CORONARY VASCULAR DISORDERS
arterial walls that may decrease the dispensability
Coronary Artery Disease
Narrowing or obstruction of the coronary arteries,
resulting in a reduction of blood supply to the
myocardium, then there will be ischemia, injury and
infarction
Atherosclerosis​-a disorder of the lipid metabolism
characterized by
a) development of fat-containing substances along
the intima of the blood vessels
b) Smooth muscle cell proliferation
Atherosclerosis affects the intima of the large and
medium sized arteries.
The intima lining of blood vessels accumulates the fatty
deposits in the coronary arteries. Can be partial or
completely blocked.
Risk Factors
Modifiable
1. Pathologic – hypertension, DM, hyperlipidemia,
elevated homocysteine, psychosocial factors,
metabolic syndrome and premature menopause
Hypertension - related to the shearing stress
causing denoting that causes injury to the
endothelial lining. Causes narrowed, thickened
and elasticity of the vessel. More force is required
to pump blood through deceased arterial
vasculature as it reflected in a higher BP. It
increases cardiac workload that causes left
ventricular hypertrophy and decreased stroke
volume with each contraction.
DM - Causes increased connective tissue
degeneration that may account for the
development of atheroma. Have alteration in lipid
metabolism, tends to have a higher cholesterol
and triglycerides level.
Hyperlipidemia - >200 mg/dl of cholesterol and
triglycerides is correlated to obesity, physical
inactivity, high caloric intake and intake of trans
fatty acids that can be found in junk foods such
as cookies, crackers, french fries, avoid these
foods to lower risk of development of CAD.
Lipoprotein - low density lipoproteins have an
affinity for arterial walls. Whereas very low
density lipoprotein contains most of the
triglycerides that have correlation with heart
disease. That's why it is necessary to maintain
HDL and to lower down the LDL or VLDL
Example: fish oil at least twice a week that is rich
in alpha linoleic acid (flaxid, canola, soy beans)
as these helps to lower down LDL and increase
HDL.
Elevations of homocysteine level -damages the
inner lining of the blood vessels. Promotes
plaque buildup which may alter the clotting
mechanism to make clot more likely to occur.
Supplementing vitamin B complex, B6, B12, folic
acid lowers the blood level of homocysteine.
Psychosocial factor - combined with high lipid
level and smoking. Usually type A personality
which is very aggressive and competitive. They
are predisposed to develop CAD even sleep
apnea is one factor.
Metabolic syndrome - have a greater risk factor
for cardiovascular diseases especially CAD
because it may increase in blood pressure that
high in triglycerides, increase insulin level, extend
body fats that may result in CAD. Diagnosis to
this includes the following conditions like insulin
resistance which may damage the endothelium
that causes thickening of the vessel wall and
potential inflammation.
 Central obesity - waist circumference of >35
inches in female or >40 inches in male are at
great risk of developing CAD. Blood pressure
persistent of greater than 130/85 mmHg or even
the is a symptoms of lipidemia.
2. Lifestyle – Smoking, obesity, elevated LDL,
physical inactivity, Diet, Use of oral
contraceptives, Hormone replacement in women.
Smoking – increases 200% risk to develop CAD
because the tobacco contains nicotine that
causes the release of catecholamines
(epinephrine and norepinephrine) that increases
heart rate, stroke volume, cardiac output and
blood pressure. Carbon Monoxide directly
damages the inner lining of the blood.
Peripheral vasoconstriction - increases systemic
changes that occur or may decrease the blood
flow. It decreases the threshold of ventricular
defibrillation by interfering the oxygen combining
with hemoglobin therefore impairing O2 diffusion
into the mitochondria.
Obesity - increased food intake is associated with
elevation of LDL. Obese people have a high
tendency towards
hypertension and glucose intolerance. It should
not be greater than 20% of the ideal body weight.
Physical inactivity - lack of exercise is directly
associated to the decrease of HDL. In diet, the
high intake of carbohydrates and fat leads to high
serum plasma cholesterol.
Usage of oral contraceptive methods or
post-menopausal women – use of hormone
replacement or birth control may affect the
cholesterol which is lowering the good cholesterol
and increasing the risk of blood clot.
Nonmodifiable
1. Age - middle-aged men
2. Gender – attribute to sex hormones
3. Family history
4. Race
Aging - CAD in men are more prevalent than women
in the age of 60. Women’s advantage declines after
menopause because of social and economic
pressure and changes in lifestyle.
Genetics - has a major role in the development of
CAD.
Race - CAD is common in patients who are African
Americans.
Theories of Atherogenesis
1. Endothelial injury – hyperlipidemia,
hypertension and chemical irritants
2. Lipid infiltration – altered endothelial
permeability
3. Aging
4. Thrombogenic – RBC, platelets and lipids
accumulation along the intima of the arteries
5. Vascular dynamics – increase intraluminal
pressure leads to altered membrane permeability
6. Inflammation
Endothelial injury - A normal intact endothelium, is
usually non-reactive to platelets, leukocytes, coagulation
even fibrinolytic. However, if the endothelial lining was
altered it may result in the chemical injury from
hyperlipidemia, hypertension may suggest certain
bacterial and various infections that play a major role in
the damage of the endothelium to the development of
atherosclerosis.
With endothelial alteration the platelets are activated and
they release growth factors that may stimulate smooth
muscle proliferation so this may entrap the lipid which
may calcify over time and form an irritant to the
endothelium on which platelets adhere or aggregate.
Lipid infiltration - lipids from the circulations enter the
endothelium and accumulate in smooth muscle in
response to the mechanical or inflammatory trauma.
Chromoprotein is trapped and damage occurs then
endothelial permeability is altered.
Aging - atherosclerotic changes occur to everyone and
become more evident as one aged
Thrombogenic - Microthrombi form in intima lining of the
endothelium. It releases substances that may alter the
endothelial permeability then thrombus extend and
reactivate the cycle.
Vascular dynamics - mechanical factors like
hypertension, because of constant elevations in the blood
pressure, it increases the rate of atheroma formation that
alters membrane permeability which may increase lipid
infiltration.
Inflammation – has a major role in the pathogenesis of
atherosclerosis. Inflammatory reactions may be a
consequence of an infectious stimuli.
Developmental Stages in Atherosclerosis
1. Fatty streaks
➔ Earliest lesions
➔ Characterized by lipid-filled smooth
muscle cells
2. Raised fibrous plaque
➔ Beginning of progressive changes in the
arterial wall
➔ Lipoproteins transport cholesterol and
other lipids into the arterial intima
➔ Fatty streak is ​covered by collagen
forming a fibrous plaque that appears
grayish or whitish
➔ Result = ​narrowing of vessel lumen
➢ Raised fibrous plaque usually occurs at the age
of 30 or increases with age. Arterial wall changes
are initiated by chronic endothelial wall injury that
result from many factors; elevated BP, increase
in cholesterol, hereditary, carbon monoxide
produced by smoking, or immune reaction with
toxic substances within the blood vessels.
➢ Normally, the endothelium repairs itself
immediately but not in patients with CAD because
it allows the LDL and growth factor from platelets
to stimulate smooth muscle proliferation and it
thickens the arterial wall. Once this endothelial is
injured, the lipoprotein transport cholesterol and
other lipids into arterial intima.
➢ In the 2nd stage, the lipid directly damages the
smooth muscle and contributes to plaque
thickening and stability. As the lipids pass
through the vessel, they may adhere causing the
lesions build up or structure abnormalities. Even
platelets also may acquire in the hypertrophy of
the smooth muscle cells. The large number of
platelets accumulate in the internal wall of the
artery it may lead to thrombosis causing the
narrowing of the artery.
Progression of Atherosclerosis
❏ Fatty Streak yellow thick appears in the intima
lining of the arterial wall so there are lipid
accumulations wherein the platelet also attaches
to the endothelium and the migrations of smooth
muscles into the intima. Then fibrous plaque,
wherein the development of atheroma, there’s an
enlargement of the plaque. The collagens are
also trapped forming fibrous plaque that appears
grayish or whitish which may also narrow the
vessel lumen.
❏ Complicated Lesion Phase Is the 3rd stage and
the final stage in the development of
atherosclerosis with the incorporations of lipid,
thrombus/thrombi, damaged tissue and
accumulation of calcium. The growing lesions
become complex, as it grows the necrotic tissue
that is hardened in the arteries causing rigidity
and hardening that may partially occlude the
arteries, then thrombus formation may develop.
Complicated Lesion Phase
❖ Continued inflammation can result in plaque
instability, ulceration, and rupture
❖ Platelets accumulate and thrombus form
❖ ​Increased narrowing or total occlusion of lumen
Collateral Circulation
● Arterial branching exists within the coronary
circulation. Attributed to inherited predisposition
and presence of chronic ischemia.
● When an atherosclerotic plaque occludes the
normal flow of blood through the coronary artery,
the ischemia is chronic then increased collateral
circulations develop. Then occlusions of the
coronary arteries occur slowly over a long period,
there’s a greater chance of adequate collateral
circulations developing and the myocardium may
still receive an adequate amount of oxygen.
● However, rapid onset CAD or coronary spasm is
inadequate for collateral development and a
decrease in arterial flow results in more severe
ischemia or infarction. That’s why younger people
will have more severe M.I. because of inadequate
collateral formation.
Pathophysiology of CAD
Predisposing factors
➔ arterial narrowing and ​occlusions of the arterial
wall​.
➔ Narrowing of the arteries/arterial blood
lumen/arterial wall.
➔ There will be ​vascular changes which may affect
the functional ability of the coronary arteries to
dilate, this leads to the decreased blood flow to
the myocardium which may cause ​angina
 insufficiency to the patient and will result in May increase luminal size of at least 20%
myocardial​ ischemia​.
➔ M. ischemia the patient may have angina
pectoris, acute coronary syndromes/ acute
myocardial infarction and sudden cardiac death.

