left anterior descending (or LAD) artery, and

 Circumflex artery

Together, they supply blood and oxygen to the:

 Left atrium
 And remaining walls of the left ventricle

During diastole, the right and left coronary arteries and their branches fill with oxygenated blood from the
aorta. Then they nourish the heart's tissue layers with blood and oxygen.
In CAD, low-density lipoproteins (or LDLs) and other substances enter the artery's endothelium and form
plaques.In later stages of CAD, this plaque calcifies, ulcerates, and attracts thrombi. Eventually, the arterial
wall weakens, and the plaque ruptures. The ruptured plaque attracts more thrombi and platelets, which may
trigger a vasospasm.
This combination of thrombi, platelets, and vasospasm may partially or totally block the affected artery,
disrupting blood flow and cellular oxygenation. These events typically cause angina. If the myocardial blood
flow is interrupted for more than 20 minutes, tissue injury and infarction ensue.
in cad low density lipoproteins
0:04
or ldls and other substances
0:07
enter the arteries endothelium and form
0:10
plaques
0:12
in later stages of cad this plaque
0:15
calcifies
0:17
ulcerates and attracts thrombi
0:20
eventually the arterial wall weakens
0:23
and the plaque ruptures the ruptured
0:27
plaque
0:28
attracts more thrombi and platelets
0:30
which may trigger
0:32
a vasospasm
0:35
this combination of thrombi platelets
0:37
and vasospasm
0:39
may partially or totally block the
0:41
affected artery
0:43
disrupting blood flow and cellular
0:45
oxygenation
0:47
these events typically cause angina
0:51
if the myocardial blood flow is
0:53
interrupted for
0:55
more than 20 minutes tissue injury and
0:58
infarction ensue

For some patients, collateral circulation may avert myocardial injury and infarction. In such patients blood
vessels connect adjacent coronary arteries or parts of the same coronary artery. Then as atherosclerotic
plaque builds up, the body compensates by dilating the collateral blood vessels. This diverts blood flow
around the blockage, preserving myocardial tissue perfusion.
If the patient doesn’t have collateral circulation or if it can’t supply enough blood and oxygen to the
myocardium, cellular ischemia occurs. Without oxygen, myocardial cells switch from aerobic to anaerobic
metabolism, causing hydrogen ions and lactic acid to accumulate in the blood. As oxygen deprivation
persists, the cells mitochondria can't produce adenosine tri-phosphate (or ATP) for energy.
Then the cells must burn stored glycogen for energy. When they've used all the available glycogen, they
stop functioning. When this happens, sodium and calcium accumulate in the cells, attracting water. This
causes the cells to swell and lose intracellular potassium. The combination of oxygen deprivation,
intracellular potassium loss, and lactic acidosis causes the affected heart muscle to lose contractility and
possibly develop arrhythmias. Unless the blood and oxygen supply is restored, permanent damage will
occur, including cell death and tissue necrosis.
for some patients collateral circulation
0:03
may avert myocardial injury and
0:06
infarction
0:09
in such patients blood vessels connect
0:12
adjacent coronary arteries or
0:14
parts of the same coronary artery
0:18
then as atherosclerotic plaque builds up
0:22
the body compensates by dilating the
0:24
collateral blood vessels
0:26
this diverts blood flow around the
0:29
blockage
0:30
preserving myocardial tissue perfusion
0:35
if the patient doesn't have collateral
0:37
circulation
0:38
or if it can't supply enough blood and
0:41
oxygen to the myocardium
0:43
cellular ischemia occurs
0:48
without oxygen myocardial cells switch
0:51
from
0:51
aerobic to anaerobic metabolism
0:55
causing hydrogen ions and lactic acid
0:58
to accumulate in the blood
1:02
as oxygen deprivation persists the
1:05
cell's mitochondria can produce
1:07
adenosine triphosphate or atp
1:10
for energy then the cells must burn
1:14
stored glycogen for energy when they've
1:17
used all the available glycogen
1:20
they stop functioning
1:24
when this happens sodium and calcium
1:27
accumulate in the cells
1:28
attracting water this causes the cells
1:32
to swell
1:33
and lose intracellular potassium
1:38
the combination of oxygen deprivation
1:41
intracellular potassium loss
1:43
and lactic acidosis causes the affected
1:46
heart muscle to lose contractility
1:48
and possibly develop arrhythmias
1:52
unless the blood and oxygen supply is
1:55
restored
1:56
permanent damage will occur including
1:58
cell death
1:59
and tissue necrosis

In an Ml, cell damage occurs in three distinct zones:

 The zone of ischemia reflects temporary interruption of the blood supply

 The zone of injury indicates prolonged blood supply interruption and cell damage
 The zone of infarction denotes complete blood supply interruption and cell death

If treatment restores blood flow to the affected area of the heart, zones of ischemia and injury may escape permanent
damage. Within 24 hours of an MI white blood cells and proteolytic enzymes move into the area to begin healing.
Within 2 weeks, a soft layer of collagenous scar tissue replaces the necrotic tissue. During this time,
myocardial rupture, a deadly complication of Ml, is most likely to occur. Within 6 weeks, new, permanent scar
tissue forms. This tissue is stronger, but less pliable.
Remember that an Ml may affect one or more walls of the right and left ventricles depending on the location
of the coronary artery lesion.

For example, this patient has an occlusion in the proximal part of his LAD artery. So the anterior wall of his
left ventricle and part of his interventricular septum has sustained myocardial injury and infarction. Because
the anterior wall forms a large part of the left ventricle, the patient may suffer complications related to loss of
myocardial function.
For any patient with an Ml, the number and severity of complications, and his chance of survival, depend on
the extent of muscle damage. And the extent of muscle damage depends, in part on your prompt
intervention.
in an mi cell damage occurs in three
0:09
distinct zones the zone of ischemia
0:13
reflects temporary interruption of the
0:15
blood supply
0:17
the zone of injury indicates prolonged
0:20
blood supply
0:21
interruption and cell damage the zone of
0:24
infarction
0:25
denotes complete blood supply
0:27
interruption and
0:28
cell death if treatment restores blood
0:33
flow to the affected area of the heart
0:35
zones of ischemia and injury may escape
0:38
permanent damage
0:42
within 24 hours of an mi
0:46
white blood cells and proteolytic
0:48
enzymes move into the area to begin
0:50
healing
0:51
[Music]
0:56
within two weeks a soft layer of
0:58
collagenous scar tissue replaces the
1:01
necrotic tissue
1:03
during this time myocardial rupture a
1:06
deadly complication of mi
1:08
is most likely to occur
1:12
within six weeks new permanent scar
1:15
tissue forms
1:16
this tissue is stronger but less pliable
1:21
remember that an mi may affect one or
1:24
more walls
1:25
of the right and left ventricles
1:27
depending on the location of the
1:28
coronary artery lesion
1:32
for example this patient has an
1:34
occlusion in the proximal part of his
1:36
led artery so the anterior wall of his
1:40
left ventricle
1:41
and part of his interventricular septum
1:44
have sustained myocardial injury and
1:46
infarction because the anterior wall
1:51
forms a large part of the left ventricle
1:54
the patient may suffer complications
1:56
related to loss of myocardial function
2:00
for any patient with an mi the number
2:03
and severity of complications
2:06
and his chance of survival depend on the
2:09
extent of muscle damage
2:11
and the extent of muscle damage depends
2:14
in part
2:15
on your prompt intervention

Because a patient with an Ml faces a very real risk of sudden death, your rapid, effective care is critical.
Suppose you're caring for this patient, who has had an infarction in the anteroseptal wall of his left ventricle.
As soon as he's admitted to your unit, obtain a blood specimen for testing and perform a rapid, focused
assessment.
This includes:

 Taking his blood pressure,

 Measuring his heart and respiratory rates, and
 Obtaining a 12-lead electrocardiogram (or ECG) tracing

His blood pressure and heart and respiratory rates are likely to be elevated because pain and stress trigger the sympathetic
nervous system to release epinephrine and norepinephrine.
Expect the 12-lead ECG to show signs of ischemia, injury and infarction. For example, suspect myocardial
ischemia if you see inverted T waves in the leads for the affected area of the heart. This is because T waves
represent ventricular repolarization, and ischemic tissue tends to re-polarize later than healthy tissue.
Suspect myocardial injury if you detect ST segment elevation. For example, this patient's ECG tracing shows
elevated ST segments in leads V1, V2, V3, and V4, which suggests myocardial injury in the left ventricle's
anterior wall and part of the interventricular septum. If you also note Q waves, suspect irreversible infarction
in the heart's walls. Q waves result from scar tissue that can’t depolarize.

The heart’s wall has three layers:

 The inner endocardium,

 The muscular myocardium, and
 The outer epicardium

These layers are surrounded by an elastic, two-layer sac called the pericardium. An Infarction may extend through one, two,
or all three layers, from the endocardium out to the epicardium. If the Ml doesn't affect all three layers, it’s called a non-Q
wave MI, named for the absence of pathologic Q waves on the ECG tracing. Although non-Q wave MIs causes ST segment
depression, they cause less tissue damage and usually are less serious.

because a patient with an mi faces a

0:21
very real risk of sudden death
0:24
your rapid effective care is critical
0:27
suppose you're caring for this patient
0:29
who has had an infarction in the
0:31
anteroceptal wall of his left ventricle
0:35
as soon as he's admitted to your unit
0:37
obtain a blood specimen for testing
0:39
and perform a rapid focused assessment
0:43
this includes taking his blood pressure
0:46
measuring his heart and respiratory
0:48
rates
0:50
and obtaining a 12 lead
0:52
electrocardiogram
0:53
or ecg tracing
0:58
his blood pressure and heart and
1:00
respiratory rates are likely to be
1:02
elevated
1:02
because pain and stress trigger the
1:04
sympathetic nervous system
1:06
to release epinephrine and
1:08
norepinephrine
1:11
expect the 12 lead ecg to show signs of
1:15
ischemia
1:16
injury and infarction for example
1:20
suspect myocardial ischemia if you see
1:23
inverted t
1:24
waves in the leads for the affected area
1:26
of the heart
1:27
this is because t waves represent
1:30
ventricular repolarization
1:32
and ischemic tissue tends to repolarize
1:35
later than healthy tissue suspect
1:38
myocardial injury if you detect st
1:42
segment elevation for example this
1:45
patient's ecg tracing
1:46
shows elevated st segments in leads v1
1:50
v2 v3 and v4 which suggests
1:54
myocardial injury in the left
1:56
ventricle's anterior wall
1:58
and part of the interventricular septum
2:02
if you also note q waves suspect
2:05
irreversible
2:06
infarction in the heart's walls q waves
2:09
result from scar tissue
2:11
that can't depolarize
2:15
the heart's walls have three layers the
2:18
inner endocardium the muscular
2:21
myocardium
2:23
and the outer epicardium these layers
 2:27
are surrounded by
2:28
an elastic two-layer sac called the
2:30
pericardium
2:32
an infarction may extend through one two
2:36
or all three layers from the endocardium
2:39
out to the epicardium
2:42
if the mi doesn't affect all three
2:45
layers
2:45
it's called a non-q wave mi
2:49
named for the absence of pathologic q
2:51
waves on the ecg
2:53
tracing although non-q wave mis cause
2:57
st segment depression they cause less
3:00
tissue damage
3:02
and usually are less serious

To limit the size and severity of your patient's Ml and to reduce his pain, begin treatment promptly, as ordered.
First, administer supplemental oxygen therapy by nasal cannula or mask. This helps deliver more oxygen to
ischemic cells. Also check his oxygen saturation, which should be above 92%. If it’s not, determine why and
expect to administer more oxygen.
Next, maintain nitroglycerin therapy, as prescribed. Nitroglycerin works by dilating the coronary arteries,
which increases the blood flow to the myocardium. Also give morphine sulfate intravenously to quickly
relieve chest pain, reduce anxiety, and decrease preload (which is ventricular wall tension at the end of
diastole).

If prescribed, administer aspirin. Expect to give one chewable aspirin immediately for fast absolution, and a
regular aspirin tablet (swallowed whole) for slower absorption.Aspirin blocks the formation of thromboxane;
A2, a powerful vasoconstrictor that is released by platelets when they accumulate in the injured arterial walls.
By inhibiting thromboxane A2, aspirin prevents further platelet aggregation and coronary vasoconstriction.
Prepare for administration of a thrombolytic drug, such as streptokinase, urokinase, or recombinant tissue
plasminogen activator, unless contraindicated by active bleeding or another condition. When given within 6
hours of the start of the MI, thrombolytic drugs open blocked coronary arteries. They do this by converting
plasminogen to plasmin, which breaks down fibrin and dissolves the thrombus.
To prevent new thrombus formation, give heparin as prescribed. This drug works by preventing the
conversion of fibrinogen to fibrin and pro-thrombin to thrombin.

Also administer an oral or intravenous beta adrenergic blocker, such as metoprolol. By displacing
epinephrine and norepinephrine from beta adrenergic sites, beta-blockers decrease the sites sensitivity to
these catecholamines.
This reduces myocardial contractility and the heart rate, which causes the heart to use less oxygen and limits
the amount of tissue damage.
cause less tissue damage and usually are
 0:03
less serious to limit the size and
0:07
severity of your patient's mi
0:09
and to reduce his pain begin treatment
0:12
promptly
0:13
as ordered first administer
0:16
supplemental oxygen therapy by nasal
0:19
cannula
0:20
or mask this helps deliver more oxygen
0:23
to
0:23
ischemic cells also
0:26
check his oxygen saturation which should
0:29
be above
0:30
92 percent if it's not determine
0:33
why and expect to administer more oxygen
0:38
next maintain nitroglycerin therapy as
0:41
prescribed
0:43
nitroglycerin works by dilating the
0:46
coronary arteries
0:47
which increases the blood flow to the
0:49
myocardium
0:52
also give morphine sulfate intravenously
0:56
to quickly relieve chest pain reduce
0:59
anxiety
1:00
and decrease preload which is
1:02
ventricular
1:03
wall tension at the end of diastole
1:07
if prescribed administer aspirin
1:10
expect to give one chewable aspirin
1:13
immediately for
1:14
fast absorption and a regular aspirin
1:17
tablet
1:17
swallowed whole for slower absorption
1:22
aspirin blocks the formation of
1:24
thromboxane
1:25
a2 a powerful vasoconstrictor
1:28
that is released by platelets when they
1:30
accumulate in the injured arterial walls
1:34
by inhibiting thromboxane a2 aspirin
1:38
prevents further platelet aggregation
1:40
and coronary vasoconstriction
1:44
prepare for administration of a
1:46
thrombolytic drug
1:47
such as streptokinase urokinase or
1:51
recombinant tissue plasminogen activator
1:53
unless contraindicated by active
1:56
bleeding or
1:57
another condition when given within six
2:00
hours of the start of the mi
2:02
thrombolytic drugs open blocked coronary
2:05
arteries
2:06
they do this by converting plasminogen
2:08
to plasmin
2:09
which breaks down fibrin and dissolves
2:12
the thrombus
2:14
to prevent new thrombus formation give
2:17
heparin as prescribed this drug works by
2:21
preventing the conversion of fibrinogen
2:23
to fibrin
2:24
and prothrombin to thrombin
 2:29
also administer an oral or intravenous
2:32
beta adrenergic blocker
2:33
such as metoprolol by displacing
2:36
epinephrine and norepinephrine from
2:39
beta adrenergic sites beta blockers
2:42
decrease
2:42
the site's sensitivity to these
2:44
catecholamines
2:46
this reduces myocardial contractility
2:49
and the heart rate which causes the
2:52
heart to use less oxygen
2:54
and limits the amount of tissue damage

When treating a patient with an MI be alert for Iife-threatening arrhythmias, such as ventricular tachycardia.
Arrhythmias commonly occur after an MI. That’s because ischemic cardiac cells develop abnormal
automaticity, which is the ability to initiate cardiac impulses.
Normally, the SA node initiates these Impulses. For the impulse to travel, sodium and potassium must move
in a way that activates and deactivates (or depolarizes and re-polarizes) each cell.
In ischemic cells, sodium and potassium don’t move properly, raising the intracellular sodium and extra
cellular potassium levels. When this happens, cells outside the SA node begin to fire abnormal impulses,
causing atrial and ventricular arrhythmias.

If a ventricular arrhythmia causes light-headedness or other symptoms, expect to administer lidocaine.

Lidocaine stabilizes the cardiac cell membrane, which reduces automaticity and conduction. In ischemic
cells, this suppresses arrhythmias, such as premature ventricular contractions and ventricular tachycardia.
the heart rate which causes the heart to
0:02
use
0:03
less oxygen and limits the amount of
0:05
tissue damage
0:07
when treating a patient with an mi be
0:09
alert for
0:10
life-threatening arrhythmias such as
0:12
ventricular tachycardia
0:15
arrhythmias commonly occur after an mi
0:19
that's because ischemic cardiac cells
0:21
develop
0:22
abnormal automaticity which is the
0:24
ability to
0:25
initiate cardiac impulses
0:28
normally the sa node initiates these
0:32
impulses
0:33
for the impulse to travel sodium and
0:36
potassium must move in a way
0:38
that activates and deactivates or
0:41
depolarizes and repolarizes
0:43
each cell in
0:46
ischemic cells sodium and potassium
0:49
don't move
0:50
properly raising the intracellular
0:53
sodium
0:53
and extracellular potassium levels
0:57
when this happens cells outside the sa
1:00
node begin to fire
1:01
abnormal impulses causing atrial and
1:04
ventricular arrhythmias
1:07
if a ventricular arrhythmia causes
1:09
lightheadedness or other symptoms
1:12
expect to administer lidocaine
1:15
lidocaine stabilizes the cardiac cell
1:18
membrane
1:19
which reduces automaticity and
1:21
conduction
1:23
in ischemic cells this suppresses
1:26
arrhythmias
1:27
such as premature ventricular
 1:29
contractions and ventricular tachycardia

Once your patient’s condition is stable, perform a complete physical assessment. First, ask about angina. If
your patient continues to have angina, his Ml could be extending. Extension occurs when coronary blood
flow is interrupted again, causing new tissue necrosis. In this complication, necrosis may extend through
additional tissue layers, such as when a non-Q wave MI becomes a Q wave Ml. Or it may extend laterally,
widening the necrotic area.
Next auscultate your patient's heart, listening closely to detect rate or rhythm changes or murmurs. The heart
rate may sound unusually fast or slow. If the Ml damaged the patient’s SA node, AV node, or bundle of His
you're likely to detect tachy-arrhythmias, such as atrial fibrillation.
If the Ml caused an AV block, you may note brady-arrhythmias. During auscultation, you may hear a heart
murmur caused by mitral valve regurgitation, which results from papillary muscle ischemia. Or you may
notice a loud, holosystolic murmur at the left sternal border, a cardinal sign of interventricular septal rupture.