Three Major Clinical Manifestations of CAD

1. Angina pectoris
2. Acute coronary syndrome (ACS)
3. Sudden cardiac death
4. Rapid pulse
5. Shortness of breath
6. Palpitations
7. Weakness

Diagnostic study Advantages of PTCA

●​ ​ECG 1. Provides an alternative to surgical procedure

●​ ​exercise stress test 2. Ambulatory 24 hours after the procedure
●​ ​2d-echo
3. Shortened the length of hospitalization
●​ ​coronary angiography 4. Rapid resumption of work in one week after the
●​ ​MRA procedure

Management of CAD Catheter is equipped with an inflatable balloon tip

1. Reduce risk factors
❏ Stop smoking, regular exercise, diet, reduce
weight, control HPN, DM, and cholesterol
❏ Diet; reduce sodium/ low sodium intake, avoid
alcohol, avoid trans fatty acids
❏ Restore blood supply (PCI)
❏ ​Revascularization is the restoration of perfusion
to a body part or organ that has suffered
ischemia through Percutaneous Coronary
Intervention (PCI) formally known as Angioplasty
and Stenting which may improve blood flow and
restore blood supply
which is inserted to the coronary arteries which pass
to the lesions and the atherosclerotic plaque is
compressed resulting in vessel dilations.
● ​Intracoronary stent placement – a stent used to
maintain vessel patency by compressing the
arterial walls and resisting vasoconstriction.
●​ ​Usually in conjunction with Angioplasty
●​ ​An expandable mesh like structure.
● ​Used to treat an abrupt closure and restenosis
following PCI
Stent is thrombogenic – antiplatelet agents (aspirin,
clopidogrel (Plavix), ticlopidine (Ticlid)) is prescribed.

Complications: hemorrhage, vascular

injury and arrhythmias

✔ ​Percutaneous Transluminal Coronary

Angioplasty (PTCA) – restores luminal patency
by compressing atheromatous plaques within the
coronary arteries.
 ✔ ​Atherectomy – the plaque is shaved OFF ✔​ ​↓ strength of the heart muscle contraction
using a type of rotational blade. It decreases the
incidence of abrupt closure as compared with ✔​ ​Relax blood vessel
percutaneous coronary intervention (PCI).
4. Antiplatelet – aspirin (prevent platelet aggregation
☝ Limited to proximal and middle portion of a that impedes the blood flow), heparin (Prevent
vessel greater than 3 mm in diameter formations of blood clot)
➔ ​↓ contractility, cause arterial
☝​ L
​ ess than 15 mm long construction, ↓BP, peripheral vascular
resistance.
☝​ ​NOT heavily calcified
Surgical Management
☝ ​re..ing blocked vasculature via a needle
puncture in the skin. a) Myocardial revascularization or CABG – graft
from saphenous vein, internal mammary artery,
☝ ​Improves blood flow to the ischemic limb or radial artery, gastroepiploic artery.
peripheral arterial blood vessels
Construction of conduit between the aorta and
arteries to improve quality of life, good survival
and cardiac related mortality.

Palliative procedure only and is not a cure for

CAD

Indications:

➢ If the left main coronary artery stenosis is greater

than 50% may undergo CABG
➢ Stenosis of proximal left anterior descending and
proximal circumflex >70%
Pharmacologic therapy ➢ Three vessel disease which is asymptomatic with
mild or stable angina for patients with proximal
1. Vasodilator – Nitroglycerin (NTG) left anterior descending stenosis with poor left
➔ Reduce myocardial oxygen consumption ventricular functions
➔ Decrease ischemia and relieves pain ➢ ​Patients who have ongoing ischemia of non-ST
➔ ​Dilates vessels and ↑ perfusion segment elevation, MI that is unresponsive to
➔ Helps ↑ coronary blood flow, prevent medical therapy.
vasospasm
Contraindications:
2. β-adrenergic blocker – atenolol ➔ Asymptomatic patients who are at low risk of
➔ ​↓ myocardial oxygen consumption by MI or death
blocking the β-adrenergic sympathetic ➔ Advanced age is not a contraindication but is
stimulation of the heart less commonly done in the elderly because they
➔ ↓ HR, BP and myocardial contractility have a shorter life expectancy and CABG may
not be necessary to prolong survival. They may
➔ ​↓cardiac workload, excitability, ↓renin
likely to experience perioperative complications
release
after CABG
➔ Check BP and HR before administration
➔ B’s of β-adrenergic blocker​;
Preoperative tests:
B​radycardia, ↓​B​P, ​B​ronchial constriction, ❏ ​Full blood count; CBC
↓ ​B​lood glucose
❏ Screening for clotting, creatinine and electrolytes
to correct any abnormalities
3. Calcium channel blocker – nifedipine, diltiazem,
❏ Liver function test
verapamil
❏ Chest X-ray, ECG, 2D echo, coronary
✔​ ​↓ SA node automaticity and AV node angiography
 ➔ Stop all activity
➔ Bed rest
Nursing care: ➔ Observe signs of respiratory depression
➔ ​NTG
● Care for the 2 surgical sites; chest, arm, nape or ➔ Monitor vital signs
acromion 2. Reducing activity
● They use the radial artery so observe for the side 3. Health education on reducing risk factors
thumb and finger for the perfusion and oximetry 4. Teach stress reduction techniques
of the distal finger
● Monitor for hypertension because it may cause Relationship Between CAD, Chronic Stable Angina,
collapse of vein graft, if there’s increase in blood and ACS
pressure, it increases pressure that promotes
leakage from the suture line and may cause
bleeding
● May give Calcium channel blockers to decrease
the incidence of the arterial spasm of heart and
anastomosis sites especially the radial artery
● ​Prevent pulmonary complications
● Restrict fluids because clients usually have
edema