This murmur occurs when an Ml weakens the muscle fibers in the interventricular septum. Then when the
ventricular pressure rises, the septum ruptures, letting blood move freely between the ventricles. If you
detect this murmur, assess for common related findings, such as a pre-cordial thrill and sudden pressure
elevation on the right side of the heart.
Now with the patient leaning forward, listen for a pericardial friction rub, with the stethoscope's diaphragm in
the third inter-costal space at the left sternal border. In some patients, an Ml causes the pericardium to
become inflamed over the necrotic tissue. When the inflamed surfaces slide over each other during systole,
they produce the characteristic rub sound.
Next observe your patient's breathing pattern to detect dyspnea, which may occur when the alveoli fill with
fluid. Also auscultate his breath sounds, noting any crackles, which reflect left ventricular dysfunction. To
complete your assessment, review the results of blood test, such as cardiac enzyme analysis.
is arrhythmias such as premature
0:02
ventricular contractions
0:04
and ventricular tachycardia once your
0:07
patient's condition is stable
0:09
perform a complete physical assessment
0:12
first
0:13
ask about angina if your patient
0:15
continues to have angina
0:17
his mi could be extending
0:22
extension occurs when coronary blood
0:25
flow is interrupted again
0:27
causing new tissue necrosis
0:30
in this complication necrosis may extend
0:33
through
0:33
additional tissue layers such as when a
0:36
non-q wave
 0:37
mi becomes a q-wave mi
0:41
or it may extend laterally widening the
0:44
necrotic area
0:46
next auscultate your patient's heart
0:49
listening closely to detect
0:51
rate or rhythm changes or murmurs
0:56
the heart rate may sound unusually fast
0:59
or
0:59
slow if the mi damaged the patient's
1:03
sa node av node or bundle of hiss
1:06
you're likely to detect tachyarrhythmias
1:09
such as
1:10
atrial fibrillation
1:12
[Music]
1:13
if the mi caused an av block you may
1:16
note
1:16
brady arrhythmias during auscultation
1:20
you may hear a heart murmur caused by
1:23
mitral valve regurgitation
1:25
which results from papillary muscle
1:27
ischemia
1:30
or you may notice a loud polo systolic
1:33
murmur
1:33
at the left sternal border a cardinal
1:36
sign of
1:36
interventricular septal rupture
1:40
[Music]
1:42
this murmur occurs when an mi weakens
1:44
the muscle fibers
1:46
in the interventricular septum then
1:49
when the ventricular pressure rises the
1:52
septum
1:52
ruptures letting blood move freely
1:55
between the ventricles
1:59
if you detect this murmur assess four
2:02
common related findings
2:03
such as a precordial thrill and sudden
2:06
pressure elevation on the right side of
2:08
the heart
2:11
now with the patient leaning forward
2:13
listen
2:14
for a pericardial friction rub with the
2:16
stethoscope's diaphragm in the third
2:19
intercostal space at the left sternal
2:21
border
2:24
in some patients an mi causes the
2:26
pericardium to become inflamed
2:29
over the necrotic tissue when the
2:31
inflamed surfaces slide over each other
2:34
during systole
2:35
they produce the characteristic rub
2:38
sound
2:41
next observe your patient's breathing
2:43
pattern to detect dyspnea
2:45
which may occur when the alveoli fill
2:48
with fluid
2:49
also auscultate is breath sounds noting
2:52
any crackles
2:53
which reflect left ventricular
 2:55
dysfunction
2:58
to complete your assessment review the
3:00
results of blood
3:01
tests such as cardiac enzyme analysis

Now, suppose you're caring for this patient, who has had an infarction in the inferior wall of her left ventricle
and in her right ventricle. An inferior wall Ml usually occurs when a blockage affects the right coronary artery
or one of its branches.
Because the right coronary artery also feeds the right ventricle, a blockage in this artery commonly causes
an infarction in the right ventricle. If you suspect your patient has an inferior wall and right ventricular Ml,
work quickly to stabilize her condition.

After obtaining a blood specimen for testing, check her:

 Vital signs, and

 12-lead ECG tracings as you would for a patient with an anteroseptal MI

On a 12-lead ECG tracing, an inferior wall Ml produces ST segment elevation and Q wave formation in leads II, III, and aVF.
Signs of right ventricular infarction are harder to spot. That's because a routine 12 lead ECG evaluates the
left ventricle. It doesn't reveal signs of ischemia, injury, and infarction in the right ventricle. To detect these
signs, perform a right-sided ECG by placing the pre-cordial leads on the right side of the chest then look for
ST segment elevation and Q wave formation in the V leads, especially in V3R and V4R.

As you provide initial care for your patient, be alert for signs of cardiogenic shock, which include:

 Low blood pressure,

 Low cardiac output, and
 High right-sided heart pressures such as central venous pressure

A dangerous complication of Ml, cardiogenic shock can result from a decrease in:

 The heart's pumping ability,

 The heart rate, or
 Blood volume and preload

When myocardial injury decreases the right or left ventricle's pumping ability, the heart can’t supply enough oxygenated
blood to meet the body's needs.

now suppose you're caring for this

0:13
patient
0:13
who has had an infarction in the
0:15
inferior wall of her left ventricle
0:18
and in her right ventricle
0:23
an inferior wall mi usually occurs when
0:26
a blockage affects the right
0:28
coronary artery or one of its branches
0:31
because the right coronary artery also
 0:34
feeds the right ventricle
0:36
a blockage in this artery commonly
0:38
causes an infarction in the right
0:40
ventricle
0:42
if you suspect your patient has an
0:44
inferior wall
0:45
and right ventricular mi work quickly to
0:48
stabilize her condition
0:51
after obtaining a blood specimen for
0:53
testing check her vital signs and 12
0:56
lead ecg
0:57
tracings as you would for a patient with
1:00
an anteroceptal mi
1:04
on a 12 lead ecg tracing an inferior
1:07
wall mi
1:08
produces st segment elevation and q
1:11
wave formation in leads 2 3
1:15
and avf signs of right ventricular
1:19
infarction are harder to spot that's
1:22
because a routine 12 lead ecg
1:24
evaluates the left ventricle it doesn't
1:27
reveal signs of ischemia
1:29
injury and infarction in the right
1:31
ventricle
1:32
to detect these signs perform a
1:35
right-sided ecg
1:37
by placing the pre-cordial leads on the
1:39
right side of the chest
1:41
then look for st segment elevation and q
1:44
wave formation
1:46
in the v leads especially in v3r and v4r
1:52
as you provide initial care for your
1:54
patient be alert for signs of
1:56
cardiogenic shock
1:58
which include low blood pressure low
2:00
cardiac output
2:02
and high right-sided heart pressures
2:05
such as central venous pressure
2:08
a dangerous complication of mi
2:10
cardiogenic shock can result from a
2:13
decrease in the heart's pumping ability
2:16
the heart rate or blood volume and
2:20
preload when myocardial injury decreases
2:24
the right or left ventricles pumping
2:26
ability
2:26
the heart can't supply enough oxygenated
2:29
blood to meet the body's needs

To treat this cause of cardiogenic shock, expect to administer an inotropic agent, such as dobutamine, to increase
myocardial contractility and improve cardiac output.
If cardiogenic shock is caused by a decreased heart rate, as when an inferior wall Ml affects the SA node,
take measures to raise the heart rate. Expect to give an anti-arrhythmic drug, such as atropine. These drugs
work by increasing SA node automaticity and raising the heart rate; if drug therapy is contraindicated or
ineffective, a temporary pacemaker may be needed. If so, adjust the transvenous pacemaker or apply an
external transcutaneous pacemaker.
These temporary pacemakers work by electrically stimulating the ventricular muscle at a fixed rate. After the
heart's natural pacemaker (the SA node) recovers from injury, plan to remove the temporary pacemaker.

Decreased blood volume and preload produce cardiogenic shock in a different way and require different
treatment. Because the pressure on the left side of the heart normally is greater than that on the right side,
the right ventricle must contract forcefully to move blood through the pulmonary vascular bed to the left side
of the heart.
When an Ml damages the right ventricle, it must work even harder to move blood forward. When a factor,
such as dehydration or a nitrate or diuretic, reduces blood volume or preload, it also reduces myocardial fiber
stretching. When the myocardial fibers can’t stretch fully, they snap back less forcefully, reducing
contractility.
So when cardiogenic shock arises from decreased blood volume or preload, expect to correct it by
discontinuing any nitrates or diuretics and by giving I.V. fluids.
If thrombolytic therapy is contraindicated and you need to rapidly unblock a coronary artery, prepare your
patient for percutaneous transluminal coronary angioplasty (or PTCA).
In this procedure, a balloon-tipped catheter is inserted into the femoral artery, threaded over a guide wire,
and advanced into a coronary artery until it reaches the blockage. Then, the balloon is inflated several times.
This pushes the plaque against the artery wall, which widens the arterial lumen and improves myocardial
blood flow.

When your patient's condition is stable, perform a thorough physical assessment as you would for a patient
with an anteroseptal Ml. However, check for other specific signs. For example, when asking about angina,
check for related symptoms.
In a patient with an inferior wall MI nausea and vomiting are common because the Ml stimulates the
parasympathetic nervous system and vagus nerve, which produce these symptoms. When auscultating your
patient's heart, listen for extra heart sounds, such as a right-sided S4. This sound is caused by the right
atrium’s forceful contraction against the stiffened right ventricle.
Also assess for jugular vein distention, which occurs when the damaged right ventricle can't move blood
effectively to the left side of the heart. Then, check for peripheral edema, which also stems from venous
blood stasis.

Finally, check the results of blood tests, such as cardiac enzyme analysis. Suspect right ventricular infarction
if the CK-MB levels are higher than you'd expect for a patient with an inferior wall Ml. This indicates
increased myocardial tissue destruction.

When you're caring for a patient with any type of Ml, individualize your interventions based on her condition
and prescribed treatments. But expect to include these general measures in your plan of care:

 Frequently monitor the patient's vital signs, noting the effects of the prescribed drugs on her heart rate and blood
pressure,
 Auscultate her heart and breath sounds to detect abnormalities that could signal a complication, such as an
arrhythmia or heart failure,
 Establish and maintain I.V. access, and use the access device to give thrombolytic agents or other drugs, as
prescribed,
 Administer oxygen, if prescribed, to help deliver extra oxygen to ischemic cells, also
 Limit her physical activity, especially for the first few days after the MI. You'll reduce her myocardial oxygen demand

On the third day after the Ml, help your patient walk at a slow pace and encourage her to gradually increase her walking
distance so that she can climb a short flight of stairs by the time she is discharged.
If your patient has been referred to an outpatient cardiac rehabilitation program, explain that she can build
exercise tolerance in a supervised, ECG monitored environment.

Before your patient is discharged, teach her and her family the information that she'll need for a full recovery
at home.
Be sure to provide instructions about:

 Drugs, including their dose frequency, and side effects,

 Energy conservation and gradual return to daily activity, work, and exercise,
 Lifestyle changes, such as weight loss, smoking cessation, and stress reduction,
 Signs and symptoms to report to the physician, and
 Follow-up care, including cardiac rehabilitation

As this video has shown, Ml occurs when atherosclerotic plaque and thrombi block coronary arteries, decreasing myocardial
blood flow and causing tissue death. By understanding the pathophysiology of an Ml, you can:

 Provide immediate care that limits the size and severity of the infarct,
 Assess your patients with pinpoint accuracy,
 Individualize their treatment effectively, and
 Anticipate or prevent life-threatening complications
For your patients, this knowledge can help them survive, and even thrive, after an Ml.

LESSON 2
Diabetes mellitus is one of the most complex and most common disorders in the nation affecting nearly 16
million Americans. But many of them don't realize that they have diabetes.
So the disorder goes unrecognized until the patient seeks care for another problem such as blurred vision.
Yet because diabetes can affect virtually all body systems. The patient runs a high risk of developing a life-
threatening or debilitating complication even before the disease is diagnosed. That's why you need to be
able to spot the clues that point to diabetes.
For example, this patient was just admitted to the emergency department. He's lethargic and confused and
his breath has a strong alcohol-like odor. Although you rnight think alcohol and toxication is the cause of this
patient's condition you should also suspect diabetic ketoacidosis (or DKA) as the cause.

But do you know why? Can you relate this patient's assessment findings to the pathophysiology of diabetes?
And do you know how your interventions can help him control the disorder?
This video will help you answer these questions with confidence. It will clearly explain the pathophysiology of
diabetes. Show you how to identify and control the disorder and demonstrate ways to recognize and prevent
its complications.

Diabetes mellitus is characterized by:

 Insulin deficiency
 Which alters the metabolism of glucose (the body's main source of energy).

Before you can manage diabetes and its complications you need to understand normal glucose metabolism.

Normally, insulin is produced in the pancreas by beta cells in the islets of Langerhans. Insulin lowers the
blood glucose in three ways. First, it shifts glucose from the blood stream into the body's cells by binding to
insulin receptors on the cells' membrane. Once bound insulin and the attached receptor move into a cell
creating an entry way for glucose.
Second, insulin promotes the storage of excess glucose. To do this it activates the enzyme glucokinase
which breaks down glucose into glucose-6-phosphate (or G-6-P). Then insulin activates glycogen synthase.
This enzyme converts G6P into glycogen which is stored in the liver and muscles.
Third, when the glycogen stores are full insulin stimulates the enzyme lipoprotein lipase to convert excess
glucose into free fatty acids. These fatty acids are absorbed by fat cells where they combine with glucerol-3-
phosphate (or G-3-P) to form triglycerides.

Two types of diabetes mellitus have been identified but each develops differently.

 Type 1 diabetes is characterized by the destruction of all beta cells.

 In idiopathic type 1 diabetes the cause of beta cell destruction is unknown.
 In auto immune type 1 diabetes the immune system recognizes beta cells as foreign and slowly destroys them.

In both forms of type 1 diabetes insulin production eventually comes to a halt. Without insulin the patient
develops hyperglycemia (or excess blood glucose).

Type 2 diabetes is characterized by:

 Decreased insulin production,

 Cell resistance to insulin, or
 Both

Decreased insulin production usually occurs with age. In fact, the risk of developing type 2 diabetes
increases with each decade of life.

Insulin resistance occurs when insulin receptors have difficulty recognizing insulin molecules. As a result
fewer insulin molecules bind to receptor sites allowing fewer glucose molecules to enter the cells.
Several factors may increase the risk of developing insulin resistance.

 A family history of type 2 diabetes, or

 An ethnic background that's African-American Hispanic or Native American may increase the risk because of genetic
factors,
 Obesity raises the risk because it increases the number of fat cells, and the receptors on fat cells resist insulin more
than the receptors on other cells,
 A sedentary lifestyle can compound the risk because the patient doesn't gain the benefit of regular exercise which
lowers the cells insulin resistance and helps prevent obesity

To compensate for insulin resistance beta cells produce more insulin. At first, this helps glucose enter the body's cells
lowering the blood glucose level. Eventually, the beta cells become overworked and produce less insulin.
This reduces the amount of glucose that enters the cells causing the blood glucose level to rise. Without
treatment severe complications can occur.

An acute complication DKA typically strikes patients with type 1 diabetes who don't take insulin as prescribed
or who have an illness such as pneumonia.
The stress of illness increases the secretion of hormones such as:

 Epinephrine,
 Norepinephrine, and
 Glucagon

These hormones raise the blood glucose level by increasing glucose production or reducing glucose movement into muscle
cells then glucose builds up in the blood because it can't enter the cells without insulin. The cells soon become starved for
glucose to fuel metabolism.
So the brain, signals the alpha cells in the pancreas to produce the hormone glucagon which converts
glycogen into glucose in the liver. When the glycogen stores are depleted the liver converts free fatty acids
and protein into glucose raising the blood glucose level even further.
The conversion of free fatty acids into glucose creates ketones as a by-product because ketones are acidic
they disturb the acid-base balance when they accumulate in the blood.
Eventually, ketone accumulation and hyperglycemia lead to DKA— a type of metabolic acidosis.

If you suspect DKA in your type 1 diabetic patient, assess him quickly so that you can provide appropriate critical care.
First measure your patient's blood glucose level. Repeat this measurement at least every hour until his
condition is stable. In DKA, the glucose level may increase to 800 milligrams per deciliter or more.
Also check your patient's urine for ketones which appear in DKA. Remember to recheck for them every two
to four hours or as ordered until they're no longer present in the urine. Next, obtain blood samples to assess
fluid electrolyte and arterial blood gas (or ABG) levels which you'll review later.

Then check for signs of fluid and electrolyte imbalances.

You're likely to detect signs of dehydration such as:

 Poor skin turgor, and

 Dry skin and mucous membranes

You're also likely to see signs of electrolyte imbalances such as cardiac arrhythmias. In DKA, severe fluid
and electrolyte loss usually results from osmotic diuresis.

When the blood glucose level rises the kidneys try to compensate by excreting excess glucose which takes
water, sodium, potassium, and other electrolytes with it. As large amounts of fluid move from the
intravascular space into the urine, the blood volume decreases.
At first, this hemo concentration causes falsely elevated electrolyte levels. However, when the fluid is
replaced the blood becomes less concentrated. This makes the electrolyte levels fall often to below-normal
levels.
Next, take the patient's vital signs being alert for Kussmaul's respirations. These rapid deep respirations
develop when the lungs try to remove excess acid by exhaling additional carbon dioxide. And because the
acidosis is caused by ketones the patient's breath smells sweet and like alcohol.
Also check for low blood pressure and tachycardia. Low blood pressure results from low blood volume. And
tachycardia occurs when the body tries to raise cardiac output while the blood volume is low.

Now assess for signs of GI complications such as:

 Absent bowel sounds,

 Nausea,
 Vomiting, and
 Abdominal pain or tenderness

GI complications are common in DKA because metabolic acidosis slows intestinal function which may lead to paralytic ileus
or intestinal paralysis. When the test results are ready check the ABG levels.

DKA typically causes:

 A partial pressure of carbon dioxide (or PC02) of less than 35 millimeters of mercury indicating the lungs attempt to
compensate,
 A bicarbonate level of less than 28 milliequivalent per liter indicating the kidneys attempt to compensate, and
 A pH of less than 7.35 indicating acidosis

To treat DKA, first replace the lost fluid with normal saline. Administer each liter over 30 to 60 minutes as prescribed.
During fluid replacement, recheck the electrolyte levels every hour and administer specific electrolytes as
needed. If your patient's pH level is below 7 start a bicarbonate infusion as prescribed. To prevent rebound
alkalosis be sure to infuse it slowly.
To lower the patients glucose level expect to administer insulin intravenously. After administering a bolus of
regular insulin begin a continuous infusion of 0.1 to 0.2 units per kilogram per hour based on the blood
glucose level.

During insulin therapy, monitor your patient's glucose level closely. Make sure that it doesn't fall faster than
100 milligrams per deciliter per hour because this can cause complications.
How? As glucose moves from the blood into the cells it takes water with it. This may cause cellular edema
and organ swelling. If swelling affects the brain, increased intracranial pressure may lead to herniation and
death.

Also, watch for early signs of hypoglycemia (or low blood glucose) such as diaphoresis, tachycardia and
tremors. In this dangerous complication the blood glucose level falls below 60 milligrams per deciliter.
When intracellular glucose levels fall the brain signals the alpha cells in the islets of Langerhans to secrete
the hormone glucagon. Glucagon causes glycogenolysis by triggering enzymes to break glycogen into
glucose. Glucagon also causes gluconeogenesis by stimulating the conversion of protein and free fatty acids
into new glycogen.
The brain also signals the adrenal glands to release epinephrine which prompts the breakdown of glycogen
and fats to glucose.

The release of epinephrine causes the early autonomic signs of hypoglycemia such as:

 Diaphoresis,
 Tremors, and
 Tachycardia

If the blood glucose level continuous to fall the patient develops late, neuroleptic signs of hypoglycemia including:

 Poor coordination,
 Slowed thinking, and
  Loss of consciousness

If your patient has hypoglycemia, is conscious and can swallow. Provide 15 grams of an easily absorbed carbohydrate such
as 4 ounces of orange juice. Repeat this treatment every 15 minutes until his hypoglycemia resolves.
If you're hypoglycemic patient is unconscious or can't swallow, administer 25 to 50 grams of dextrose 50% in
water by I.V. bolus. If he doesn't have an I.V. access device, inject glucagons intramuscularly. Remember to
turn the patient on his side to prevent aspiration, because glucagon can cause vomiting.
To prevent hypoglycemia, change the I.V solution to dextrose 5% in water and half-normal saline. When the
patient's glucose level falls below 250 milligrams per deciliter. If your patient with DKA has abdominal pain,
nausea, vomiting and absent bowel sounds, give him nothing by mouth and prepare to insert a nasogastric
tube to relieve distention.

Once you're patient's condition is stable perform a complete physical assessment. First, obtain a full
description of his symptoms.
You're patient is likely to report:

 Polydypsia (or increased thirst),

 Polyuria ( or excesss urine output ),
 Polyphagia ( or increased hunger ), and
 Weight Loss

All of these classic effects of diabetes are caused by hyperglycemia.

Polydypsia results from dehydration. As excess water is excreted in the urine the fluid volume decreases.
Then the brain's thirst mechanism alerts the patient to drink more fluid.
Polyuria results from osmotic diuresis. As the blood glucose level rises the kidneys try to compensate by
excreting glucose into the urine. Because glucose is a large molecule. It pulls water with it. This produces
large amount of dilute urine.
Polyphagia stems from cellular glucose deprivation. Because glucose can't enter the cells, they signal the
brain's appetite center to increase food intake. But eating more food worsens the hyperglycemia by causing
more glucose to enter the blood from the GI tract.

Weight loss is caused by dehydration and fat breakdown. The latter occurs when the glycogen stores are
depleted and the cells desperate for fuel signal the liver to convert fat to glucose.
Also ask about other signs of hyperglycemia, including:

 Frequent infections,
 Vision disturbances, and
 Paresthesias in the hands and feet

Among diabetic patients, infections occur frequently and typically include infections of the:

 Skin,
 Urinary tract,
 Vagina, and
 Wounds

No one knows exactly why diabetes increases the risk of infection. However, some experts believe that hyperglycemia
impairs phagocytosis which is microorganism destruction by white blood cells.
Others believe that hyperglycemia and acidosis lead to infection by creating an environment that promotes
microorganism over growth.
Diabetes may cause vision disturbances such as blurred vision because hyperglycemia alters eye structures
such as the:

 Lens,
 Aqueous humor, and
 Cornea

Paresthesias occur when excess glucose coats the nerve fibers. Over time the coating interferes with nerve function causing
abnormalities such as:

 Numbness, and
 Tingling in the hands and feet

Finally, assess your patient for signs of chronic complications of diabetes which can affect nearly all of the body's organs.
That's because uncontrolled hyperglycemia damages the arteries that supply those organs with blood.
Here's how:

 First, hyperglycemia increases the risk of hypertension and hyperlipidemia. In the arteries these conditions tend to
injure the endothelial lining allowing lipids to invade it,
 Second, hyperglycemia and other factors lead to smooth muscle cell proliferation in the injured arteries this narrows
the arterial lumen.
 Third, hyperglycemia makes platelets stickier which increases platelet aggregation at the injury site. This impedes
blood flow even further.

All three events raise the blood pressure and impair blood circulation by increasing arterial resistance.

Most chronic complications of diabetes are macrovascular or microvascular.

Macrovascular complications result from changes in large blood vessels. To detect them, assess for signs of:

 Heart disease especially coronary artery disease,

 Cerebrovascular disease such as cerebrovascular accident, and
 Peripheral vascular disease such as arterial occlusive disease which can lead to foot ulcers

Microvascular complications stem from changes in small blood vessels.

To spot them, be alert for signs of:

 Retinal disease,
 Kidney disease, and
 Nerve disorders

To evaluate the effectiveness of treatment prepare your patient for diagnostic tests. When the tests are completed review
the results.
In a diabetic patient the blood glucose test is likely to show a level that exceeds 126 milligrams per deciliter
on a fasting glucose test and 200 milligrams per deciliter on a 2-hour postprandial glucose test.
In a patient without diabetes, the glycosylated hemoglobin test shows that 4 to 7 per cent of glucose is bound
to hemoglobin. In a diabetic patient the test may reveal that 10 to 20 percent of glucose is bound to
hemoglobin.

That's because in poorly controlled diabetes the blood glucose level remains higher for a longer time
allowing more glucose to bind to hemoglobin in red blood cells.
The glycosylated hemoglobin test reflects glucose control and treatment compliance over several months
because glucose stays bound to hemoglobin for the red blood cells for the entire life span which is several
months.
The urine ketone test may show ketones in the urine. When accompanied by a high blood glucose level this
is abnormal and signals ketoacidosis.
After reviewing the test results and other findings with the patient's physician, work together to maximize the
effectiveness of the treatment plan. Then discuss the plan with your patient.
Treatment for diabetes mellitus consist of:

 Drugs,
 Diet, and
 Exercise

A patient with type 1 diabetes typically receives insulin subcutaneously every day to control his blood glucose level. Because
this drug mimics endogenous insulin it promotes glucose storage and helps prevent the breakdown of glycogen, protein, and
fat.
Depending on your patient's response to insulin he may need:

 Rapid-acting,
 Intermediate-acting,
 Long-acting insulin, or
 A combination of insulins

A balanced diet is a vital part of therapy for type 1 diabetes. Your diabetic patient should eat a diet that provides nutrients
from all food groups. Is low in sodium and cholesterol and is high in fiber.
A balanced diet typically includes:

 50 to 55 percent carbohydrates,
 30 to 35 percent fat, and
 10 to 20 percent protein

Your patient also should follow a regular exercise program to enhance the body's use of insulin.

This patient with type 2 diabetes mellitus was admitted to your unit today for treatment of pneumonia. During
your rounds, you notice that she's lethargic and difficult to arouse. You suspect that she may have
hyperglycemic hyperosmolar nonketotic ( HHNK) syndrome an acute complication of type 2 diabetes
mellitus.
In a type 2 diabetic patient, surgery or another stressor increases the body's need for insulin. Because such
a patient can't produce extra insulin or use it effectively. The cells don't receive enough glucose for energy.
Insufficient intracellular glucose triggers gluconeogenesis which converts fat and protein into the glucose that
the cells need. But without sufficient insulin to help glucose move into the cells the blood glucose level
climbs.

If untreated HHNK syndrome occurs raising the blood glucose level dramatically. However, this syndrome
does not cause ketosis. That may be because the pancreas still produces some insulin which prevents the
breakdown of fat into ketones.
However, the pancreas doesn't produce enough insulin which means that too little glucose reaches the cells.
And this causes the liver to convert glycogen into glucose raising the glucose level even higher than in DKA.
That's why HHNK syndrome causes severe dehydration and neurologic dysfunction killing about half of the
patients it strikes.

HHNK syndrome requires critical care and prompt treatment. So if you suspect this syndrome work quickly to
assess the patient and intervene rapidly.

First check the blood glucose and urine ketone levels. In a patient with HHNK syndrome expect the blood
glucose level to exceed 800 milligrams per deciliter.
Next assess the patient for signs of fluid and electrolyte imbalances which occur when the kidneys excrete
water and electrolytes along with glucose. Then replace the lost fluid by administering normal saline at the
prescribed rate.
During fluid replacement therapy monitor the patient's urine output closely. When it reaches 60 milliliters per
hour expect to switch to half-normal saline solution to prevent hypernatremia.
Plan to administer insulin as prescribed usually at 0.1 units per kilogram per hour. When the patient's blood
glucose level reaches 250 milligrams per deciliter prevent hypoglycemia by switching to an I.V. solution that
contains dextrose. As fluids are replaced check the electrolyte levels and administer electrolytes if needed.

When the patient's condition is stable perform a complete assessment and review all test results as you
would for a patient recovering from DKA. Be alert for signs of diabetes and its chronic complications.
Also discuss your findings and the treatment plan with the physician and your patient. If a balanced diet and
regular exercise don't control the blood glucose level your type 2 diabetic patient may need drug therapy.
Occasionally, she may need insulin. But usually, she just needs an oral hypoglycemic drug.
Sulfonylureas such as glyburide stimulate beta cells to produce more insulin. They also increase cell
receptor sensitivity to insulin in peripheral tissues which allows more insulin to bind with insulin receptors.
Both mechanisms let more glucose enter the cells which lowers the blood glucose level.

Like sulfonylureas, biguanides (such as metformin) increase cell receptor sensitivity to insulin. In addition,
they suppress glycogen formation in the liver, which reduces gluconeogenesis. Alpha-glucosidase inhibitors
such as acarbose delay carbohydrate breakdown and GI tract absorption which lowers the blood glucose
level.
When used in combination therapy these drugs may let the patient receive smaller dosages of other oral
hypoglycemics or insulin.

Whether your patient is recovering from DKA or HHNK syndromes. Individualize her nursing care. But expect
to perform these general nursing interventions:

 Check the patient's blood glucose and urine ketone levels at least every four hours,
 Assess electrolyte and ABG levels as well as the results of other tests,
 Monitor the patients fluid intake and output to evaluate fluid replacement,
 Watch for signs of complications such as hypoglycemia, and
 Ensure that the patient receives a balanced diet

Before your patient is discharged teach her and her family how to control diabetes and prevent complications.

Be sure to cover:

 Medication use and side effects,

 Diet and exercise changes,
 Blood Glucose and urine ketone testing,
 Signs, symptoms, and treatment of hyperglycemia and hypoglycemia,
 Health maintenance activities such as eye and foot care, and
 Follow-up care

As you have just seen diabetes mellitus as a complex disorder that affects all body systems. If uncontrolled it can lead to
life-threatening complications such as DKA and HHNK syndrome.
By understanding the pathophysiology of diabetes you can:

 Recognize its complications swiftly and accurately,

 Intervene with confidence,
 Evaluate the treatment's effectiveness expertly,
 Help your patient control the disorder

Armed with this knowledge you can provide the best possible care for your patient and help her live longer
and better with diabetes.

LESSON 3
Sam Drake, age 54, developed acute renal failure after an episode of severe hypotension during surgery
yesterday. Despite receiving dopamine at 5 micrograms per kilogram per minute, his condition has
worsened. Today, he's been vomiting and reports lethargy, weakness, and nausea.
The results of his diagnostic test reveal a blood urea nitrogen (or BUN) level of 100 milligrams per deciliter
and a serum creatinine level of 4.1 milligrams per deciliter, reflecting uremia. They also show a potassium
level of 7.2 milliequivalents per liter, indicating severe hyperkalemia.

As you evaluate Mr. Drake's electrocardiogram (or ECG) tracing, you'll notice widened QRS complexes and
no discernable P waves. Suddenly, you spot the characteristic fibrillatory waves of ventricular fibrillation on
the cardiac monitor. You immediately activate the code team and prepare for emergency cardiac life support.
After quickly opening Mr. Drake's airway, you check for respirations and a pulse, which are absent because
he's in cardiopulmonary arrest, you begin cardiopulmonary resuscitation (or CPR). In addition to supporting
his circulation and respirations and restoring a normal sinus rhythm, you know that you'll need to provide life
saving drug therapy.

To help you get the most from these powerful drugs, this video will present every vital aspect of care for your
patients with cardiopulmonary arrest. You'll see how to:

 Provide immediate therapy that restores circulation,

 Raise the blood pressure to promote vital organ perfusion,
 Suppress life-threatening arrhythmias, such as ventricular fibrillation, and
 Correct the underlying causes of the arrhythmias

For Mr. Drake, you must work quickly and skillfully to restore a normal sinus rhythm and prevent cardiopulmonary arrest
from leading to death. To do this, your goals are to:

 Restore normal sinus rhythm,

 Restore circulation,
 Lower the defibrillation threshold, suppress myocardial irritability, and
 Correct hyperkalemia

To achieve these goals with skill and confidence, you need to understand how hyperkalemia can lead to ventricular
fibrillation and cardiopulmonary arrest.

Normally, potassium ions move across myocardial cell membranes in exchange for sodium and other ions.
This movement causes cell depolarization and repolarization. The kidneys help keep potassium at its optimal
blood level about 3.5 to 5 milliequivalents per liter by excreting excess potassium through the nephrons'
distal tubules and collecting ducts.
In acute renal failure, the nephrons are suddenly damaged by low blood perfusion or another factor. Then
they can’t excrete potassium effectively, causing its blood level to rise. As the blood potassium level rises,
fewer potassium ions leave myocardial cells, reducing the cells' negative charge. At first, because of the
reduced negative charge, myocardial cells are more excitable and need less energy to depolarize.

The excitable myocardial cells can trigger chaotic impulses in the atria and ventricles, causing them to quiver
(or fibrillate) instead of contracting rhythmically. As a result, cardiac output drops dramatically, and little or no
blood leaves the heart to perfuse vital organs. If the blood potassium level continues to rise, myocardial cell
conduction slows because there's not enough difference between intracellular and extracellular charges. If
the cells are deprived of oxygen, fibrillation can progress to a systole. Before you can correct your patient's
potassium level, however, you must begin emergency life support.
If a defibrillator isn’t immediately available, begin CPR to help perfuse the organs and deliver oxygen to the
lungs. Using a defibrillator, deliver one shock at 200 joules on a biphasic defibrillator or 360 joules on a
monophasic. Immediately resume CPR beginning with chest compressions for 5 cycles. After 5 CPR cycles,
check the patient's rhythm. If ventricular fibrillation persists prepare to administer drugs, while other team
members perform endotracheal intubation and continue CPR.
Immediate drug therapy for cardiopulmonary arrest usually includes:

 A vasoconstrictor and cardiac stimulant, such as epinephrine or vasopressin,

 Calcium chloride as well as one or more potassium-lowering drugs, such as sodium bicarbonate or insulin with
glucose if the arrest was caused by hyperkalemia, and
 An antiarrhythmic, such as amiodarone

To begin immediate therapy, prepare to administer the powerful vasoconstrictor and cardiac stimulant, epinephrine,
preferably by I.V. bolus.
First, try to choose an I.V. line or port of a central line that hasn't been used for an alkaline solution, such as
sodium bicarbonate. That's because epinephrine can form a precipitate when mixed with such a solution.
Then rapidly inject 1 milligram of epinephrine, followed by sterile saline solution to flush the line. Repeat this
every 3 to 5 minutes during resuscitation. Or he may prescribe an epinephrine infusion. If so, prepare it by
mixing 1 milligram of epinephrine in 250 milliliters of normal saline or 5% dextrose and water solution.
To avoid tissue necrosis from extravasation, plan to connect the epinephrine infusion to a central line. If a
central line isn’t available or patent or intraosseous cannulation is not possible, plan to give epinephrine (and
certain other drugs) through the endotracheal tube.

If administering epinephrine, expect to give 2 to 2.5 milligrams through the endotracheal tube. The
endotracheal route can be effective because these drugs, when given in higher doses, cross the alveolar
capillary membrane and enter the blood, though not as quickly as when given by the I.V. route. When using
a central line, set the I.V. pump to deliver 1 microgram of epinephrine per minute. If prescribed, increase the
infusion rate up to 4 micrograms per minute.
Epinephrine stimulates alpha-1 receptors on smooth-muscle cell membranes. This action constricts
peripheral vascular smooth muscles, which increases the blood pressure. By causing vasoconstriction,
epinephrine also diverts blood to the heart and brain, thereby preserving coronary and cerebral blood flow.
In the fibrillating heart, epinephrine may improve the myocardial response to defibrillation, and increase
myocardial cell automaticity (or impulse generation). However, the drug may cause myocardial ischemia
after circulation has been restored. This can occur because epinephrine increases the heart rate and blood
pressure, which can increase the myocardial oxygen demand while decreasing the myocardial blood flow.

Instead of epinephrine, the physician may prescribe a single dose of vasopressin as a vasoconstrictor and
cardiac stimulant like epinephrine; vasopressin can cause tissue necrosis if it infiltrates soft tissue. So plan to
use a central line and administer vasopressin as an I.V. bolus of 40 units.
This natural antidiuretic hormone stimulates vasopressin-1 (or V1) receptors on smooth-muscle cell
membranes. In peripheral blood vessels, this action promotes vasoconstriction, which helps divert blood to
the coronary and cerebral blood vessels and preserve circulation to the heart and brain.
Unlike epinephrine, vasopressin doesn't cause myocardial ischemia when the circulation is restored. That's
because vasopressin doesn't increase the heart rate even though it increases the blood pressure. So the
myocardial oxygen demand doesn’t increase.