b) Transmyocardial laser revascularization

(TMR)
➢ Uses a laser to create a channel between the left
ventricular cavity and the coronary Angina Pectoris (chest pain)
microcirculation. The channel allows blood to flow
● A clinical syndrome characterized by episodes of
into the ischemic area.
➢ This can be done during cardiac catheterization pain or pressure in the anterior chest due to
and using elect anterior thoracotomy incision. insufficient coronary blood flow.
● The patients may experience A.P. due to
Complications: imbalance myocardial O2 supply and demand.
Usually occurs in coronary atherosclerosis.
● ​Ventricular arrhythmia
● Causes of Angina can also be: vessel factors;
● Post operative bleeding
atherosclerosis, arterial spasm from smoking or
● Cardiac tamponing emotional stress, circulatory factors; hypotension,
● Low cardiac output aortic stenosis because of ↓ in filling, ↓ venous
return, blood factors; anemia, hypoxemia,
CABG Surgery polycythemia.
● The mentioned factors contribute to the ↓ O2
supply.

PQRST Assessment of Angina

1. P​recipitating factors (activity, exercise, resting)

2. Q​uality (dull, aching, sharp, tight)
3. R​adiation of pain (back, arms, jaw, shoulder)
4. S​everity - using 0 – 10 pain scale
5. T​iming – 5 seconds to 30 minutes

Nursing Management

1. Treat pain

Location of Chest Pain (Angina)
Precipitating Factors of Angina
1. Physical exertion
➔ ​↑ HR that ↓ hearts time to diastole
2. Extreme temperature
➔ ​Cold ↑ workload of the heart, Blood
vessels constrict in response to a cold
stimulus; B.V. dilate and blood cools in
the skin in response to a hot stimulant
3. Strong emotion
➔ Stimulate the sympathetic nervous sys.
That may increase the workload of the
heart.
4. Consumption of heavy meal
➔ ↑ workload of the heart during the
digestive process, the blood is delivered
to the G.I. sys. Causing a ↓flow rate in
the coronary artery.
5. Cigarette smoking
➔ ​Nicotine stimulate catecholamine release
it may cause vasoconstriction and ↑ HR,
it may also ↓ 02 available by ↑ CO2
6. Sexual activity
➔ ↑ cardiac workload and ↑ sympathetic
stimulation, that’s why Nitroglycerin is
prescribed before engaging in this
activity.
7. Stimulants
➔ cocaine, amphetamines ↑ HR and
subsequently myocardial O2 demand.
8. Circadian rhythm patterns
➔ related to the occurrence of stable angina
or prinzmetal angina or sometimes it may
MI or sudden death.
➔ Include the quality of Angina Pectoris
➔ how does it feel? (Quality) There’s a
sensation of pressures and heavy weight
on the chest.
➔ Burning sensation, feeling of tightness or
squeezing, choking or suffocating
sensation (Sensation)
➔ Patients who have Angina located in the
left shoulder, jaw, left interscapular/
suprascapular area, median aspect of the
left arm (Location)
➔ Duration is about 5 s -30 mins.
➔ The manifestation of CAD tends to occur
in the early morning after awakening
➔ ​Severity of pain using pain scale
Types of Angina
1. Stable angina
2. Unstable angina
3. Intractable : severe incapacitating chest pain
4. Variant angina – due to coronary vasospasm
5. Silent ischemia : objective evidence of ischemia
but patient reports no symptoms
6. Nocturnal : associated with rapid eye movement
sleep during dreaming
7. Angina decubitus - characterized by the onset of
chest pain when the patient is resting or lying
down.
Stable Angina
❏ Described as a crushing, tightness or squeezing
sensation in the chest
❏ Down sloping ST segment indicate CAD
❏ Stress test or treadmill exercise test
 ❏ Characterized by effort induced chest discomfort ❏ Myocardial O2 demand and supply coronary
with or without radiation that lasts from 5 s – 15 artery spasm, and it is also stress related
mins. catecholamine release and platelet aggregation.
❏ Usually arises when the lumen stenosis is greater ❏ Unstable angina is the 1st clinical manifestation
than 70% which may incur blood supply to the of CAD
heart only during exertion or increase metabolic ❏ This unstable lesion ↑ the risk of complete
demands. thrombosis of the lumen with progressions to MI.
❏ Generally relieved by rest, removal of provoking That’s why patients with unstable angina require
factors, or taking of sublingual vasodilators immediate hospitalization for ECG monitoring and
❏ ​It is predictable; so, medications may be given to bed rest.
provide relief. So strenuous activities, cold
weather, heightened emotional stress may trigger VARIANT OR PRINZMETAL’S ANGINA
angina which can be relieved by NTG or rest
● NOT directly related to atherosclerosis but
Important Treatment /Elements of Stable Angina caused by coronary ​vasospasm
● NOT precipitated by exertion or stress
✔​ ​A – aspirin, antianginal therapy ● Occurs at the same time everyday
● Treatment – Nitrates, Calcium channel blocker
✔​ ​B – β-adrenergic blocker, blood pressure
❏ This is characterized by chest pain that occurs at
✔​ ​C – cigarette smoking, cholesterol rest in the early hours of the morning. It is often
associated with ST elevations in the ECG. And
✔​ ​D – Diet, diabetes the underlying cause is thought to be coronary
artery spasm due to the sudden reduction in
✔​ ​E – education, exercise
coronary blood flow brought on bi… spasm and
not on ↑ myocardial O2 demand.
Nursing Management (Stable Angina)
❏ It has been suggested that the spasm is caused
by a stroke (?) contraction of the smooth muscles
Acute Interventions for ​anginal attack
in coronary arteries, caused by ↑ intracellular
➢ Administration of supplemental oxygen calcium
❏ The ↓ in the myocardial consumptions that occur
➢ 12-lead ECG
➢ Prompt pain relief first with a nitrate followed by during sleep or rest may lead to coronary artery
an opioid analgesic if needed vasoconstriction that are responsible for the
➢ ​Auscultation of heart sounds spasm. Frequent between midnight and 8 am and
➢ Comfortable positioning of the patient to increase may disappear spontaneously or some point of
exercise, may have dysrhythmia and conduction
cardiac workload
abnormalities
Unstable Angina
Comparison of Types of Angina
➔ Pain last longer and more frequent and NOT
relieved by rest,
➔ Unpredictable
➔ Treatment: aspirin, heparin and antiplatelet
agents
❏ Also known as pre infarction or acute coronary
insufficiency
❏ Associated with deterioration of once stable
atherosclerotic plaque. Once the stable plaque
ruptured, exposing the intima to blood, and
stimulating the platelet aggregation and local
vasoconstriction with thrombus formation.
❏ It may be precipitated by factors other than effort
or activities. This is more severe than stable
angina. Frequency preceding with myocardial
infarction because of the imbalance between
Clinical Manifestation of Angina 10. Notify MD if Chest pain persists not relieved by
rest/Nitroglycerin
1. Chest discomfort and may experienced
epigastrium (upper central abdomen), back, neck
area, jaw, or shoulder ACUTE CORONARY SYNDROME
➔ When taking care of the elderly be sure
•A group of symptoms arise when vessel or coronary
to take the history properly because in
arteries becomes occluded or obstructed by thrombus
elderly with angina, it may not exhibit the
typical pain total, because of the ➔ When oxygen supply is decreased for a long
diminished responses of period of time which not immediately reverse,
neurotransmitters that occur with aging. then it can cause acute coronary symptoms
Most of the time the presenting symptom ➔ Usually precipitated by ​blood​ ruptured and blood
in the elderly is dyspnea. formation.
➔ Sometimes there are no symptoms ➔ Also associated with coronary thrombosis
making diagnosing and recognition as a
clinical challenge •Primary symptom is ​chest pain
2. Shortness of breath
➔ In which radiating from left arm or angle of the
3. Cold sweat
jaw which is very common and caused by
4. Weakness
atherosclerosis
5. Diaphoresis
➔ Cardiac chest pain can be precipitated by
6. Dizziness
anemia, bradycardia or tachycardia.
7. Nausea and vomiting
•​Etiology​: Atherosclerosis
Diagnostic Studies
NOTE: The acute ischemia is usually related to this
1. ECG or Holter monitoring syndrome raging from unstable angina to myocardial
2. Treadmill exercise test infarction with or w/o ST elevation
3. Nuclear imaging – myocardial perfusion
4. Positron Emission tomography Subtypes of ACS
5. 2-D echocardiography
Acute Coronary Syndrome - ​serve as an umbrella to the
6. Coronary angiography
7. Electron beam CT – assess CAD in all stages unstable angina, NSTEMI or STEMI.