Next, expect to provide calcium chloride, as prescribed, to antagonize the effects of hyperkalemia on
myocardial cells. To do this, inject 500 to 1,000 milligrams of calcium chloride slowly over 3 to 5 minutes
through a central line. To understand how calcium chloride reverses the effects of hyperkalemia, consider
how a high blood potassium level can depress myocardial cells ability to depolarize.
Normally, the cell's threshold potential (which is the minimum energy needed to depolarize the cell) exceeds
the cell's resting membrane potential (which is the cell membrane's electrical charge at rest). When the
extracellular potassium level rises, the cell's threshold potential and resting membrane potential equalize,
preventing depolarization.

Calcium chloride raises the threshold potential, making it higher than the resting membrane potential. And
this allows the cells to depolarize. Calcium chloride also shortens cardiac muscle fibers, or myofibrils, which
increases the force of myocardial contractions.

If ventricular fibrillation persists, despite epinephrine or vasopressin and calcium chloride therapy, defibrillate
the patient again with one shock at 200 joules on a biphasic defibrillator or 360 joules on a monophasic.

When the patient has been resuscitated, expect to provide a potassium-lowering drug to treat his
hyperkalemia. If his blood potassium level exceeds 7 milliequivalents per liter and he has acidosis,
administer sodium bicarbonate, as prescribed. To do this, inject 50 milliequivalents over 5 minutes, as
prescribed, through a dedicated I.V. line. This drug lowers the potassium level by raising the pH.
Here's how. In acidosis, excess hydrogen ions move into myocardial cells in exchange for potassium ions.
This shift raises the blood potassium level, resulting in hyperkalemia. Sodium bicarbonate buffers the excess
hydrogen ions in the blood, which raises the pH. And this forces potassium ions to stay inside myocardial
cells, which reduces the blood potassium level.
Whenever your patient receives sodium bicarbonate, check his arterial blood pH regularly to monitor the
drug's effectiveness and avoid alkalosis.

In addition to, or instead of sodium bicarbonate, the physician may prescribe regular insulin and glucose to
shift potassium ions into the cells. As prescribed, administer a mixture of 10 units of regular insulin and 25
grams of glucose through a central venous catheter. Plan to infuse the mixture over 15 to 30 minutes. Insulin
increases the activity of adenosine triphosphates (or ATPase), an enzyme that moves potassium and other
ions into and out of cells. By increasing ATPase activity, potassium ions move from the extracellular fluid to
the intracellular fluid, lowering the blood potassium level.
Glucose is given with insulin to help prevent hypoglycemia. But be certain to check your patient's blood
glucose level as prescribed, because life-threatening hypoglycemia may occur.
In the pancreas, glucose stimulates beta cells to release endogenous insulin. Then this insulin drives
potassium into the cells. To help suppress ventricular fibrillation and prevent new ventricular arrhythmias
from occurring, the physician may prescribe an antiarrhythmic, such as amiodarone. Expect to give two
loading doses.

For the first dose, dilute 150 milligrams in 20 to 30 milliliters of normal saline or dextrose and water and
administer over 10 minutes. For the second dose, infuse amiodarone at 1 milligram per minute for 6 hours.
Also plan to provide a maintenance dosage, infusing .5 milligram per minute, for up to 96 hours or until
rhythm is stable.
A class-III antiarrhythmic, amiodarone blocks potassium from leaving myocardial cells through potassium
channels in their membranes. This action prolongs the cells refractory period, which reduces their ability to
respond to impulses. Amiodarone also reduces automaticity in the Purkinje fibers.
During amiodarone therapy, monitor for hypotension and breakthrough arrhythmias. If you detect
breakthrough ventricular tachycardia, notify the physician and expect to infuse another 150 milligrams of
amiodarone. After your patient has been resuscitated, closely monitor him for a recurrence of ventricular
fibrillation.

Also prepare for continuing therapy, which may include:

 An I.V. or oral antiarrhythmic, and

 A potassium-lowering drug, such as a cat-ion exchange resin

If amiodarone or another antiarrhythmic helped convert ventricular fibrillation into a normal sinus rhythm, prepare to continue
the infusion. And if ventricular arrhythmias are likely to recur, plan to administer the oral form of that drug. To further reduce
the blood potassium level, administer a cat-ion exchange resin, such as sodium polystyrene sulfonate, orally or rectally as
prescribed.
This potassium-lowering drug works by exchanging its sodium ions for potassium ions in the intestinal wall.
Then the excess potassium is excreted in the stool. If your patient's renal failure and hyperkalemia persist
prepare him for dialysis as soon as he's hemodynamically stable.

Marvin Greene, age 78, was admitted to your unit today with severe dehydration caused by several days of
vomiting and diarrhea. Mr. Greene's medication history shows daily use of the loop diuretic furosemide to
treat hypertension.
As you begin to assess Mr. Greene, you notice that he's lethargic and barely responds to voice commands.
When you can’t auscultate his blood pressure, you palpate his systolic pressure, which is about 60
millimeters of mercury. Although the cardiac monitor reveals sinus tachycardia at 120 beats per minute, you
can’t detect a radial or carotid pulse. When your assessment reveals that Mr. Greene isn't breathing, you
quickly identify cardiopulmonary arrest caused by pulseless electrical activity (or PEA) and hypovolemic
shock.
So you instantly activate the code team and prepare for emergency cardiac life support. In addition to
performing CPR to restore Mr. Greene's circulation, you should expect to administer drugs, including fluids.

With drug therapy for PEA and hypovolemic shock, your goals are to:

 Stimulate myocardial contractions to restore circulation

 Replace fluids to correct hypovolemia, and
 Raise the blood pressure to promote vital organ perfusion

Let’s see how hypovolemic shock can lead to PEA. Normally, the heart perfuses the other organs with oxygen-rich blood. To
do this, its output must be adequate, which requires an optimal heart rate and stroke volume. When the blood volume falls,
so does the stroke volume, which is the amount of blood ejected by the heart with each ventricular contraction.
To compensate for this, tachycardia and vasoconstriction occur and antidiuretic hormone (or ADH) is
released. These actions temporarily raise the blood volume and blood pressure so that the vital organs can
continue to receive blood and oxygen. When the blood volume falls by 25% or more, the compensatory
mechanisms begin to fail and the vital organs receive less blood and oxygen.
If the heart’s oxygen demand exceeds its supply, myocardial cells can become ischemic and may die.
Eventually, myocardial contractions grow extremely weak or come to a halt. A pulse isn’t palpable even
though the hearts electrical activity may continue.

For your patient with PEA and hypovolemic shock, expect to administer immediate drug therapy, which
includes:

 A vasoconstrictor and cardiac stimulant such as epinephrine, and

 A crystalloid solution, such as lactated Ringer's

Once adequate fluid resuscitation has occurred, expect to administer a vasopressor, such as norepinephrine or dopamine.
Before beginning drug therapy, make sure that a code team member performs chest compressions while another member
performs endotracheal intubation. Also check that the patient has a large bore I.V. catheter or central line in place so you
can administer I.V. fluids and drugs.
Then administer the vasoconstrictor and cardiac stimulant epinephrine, by I.V. bolus as you would for a
patient in cardiac arrest. As prescribed, rapidly inject 1 milligram of epinephrine. Then flush the line with 20
milliliters of sterile saline solution. During resuscitation, repeat this sequence every 3 to 5 minutes.
By stimulating alpha-1 receptors on cell membranes, epinephrine affects peripheral vascular smooth
muscles, causing vasoconstriction and increased blood pressure. By constricting peripheral vessels,
epinephrine also improves coronary and cerebral blood flow by shifting more blood to the heart and brain.

Next, administer an I.V. crystalloid solution, such as lactated Ringer's, as prescribed. Expect to individualize
the dosage. By replacing lost fluids and electrolytes, lactated Ringer's solution helps expand blood volume
and correct hypovolemic shock.
If a crystalloid solution doesn’t raise your patient's systolic pressure above 70 millimeters of mercury despite
adequate fluid replacement, expect to administer a vasopressor, such as dopamine. For this infusion, use
400 milligrams of dopamine mixed in 250 milliliters of 5% dextrose and water solution, and plan to give it
through a central venous catheter. Then set the infusion pump to deliver 2 to 20 micrograms per kilogram
per minute.
At this dosage, dopamine stimulates alpha-1 receptors on vascular smooth-muscle cell membranes. By
stimulating alpha-1 receptors dopamine like norepinephrine constricts peripheral blood vessels and raises
the blood pressure.

If the patient’s systolic blood pressure remains below 70 millimeters of mercury, discontinue the dopamine
infusion and administer a more potent vasopressor such as norepinephrine.
Norepinephrine stimulates alpha-1 receptors on smooth-muscle cell membranes. This action constricts
peripheral vessels, which raises the blood pressure and diverts blood and oxygen to the heart and brain.
Because norepinephrine causes peripheral vasoconstriction, closely monitor your patient for signs of
peripheral and GI ischemia. For example, palpate and document the location and strength of his peripheral
pulses. And monitor for signs of bleeding in his stool and vomitus.

As your patient's condition improves, wean him off the vasopressor, as prescribed, to keep his systolic
pressure above 100 millimeters of mercury. Also, closely monitor him for the adverse effects of low blood
perfusion. For example, measure his fluid intake and output every hour to assess for renal dysfunction and
increased fluid requirements.
Finally, prepare your patient for discharge by reviewing the signs and symptoms of dehydration and
hypotension. Also teach him about any changes in his prescribed drug regimen, such as discontinuation of a
diuretic.

When your patient develops cardiopulmonary arrest, you need to intervene without hesitation to administer
the most effective drugs swiftly and confidently.
As this video has just shown, you need to be ready to:

 Provide drug therapy and other care to resuscitate your patient in cardiopulmonary arrest
 Recognize and treat the underlying causes, and
 Minimize adverse drug reactions and drug interactions

With powerful drug therapy and your life-saving interventions, you can rescue your patient from a life-threatening condition
and put him on the road to recovery.

LESSON 4
Central Venous Access Devices

Changing a Peripherally Inserted Central Catheter (PICC) Line Dressing

1. Gather equipment and verify physician's order (many times this will be a standing protocol).
2. Explain procedure to the patient.
3. Perform hand hygiene.
4. If agency requires, apply a mask and have patient also put on a mask. Don clean gloves. Set up sterile field
on area to be used. Have patient place arm in the middle of the sterile field. Open dressing kit using sterile
technique and place on sterile towel.
Assess PICC insertion through old dressing. Remove old dressing by lifting it distally and then working
5.
proximally. Remove gloves and dispose of properly. Put on sterile gloves.
6. Starting at insertion site and continue in a circle, wiping off any old blood or drainage with a sterile alcohol
wipe. Clean accordingly to agency policy such as using the alcohol swab sticks, one at a time, and move in a
circular fashion from the insertion site outward (2- to 3-inch area). Allow to dry.
Follow alcohol cleansing with povidone-iodine swabs using the same technique. Allow to dry. If needed, you
7.
can then apply skin-protectant pad to this area, working from the insertion site out. Allow to dry.
Reapply sterile dressing or secure device according to agency policy. Secure tubing or lumens to prevent
8.
tugging on insertion site.
9. Note date, time of dressing change, size of catheter, and initials on tape or dressing.
10.Discard equipment properly and perform hand hygiene.
Clamp all lines of the PICC and remove injection caps. Cleanse the catheter ends with alcohol and then apply
11.
new injection caps. Tape the distal ends down securely.
12.Cleanse the injection cap with alcohol and insert the syringe with normal saline.
Open the clamp and push down on the syringe plunger flushing the device with 3 to 5 mL of saline, while
13.
observing for fluid leak and/or infiltration. It should flush easily, without resistance.
Cover the entire needle and port with the transparent dressing, leaving the ports of the extension tubing
14.
uncovered for easy access.
15.Remove gloves and discard. Perform hand hygiene.
16.Document the time, date, of procedure.

Accessing an Implanted Port

1. Gather equipment and verify physician's order (many times this will be a standing protocol).
2. Explain the procedure to the patient.
3. Perform hand hygiene.
4. Raise the bed to a comfortable working height.
5. Open the kit using sterile technique. Don the mask and the first pair of sterile gloves. Set up your sterile field.
6. Attach the needleless injection cap to the end of the extension tubing and connect it.
7. Take the pre-filled normal saline syringe and prime the tubing with normal saline.
Cleanse according to agency policy. For example, using the alcohol swab sticks, wipe in a circular fashion
8.
from the insertion site outward (2- to 3-inch area). Use each swab once and discard. Allow to dry.
9. Follow alcohol cleansing with povidone-iodine swabs using the same technique. Allow to dry.
Locate the port septum by palpation. With your nondominant hand, hold the port stable, keeping the skin taut
10.
but without touching the port side.
Visualize the center of the port. Push the Huber needle (noncoring 90 degree) to the skin into the portal
11.
septum until it hits the back of the port septum.

12.Cleanse the injection cap with alcohol.

Connect the intermittent injection cap to the extension tubing on the Huber needle. Attach the 10-mL syringe
13.
to the intermittent injection cap and flush the needle with tubing.
Pull back on the syringe plunger to aspirate for blood return. Aspirate only a few milliliters of blood; do not
14.
allow blood to enter syringe.
15.Flush with the remainder of saline in syringe.
Clamp the tubing, remove the syringe, and attach the heparin-filled syringe (if appropriate for the institution).
16.
Clamp the tubing while maintaining positive pressure on the syringe barrel at the end of the flush.
If needed, you can then apply skin-protectant pad to this area, working from the insertion site out. Allow to
17.
dry.
18.Apply tape or Steri-Strips in a star-like pattern over the needle to secure it.
19.Apply a transparent occlusive dressing.
20.Label the dressing with the date, time, size needle used, and your initials, according to agency policy.
Document the time, date, type and location of port, condition of skin at site, size needle used, the presence of
21.
a blood return, and any difficulties encountered.

Flushing a PICC Line

Gather equipment and verify physician's order. Fill lock adapter device with normal saline or heparin flush
1. according to agency policy.
2. Explain procedure to the patient.
3. Perform hand hygiene.
4. Assess the IV site.
5. Clamp off primary IV tubing.
6. Don clean gloves according to the hospital policy. Clamp the extension tubing if a clamp is present. Remove
the primary IV tubing from the extension set and attach the lock or adapter device. Cleanse the cap of the
lock of adapter device with an alcohol swab.
Unclamp the extension set and insert a saline filled syringe into the cap and flush the line according to
7.
agency policy. Remove the syringe.
Insert the heparin-filled syringe and flush the tubing. Remove the syringe carefully and reclamp the extension
8.
tubing.
9. Remove gloves and dispose of them appropriately.
10.Perform hand hygiene and ensure the patient is comfortable.
11.Chart on IV administration record or medication Kardex per institutional policy.

Deaccessing an Implanted Port

1. Gather equipment and verify physician's order (many times this will be a standing protocol).
2. Explain the steps to the patient.
3. Perform hand hygiene.
4. Raise the bed to a comfortable working height.
5. Don gloves.
Begin to gently pull back transparent dressing, beginning with edges and proceeding around the edge of the
6.
dressing. Carefully remove all the tape that is securing the needle in place.
Clean the injection cap and insert the saline filled syringe. Unclamp the catheter's extension tubing and begin
7.
to flush with a minimum of 10 mL normal saline.
8. Remove the syringe and insert the heparin-filled syringe, flushing with 5 mL of heparin (100 u/mL or agency's
policy). Clamp the extension tubing while maintaining positive pressure on the barrel of the syringe. Remove
the syringe.
9. Secure the port on either side with the fingers of your nondominant hand. Grasp the needle/wings with the
fingers of your dominant hand. Firmly and smoothly, pull the needle straight up at a 90-degree angle from the
skin to remove it from the septum.
Apply gentle pressure with the gauze to the insertion site. A Band-Aid may be applied over the port if any
10.
oozing occurs.
Remove gloves and place bed in the lowest position. Make sure that the patient is comfortable before you
11.
leave the room.
12.Perform hand hygiene.
Document the date and time of deaccessing, the appearance of the site, ability to flush, and medication used
13.
to flush.

Assessing a Peripherally Inserted Central Catheter (PICC) Line Site

1. Monitor IV infusion several times a shift. More frequent checks maybe necessary if medication is being
infused:

1. Check physician's order of IV solution

2. Check drip chamber and time drops if IV is not regulated by an infusion control device
3. Check tubing for anything that might interfere with flow. Be sure that clamp is in the open position.
Observe dressing for leakage of IV solution
4. Observe settings, alarm, and indicator lights on infusion control device if one is being used

Inspect site swelling, pain, coolness, or pallor, which may indicate infiltration. This necessitates removing IV
2.
and restarting at another site.
Inspect site for redness, swelling, heat, and pain, which my indicate phlebitis. IV will need to be discontinued
3.
and restarted at another site. Notify physician if you suspect phlebitis.
Check for local or systemic manifestations that indicate an infection is present at the site. IV should be
4. discontinued and physician notified. Be careful not to disconnect IV tubing when putting on patient's hospital
gown.
If possible, instruct patient to call for assistance if any discomfort is noted at site. Solution container is nearly
5.
empty, flow has changed in any way, or pump alarm sounds.
6. Document IV infusion, any complications of therapy, and patient's reaction to therapy.

Obtaining Blood Samples from a CVAD

1. Gather equipment and verify physician's order (many times this will be a standing protocol).
2. Explain the steps to the patient.
3. Perform hand hygiene.
4. Raise the bed to a comfortable working height.
 5. Don gloves, mask, and protective eyewear.
6. If IV fluids are infusing through the central venous access device (CVAD), stop the flow of fluids. Depending
on facility policy, it could take up to 1 minute for standard IV fluids and up to 5 minutes for total parenteral
nutrition, heparin, or any other solutions that may alter laboratory results.
7. Position the patient for easy access to the CVAD, draping them if necessary to expose only the CVAD site.
8. If more than one lumen is present, draw blood samples from the proximal lumen if possible.
9. Cleanse the injection cap with alcohol and allow to air dry.
10.Place the Vacutainer adapter with the needleless cannula into the injection cap.
Insert the discard tube into the Vacutainer and snap it into place. Fill the tube; 5 mL is the minimum for
11.
discard. Remove the discard tube from the sleeve and quickly insert and fill the desired collecting tubes.
When the last tube of blood is obtained, remove the tube from the sleeve. Remove the Vacutainer cannula
12.
from the injection cap.
13.Flush the lumen. If the lumen is not going to be used at present, flush with the appropriate saline and then
heparin flush (if heparin is agency policy). If IV fluids are to be resumed, flush the lumen with 10 mL normal
saline and resume IV fluids. Dispose of your equipment.
Remove your gloves and place the bed in the lowest position. Make sure the patient is comfortable before
14.
you leave the room.
15.Label the specimen tubes according to facility policy.
16.Document the procedure according to agency policy and send the specimen to the laboratory.