● Unstable angina​ – when atherosclerotic plaque

May also include ​blood test​, ​lipid profile​ & ​cardiac enzyme
shoot of embolus downstream to cause
Goals for Management of Angina microinfarct
➔ Reduced blood flow in the coronary
1. Alleviate manifestations artery dues to ruptured of an
2. Prevent the progression of coronary heart atherosclerotic plaque
disease and myocardial infarction ➔ A plaque begin to form at top of coronary
3. Relieve acute attacks but artery not completely occluded
➔ This acute situation can result into chest
Nursing Management for Angina pain that may referred as preinfarction
angina because the patient is likely to
1. Oxygen as ordered have a myocardial infarction and
2. Pain relief – nitrates, narcotics, ​nitroglycerin interventions do not occur
(sublingual)
3. VS & assess cardiac function ● NSTEMI​ – when necrosis confined to endocardial
4. ECG layers (most susceptible to ischemia)
5. Semi-High fowler – to decrease myocardial ➔ Non-ST Segment Elevation Myocardial
demands Infarction
6. Emotional support – to reduce anxiety (eg. music ➔ If ECG does not show typical changes,
therapy) this called Non ST Segment Elevation
7. Minimize precipitating events ACS
8. Gradual increase in exercise ➔ However, patient may still suffered from
9. Allow for rest periods Non St elevation myocardial infarction
 ➔ Occlusion is about 25% or partial block in
the coronary artery but still there is blood
perfusion to the block artery
➔ The presence of collateral circulation is
very important so no ST or P-wave
alteration on the ECG when necrosis
confined​ to ​endocardial layer therefore,
more susceptible to ischemia
➔ Can be a positive or negative cardiac
enzyme depending on the size that is
affected.
➔ TREATMENT: Conventional lifestyle
modification.
➔ MEDICATION: Aspirin, Clopidogrel or
Heparin. Revascularization like
Percutaneous Transduminal Coronary
Angioplasty.
● STEMI ​– when full thickness necrosis of the
ventricular wall occurs
➔ There is a sudden occlusion in the
coronary artery that caused ischemia
➔ There is a presence of clot
➔ If the ECG confirm changes suggest
Myocardial Infarction
➔ 30% of Transmural Infarction of the
Myocardium undergoes necrosis that
may results to ST Elevation in which also
release cardiac enzyme
➔ There is (+) cardiac enzyme and ST
changes in the ECG
➔ P wave inversion and pathologic P Wave
➔ This is emergency situation that needs
Revascularization of the occluded artery
so it must done immediately
➔ TREATMENT: Thrombolytic or
Angioplasty
NOTE: NSTEMI and STEMI are named according to the
appearance in the ECG classified as acute coronary
artery.
UNSTABLE NSTEMI STEMI
ANGINA
Non occlusive Non-occlusive Complete
thrombus thrombus thrombus
sufficient to occlusion
Non specific cause tissue
ECG damage & mild ST elevations
myocardial on ECG or new
necrosis LBBB
Normal cardiac Elevated cardiac
enzymes ST depression enzymes
+/-
More severe
T wave symptoms
inversion on
ECG
Elevated cardiac
enzymes
Signs and Symptoms of ACS
1. Palpitations - refers to patient with dysrhythmia
2. Pain – pressure, squeezing, or a burning
sensation across the precordium and may radiate
to the neck, shoulder, jaw, back, upper abdomen,
or either arm
➔ Cardinal signs of decreased blood flow to
the heart and pain radiates to the left
arm. A pressure like in character or
associated with nausea and vomiting due
to vagal stimulation. Sweating because of
sympathetic discharge
3. Exertional dyspnea that resolves with pain or rest
4. Diaphoresis from sympathetic discharge
5. Nausea from vagal stimulation
6. Decreased exercise tolerance
7. Jugular venous distention
➔ Also evidence also in patient who have
acute coronary syndrome
8. Cool, clammy skin
➔ Because of sympathetic system
stimulation
➢ Patients might also experience the feeling of
acute ill.
➢ The presence of S3 and S4 in Heart sound.
➢ Presence of rales in Pulmonary examination -
suggestive of left ventricular dysfunction or mitral
devitations.
➢ HYPOTENSION - decreased in blood pressure
indicates ventricular dysfunction due to
myocardial ischemia or infarction.
➢ HYPERTENSION - it may precipitate angina or
elevated in catecholamine level due to anxiety or
exogenous​ sympathomimetic stimulation
DIAGNOSTIC STUDIES
1. ECG
➔ Indicates acute heart damage
➔ Elevation in the ST Segment or​ New Left
Bundle branch block
 2. Chest X-ray
3. Troponin I and T
➔ Cardiac markers
➔ Pulmonary embolism is suspected - need
to place the patient in telemetry unit to
monitor the heartbeat
4. Brain natriuretic peptide (BNP) – provide
information to develop MI
5. C-reactive protein (CRP) – systemic inflammation
6. Interleukin-6 – major determinant of acute-phase
risk of unstable angina

MANAGEMENT OF ACS
THREE ZONES OF TISSUE DAMAGE
1. Monitor and treat arrhythmia
2. Correct electrolyte imbalances – potassium, 1. Ischemia – T wave inversion
magnesium ➔ There is a greater chance of viability of
3. Provide oxygen therapy – to correct hypoxemia the myocardial cells, unless the Ischemia
4. Pharmacologic therapy – aspirin, clopidogrel persists or worsens.
➔ It will take about 20 minutes
2. Injury – ST elevation
MYOCARDIAL INFARCTION (MI)
➔ Surrounding of necrotic tissue that
causes injury on the myocardial cells that
● Complete or nearly complete occlusion of a
potentially viable if adequate circulation is
coronary artery usually precipitated by rupture of
quickly restored
a vulnerable atherosclerotic plaque and
➔ ECG tracing - ST elevation, shows injury
subsequent thrombus formation with cause
in bipolar leads
abrupt cessation of blood and oxygen to the heart
3. Infarction – deep Q waves
➔ Myocardial - pertains to myocardium
➔ Sometimes called Central Area
➔ Infarction - there is a decrease in
➔ Consists of necrotic myocardial cells,
coronary p[erfusion that affect according
capillaries and connective tissue
to myocardial layer
➔ Causes the presence of the Q wave due
to the inability of this necrotic muscle to
Basic Types of MI Based on Pathology
conduct an impulse
1. Transmural – all layers is affected; complete
occlusion
➔ Extends from endocardium to
pericardium with results complete
occlusion of the areas blood supply
2. Subendocardial – small areas; susceptible to
ischemia
➔ Generally it confined a small part of
myocardium or the sub endocardial wall
of the left ventricle, ventricular septum or
papillary muscles
➔ Majority of this involve the left ventricle