Unexpected Situations

LESSON 5
Shock. This deadly disorder can strike suddenly and progress rapidly, depriving your patient's organs,
tissues, and cells of vital blood and oxygen. And without your expert care, it can lead to irreversible organ
damage and death. Like no other disorder, shock can challenge your knowledge and clinical skills.
To help you rise to the challenge, this video will show you how cardiogenic and hypovolemic shock develop.
And it will show you how to:

 Detect early and late signs of shock,

 Intervene skillfully to prevent complications, and
 Provide effective follow-up care

An hour ago, this patient arrived with severe, crushing, chest pain that radiated to his left arm. Because his 12-lead
electrocardiogram (or ECG) tracing suggested an anterior wall myocardial infarction (or Ml), he received nitroglycerin,
aspirin, and morphine.
Now on your unit, the patient seems lethargic. He reports another episode of chest pain, and has a blood
pressure of 80 over 50 millimeters of mercury.
Another patient on your unit was admitted yesterday with abdominal pain, melena, weakness, and a history
of rheumatoid arthritis and corticosteroid use. Now she is vomiting large amounts of frank blood, and her skin
is pale and clammy. Also her blood pressure is low at 80 over 50 millimeters of mercury and her heart rate is
fast at 120 beats per minute.

These two patients are developing two different types of shock. But their conditions will follow the same life-
threatening course unless you intervene. To provide informed care, consider the causes of shock. Three key
conditions must exist for oxygenated blood to perfuse the body's cells, tissues, and organs.
Perfusion depends on:

 Optimal myocardial function,

 Adequate blood volume, and
 Sufficient vascular tone

Altered myocardial function can produce cardiogenic shock. It's most common cause is an MI. Inadequate blood volume can
result in hypovolemic shock. Although trauma is a common cause, it also may result from GI bleeding and other disorders.
Excessive vasodilation can lead to other types of shock, such as septic shock.
Without treatment, all types of shock typically progress through four phases:

 The initial phase, when cellular perfusion falls,

 The compensatory phase, when mechanisms maintain cardiac output and cell perfusion,
 The decompensated phase, when compensatory mechanisms fall and cell perfusion falls further, and
 The irreversible (or refractory) phase when death ensues

Let's see how these phases can occur in a patient with cardiogenic shock. First, if 40 to 50 percent of the left ventricle is
damaged, as can happen with an anterior wall Ml, the heart can no longer pump blood effectively.
In the initial phase of shock, this reduced myocardial contractility lowers the cardiac output (the amount of
blood ejected from the left ventricle) and the blood pressure.
This dramatically reduces blood and oxygen delivery to the cells.
In response, the compensatory phase occurs. Baroreceptors in the aortic arch and carotid arteries sense
reduced blood pressure and cause the medulla to transmit sympathetic nerve signals to the heart and blood
vessels.

In addition, the adrenal glands secrete epinephrine and norepinephrine. Both actions boost the heart rate
and cardiac output and cause the arteries to constrict which raises the blood pressure.
Unfortunately, the faster heart rate shortens diastole, which decreases the left ventricle's filling time and the
amount of oxygen-rich blood that reaches the coronary arteries and myocardium.
Decreased coronary artery perfusion worsens myocardial ischemia, further reducing contractility and cardiac
output. This leads to the decompensated phase of shock. In this phase, less blood leaves the left ventricle,
and organ, tissue, and cell perfusion falls, which impairs organ function.

In the cells, mitochondria switch from aerobic to anaerobic metabolism, to maintain the production of
adenosine triphosphate (or ATP). This makes the cell use glucose less efficiently, which produces lactic acid.
When the cells' lactic acid level rises, its pH falls.
The drop in pH results in metabolic acidosis further impairing cell and organ function. And the lack of ATP
prevents the cell's sodium-potassium pump from working. So sodium, chloride, and water accumulate inside
the cell, while potassium leaks out.
Eventually, the cell bursts and dies releasing enzymes that destroy adjacent cells. In the irreversible phase
of shock, cell destruction and organ dysfunction progress despite treatment, leading to death.

For your patient in shock, rapidly perform a focused assessment and provide priority care. Be sure to monitor
his heart rate and rhythm, blood pressure, and oxygenation with a continuous cardiac monitor, automatic
blood pressure cuff, and pulse oximeter.
And as ordered, intervene by:

 Ensuring adequate I.V. access,

 Administering supplemental oxygen,
 Obtaining a 12-lead ECG tracing and chest X-ray, and
 Drawing blood for arterial blood gas (or ABG) analysis, cardiac enzyme and blood lactic acid levels, and other tests

Then continue the assessment by measuring your patient's heart rate and blood pressure. His heart rate is
likely to be relatively rapid because the body compensates for low perfusion by raising the heart rate to
increase cardiac output. And his blood pressure is likely to be relatively low because his cardiac output is
low.

Now auscultate your patient's heart to detect extra sounds.

To hear these low-pitched sounds more clearly:

 Turn your patient to his left to bring the heart closer to the chest wall, and
 Place the bell of your stethoscope in the fifth intercostal space at the midclavicular line

In a patient with cardiogenic shock, you'll probably notice an S3, or ventricular gallop. This soft sound (heard
immediately after S2) is caused by overfilling of the left ventricle. When the left ventricle fails, it can't eject the
usual amount of blood at the end of systole.
Then in early diastole, blood enters the overfilled ventricle and abruptly decelerates. This makes the
ventricular walls vibrate, producing an S3. You're also likely to hear an S4, a low-pitched heart sound just
before S1. When an Ml damages the left ventricle, its stiffened walls must distend to receive blood from the
atria at the end of diastole. Then the walls vibrate, producing an S4.
In a patient with cardiogenic shock, you may even hear all four heart sounds in a summation gallop. In a
patient with hypovolemic shock, you're likely to hear a rapid heart rate but not extra heart sounds.

Next auscultate your patient's lungs, especially if he has dyspnea. In a patient with cardiogenic shock, you
may hear fine crackles, suggesting pulmonary congestion.
Crackles can occur when the damaged left ventricle can't pump blood forward. If blood backs up into the
pulmonary vessels, it can increase the pulmonary capillary hydrostatic pressure and cause fluid to leak into
the alveoli. Then when air enters the fluid-filled alveoli during inspiration, it produces crackles.

In a patient with hypovolemic shock, you may not detect pulmonary congestion, but are likely to find a rapid
respiratory rate, signaling an attempt to compensate for poor tissue perfusion.
Here's why.
When blood loss occurs, as with Gl bleeding, the number of red blood cells falls. In red blood cells,
hemoglobin has four oxygen-binding sites. When the oxygen saturation in arterial blood is normal, oxygen
molecules bind to all four sites. When red blood cells reach the tissues they release this oxygen before
returning to the lungs to pick up more.
When blood loss exceeds 30 percent, fewer red blood cells are available to bring oxygen to the tissues.
Sensing this, the brain signals the lungs to increase the respiratory rate to draw in more oxygen to bind with
hemoglobin.

Next, check for edema and other signs of fluid retention, which may result from activation of the renin-
angiotensin-aldosterone system. When the nephrons' juxtaglomerular cells sense decreased blood flow, they
release renin.
In the blood, renin prompts the conversion of angiotensinogen to angiotensin I. Then in the lungs,
angiotensin-converting enzyme (or ACE) converts angiotensin I to angiotensin II. From the adrenal cortex,
angiotensin II triggers the release of aldosterone, causing sodium and water retention in the blood.
Also, the posterior pituitary gland releases antidiuretic hormone (or ADH), which makes the renal tubules
more permeable, so that more water is reabsorbed into the blood. Remember to assess your patient's urine
output which is likely to be reduced. This sign of fluid retention is expected as the nephrons excrete less
sodium and water into the urine.
Also evaluate your patient's level of consciousness and skin temperature and color. Lethargy and cold, pale,
clammy skin point to reduced perfusion of the brain and periphery, caused by diminished cardiac output.
Then assess the amplitude of the peripheral pulses. Weak, thready pulses also reflect reduced cardiac
output and perfusion. Recheck the patient's blood pressure regularly. A systolic pressure that falls below 80
millimeters of mercury may mean that shock has progressed to the decompensated phase.

To assess the patient's hemodynamics more closely and guide I.V. drug therapy, assist the physician with
pulmonary artery catheter and arterial line insertion. Once a chest X-ray confirms catheter placement
prepare to take and interpret hemodynamic readings.
Expect a patient with cardiogenic shock to have:

 A cardiac index below 2.2 liters per minute per square meter,
 High intracardiac pressures, such as a right atrial pressure above 8 millimeters of mercury, and
 Pulmonary artery wedge pressure (or PAWP) above 18 millimeters of mercury, which reflects the left atrial pressure

In hypovolemic shock, expect:

 A cardiac index below 2.2 liters per minute per square meter,
 A right atrial pressure below 4 millimeters of mercury, and
 A PAWP below 4 millimeters of mercury

Unlike cardiogenic shock, which reduces cardiac output when the heart can't pump enough blood,
hypovolemic shock reduces cardiac output when there isn't enough blood to be pumped. This reduces
preload and blood flow to the heart and accounts for the different hemodynamics in these two types of
shock.

Also, check the results of blood tests, which may be altered in both types of shock.
For example, anticipate ABG levels with:

 A partial pressure of oxygen (or PaO2) below 80 millimeters of mercury, reflecting hypoxemia,
 A partial pressure of carbon dioxide (or PaCO2) below 35 millimeters of mercury, indicating hypocapnia,
 A bicarbonate level (or HCO3) below 21 milliequivalents per liter, showing renal compensation, and
 A pH above 7.45, suggesting respiratory alkalosis

Early in both types of shock, expect respiratory alkalosis to occur because the body compensates for low oxygen and pH
levels by raising the respiratory rate. With every breath, this brings in more oxygen and forces out more carbon dioxide,
reducing its blood level and raising the pH.
Late in shock, expect the pH to drop as lactic acid (the by-product of anaerobic metabolism) accumulates in
the blood faster than the lungs can compensate.

To manage cardiogenic shock, expect to intervene by administering a vasopressor, such as dopamine, to

help raise the blood pressure. For this drug, plan to infuse 400 to 800 milligrams of dopamine at 10 to 20
micrograms per kilogram per minute. Then titrate the infusion based on the patient's blood pressure, as
ordered.
At this dosage, dopamine stimulates alpha-1 receptors on vascular smooth-muscle cell membranes. By
stimulating alpha-1 receptors, dopamine constricts peripheral blood vessels, which increases the blood
pressure.
If dopamine raises the systolic pressure to 100 millimeters of mercury, expect to give an inotropic drug, such
as dobutamine, to improve myocardial contractility. Begin a dobutamine infusion at 2.5 to 5 micrograms per
kilogram per minute. Increase the dosage as prescribed, until the cardiac index is at least 2.5 liters per
minute per square meter.

When dobutamine reaches myocardial cells, it stimulates their beta-1 adrenergic receptors. This increases
the heart rate, the force of myocardial contraction, and ultimately the cardiac output. Dobutamine also
stimulates beta-2 adrenergic receptors in the peripheral blood vessels. This causes vasodilation and reduces
afterload (the resistance the heart must pump against to eject blood into the aorta).
If your patient's systolic pressure remains above 100 millimeters of mercury and his PAWP stays high,
expect the physician to order a vasodilator, such as nitroglycerin, to improve cardiac output. As prescribed,
start the nitroglycerin infusion at 5 micrograms per minute. Then increase the dosage, as ordered. In the
blood, nitroglycerin is metabolized into nitric oxide (or NO).
Nitric oxide activates guanylate cyclase, which increases the level of cyclic guanosine monophosphate (or
cGMP). cGMP forces calcium out of vascular smooth muscle cells, causing them to relax. Smooth muscle
relaxation causes vasodilation, which improves cardiac output in two ways. First, vasodilation reduces
afterload. Second, it dramatically reduces preload.
This occurs because dilated veins hold more fluid, which reduces the venous return to the heart and the
filling pressures in the ventricles.

If the patient's chest pain persists and his blood pressure and cardiac output continue to fall despite drug
therapy, expect the physician to place the patient on intra-aortic balloon counter pulsation therapy.
After the physician threads a balloon-tipped catheter through the femoral artery and into the descending
thoracic aorta, therapy begins. During diastole after the aortic valve closes, the balloon inflates, forcing blood
from the aorta into the coronary arteries. This improves myocardial blood flow.
When the balloon deflates during systole, it creates a vacuum in the aorta that reduces myocardial oxygen
demand and afterload. This makes it easier for the left ventricle to pump blood to the aorta.

To restore blood volume and treat hypovolemic shock, plan to intervene by replacing fluid with a crystalloid
solution, such as normal saline. Expect to infuse about 300 milliliters of normal saline for every 100 milliliters
of estimated fluid loss.
To optimize fluid replacement plan to:

 Use a large-bore catheter, such as a 16-gauge or central line catheter,

 Use unbifurcated tubing with a pressure bag to maximize the infusion rate,
 Warm the I.V. solution to prevent hypothermia and arrhythmias, and
 Infuse the solution through a large vein, such as the external jugular or antecubital vein

If the patient's estimated blood loss exceeds 30 percent, anticipate administering whole blood or packed red
blood cells. This not only boosts blood volume, but also increases the number of red blood cells available to
bring oxygen to the tissues.

Once your patient's condition is stable, provide follow-up care as you prepare for treatment of the underlying
cause. Expect to monitor the patient's vital signs and hemodynamic readings at least every hour and titrate
his drugs accordingly.
For your patient with cardiogenic shock, look for signs of improved myocardial function, including an:
  Increased blood pressure and cardiac index, and
 Decreased right atrial pressure and PAWP

If your patient is recovering from hypovolemic shock, expect an:

 Increased blood pressure and cardiac index, and

 Increased right atrial pressure and PAWP

Also, at least every four hours, listen for the resolution of abnormal heart and breath sounds. Check the
patient's urine output, which should exceed 30 milliliters per hour. And as appropriate, ask your patient about
chest pain and dyspnea or signs of Gl bleeding, which should resolve.

As this video has just shown, for patients with cardiogenic or hypovolemic shock, you need to:

 Quickly assess their signs and symptoms,

 Intervene effectively , and
 Provide appropriate follow-up care

With this knowledge, you can increase the chance of survival, and recovery, for your patients with shock.

LESSON 9
Hypertension, or high blood pressure, is the nation's most common chronic health problem, affecting about
50 million people. But can you identify which ones have hypertension? It's not as easy as you may think.
Many patients with hypertension have no symptoms. Yet because the disease affects the blood supply to all
the major organs, these patients may be at risk of organ damage and death. That's why hypertension is
often called the silent killer.
This video will help you identify patients with hypertension and those at risk. By linking the pathophysiology
of hypertension with its acute and chronic complications, it also will help you effectively treat patients with
hypertension before complications can occur.

This patient saw his primary care physician because he had a dull headache, blurred vision, and right-sided
weakness that resolved. At the time, his blood pressure was high; 220 over 110 millimeters of mercury.
Now, he's being admitted to your unit for evaluation because his symptoms suggest an acute complication of
hypertension. But do you know what causes high blood pressure and how the body normally controls it?

Hypertension is the persistent elevation of systemic arterial blood pressure. It may be primary or secondary.

 Primary (or essential) hypertension has no known cause, although it's linked to several risk factors,
 Secondary hypertension has an identifiable cause, such as a disease or drug

Several factors increase the risk of developing primary hypertension. Some risk factors can't be modified. But others can
with lifestyle changes.
Unmodifiable risk factors include:

 A family history of hypertension,

 African-American heritage, and
 Advancing age
Modifiable risk factors include:

 Obesity,
 Uncontrolled diabetes mellitus,
 Sedentary lifestyle,
 High-sodium diet,
 Excess alcohol intake,
 Stress, and
 Smoking

To understand how modifiable and unmodifiable factors increase this patient's risk for hypertension, you must first
understand the mechanisms that normally control blood pressure. Blood pressure is the force exerted by blood against the
arterial walls. It helps propel blood through a vast network of vessels to reach the body's organs.
During ventricular contraction (or systole), the peripheral arteries expand as blood is ejected from the aorta.
When this occurs, the pressure in the arteries is called the systolic blood pressure.
During ventricular relaxation (or diastole), the peripheral arteries constrict slightly as the ventricles fill with
blood. When this happens, the pressure in the arteries is called the diastolic blood pressure.

Two major forces work to control blood pressure.

They are:

 Peripheral vascular resistance, which is the arteries' resistance to blood flow, and
 Cardiac output, which is the amount of blood ejected from the heart in one minute

These forces are affected by various factors. For example, peripheral vascular resistance is affected by:

 Vessel diameter and elasticity, and

 Blood viscosity

Cardiac output is affected by:

 Blood volume
 Ventricular contractility, and
 Heart rate

Changes in these factors can alter peripheral vascular resistance or cardiac output, which can affect blood pressure.
For example, as vessel diameter decreases, peripheral resistance to blood flow increases. The body controls
vessel diameter by constricting and dilating the vessels.

Vasoconstriction can occur when stress causes the adrenal medulla to release the catecholamines,
epinephrine, and norepinephrine, which stimulate the sympathetic nervous system. When released in large
amounts, catecholamines stimulate alpha1-receptors in the peripheral arteries. This makes the vessels
constrict, quickly raising the blood pressure.
When catecholamines are released in smaller amounts or when they act on beta2-receptors in blood
vessels, the arteries dilate, which lowers the blood pressure.
Vessel diameter also can increase when chemicals in the blood, such as:

 Carbon dioxide,
 Potassium,
 Nitric oxide, and
 Hydrogen, cause the arteries to dilate

Decreased vessel elasticity occurs when atherosclerosis stiffens and blocks the arteries. Because they no longer stretch
easily, the arteries can’t expand to accommodate increased blood volume. And this elevates the blood pressure.
Increased blood viscosity also causes the blood pressure to rise. This occurs when the hematocrit is
abnormally high, as in polycythemia vera and other disorders.
Increased blood volume can occur when the catecholamines stimulate beta1-receptors in the kidneys. This
activates the renin-angiotensin-aldosterone system, which raises the blood pressure slowly.

In this system, the release of renin causes an enzyme in the lungs to convert angiotensin I to angiotensin II.
Then angiotensin II triggers the release of aldosterone.
In the kidneys, angiotensin II and aldosterone prevent sodium and water from entering the loop of Henle,
which increases sodium and water reabsorption into the bloodstream. This raises blood volume and the
blood pressure.
Catecholamine release also affects ventricular contractility. By stimulating beta1-receptors, catecholamines
increase contractility, which raises cardiac output and blood pressure. This stimulation also increases the
heart rate, which boosts the cardiac output and blood pressure in yet another way.

This patient has several unmodifiable risk factors for primary hypertension.

 First, he has close relatives with hypertension. This family history greatly increases his chance of developing the
disorder himself
 Second, he is African-American. And this heritage is associated with higher blood pressure readings and a higher
incidence of hypertension

These two factors may increase the risk for hypertension because of specific genes or shared environmental
factors, such as lifestyle and diet. Also, an African-American heritage is linked to sodium sensitivity.

In this condition, the kidneys don’t excrete sodium effectively. As a result the blood retains more sodium and
water, increasing the blood volume and blood pressure.
In addition, this patient is over age 50. With advancing age, the arterial walls lose their elasticity. When this
occurs, the arteries narrow and can’t expand fully during systole, increasing the peripheral vascular
resistance.
This leads to isolated systolic hypertension, in which the systolic pressure is increased, but the diastolic
pressure is not.

Fortunately, this patient can reduce his risk of developing hypertension (or the severity of it) by changing his
modifiable risk factors.
For example, he can control his weight and blood glucose level. Obesity and uncontrolled diabetes mellitus
may increase the risk of hypertension because they are associated with insulin resistance. In this condition,
glucose can't readily enter the cells because their insulin receptors are too few or dysfunctional. In response,
the body produces more circulating insulin.

The rise in insulin may increase catecholamine secretion leading to:

 Vasoconstriction,
 Sodium and water retention, and
 Vascular hypertrophy

Eventually, peripheral vascular resistance and the blood volume climb, raising the blood pressure.

Another way this patient can reduce his risk is by engaging in regular physical exercise. A sedentary lifestyle
may promote hypertension in two ways.
First, it can lead to obesity. And second, it doesn't offer the protection of regular physical exercise, which
raises the amount of high-density lipoproteins (or HDLs) that remove cholesterol from the blood. Without
exercise, the cholesterol levels stay high and may impair vasodilation by blocking nitric oxide.
Your patient could reduce his risk by changing his diet because a high-sodium diet is associated with
hypertension. In some patients, the kidneys’ ability to excrete sodium is impaired. If such a patient eats a
high-sodium diet, his body retains sodium and water. This increases the blood volume, which ultimately
raises the blood pressure. A low-potassium diet tends to worsen sodium-induced hypertension.

Your patient also can reduce his risk of hypertension by avoiding excess alcohol intake. Having more than
three alcoholic drinks per day may raise the systolic blood pressure by:

 Stimulating renin production, which causes vasocontriction and sodium and water retention,
 Inducing insulin resistance, as in obesity and diabetes, and
 Damaging smooth muscle cell membranes

This lets calcium enter the cells, preventing smooth muscle relaxation and causing vasoconstriction. By reducing stress,
your patient can also decrease his risk of hypertension. During stressful episodes, the adrenal medulla secretes
catecholamines to raise the blood pressure in a fight-or-flight response.
However, with prolonged stress, the catecholamine release becomes sustained, and blood pressure remains
elevated. In addition, baroreceptors in the aorta, heart, and lungs become desensitized. When
overstimulated, these pressure sensors lose their ability to detect high blood pressure and signal the nervous
system to correct it. So blood pressure remains high even when the patient isn’t feeling stressed.
Finally, your patient can decrease his risk by not smoking. Cigarette smoking may raise the blood pressure
by providing nicotine, which stimulates the sympathetic nervous system.

In a patient with secondary hypertension, the cause is a disease or drug. For example, this patient has
secondary hypertension caused by renal artery stenosis.
The narrowed renal artery slows blood flow to the kidneys, which triggers the release of renin. This activates
the renin-angiotensin aldosterone system, which produces the end-products, angiotensin II and aldosterone.
Angiotensin II causes vasoconstriction; aldosterone causes sodium and water reabsorption, which increases
blood volume. Together, they raise the blood pressure.

Other causes of secondary hypertension include:

  Renal parenchymal diseases,
 Endocrine disorders,
 Catecholamine-secreting tumors,
 Pregnancy,
 Coarctation of the aorta, and
 Drugs, such as oral contraceptives or cyclosporine

Patients with hypertension usually don't develop symptoms until chronically high blood pressure leads to complications,
such as:

 Vascular changes, or
 Organ damage

Vascular changes affect the arteries, which supply oxygenated blood to the organs.
Normally, arteries have four, intact layers:

 The outer tunica adventitia,

 The elastic membrane,
 The muscular tunica media, and
 The inner tunica intima

In hypertension, prolonged vasoconstriction and increased pressure causes the tunica media's smooth muscle cells to
enlarge and multiply. This permanently narrows the artery.
Hypertension also thickens and causes breaks in the tunica intima's endothelial layer allowing lipids, plasma
proteins, and calcium to enter. All of these changes permanently damage the arterial wall and promote
atherosclerosis.

Certain organs are prone to damage from high blood pressure. These target organs include the:

 Brain,
 Eyes,
 Heart,
 Peripheral vessels, and
 Kidneys

When you need to assess a patient with hypertension, remember to check all the body systems especially the target organs
for complications. Begin by measuring the patient's blood pressure, keeping in mind that a diagnosis of hypertension usually
is based on two or more seated blood-pressure readings in at least two sequential office visits.

To classify your patient's blood pressure, consider the national standards for blood pressure:

 A normal blood pressure produces a systolic reading less than 120 millimeters of mercury and diastolic reading less
than 80 millimeters of mercury
 Prehypertension is characterized by a systolic reading of 120 to 139 millimeters of mercury and a diastolic reading of
80 to 89 millimeters of mercury
 Stage I hypertension is characterized by a systolic reading of 140 to 159 millimeters of mercury and a diastolic
reading of 90 to 99 millimeters of mercury, and
 Stage II hypertension is characterized by a systolic reading at or greater than 160 millimeters of mercury and a
diastolic reading at or greater than 100 millimeters of mercury

Be alert for hypertension that progresses rapidly and produces a diastolic pressure of 140 millimeters of mercury or more.
This signals hypertensive crisis, a life-threatening complication. Hypertensive crisis damages target organs and causes
emergencies, such as hypertensive encephalopathy and cerebrovascular accident (or CVA).
When examining the patient's nervous system, ask about headaches, which may be the only symptoms of
hypertension. Hypertension usually produces throbbing occipital or frontal headaches that are severe in the
morning, but diminish as the day progresses.
These headaches typically result from vasodilation, which stimulates certain nerves to transmit pain signals.

Also, carefully assess the patient's level of consciousness, which may be decreased. A decreased level of
consciousness primarily results from cerebral edema. Normally, cerebral arterioles constrict to protect the
delicate brain tissue from high arterial pressure.
However, as the arterial pressure climbs, it overcomes the arterioles, causing them to dilate. This results in
high capillary hydrostatic pressure and increased capillary permeability. Eventually, fluid leaks from the
capillaries into the interstitial space, causing cerebral edema.
If untreated, edema can progress to cerebral ischemia or a CVA. If you suspect cerebral ischemia, assess
for weakness in the patient's arms or legs, changes in her speech or behavior, and difficulty swallowing.

When assessing your patient's eyes, ask about symptoms, such as blurring or loss of vision. Then using an
ophthalmoscope, assess the retina. Here, vascular changes are easy to see and reflect the severity of the
hypertension.
Signs of irreversible retinal damage begin in stage 2 hypertension, when the retinal arteries narrow and
thicken to protect the delicate retinal structures from high pressure. This causes A-V nicking, in which retinal
veins appear nicked, or cut, where they cross retinal arteries.
As the high blood pressure overcomes the arteries, bloody fluid leaks into the retina, forming retinal
hemorrhages and soft, white exudates, known as cotton-wool patches. Then the optic disk swells, resulting
in papilledema.

Continue by asking the patient about epistaxis (or nosebleeds). Epistaxis occurs when high blood pressure
ruptures the small, fragile blood vessels in the back of the nose.
When assessing the cardiovascular system, begin by palpating the precordium. As you palpate, note the
apical impulse. Normally, it’s short and gentle.
In hypertension, it's longer and much more forceful. That’s because the left ventricle must increase its force
of contraction to overcome the increased blood pressure in the aorta. Over time, this thickens the myocardial
muscle fibers, leading to left ventricular hypertrophy.

Next, auscultate the patient's heart sounds, evaluating the heart rate and rhythm, and listening for extra
heart sounds and murmurs.
Assess for signs and symptoms of myocardial ischemia, such as chest pain, and peripheral ischemia, such
as pain or claudication in the arms and legs. These symptoms occur because arteries damaged by high
pressure commonly develop atherosclerosis.
Next, palpate the peripheral pulses. Like pain, a weak pulse can result from atherosclerosis. Also, auscultate
the aorta and carotid, renal, and femoral arteries to detect bruits. These murmur-like sounds are caused by
turbulent blood flow in arteries that are narrowed by atherosclerosis.

As you assess the patient’s respiratory system, ask about dyspnea, and auscultate the lungs for crackles.
Both findings can occur when chronic, uncontrolled hypertension leads to left ventricular hypertrophy and
heart failure. As blood backs up into the left atrium and pulmonary vessels, high pulmonary capillary
pressure causes fluid to leak into the interstitial space.
Eventually, interstitial hydrostatic pressure forces interstitial fluid into the alveoli. With each inhalation air
enters the fluid filled alveoli, producing crackles and dyspnea.

During the assessment, check the appearance of the patient's urine. It may look dark and cloudy. That's
because, as renal damage progresses, increased arterial permeability, lets protein and red blood cells leak
into the urine, changing its appearance.
Finally, check for peripheral edema, which results from fluid movement into the interstitial space.

To detect complications of hypertension or to identify its cause, prepare your patient for diagnostic tests as
needed. When the tests are completed, review their results.
Your patient’s urinalysis may detect:

 Red blood cells, protein, or hyaline casts, suggesting kidney damage, or

 It may reveal glucose or ketones, indicating diabetes mellitus

If your patient undergoes 12-lead electrocardiography, it may show signs of myocardial ischemia or infarction, such as:

 T wave inversion,
 ST segment elevation, or
 Q wave formation, or
 It may display tall QRS complexes, indicating left ventricular hypertrophy

If he has a chest X-ray, it may reveal an enlarged heart or pulmonary congestion. Either may signal left-sided heart failure or
pulmonary edema. Other tests may identify the cause of secondary hypertension.
For example:

 Elevated urine catecholamine and vanillylmandelic acid levels may indicate pheochromocytoma,
 Renal angiography may show renal artery stenosis, or
 Ultrasonography may detect coarctation of the aorta

After reviewing the test results and other findings with the patient's physician, work together to develop his treatment plan.
To control hypertension, treatment usually follows a stepped-care approach.
Step 1, calls for lifestyle changes, such as:

 Weight loss,
 Regular exercise,
 Sodium and alcohol restriction, and
 Stress management

If these don't control blood pressure, treatment moves to step 2, which adds antihypertensive therapy with:

 A diuretic,
 Beta-adrenergic blocker,
 Calcium channel blocker, or
 Angiotensin-converting enzyme (or ACE) inhibitor
If these don't control blood pressure, treatment advances to step 3, in which:

 The drug dosage is increased, or

 A second drug is substituted for or added to the first

If this doesn't control blood pressure, treatment continues to step 4. Here, a:

 Drug from a third class is added, or

 Substituted for the second

Drugs from seven different classes are used to treat hypertension. Each works in a different way to control blood pressure.
Diuretics act by increasing sodium and water excretion. This reduces the blood volume, which lowers the
blood pressure.
Beta-adrenergic blockers, such as propranolol, prevent the heart's beta adrenergic receptors from being
stimulated by catecholamines. This promotes vasodilation, lowering the blood pressure.

Calcium channel blockers, such as diltiazem, work by preventing calcium ions from entering smooth muscle
cells. This results in smooth muscle relaxation and vasodilation ultimately reducing blood pressure.
ACE inhibitors and angiotensin-II (AT-II) receptor antagonists block an enzyme from converting angiotensin I
to angiotensin II in the lungs. This prevents sodium and water retention and vasocontriction, reducing the
blood pressure.
Vasodilators, such as nitrates and hydralazine, primarily work by dilating the arteries and veins, which lowers
the blood pressure.

Alpha-adrenergic blockers, such as prazosin, act by preventing catecholamines from entering

alpha1 receptors site in the arterial smooth muscle. This causes vasodilation and reduced blood pressure.
Central-acting agent, such as clonidine, blocks the signal from the brainstem that causes the release of
catecholamines which stimulate beta cells in the kidneys. This causes vasodilation and reduces the blood
volume and blood pressure.

For a patient with hypertension individualized your nursing care based on her condition and prescribed
treatments. But expect to perform these general nursing interventions. Check the patient’s heart rate and
blood pressure every four hours or more frequently.
To obtain an accurate blood pressure reading, make sure the patient hasn’t had caffeine or smoked a
cigarette in the last 30 minutes.

Also help her feel relaxed. And be sure to use the correct-size blood pressure cuff. A cuff that’s too small will
give a falsely elevated reading.
In addition, be sure to:

 Insert and maintain an I.V. access device to administer drugs,

 Place your patient on a cardiac monitor, and be alert for life-threatening arrhythmias, and
 Maintain your patient on a low-sodium diet
Remember to evaluate the effectiveness of the patient’s drug therapy by measuring his fluid intake and
output and checking for a negative balance. Also monitor your patient’s heart and breathe sounds at least
every four hours. Listen for resolution of abnormal heart sounds and crackles.

Before your patient is discharged, meet with him and his family to review the information he needs to control
hypertension at home.
Be sure to reinforce instructions about:

 Drugs, including their dose, frequency and side effects,

 Lifestyle changes, such as losing weight, following a low-sodium diet, and limiting alcohol intake,
 Signs and symptoms to report to the physician, and
 Follow up care

In this video, you saw how hypertension causes vascular changes and organ damage while producing few symptoms, if any.
By understanding the pathophysiology of this silent killer, you can:

 Assess your patients expertly,

 Evaluate their treatments effectiveness confidently, and
 Anticipate or prevent a wide range of complications

In your practice, keep this information in mind so you can "see through" to the causes of hypertension and
plan your care with a full understanding of its effects. For your patients with hypertension, your knowledge
and expert care could put them on the road to recovery.

LESSON 10
Gerald Moore, age 46, has had primary (or essential) hypertension for three years. Until recently, metoprolol
and hydrochlorothiazide controlled his blood pressure. Three days ago, he stopped taking these drugs
because he neglected to refill his prescriptions. This morning, Mr. Moore awoke with a severe headache and
uncontrolled epistaxis. When he reached the emergency room, his blood pressure was 220 over 128
millimeters of mercury.
Because Mr. Moore's diastolic pressure exceeds 120, he is diagnosed with hypertensive emergency, which
is a type of hypertensive crisis. To treat the immediate crisis and limit damage to his vital organs, you must
provide rapid, effective drug therapy.
And when the crisis resolves, you need to guide your patient through long-term antihypertensive therapy to
prevent serious complications, such as cerebrovascular accident (or CVA). Yet antihypertensive therapy can
include a vast array of drugs with powerful and sometimes dangerous effects. And you need to administer
them quickly, confidently, and safely.

To help you meet the challenges of antihypertensive therapy, this video will show you:

 Which drugs are prescribed for different hypertensive patients,

 How these drugs reduce blood pressure,
 How you can detect and prevent adverse reactions, and
 How you can provide the safest, most effective drug therapy for your patients

When faced with a hypertensive emergency, you must work quickly to limit damage to vital organs, such as the brain, eyes,
heart, and kidneys.
Treatment for a hypertensive emergency always calls for I.V. drugs. That’s because these drugs can:

 Begin reducing the blood pressure within minutes,

 Prevent cerebral ischemia by reducing mean arterial pressure slowly by no more than 25% during the first two hours,
and can
  Limit damage to other vital organs

To understand how antihypertensive drugs produce these effects, you need to know how hypertension develops and leads
to a hypertensive emergency.
Blood pressure is the force that blood exerts against artery walls. This pressure helps propel blood to all of
the body's organs. It normally rises and falls as a result of physical activity, emotions, and other factors.
When blood pressure at rest remains consistently high, hypertension occurs.
Primary hypertension has no known cause, although such factors as African-American race and obesity may
increase the risk of developing it.

In a hypertensive emergency, the diastolic blood pressure rises rapidly and exceeds 120 millimeters of
mercury. It can result from various causes, including abrupt withdrawal of antihypertensive drugs. The sharp
rise in pressure damages the arteries' intimal and medial layers, which eventually weaken and may rupture.
If arterial damage is severe, hemorrhage may occur, destroying tissues in the kidneys, heart, and other vital
organs.

To limit such damage, immediate drug therapy typically includes a powerful, fast-acting vasodilator, such as
sodium nitroprusside. This drug lowers the blood pressure within minutes, and its short half-life allows for
relatively safe titration.
To prepare sodium nitroprusside, mix 50 milligrams in 2 milliliters of 5% dextrose in water and then add to
250 to 500 milliliters of 5 percent dextrose in water, as prescribed. Then place an opaque cover over the I.V.
bag to protect the nitroprusside from Iight, which can cause it to break down. Arrange to use an infusion
pump to deliver the drug safely and accurately. And plan to use intra-arterial monitoring to check the
patient's blood pressure continuously during therapy.
As prescribed, begin the infusion at .3 micrograms per kilogram per minute. Expect to gradually titrate
upward every few minutes until desired effect occurs or rate of infusion reaches 10 micrograms per kilogram
per minute.

To understand how nitroprusside and other antihypertensives work, consider the two major forces that
control blood pressure:

 Peripheral vascular resistance, and

 Cardiac output

Any factor that increases peripheral vascular resistance automatically increases blood pressure. Any factor that raises
cardiac output also raises blood pressure. Similarly, any factor that decreases peripheral vascular resistance or cardiac
output also decreases blood pressure.
Upon infusion, nitroprusside is converted into nitric oxide in the blood. Nitric oxide activates guanylate
cyclase, which increases the level of cyclic guanosine monophosphate (or cyclic GMP). Cyclic GMP forces
calcium out of vascular smooth muscle cells, causing them to relax. Smooth muscle relaxation causes
arteries and veins to dilate, which reduces peripheral vascular resistance and blood pressure.