NOTE: In the clinical picture of MI, if there is P wave

infarction that means it is a conversion of oxygen to the
cells therefore it becomes necrosis within 5-6 hours after
occlusion.
If there is a presence of deep P wave in the ECG training
that means it is permanent and also indicates sustained
coronary occlusion and extensive necrosis.
SITE OF INFARCTION

1. Anterior wall of the left ventricle near the apex –

common
➔ It results from thrombosis of the
descending arch branch of the left
coronary artery.
2. Posterior wall of the left ventricle near the base
➔ results from the occlusion of the right
coronary artery or circumflex branch of
the left coronary artery
3. Inferior surface of the heart
➔ Results from the right coronary artery The affected Myocardial cells do not regenerate after an
occlusion infarction so healing requires the formation of the scar
4. Lateral – left circumflex artery tissue that replaces the nuclotic myocardial muscles.

NOTE: The severity of MI depending on 3 factors:
1. The level of occlusion in the coronary arteries
2. The lent of time of occlusion
3. Absence collateral circulation
ETIOLOGY OF MYOCARDIAL INFARCTION
1. Coronary artery spasm can cause acute
occlusion
2. Decrease oxygen supply from acute blood loss,
anemia or low blood pressure
3. Unstable angina
4. Plaque rupture
NOTE: The main problem is that there is insufficient blood
supply in the Myocardium so there is a decreased supply
of oxygen and nutrients to the Myocardium.
If there is a deprivation of the Oxygen to the Myocardial
cells then Ischemia may develop because of prolonged
lack of oxygen it may result in Infarction of the death of
myocardial cells.
The enzymes it may (​di ko maintindihan sorry​) the
different intramyocardial cellular enzymes such as the
CGK or CK-MB, Myoglobin or Troponin that resulted in
patient develop or complaining of chest pain.
The morphology changes will be ranging from there is no
apparent cellular change within the first 6 hours total
replacement by scar tissue.
When there is scar tissue it may inhibit the contractility
and cause slow conduction of electrical impulse that may
trigger reentry mechanism that results in ventricular
defibrillation.
As the contractility falls, the failure of the myocardial to
contract may cause heart failure so the body starts to use
the compensatory mechanism in attempt to maintain
cardiac output.
CLINICAL MANIFESTATIONS OF MI
1. Chest pain – sudden and continuous (primary)
➔ Substernal pain despite of medication
and rest
➔ Ask for the quality of chest pain, if it is
severe, squeezy, heavy, pressure
sensations or chest tiredness
➔ Usually, it is intense and not relievable for
about 30-60 minutes and there is
radiation from the substernal to the neck,
shoulder, jaw and down the left arm.
➔ Blood pressure is initially elevated bc of
chest pain, peripheral vasoconstriction
that results from adrenergic response to
pain ventricular dysfunction
2. Unexplained anxiety
3. Restless
4. Stomach, back and abdominal pain (epigastric
pain or indigestion)
5. SOB and dyspnea
6. Weakness
7. Diaphoresis or sweating
8. Syncope – without cause
9. Cognitive impairment – without cause
10. Sinus Bradycardia
11. Nausea and vomiting