For the first one to two hours of nitroprusside therapy, titrate the dosage to reduce the diastolic pressure to
no less than 100 millimeters of mercury. Avoid reducing the blood pressure any faster because that can have
deadly results.
Here's how.
For adequate perfusion, the brain normally needs a mean arterial pressure of at least 60 millimeters of
mercury. In hypertension, an autoregulatory mechanism constricts the cerebral blood vessels to protect the
brain from the high pressure. This gradually shifts the mean arterial pressure needed for brain perfusion to
about 120 millimeters of mercury.
If sodium nitroprusside reduces the mean arterial pressure too much or too rapidly, the autoregulatory
mechanism can’t adjust quickly enough to keep the brain well perfused. If perfusion drops suddenly, cerebral
ischemia or CVA may occur.

So monitor your patient's blood pressure continuously during nitroprusside therapy to assess his response to
the drug and determine how quickly and how far his blood pressure falls. If his blood pressure drops too low,
stop the infusion immediately. This action usually reverses hypotension within minutes because nitroprusside
has a short half-life.

If your patient receives nitroprusside for two days or more or has renal insufficiency, be aware that he's at
risk for cyanide and thiocyanate toxicity. This dangerous adverse reaction may occur when the iron in
nitroprusside molecules reacts with the sulfhydryl groups in the hemoglobin of red blood cells, forming
cyanide.
Once cyanide reaches the liver, it's metabolized into thiocyanate which the kidneys filter out and excrete in
the urine. If too much cyanide accumulates in the blood, or if more thiocyanate forms than the kidneys can
remove, these substances can reach toxic levels.

So watch for signs of cyanide and thiocyanate toxicity, such as:

 A rise in the anion gap,

 A thiocyanate level that exceeds 10 milligrams per deciliter, or
 Nausea, vomiting, and confusion

If you detect any of these signs, stop the nitroprusside infusion and administer a 3% solution of sodium
nitrite, as prescribed. Sodium nitrite neutralizes cyanide and converts the hemoglobin in red blood cells into
methemoglobin. This conversion prevents the nitroprusside's iron from linking with the blood cells’ sulfhydryl
groups to form more cyanide.
After administering sodium nitrite, give sodium thiosulfate, as prescribed. This drug converts the remaining
cyanide into thiocyanate so it can be excreted in the urine.

Once your patient's blood pressure reaches the target range, expect to continue therapy with oral drugs as
you taper off the I.V. drug dosage.
Continuing therapy may include a:

 Diuretic,
 Beta blocker,
 Angiotensin-receptor blocker,
 Central-acting drug (or alpha agonist), or
 A combination of these antihypertensive drugs

Therapy for hypertension is individualized, based on your patient's blood pressure and the presence of
hypertensive complications or other disorders. Generally, if a patient's systolic blood pressure is between
120 and 140 millimeters of mercury and the diastolic blood pressure is between 80 and 90 millimeters of
mercury and if he has no complications (such as retinopathy) or other disorders (such as diabetes), therapy
may include moderate exercise, sodium restriction, and other lifestyle changes.
If lifestyle changes don’t reduce the blood pressure, the physician may prescribe drug therapy. He also may
order drugs if the patient has hypertensive complications or risk factors for cardiovascular disease, such as
diabetes or cigarette smoking.

If the patient's blood pressure remains high after a few months of drug therapy, the physician may:

 Increase the drug's dosage,

 Add a drug from a different class, or
 Substitute a drug from another class

For Mr. Moore, the physician originally prescribed the thiazide diuretic, hydrochlorothiazide. Diuretics are first line oral
antihypertensives. Diuretics are particularly effective in sodium sensitive African-Americans. These patients tend to retain
sodium and water, which causes fluid retention that boosts blood pressure.
Thiazide diuretics are highly effective at reducing blood volume caused by fluid retention. In the distal
convoluted tubule, these diuretics prevent sodium and water reabsorption into the blood, causing them to be
excreted in the urine. This action reduces the blood volume and cardiac output. By reducing cardiac output it
decreases blood pressure. Diuretics may also directly affect arterial smooth muscles, causing vasodilation.
By reducing peripheral vascular resistance, vasodilation lowers blood pressure.
Whenever you administer a diuretic, check for signs of electrolyte imbalances, such as hypokalemia and
hypomagnesemia. These imbalances occur when potassium and magnesium ions are excreted in the urine,
along with sodium and water.

When Mr. Moore's blood pressure didn’t respond to hydrochlorothiazide alone, the physician added the beta
blocker metoprolol to his regimen. Beta blockers shield beta receptors in cell membranes from the
catecholamines epinephrine and norepinephrine. This reduces blood pressure in several ways.
In the heart, beta blockers prevent the stimulation of beta1 receptors. This slows the heart rate and reduces
cardiac contractility which lowers the cardiac output and blood pressure.

In the kidneys, beta blockers prevent the stimulation of beta1 receptors, reducing the release of renin. This
prevents the formation of angiotensin II and the resulting release of aldosterone. A decreased angiotensin II
level allows vessels to dilate, which reduces both peripheral vascular resistance and blood pressure. A
decreased aldosterone level allows sodium and water excretion, which reduces the blood volume. This, in
turn, reduces both cardiac output and blood pressure.

If your patient must receive a beta blocker, document his heart rate and blood pressure before therapy
begins. Later, you'll use these numbers as a baseline for comparing future readings. Also, ask if he has
asthma because some beta blockers can worsen its symptoms.
Here's how.
Beta1-selective blockers, such as metoprolol, primarily block catecholamines from stimulating beta 1-receptor
sites. Unlike these drugs, nonselective beta blockers, such as propranolol, block catecholamines from
stimulating beta1- and beta2-receptor sites.
In the lungs, blockage of beta2 receptors can trigger bronchoconstriction and worsen asthma symptoms.

Before therapy begins, also ask if your patient has depression because some beta blockers can exacerbate
the problem.
Here's how.
Highly lipid-soluble beta blockers, such as propranolol and metoprolol, cross the blood-brain barrier more
readily than less lipid-soluble beta blockers, such as atenolol. So these lipid-soluble drugs can affect the
central nervous system, causing depression and lethargy.
When therapy begins, instruct the patient not to suddenly stop taking the beta blocker. Otherwise, he may
suffer life-threatening adverse reactions. Such reactions may occur because blocked beta receptors
compensate by multiplying and becoming more sensitive to catecholamines. So if a beta blocker is halted
suddenly, catecholamines can stimulate many more receptors and to a greater degree.

Increased beta-receptor stimulation can cause:

 Rebound hypertension,
 Tachycardia, and
 Increased myocardial oxygen consumption

In a patient with coronary artery disease, this can lead to myocardial ischemia or infarction.

If a beta blocker and a diuretic don't control your patient’s blood pressure, expect the physician to add or
substitute a different antihypertensive drug. Although the physician may choose from many classes of drugs,
for this patient he prescribes the angiotensin-receptor blocker Losartan (losartan potassium). Losartan
(losartan potassium) prevents the powerful vasoconstrictor, angiotensin II, from attaching to its receptors on
arterial cell membranes.
By blocking angiotensin II, Losartan (losartan potassium) causes smooth muscle relaxation and vasodilation.
Vasodilation reduces peripheral vascular resistance and blood pressure. And because Losartan (losartan
potassium) also suppresses aldosterone production, less sodium and water is reabsorbed into the blood,
which reduces the blood volume, cardiac output, and blood pressure.
Before administering Losartan (losartan potassium), expect to reduce the diuretic dosage for 2 to 3 days to
prevent first-dose hypotension caused by blood volume depletion. Also advise the patient to change
positions slowly to prevent falls caused by orthostatic hypotension. And if the patient is receiving a
potassium-sparing diuretic, monitor his blood potassium level closely because both drugs can cause
hyperkalemia.

If these drugs don't control your patient's hypertension, the physician may substitute or add a central-acting
drug, such as clonidine.
To administer clonidine, expect to apply a transdermal patch or give it by mouth, as prescribed. If a
transdermal patch is ordered, select a spot that’s clean, dry, and free of hair and open cuts. Then place the
patch on or near the patient’s torso. This avoids areas with poor peripheral circulation, which can reduce
drug absorption.
Once clonidine reaches the blood, it stimulates alpha receptors in the brain, which block brain signals that
trigger the release of catecholamines. By doing this, clonidine reduces blood pressure in two ways. First, it
causes vasodilation, which decreases peripheral vascular resistance. And second, it slows the heart rate,
which decreases cardiac output.

During clonidine therapy, warn the patient about adverse reactions, such as dry mouth and constipation. If
dry mouth occurs, encourage good oral hygiene and frequent mouth rinsing. Reassure the patient that
drowsiness, lethargy, and other central nervous system reactions tend to resolve after a few weeks. These
reactions occur because clonidine also stimulates the brain's opiate centers. Also, advise the patient not to
drink alcohol because it can exacerbate clonidine's sedating effects.
Throughout continuing therapy for hypertension, monitor your patient's blood pressure and heart rate at least
every four hours. When assessing the effectiveness of antihypertensive therapy, remember the national goal
for blood pressure, which is: less than 120 over 80 millimeters of mercury for most patients.
Also monitor for adverse reactions, such as:

 Constipation,
 Dizziness,
 Lethargy, and
 Dry mouth

If adverse reactions are extremely unpleasant consult the physician about switching the patient to an antihypertensive that’s
better tolerated. This simple adjustment can improve his compliance and quality of life.

For Ann Carlton, age 63, primary hypertension is complicated by diabetes mellitus and renal insufficiency. Although she has
been taking lisinopril, her blood pressure was 200 over 130 millimeters of mercury upon admission to the hospital. At that
time, she reported blurred vision, but no other symptoms. Mrs. Carlton is diagnosed with hypertensive emergency, caused
by worsening of her hypertension.
To reduce her blood pressure, you'll need to prepare for drug therapy. But because this patient also has
diabetes mellitus and renal insufficiency, you'll need to work closely with the physician to administer drugs
that will lower her blood pressure without worsening her diabetes or renal function.

To reduce this patient’s blood pressure to the target range safely, immediate therapy typically calls for I.V.
drugs, including a:

 Vasodilator, such as fenoldopam, and

 Possibly a diuretic, such as furosemide

For most patients with hypertensive emergency, sodium nitroprusside is the vasodilator of choice. But for patients with renal
insufficiency, this drug isn’t recommended because their kidneys can’t eliminate its toxic metabolites, which increases the
risk of toxicity.
So, plan to administer the vasodilator fenoldopam because this dopamine1-receptor agonist is safe for
patients with renal insufficiency.

First, mix the drug with normal saline solution or 5% dextrose in water. Next, set up an automatic blood
pressure cuff to monitor the patient’s response frequently. Then, administer fenoldopam as a continuous
infusion of .01 to .3 micrograms per kilogram per minute, as prescribed.
In vascular smooth muscle cells, fenoldopam stimulates postsynaptic dopaminergic receptors. This relaxes
vascular smooth muscles and dilates the arteries, which reduces peripheral vascular resistance and blood
pressure.
In the kidneys, fenoldopam dilates renal arteries, which improves blood flow. The drug also increases
sodium and water excretion, which increases diuresis. This decreases the blood volume, cardiac output, and
blood pressure.

During fenoldopam therapy, check your patient's blood pressure at least every 15 minutes. And increase the
dosage slowly by .05 to .1 micrograms per kilogram per minute every 15 minutes, or as prescribed. This
prevents cerebral ischemia caused by too-rapid blood pressure reduction. However, if your patient develops
hypotension, expect to decrease the dosage.
Because fenoldopam has a short half-life, the blood pressure should rise within 5 minutes. Throughout
fenoldopam therapy, assess for reflex tachycardia, a common adverse reaction to high drug dosages.

If needed, the physician may also prescribe a loop diuretic, such as furosemide.
For a patient with renal insufficiency, loop diuretics are better than thiazide diuretics because they're more
effective when the glomerular filtration rate is low. Also, loop diuretics don't antagonize insulin and other
antidiabetic drugs or gradually induce hyperglycemia the way thiazide diuretics can.
If furosemide is prescribed, plan to administer 20 to 40 milligrams by I.V. push. To prevent transient
deafness, inject each 20 milligrams over one to two minutes. Near the ascending limb of the loop of Henle,
furosemide prevents sodium and water reabsorption. This promotes diuresis which reduces the blood
volume, cardiac output, and blood pressure.

As your patient's condition stabilizes, expect to begin oral drug therapy as you taper off the I.V. drug
dosages.
Continuing therapy may include an oral diuretic and one or more antihypertensive drugs, such as an:

 Angiotensin-converting enzyme (or ACE) inhibitor,

 Calcium channel blocker, or
 Alpha blocker

Before admission, Mrs. Carlton had been taking the ACE inhibitor Iisinopril. Because it was no longer
controlling her hypertension, the physician may increase the dosage or switch her to a different ACE
inhibitor.
For patients with hypertension and diabetes, ACE inhibitors may protect the kidneys while reducing the blood
pressure.
Here's how.
In the kidneys, hypertension raises the pressure in the glomeruli. This high pressure damages basement
membranes, reducing the amount of healthy filtrate that can remove urea, creatinine, and other toxins from
the blood.

In diabetes mellitus, excess glucose damages the glomeruli further, causing protein and other substances to
leak into the urine. ACE inhibitors, such as lisinopril, reduce pressure in the glomeruli, preventing basement
membrane damage and protein leakage. These drugs also control blood pressure by blocking the enzyme
that converts angiotensin I to angiotensin II.
Without angiotensin II, the blood vessels relax, which reduces peripheral vascular resistance and blood
pressure. Also without angiotensin II, the adrenal cortex can't release aldosterone. The lack of aldosterone
prevents sodium and water reabsorption. This reduces the blood volume, which decreases cardiac output
and blood pressure.
Before ACE inhibitor therapy, expect the physician to reduce the diuretic dosage to prevent first-dose
hypotension caused by blood volume depletion.

If your patient's blood pressure remains high after one or two months, the physician may also prescribe a
calcium channel blocker, which may be a dihydropyridine or a nondihydropyridine.
Dihydropyridine drugs, such as amlodipine, block calcium from moving into vascular smooth muscle cells.
This relaxes the artery walls, which reduces peripheral vascular resistance and blood pressure.
Nondihydropyridine drugs, such as diltiazem (diltiazem hydrochloride), also block calcium movement into
smooth muscle cells, but they don’t relax the arterial walls as much. So they're less effective than
dihydropyridines at reducing peripheral vascular resistance. Nondihydropyridines also slow cardiac
conduction and reduce cardiac contractility. This action reduces the cardiac output and blood pressure.

Whether a dihydropyridine or nondihydropyridine is prescribed don’t administer certain calcium channel

blockers such as nisoldipine, with grapefruit juice. Grapefruit juice can increase the drug's absorption and
blood level, making it more potent.
During calcium channel blocker therapy, assess for peripheral edema. This is caused by fluid retention,
which is especially common with short-acting dihydropyridines, such as nifedipine. Also check for other signs
of heart failure, such as dyspnea, crackles, and an S3 heart sound.
Heart failure can occur when a calcium channel blocker, such as diltiazem (diltiazem hydrochloride) or
verapamil, reduces myocardial contractility. Or it can result from a dangerous interaction between a beta
blocker and certain calcium channel blockers. If the patient is receiving these drugs, prepare to discontinue
one or both of them.

If the patient doesn't respond to an ACE inhibitor or calcium channel blocker, the physician may substitute an
alpha blocker, such as prazosin. These drugs block the effects of norepinephrine on postsynaptic
alpha1 receptors in vascular smooth muscle. By blocking these receptors, prazosin causes vasodilation,
which reduces peripheral vascular resistance and blood pressure.
After administering prazosin, instruct the patient to remain supine or seated for 30 to 60 minutes or give the
drug at bedtime to avoid orthostatic hypotension, which commonly occurs with the first dose. After 60
minutes, help the patient rise slowly to avoid syncope. Then evaluate her response to therapy by comparing
her supine and standing blood pressure readings.
During prazosin therapy, tell the patient not to take sedatives or drink alcohol because they can decrease her
blood pressure too much.

When your patient is ready for discharge, teach her about each prescribed drug, including its dosage and
adverse effects. Help her develop a schedule that prevents drug interactions. And tell her to avoid over-the-
counter drugs, such as cold remedies with pseudoephedrine that can interact with prescription drugs or
worsen her hypertension.
With so many drugs available to treat hypertension, administering the right ones with confidence can be
difficult. To deliver safe, effective antihypertensive therapy, you need to know which drugs are best for your
patients and what effects they may have.
By viewing this video, you've gained a deeper understanding of how antihypertensive drugs work and how
you can manage their adverse effects. You've also increased your ability to provide the best possible care
for your patients with hypertension even when the disorder is complicated by diabetes or renal insufficiency.
And you've seen how you can help your patients care for themselves and preserve their quality of life.

LESSON 11
Adam Clark, age 62, has hyperlipidemia and coronary artery disease (or CAD), which were diagnosed about
4 years ago. For the past hour, he has had crushing chest pain that radiates down his left arm. Because
nitroglycerin didn't relieve the pain, he called 911.
When Mr. Clark reached your unit, he had a heart rate of 110 beats per minute, a blood pressure of 160 over
90 millimeters of mercury and ST segment elevation in leads V1 through V4 on a 12-lead electrocardiogram
(or ECG) tracing.

Based on these findings, you and the physician suspect an anteroseptal myocardial infarction (or MI), which
requires effective drug therapy. Now you must work quickly to administer drugs that will relieve Mr. Clark's
pain and restore circulation to his injured myocardium.
To help you manage his drug therapy confidently, this video will show you:

 Which drugs produce the best outcomes for patients with an MI

 How these drugs work to halt myocardial injury
 How you can administer these drugs skillfully
 How you can minimize adverse reactions, such as bleeding
 How you can evaluate a drug's therapeutic effects
For an MI, the goals of drug therapy are to:

 Limit the infarction's size by quickly restoring coronary blood flow

 Reduce the patient's pain and anxiety
 Prevent acute and chronic complications
 Treat the MI's cause, such as hyperlipidemia

Before you pursue these therapeutic goals, let’s quickly review how an MI develops a process that usually begins with
coronary atherosclerosis.
In atherosclerosis, lipids and other substances enter a coronary artery's injured endothelial lining and form
plaque. Plaque narrows the coronary artery's lumen, which reduces blood flow. Once plaque forms, it can
harden, ulcerate, and eventually rupture. The roughened surface of the ruptured plaque site triggers a
cascade of events that leads to the formation of a fibrinous thrombus.
If the thrombus blocks the left anterior descending artery, it reduces blood flow to the anterior wall of the left
ventricle. The reduced perfusion causes myocardial ischemia, injury, and necrosis, which result in an MI.