*Some patients may experience Fever if it is greater than
1 degree celsius as early as 4-8 hours after the onset of
the MI.
DIAGNOSTIC STUDIES IN MI
1. Laboratory test
❏ CK-MB​ ​- ↑ 4 – 6 hours after onset of
chest pain (the peak is about 12 - 18
hours and normalize in 3-4 days)
❏ Troponin T and I​ ​(​Troponin T​ is about
84% sensitivity for MI, 8 hours after onset
and this is very sensitive to detect
myocardial ischemia. Whereas, the
Troponin I i​ s about 90% sensitivity to
protect high risk and unstable angina).
❏ Myoglobin​ – indicate myocardial
damage (Elevated means myocardial
damage in the absence of skeletal
muscle but sensitivity may not be reliable
after 10-12 hours because of the rapid
renal clearance).
❏ LDH​ (Increased in 12 hours after onset of
chest pain, peak is about 24-38 hours
and remains increased about 10 days
especially the isoenzyme L1 and L2
which indicates myocardial damage.
❏ CBC​ – leukocytosis (bc of muscular
injury and subsequent ischemia and
ESR (erythrocyte sedimentation rate is
also elevated bc ​reflects​ the tissue
necrosis.
❏ C-reactive protein (CRP)​ - for acute
inflammation
2. Radionuclide imaging
❏ Provides information in the presence of
coronary artery disease
❏ Location of ischemic infarcted tissue
3. MRI
❏ Help to provide or identify and extend the
MI and serves as the basis for the
assessment of the effect of perfusion
therapy.
❏ In this MRI, heart technology that
differentiate the reversible and
irreversible tissue injury.
4. Positron Emission Tomography (PET) scan​ –
cardiac metabolism and assess tissue perfusion
so it will evaluate the presence of coronary artery
disease, coronary flow reserve and even detect
MI.
5. 2-D echo
❏ Identify the different areas of abnormal
regional ​(di ko maintindihan hehe)
❏ Detecting complications associated with
MI
6. ECG
❏ ​ST elevation for AMI
❏ ST depression for ischemia
1. Once the patient recovered from MI, the first to
return to the normal is the ​ST Segment; ​it takes
1 -6 weeks.
2. P​ waves b ​ ecome large and symmetric for the 24
hours and invert within 1 to 3 days.
3. P wave​ alteration that would be permanent.
P-Waves occur or notice changes in the ECG, usually
following 36-48 hours then there would be changes in the
P-waves if there is no PROMPT treatment to the patient.
P Waves may persist as evidenced by an old infarction
and can be used to localize the effects throughout the
person's life.
MANAGEMENT
1. Hemodynamic monitoring
2. Oxygen therapy
➔ Need to measure the partial arterial
oxygen if it is hypoxemia need to
receives about 2-4 L per minute as per
doctor's order
3. Bed rest
➔ To decreased myocardial oxygen
consumption
4. Diet – liquid diet 1​st​ 4 to 12 hours (to decreased
gastric distension); saturated fat restriction and
low sodium
5. Pharmacologic therapy
6. Percutaneous coronary intervention (PCI)
-Intra-aortic balloon pump, angioplasty, stent
placement, etc.
➔ Intra-aortic Balloon Pump
 ➔ Angioplasty
➔ STEM Placement
7. Cardiac rehabilitation
➔ If the patient is already recovered from
Acute MI
➔ Long term program of medical evaluation,
indications to patients and even
counselling in order to limit the physical
and psychological effect of cardiac illness
and improve the pt’s quality of life.
➔ It has different phases
➔ Theme: Improve functional mobility, and
decreased the risk factor through
medications that is related to cardiac
inquiry
➔ Includes family that teaches how to
manage the psychological effects that
may influence recovery after MI.
INTRA-AORTIC BALLOON PUMP
➔ Mechanical devices that increase the coronary
perfusion and lowers systolic blood pressure.
➔ Reduce the afterload and improve blood flow with
pt cardiac contractile functions.
➔ Increase the cardiac output by improving the
coronary blood flow. If there is an increased in
coronary blood flow therefore, there is more
myocardial oxygen delivery
❏ Usually it will inflate during the diastole and
ventricular filling that may increase the pressure
in the aorta therefore, it may increase the blood
flow through the coronary and peripheral arteries.
❏ It is inflated just before ventricular contraction that
will lessen the pressure in the aorta before the
left ventricle contraction so that it may decrease
the amount of resistance to the heart.
PHARMACOLOGIC INTERVENTION
MYOCARDIAL INFARCTION “MONA TASS”
M MORPHINE
Analgesic drugs such as morphine are to
reduce pain and anxiety, also have other
beneficial effects as a vasodilator and
decrease the workload of the heart by
reducing preload and afterload.
O OXYGEN
To provide and improve oxygenation of
ischemic myocardial tissue ; enforced
together with bedrest to help reduce
myocardial oxygen consumption. Given via
the nasal cannula at 2 to 4 L/min.
N NITROGLYCERIN
First-line of treatment for angina pectoris and
acute MI ; causes vasodilation and increases
blood flow to the myocardium.
A ASPIRIN
First-line of treatment for angina pectoris and
acute MI ; causes vasodilation and increases
blood flow to the myocardium.
T THROMBOLYTICS
To dissolve the thrombus in a coronary
artery, allowing blood to flow through again,
minimizing the size of the infarction and
preserving ventricular function; given in
some patients with MI.
A ANTICOAGULANTS
Given to prevent clots from becoming larger
and block coronary arteries. They are usually
given with other anti clotting medicines to
help prevent or reduce heart muscle
damage.
S STOOL SOFTENERS
Given to avoid intense straining that may
trigger arrhythmias or another cardiac arrest.
S SEDATIVES
In order to limit the size of infarction and give
rest to the patient. Valium or an equivalent is
usually given.
1. Analgesics - ​Morphine
➔ Vasodilator that reduces the pain and
anxiety
➔ Reduces the blood flow of the heart, that
results into a decrease preload and
afterload
➔ Help in relaxation of the bronchioles that
enhance oxygenation
2. Thrombolytic – aspirin, heparin,
streptokinase, tPA
a. Anti-platelet aggregating agents –
aspirin
 ➔ Blocks the prostaglandin
synthesis
➔ Prevents additional platelets
activation that interferes to the
platelets adhesion
➔ Limit formation of thrombus
➔ It should not be used in client
with severe renal or liver
diseases
➔ Assess for presence of bleeding,
before administering this.
➔ CLOPIDOGREL - adjunctive
reperfusion therapy, beneficial
combination with aspirin
b. I​ ndirect thrombin inhibitor​ - ​heparin
(​Antidote: Protamine sulfate​)
➔ HEPARIN:​ Increased the ability
of antithrombin, therefore it will
not activate the circulating
thrombin and limit the formation
of thrombus formation
➔ Monitor aPTT (activated partial
thromboplastin time) levels
❏ STREPTOKINASE:​ Given during
the first attack of MI
❏ Made from streptococcus
organism
❏ Increased the amount of
plasminogen activator that
increased the amount of both
circulation clot ​blood
plasminogen
❏ Not given to patient who has
been exposed to recent
streptococcal infection or just
received a streptokinase
❏ Not being used again after 4
days of administration bc it might
cause allergic reaction, if allergic
occurs need to administer tPA
❏ Need to monitor: Heart rate and
rhythm and observe for any
bleeding.
c. Tissue-type plasminogen activator
(tPA)
➢ Activate Plasminogen on the clot
➢ Heparin is used at the same time
➢ Ex. ​Alteplase:​ breakdown the
blood clots, conversion of
plasminogen to plasmin.
3. Angiotensin-converting enzyme inhibitor
(Captopril)
a. prevent conversion of angiotensin I to II
b. ​↓ BP, kidney excrete Na and fluid to ↓ O2
demand by the heart
4. Beta blocker
a. ​reduce pain, limit infarct size
b. ​↓ HR, reduce cardiac work and
myocardial O​2​ demand
5. Nitrates
a. Reduce cardiac workload
b. Dilate coronary arteries and collateral
channels in the heart
➢ ​Adverse effect: tachycardia and
hypotension
6. Dopamine​ – improves blood flow, prevent renal
ischemia
NURSING MANAGEMENT
1. Assess the characteristics of pain including the
location, duration, quality, intensity and presence
of radiation.
2. Maintain an IV access just incase of an
emergency situation.
3. Monitor ongoing assessment - lab test, cardiac
enzyme, hemodynamic parameter if the pt is with
Swan-Ganz catheter
4. Minimize anxiety - talk with the pt
5. Minimize metabolic demands - provide a rest
period
6. Assess vital signs and peripheral edema
7. Provide calm environment - quiet environment
helps in early recovery of the patient
8. Limit visitors
9. Elevate legs and avoid pressure under the knees
10. Administer drug therapy as ordered (MONA)
11. Prepare for treatment (PTCA, CABG)
12. Support system
13. Patient teaching
14. Physical exercise - may used isometric and
isotonic
15. Resumption of sexual activity – use of nitrates
before sexual activity
16. AVOID activities - always provide a resting period
after exercise
17. Patient discharge - submit to cardiac
rehabilitation called care unit in hospital
➔ If the pt is still in the Hospital the pt needs to put
the pt in ECG monitoring.
➔ Small frequent meals is one example to decrease
cardiac workload.
➔ Avoid valsalva maneuver bc cause bradycardia
COMPLICATIONS
1. Dysrhythmias
➔ Bc of the damaged muscles which
generates abnormal current causing
abnormal cardiac contractility and the
infarct damaged of the conductive tissue
➔ This also results in predisposing factors
like tissue injury, hypoxemia, lactic
acidosis, hemodynamic abnormalities
and electrolytes imbalances.
➔ Also, because of declines in cardiac it
increases the cardiac irritability which
further compromises myocardial
perfusion.
2. Congestive heart failure (CHF)
➔ Usually, the MI comprise the myocardial
function by reducing contractility and
producing abnormal wall ​motion, ​bc of
this pt may have have cardiogenic shock
bc of the failure of the heart to pump
adequately thereby reduces cardiac
output and compromised the tissue
perfusion
➔ Usually occur in left ventricle
3. Pericarditis – pericardial friction rub
➔ Also known as Dressler Syndrome
➔ Usually pericardial is occur after a
transmural infarction
➔ Occur about 10-20% individual (after a
week of infarction)
4. Ventricular aneurysm
➔ Late complications of MI that involves
thinning, ballooning and hypokinesis of
the left ventricular wall after transmural
infarction.
➔ Aneurysm often creates paroxysmal
motion of the left ventricular wall and
ballooning of an aneurysmal segment of
the ventricular contraction.
CONGESTIVE HEART FAILURE (CHF)
● Heart Failure is NOT a heart attack
❏ Associated with various type of heart
diseases particularly with long standing
hypotension and CAD
❏ Is a type of circulatory failure which
includes hypoperfusion resulting from
extra cardiac conditions like hypovolemia,
peripheral vasodilation or inadequate
oxygenation of hemoglobin
● Heart failure means the heart is:
➔ Weakened
➔ Cannot pump enough blood to supply the
body’s needs
● The heart is unable to provide sufficient pump
action to maintain blood flow to meet the needs of
the body.
❏ The occurrence of circulatory congestion is from
decreased myocardial contractility that results
from inadequate cardiac output to maintain the
blood flow to the body organs that resulted from
cardiac causes of congestive heart failure.
❏ If it is not cardiac conditions like increased blood
volume from sodium or salt retention of primary
or decreased peripheral resistance.
COMPENSATORY MECHANISMS FOR MAINTAINING
CARDIAC OUTPUT
1. Ventricular dilation - ↑ contraction leads to ↑ CO
and maintain perfusion
➔ As the heart enlarges it can cause
pressure in the left ventricle over a
certain time, so the muscle fiber of the
heart is stretched thereby, it increases
the contractile force.
➔ Initially this may increased contraction
that may lead to increased cardiac output
and maintaining arterial blood pressure
and perfusion therefore the dilation is an
adaptive mechanism to cope with the
increasing blood volume but eventually
this mechanism become inadequate bc of
elastic elements of the muscle fiber are
overstretched like a rubber band which
made it become no longer functional and
not able to contract effectively then
resulting to a decreased cardiac output.
2. Myocardial hypertrophy – thickness response to
overwork and strain
➔ Hypertrophy means there is an increase
in the muscle mass and cardiac wall
thickness
➔ Occurs slowly bc it takes time for this
muscle tissue to develop
➔ Usually, it follows persistent or chronic
dilation and also increases the
contractive power of the muscle fiber that
will lead to increased cardiac output and
maintenance of tissue perfusion.
➔ Hypertrophic heart muscle has a poor
contractility.
3. Sympathetic Nervous System activation -
release of epinephrine and norepinephrine ↑ HR,
myocardial contractility and peripheral vascular
constriction
 ➔ Vasoconstriction may cause an
immediate increase in the preload that
initially increased the cardiac output.
➔ However. An increased venous return
(volume overload) can worsen ventricular
performance.
4. Neurohumoral response – Na and water retention
➔ Vasoconstriction secondary to
norepinephrine or epinephrine
➔ It may decrease the cardiac output by
stimulating the sympathetic nervous
system which increases the heart rate ,
BP and contractility.
➔ The release of the catecholamine
decreases renal perfusion or stimulation
of RAAS (​Renin-Angiotensin-Aldosterone
System) that causes vasoconstriction,
increased BP, vascular volume and
decreases water and sodium restriction.
If the cardiac output fails, blood flow to the kidneys
decreases glomerular blood flow therefore, the kidney
may release angiotensin 1 and 2 or also known as
angiotensin system.
Adrenal cortex will release the aldosterone then increase
in peripheral vasoconstriction and increase the arterial
BP.
RISK FACTORS OF CHF
● ​High blood pressure
● Myocardial Infarction
● High cholesterol
● Damage to heart valves
● ​Diabetes
● ​Obesity
● Advancing age
Note: Precipitating factors:
❏ Infection​ - increases oxygen demand of tissue
then stimulating increased cardiac output
❏ Stress ​- has an effect in development of heart
failure
❏ Anemia​ - bc of decreased oxygen carrying
capacity of the blood then stimulating an increase
in cardiac output to meet the tissue demands.
❏ Thyroid disorders - ​bc of changes in tissue
metabolic weight that increases the heart rate
and workload of the heart indirectly it predispose
to atherosclerosis thereby it decreases
myocardial contractility
❏ Pulmonary embolism - b ​ c of the blood clot in
the pulmonary vasculature therefore it increases
pulmonary pressure except pressure on the right
ventricle leading to hypertrophy of the right
ventricle and failure
❏ Nutritional deficiency - d ​ ecreases cardiac
function bc of decreased myocardial muscle
mass and contractility
❏ Hypervolemia ​- it increases the preloading,
therefore, causes an increased in blood volume
load in the right ventricle
FACTORS THAT CAUSES INTERFERENCE WITH THE
NORMAL MECHANISM REGULATING THE CARDIAC
OUTPUT:
1. Preloading bc of the amount of blood fills the
ventricle before contraction. (venous return and
increased elasticity of the ventricle may results to
hypertrophy or thickness of the myocardium)
2. Afterload- amount of resistance to the ejection of
the blood vessels from the ventricle that related
to stroke volume
➔ Factors that determine after, the diameter
and distance ability of the great vessels
like aorta and pulmonary artery and
➔ Even the opening of the aortic and
pulmonic valve. If the valve open easily
resistance is low therefore, hypertension
may increased resistance
3. Heart rate, myocardial contractility, metabolic
state of the individual - any alteration of these
factors can lead to decreased ventricular function
and results in manifestation of heart failure.
ETIOLOGY OF CHF
1. Abnormal loading condition – ↑ preload
(regurgitation of mitral or tricuspid valve); ↑
afterload (hypertension, aortic or pulmonic
stenosis)
➢ Even pt who have hypovolemia or pt who
has congenital defects like atrial or
ventricular septal defect
➢ High peripheral vaso resistance
2. Abnormal muscle function – MI, cardiomyopathy
➢ MI - bc of infarcted necrotic tissue
myocardium that affects the function of
the heart
➢ Cardiomyopathy - disease in myocardium
that affects contractility of the ventricles
➢ Ventricular aneurysm - bc of abnormal
muscle function
3. Limited ventricular filling – cardiac tamponade,
pericarditis
➔ Cardiac tamponade - also known as
pericardial tamponade, this a type of
pericardial effusion in which the fluids
 accumulate in the pericardium, so the
pressure on the heart muscle which
occur when the pericardial space fill up
with fluid faster than pericardial sac, if the
amount of fluid increased slowly then the
pericardial sac can expand a little then a
tamponade may occur
➔ If the fluid occurs rapidly as little as 100
ml it can cause tamponade therefore,
increased in pericardial pressure but
decreased venous return and also
decrease in cardiac output depending on
the determinants of the three
characteristics of ​extrayant in ventricular
filling:
1. Distance heart sound - bc of the fluid inside the
pericardium
2. Distended ​loop - ​bc of intravenous return of the
heart
3. Decrease pulse pressure - bc of cardiac function
and decrease in stroke volume
TYPES OF VENTRICULAR FAILURE
1. Systolic failure ​– common cause of CHF; ↓ the
left ventricular ejection fraction caused impaired
contractile function
➔ This means that inability of the heart to
pump blood
➔ There is a defect in the ventricular
contraction, so the left ventricle loses its
ability to regenerate enough pressure to
eject blood forward to the high pressure
aorta, the reason why it was called
SYSTEMIC FAILURE.