When your patient needs immediate drug therapy for an acute anteroseptal MI, prepare to give:

 nitroglycerin
 morphine sulfate
 aspirin
 another antiplatelet, such as clopidogrel bisulfate
 a thrombolytic, such as alteplase
 an anticoagulant, such as heparin
 a beta blocker, such as metoprolol

If your patient’s systolic pressure exceeds 90 millimeters of mercury, plan to give him nitroglycerin first as a sublingual tablet
or spray. In either form, nitroglycerin rapidly produces three critical effects.
First, it relaxes vascular smooth muscles in arteries and veins. In the heart; this action dilates coronary
arteries, which improves myocardial blood flow and oxygenation.
Second, the drug helps reduce the patient's chest pain by the same mechanism.
Third, it reduces preload, which is the tension on myocardial walls caused by blood at the end of diastole.
And this can decrease myocardial oxygen demand, which is the amount of oxygen needed by myocardial
cells.

Immediately after administering sublingual or aerosol nitroglycerin, prepare to give I.V. nitroglycerin. Initially
administer 5 micrograms per minute and then increase by 5 micrograms per minute every 3 to 5 minutes
until pain is relieved or 20 micrograms per minute is reached.
If pain persists at 20 micrograms per minute, increase the dosage in increments of 10 to 20 micrograms per
minute every 3 to 5 minutes until pain is relieved or 100 micrograms per minute is reached. If pain returns,
increase the infusion rate but do not exceed maximum rate of 100 micrograms per minute.
But before you do, check the patient's blood pressure because nitroglycerin can reduce it dramatically and
with dangerous effects. If the blood pressure falls too low, it can deprive myocardial cells of oxygen. And in a
patient with an MI oxygen deprivation can expand the area of infarction. So if the patient’s systolic pressure
is less than 90 millimeters of mercury or has fallen by more than 10%, contact the physician immediately.

To further reduce pain and anxiety, expect to administer morphine sulfate. As prescribed, give 1 to 3
milligrams by slow I.V. push and repeat this dose every 5 minutes as needed. During morphine therapy,
watch closely for slowed respirations and hypotension.
In the central nervous system, morphine stimulates opiate receptors, which helps reduce pain and anxiety.
This is particularly important in an MI because pain and anxiety cause the adrenal glands to produce excess
catecholamines, such as epinephrine and norepinephrine.
Catecholamines raise the heart rate and blood pressure, which increases the myocardial cells’ need for
oxygen. Because injured myocardial cells already have a decreased oxygen supply, an increased need for
oxygen can expand the infarction.

Next, work to reduce platelet aggregation by giving the patient aspirin. First, administer 160 to 325 milligrams
as a chewable tablet. Then expect to continue aspirin therapy daily for at least 30 days. Aspirin reduces
platelet aggregation and improves coronary blood flow by blocking the formation of thromboxane A 2 (or
TXA2).
In CAD, the roughened surface of the ruptured plaque site attracts platelets. When platelets adhere to the
site, they release thromboxane A2. Then thromboxane A2 causes more platelets to aggregate. It also triggers
vasoconstriction.
By blocking thromboxane A2, aspirin prevents platelet aggregation and coronary vasoconstriction. And this
improves myocardial blood flow. If the patient is allergic to aspirin, expect to administer an antiplatelet agent
such as clopidogrel, 75 milligrams orally.

To restore myocardial blood flow quickly, plan to give a thrombolytic drug, such as alteplase. For maximum
effectiveness, administer the drug as soon as possible after the onset of chest pain and ECG changes.
If used within 24 hours of the onset of these signs and symptoms, alteplase can lyse the occluding thrombus,
restore coronary blood flow and prevent necrosis of the injured myocardium.
Because of the risk of life-threatening bleeding, assess for contraindications before administering alteplase.

Contraindications include:

 Active or recent internal bleeding or known bleeding disorder

 History of cerebrovascular accident (CVA) or structural cerebral vascular lesions
 Aortic dissection
 Traumatic cardiopulmonary resuscitation (or CPR longer than 10 minutes)
 Severe, uncontrolled hypertension
 Intracranial neoplasm or aneurysm
 Recent intracranial or intraspinal surgery or trauma
 Recent closed head or facial trauma within past 3 months
 Major surgery within past 3 weeks
 Pregnancy
 Active peptic ulcer or use of prescribed anticoagulants

If the patient has no contraindications, prepare for alteplase therapy. Draw blood for baseline laboratory tests, such as
prothrombin time (or PT) and activated partial thromboplastin time (or APTT).
During therapy, plan to monitor your patient's ECG continuously to detect life-threatening arrhythmias
caused by reperfusion. And plan to check his blood pressure frequently. But don’t use an automatic cuff
because it can cause excess pressure and bruising. Also make sure the patient has at least two patent I.V.
catheters.

Now prepare the alteplase, using the accompanying transfer device. Insert one end of the device into a vial
of sterile water. Invert the powdered drug vial and insert its rubber stopper into the other end of the device.
Invert the vials to dilute the powder and then remove the transfer device. Gently swirl, don’t shake the vial to
dissolve the powder completely.

Because Mr. Clark weighs more than 147 lbs (67 kg), give 100 milligrams over 1½ hours. To do this, give 15
milligrams by I.V. bolus over 1 minute. Then using the glass vial as the delivery device, give 50 milligrams
over the first 30 minutes. Over the next hour, infuse the remaining 35 milligrams. When the infusion is
complete flush the I.V. line with normal saline solution or dextrose and water to make sure the patient
receives the full drug dose.
Alteplase, which is a tissue plasminogen activator, helps convert plasminogen to plasmin in a patient with an
MI. Plasmin breaks down fibrin, fibrinogen, and other clotting factors, which dissolves the thrombus. By
breaking down the fibrinous thrombus, the drug restores myocardial blood flow.
During alteplase therapy, assess for chest pain relief, a sign of drug effectiveness. Also review the patient's
test results to detect peaking of the creatine kinase MB isoenzyme within 12 hours. This signals that
myocardial cell death has slowed or stopped. And evaluate serial 12-lead ECG tracings. Watch for ST
segments and T waves to return to the baseline, which reflects reperfusion to injured myocardial cells.

For a patient who receives alteplase, expect the physician to prescribe the anticoagulant heparin. To
administer heparin, first give 60 units per kilogram by I.V. bolus. Then maintain a continuous infusion of 12
units per kilogram per hour for 24 to 48 hours after alteplase therapy ends.
Heparin blocks the conversion of fibrinogen to fibrin and of prothrombin to thrombin, which prevents new
thrombi from forming. This is vital because alteplase doesn't dissolve of the existing thrombus. And the
residual thrombus has a rough surface that encourages the formation of new thrombi. Plus, blood can pool in
the left ventricle because the injured myocardium can't pump blood forward as briskly as usual. And blood
pooling promotes thrombus formation on the left ventricle's wall.
Because heparin and alteplase inhibit clotting, take precautions to prevent bleeding. For example:

 Avoid unnecessary venipunctures and insert catheters only in vessels that can be easily compressed to stop
bleeding
 Monitor old venipuncture sites for oozing, and apply pressure if needed
 Look for signs of blood in the stool, urine, and other body fluids
 Frequently perform neurologic assessments to detect signs of CVA, a dangerous effect of thrombolytic and
anticoagulant therapy
 To detect excessive anticoagulation, monitor the patient's APTT every 4 hours or as ordered.

Adjust the heparin dosage to maintain the APTT at 1½ to 2 times the control. Next the physician may prescribe an I.V. beta
blocker, such as metoprolol, to prevent further heart damage. Before administering a beta blocker, check the patient's blood
pressure and heart rate. Don’t administer the drug if his systolic pressure falls below 100 millimeters of mercury or if his
heart rate is less than 55 beats per minute. Otherwise, the drug may cause profound hypotension and bradycardia, which
can worsen ischemia.

Administer 5 milligrams of metoprolol by I.V. bolus. Then repeat this dose in 2 minutes followed by another
dose 2 minutes later, if tolerated. In patients who tolerate the full intravenous dose, 15 milligrams, oral
metoprolol, 50 milligrams, should be initiated 15 minutes after the last intravenous dose and given every 6
hours for 48 hours.
Like other beta blockers metoprolol prevents further damage to the heart by reducing myocardial oxygen
demand. It does this in several ways. First, it blocks the heart's Beta 1 receptors. This slows the heart rate,
which reduces the amount of oxygen that the myocardial cells need. Second, by slowing the heart rate,
metoprolol reduces cardiac output and blood pressure. This decreases afterload, which is the amount of
resistance the heart must pump against. And this, in turn, reduces myocardial oxygen demand. And third, the
drug decreases the force of myocardial contraction, which helps the heart use less oxygen.
During I.V. beta blocker therapy, monitor for signs of heart failure, such as an S 3 heart sound, crackles,
oliguria, and peripheral edema. This life-threatening complication is especially common in patients with
anteroseptal MIs who receive beta blockers. That's because these drugs decrease myocardial contractility,
which can reduce cardiac output if an MI has already weakened the heart.

When your patient's condition is stabilized, expect to taper off the I.V. drugs, as prescribed. And plan to
continue therapy with oral drugs, such as:

 A beta blocker
 Aspirin
 A nitrate
 An angiotensin-converting enzyme (or ACE) inhibitor or angiotensin receptor blocker (ARB)
 A lipid-lowering drug
Continue the oral beta blocker therapy and assess blood pressure and heart rate before each dose. If the patient's heart rate
or blood pressure falls below these levels, be prepared to reduce the dose or withhold it for at least 12 hours as prescribed.
Also, plan to provide a daily dose of aspirin to continue to prevent platelet aggregation.
After 24 to 48 hours of I.V. nitroglycerin therapy, expect to taper off that drug and begin therapy with a topical
or oral nitrate, such as nitroglycerin paste or isosorbide, to prevent chest pain. If the physician prescribes
sublingual nitroglycerin for home use, teach the patient how to take it as needed for chest pain.

To prevent left ventricular dilation, anticipate an order for an ACE inhibitor, such as enalapril (enalapril
maleate). This type of drug is critical because injured or necrotic myocardial tissue has reduced strength for
several weeks until it heals. During this time, pressure in the left ventricle can cause it to dilate.
By reducing afterload and blood pressure, ACE inhibitors can minimize left ventricular dilation. After 6 weeks,
the physician may discontinue the ACE inhibitor unless the patient is at risk for heart failure.

Because Mr. Clark has uncontrolled hyperlipidemia, plan to administer a lipid-lowering drug, such as
lovastatin, to reduce his risk of a second MI.
By inhibiting the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (or HMG-CoA) reductase, this drug
prevents cholesterol synthesis in the liver. Over time, lovastatln can decrease the levels of:

 Total cholesterol,
 Triglycerides,
 Low-density lipoprotein (or LDL),
 Very low-density lipoprotein (or VLDL)

It can also increase the high-density lipoprotein (or HDL) level. Before the patient is discharged, advise him to consult the
physician before taking lovastatin with other drugs, such as itraconazole, cyclosporine (cyclosporin), erythromycin, or other
lipid-lowering drugs. These drug combinations can lead to muscle breakdown and possibly renal failure.

Two days ago, Molly Hooper, age 65, was admitted to your unit with pneumonia. Eight years earlier, she had
coronary artery bypass surgery. Now when you answer her call light she reports severe chest pain. A 12-
lead ECG tracing reveals T wave inversion in leads II, III, and a VF.
After receiving three sublingual nitroglycerin tablets and oxygen at 4 liters per minute, Mrs. Hooper continues
to have chest pain. A follow-up ECG tracing shows ST segment depression in leads II, III, and a VF.
Based on this information, you suspect an inferior wall MI, which the physician confirms. To open the
occluded bypass graft or coronary artery, the physician orders drug therapy and plans for percutaneous
transluminal coronary angioplasty (or PTCA) with stent placement.

To treat the patient's MI symptoms and prepare her for PTCA and stent placement, you'll need to begin drug
therapy right away. For this patient, immediate therapy may include:

 Nitroglycerin
 Aspirin
 A glycoprotein IIb-IIIa receptor antagonist, such as abciximab
 Another antiplatelet drug, such as clopidogrel
 A beta blocker
 A calcium channel blocker

To quickly relieve chest pain, administer I.V. nitroglycerin as prescribed. Titrate the dosage until the patient is pain-free. But
make sure that her systolic pressure remains above 90 millimeters of mercury.
To prevent platelet aggregation and new thrombus formation, give the patient a chewable aspirin tablet.
Besides aspirin, the physician may prescribe another antiplatelet drug, such as the glycoprotein IIb-IIIa
receptor antagonist, abciximab.
To prepare abciximab, mix the drug using a low-protein binding filter, which you'll also use for the infusion.
The filter traps nondrug particles that are part of the drug's growth medium, while it lets the protein-based
drug flow through.
Ten to sixty minutes before PTCA, administer a bolus of .25 milligrams per kilogram over 1 minute into a
dedicated I.V. line. After giving the bolus, set the pump to deliver a continuous infusion of .125 micrograms
per kilogram per minute, up to a maximum of 10 micrograms per minute.

Expect to maintain the infusion for 12 hours for maximum antiplatelet effects. Usually, when platelets gather
at the ruptured plaque site, circulating fibrinogen attaches to the platelets' glycoprotein IIb-IIIa receptors.
Then the fibrinogen converts to fibrin, which links the platelets to form a fibrinous thrombus. This thrombus
traps red blood cells and other substances, and can eventually block the vessel.
By binding to glycoprotein IIb-IIIa receptors, abciximab prevents fibrinogen from binding to the receptors.
And this alters the platelets’ ability to form thrombi. During abciximab therapy, watch for signs of bleeding
caused by altered clotting.

If bleeding becomes severe, stop the infusion and notify the physician at once. Within minutes, the bleeding
should diminish because the drug has a short half-life. Whenever you administer abciximab, be alert for
dyspnea and other signs of a hypersensitivity reaction, such as urticaria and rash.
If you detect these signs, stop the infusion immediately and prepare to give epinephrine, corticosteroids, or
an antihistamine, as prescribed. If prescribed, administer another antiplatelet drug, clopidogrel, beginning
with a single oral dose of 300 milligrams one day before PTCA. Then, plan to give 75 milligrams daily for 3 to
4 weeks.
Clopidogrel binds to adenosine diphosphate (or ADP) receptors on the surface of platelets. This action
blocks ADP, which deactivates nearby glycoprotein IIb-IIIa receptors and prevents fibrinogen from attaching
to these receptors. Without fibrinogen, platelets can’t aggregate and form thrombi.
The physician may prescribe a beta blocker to reduce myocardial oxygen consumption and prevent
ischemia-induced arrhythmias. She may also prescribe a calcium channel blocker, such as diltiazem
(diltiazem hydrochloride). Diltiazem (diltiazem hydrochloride) prevents coronary vasospasm. This is
particularly important for Mrs. Hooper because ruptured plaque attracts thrombi and platelets, which can
provoke vasospasm. And PTCA can further disrupt the plaque as it's pushed to the side of the artery.
If more plaque and thrombi migrate to the roughened coronary surface, vasospasm can worsen. A calcium
channel blocker, such as diltiazem (diltiazem hydrochloride), halts this process by preventing calcium from
entering myocardial cells through calcium channels. In this way, diltiazem (diltiazem hydrochloride) relaxes
vascular smooth muscles and can suppress vasospasm.
If the patient receives a beta blocker and a calcium channel blocker, stay alert for signs of heart failure.
That’s because both drugs can impair myocardial contractility, which reduces cardiac output.
To maintain coronary artery patency and prevent complications after PTCA, prepare to administer such
drugs as:

 Heparin
 Nitroglycerin
 An antiarrhythmic
 Electrolytes

Plan to maintain the continuous I.V. heparin infusion that was started during PTCA. Heparin stops thrombi from attaching to
the roughened arterial wall. This helps the newly opened artery stay patent. During heparin therapy, individualize the dosage
so that the APTT stays at 1½ to 2 times the control, as ordered.
Until heparin is discontinued and the APTT returns to baseline, monitor the patient closely for bleeding. Also
expect to maintain an I.V. infusion of nitroglycerin for 12 to 24 hours. This helps relieve chest pain and
prevent coronary vasospasm.

While treating the patient's MI, watch for life-threatening arrhythmias. If you detect one, quickly assess the
patient's blood pressure and heart rate and obtain a 12-lead ECG tracing. If the patient develops severe
bradycardia, light-headedness, and palpitations, or if her blood pressure falls sharply, prepare for
antiarrhythmic therapy.
Bradycardia is especially common in patients with an inferior wall MI. That's because, in this type of MI, the
right coronary artery usually is blocked so it can’t supply enough blood and oxygen to the SA node. If SA
node ischemia occurs, electrical impulses may slow to less than 60 beats per minute.

When the heart rate falls too low, cardiac output falls, and ischemia can worsen. To raise the heart rate,
administer 1 milligram of the antiarrhythmic atropine by I.V. push. Repeat this dose after 5 minutes as
needed to raise the heart rate to at least 60 beats per minute.
Atropine increases SA node automaticity, which is the ability to generate an electrical impulse. It also boosts
AV node impulse conduction. And these two actions correct bradycardia. But remember that atropine can
increase the myocardial oxygen demand by raising the heart rate. And the increased oxygen demand can
cause ischemia to worsen. The drug can also make ischemic cells more irritable and can cause other
arrhythmias, such as premature ventricular contractions.

To help prevent arrhythmias, check your patient's potassium, magnesium, and other electrolyte levels. Then
replace these electrolytes as prescribed. When your patient is stabilized, prepare her for discharge. And
teach her about continuing drug therapy, which may include:

 Aspirin
 Clopidogrel bisulfate
 A beta blocker
 Oral or sublingual nitroglycerin
 If her left ventricular function is compromised, an ACE inhibitor

Caring for a patient with an MI requires rapid decision making, swift action, and effective drug therapy. That’s why you must
be fully prepared to treat your patient with an MI. And in this video, you've seen how.
Armed with this knowledge, you'll play an important role in helping your patient live longer and better after an
MI.