2. Diastolic failure ​– impaired ability of the
ventricles to fill during diastole. ↓ filling of the
ventricles will result in ↓ stroke volume.
➔ Diastolic failure means there is a
decreased filling of blood in the ventricle
➔ Impair ability of the ventricle to fill blood
during the diastole
➔ Ventricle becomes less compliant or stiff.
Ventricular filling cannot relax because
of wall is thick and rigid therefore an
decrease in stroke volume
FORMS OF CHF
● Left​: Left ventricle has reduced capacity to pump
blood into systemic circulation -decreased CO
and backup of fluid into the pulmonary circulation
➢ Results from dysfunction, inability of the
left ventricle to function normally that
causes to back up through the left atrium
➢ If there is pressure in left atrium, the
pressure affects the pulmonary vein
➢ In the pulmonary vasculature, it may
cause an elevation of pulmonary
pressure bc of this fluid extravasation
from the pulmonary capillary bed into the
interstitium
➢ Also affects alveoli which manifests
pulmonary congestion or edema
➢ Left sided may result to pulmonary
congestion that is why the patient
experience dyspnea, exertion that
increases pressure on the blood vessels
on the lungs - called it as PULMONARY
HYPERTENSION bc of increased
pressure in the pulmonary area or
vasculature
➢ When the blood ventricle cannot pump
effectively then it blocks out the ventricles
into the aorta to the systemic circulation
that affects the cardiac output and also
impair gastric change
● Right​: the right ventricle has reduced capacity to
pump blood into pulmonary circulation causing
backup of fluid into the venous circulation
➢ The right side of the heart cannot eject
blood forward to the pulmonary
vasculature therefore it accommodates
all the blood in the right ventricles
therefore there is a tendency that
backflow of blood to the right atrium and
mini circulation might happen.
➢ Patient that has right sided heart failure
primarily produces signs and symptoms
like anxiety, hepatomegaly, peripheral
edema (Pitting edema) bc of vascular
congestion.
➢ Venous congestion causes Jugular Neck
Vein Distension.
MAJOR ALTERATION IN CHF
1. Diminished cardiac output – inadequate perfusion
of the vital organ result to deprivation
➔ Oxygen and nutrients are failed to meet
2. Pulmonary vascular bed no longer emptied
effectively by left atrium and ventricle – engorged
pulmonary vessel (that also results to pulmonary
hypertension and p. edema)
3. Increase venous pressure – engorged capillaries
leading to ascites and peripheral edema
 ➔ Move backward that increased the
venous pressure that affects liver and
other organs will be congested
DIAGNOSTIC STUDIES
CLINICAL MANIFESTATIONS PER SYSTEM
1. Cardiovascular​ – activity intolerance ​(bc of the
reduced CO & blood circulation)​, tachycardia ​(b​ c
of reduced CO & stimulation of SNS),​
palpitations, S3 and S4 heart sounds ​(in normal
pt it cannot hear)​, elevated CVP, neck vein
distention, hepatojugular reflux, splenomegaly
2. Neurologic​ ​– confusion, impaired memory,
anxiety, restlessness, insomnia
3. Genitourinary​ – decreased urine output, nocturia
(bc of the imapired renal perfusion during the day
however when the pt lies back at the night the
fluid will move from interstitial space back to the
circulatory system that increases renal blood
flow)
4. Integumentary​ – pallor or cyanosis ​(bc of
decreased supply of O2),​ cool and clammy skin,
diaphoresis ​(bc of stimulation of SNS)
5. Respiratory​ – DOE, SOB, tachypnea, orthopnea,
dry cough​ (blood stain sputum bc there is a
presence of alveoli edema herein the alveoli
lining cells are destructed and contain RBC move
in alveoli)​ ,crackles in lung base
➢ pt should be in semi or high fowler's
position to facilitate breathing bc of the
pressure in the pulmonary vasculature,
this position should be done to avoid
impaired gas exchange
6. Gastrointestina​l​ – anorexia, nausea, abdominal
distention, liver enlargement, RUQ pain
7. Musculoskeletal​ – fatigue and weakness​ (lack of
oxygen and blood supply in the muscles)
8. Metabolic processes ​ - peripheral edema and
weight gain ​(bc of fluid retention)
1. ECG​ – clue to the cause of left ventricular failure
➔ Changes in the ECG tracing
2. CXR​ – shows enlarged cardiac silhouette,
pulmonary congestion
3. 2-D echo​ – provide cardiac chamber size and
ventricular function (EF - > 55% to 70%)
4. ABG ​– respiratory alkalosis or acidosis
➔ Usually occurs in patient who have
pulmonary edema due to hyperventilation
then it may results to respiratory alkalosis
➔ Hypoventilation - acidosis
5. Laboratories​ – electrolytes ​(check the sodium,
potassium),​ blood chemistry (​increased creatinine
bc of decrease glomerular filtration and liver
function value is the liver is affected that results
to increased liver enzyme)​ ,urine studies
(decreased urine output)
➔ Hyponatremia due to water retention,
urinary sodium loss in response to
diuretics to relieve the congestions.
➔ Hypokalemia bc of excessive use of
diuretics or secondary to manifestation of
aldosteronism
 6. Nuclear imaging studies ​- areas of myocardial
perfusion
7. Cardiac Catheterization ​may be done
MANAGEMENT
1. Oxygen therapy
2. Intubation - severe case​ (severe pulmonary
edema)
3. Positioning – High Fowler’s ​(in order to increase
venous return and increase thoracic capacity
allowing for improve ventilation)
4. Monitor I and O, weigh daily
5. Fluid restrictions - less than Liter per day to
prevent more fluid that may ​ampere​ the functions
of the heart
6. Decrease Na in diet
7. Rest - bc they get easily get fatigue due to
decreased CO
8. Auscultate heart and lung sounds
9. Hemodynamic monitoring (PCWP)
10. Surgery - heart transplant; cardiomyoplasty
(severe type of heart failure)
11. Intra-aortic balloon pump - it assists the heart by
decreasing afterload or increased coronary artery
perfusion.
12. Drug Therapy
1. Nitroglycerin (NTG)​ (vasodilator)​ – improve
coronary artery circulation
❏ Reduce preload, slightly reduce afterload
and increased myocardial oxygen supply
2. Nitroprusside (Nitrate)​ (vasodilator)​ – reduces
preload and afterload
❏ Improve myocardial contraction
❏ Increases cardiac output
❏ Reducing pulmonary congestions
❏ COMPLICATIONS of IV nitrate:
Hypotension (needs dopamine to
maintain arterial blood pressure of >60
mmHg), thiocyanate toxicity
3. Morphine​ – dilates pulmonary and systemic
blood vessels to improve gas exchange
❏ Reduction of anxiety
Recommended by Expert:
4. Diuretics​ - help control symptoms
➢ Increased the rate of urine output with
patient fluid overload
➢ Reduces pulmonary venous pressures
and preloading
➢ Furosemide​ - acts on the ascending loop
of henle to promote sodium chloride and
water excretion. It is more predictable in
each response.
➢ SIDE EFFECTS: Reduces serum
potassium level
➢ THIAZIDE​ - for chronic heart failure.
Treat edema secondary to heart failure. It
is also controlling hypertension. Inhibits
sodium reabsorption in the ​distal tubule
and also promotes excretion of sodium
and water another example of this is
Hydrodiuril - oral
➢ Potassium-sparing diuretics -
promotes water and sodium excretion but
blocks potassium excretion (​Aldactone​)
5. Digoxin​ - helps control symptoms
➔ Increases the strength and force of
cardiac contraction
➔ It has a inotropic action which reduces
the conduction speed within the
myocardium and slows the heart rate
➔ Allows the complete emptying of
ventricles during diastole
➔ Need first to check the heart rate of the
patient before administering this drug.
➔ If less than 60 bpm do not give the
medication bc it slows the heart rate
furtherly
➔ DIGITALIS - increases cardiac output
and stroke volume and contractility
6. ACE Inhibitors​ - can slow disease progression
➔ Treatment for all stages of heart failure
➔ Useful systolic and diastolic heart failure
➔ First line therapy in the treatment bc this
promotes vasodilation, increasing urine
output by decreasing afterload and
preload.
➔ Ex. ​Captopril and Enalapril
 7. ​Beta-adrenergic Agonist ​ - can slow disease 1. Primary (​essential or idiopathic)​
progression a. Common form
➔ Epinephrine in which increases b. Unknown cause/ usually asymptomatic
myocardial contractility and blood flow to c. Theories:
the renal​ (di ko maintindihan)​ and i. Neural ​- contributive factor because of
coronary and cerebral vascular excessive neuro humoral stimulation
➔ Highly effective to patients who have that may increase muscle tone
heart failure because it increases the CO ii. CNS activation - increased central
and promotes diuresis. nervous activity may increase bp by
increasing the renin via releasing the
HYPERTENSION catecholamine
iii. Renin-angiotensin-aldosterone
● Abnormal elevation of the systolic arterial BP with system - (RAAS) stimulation and
age related differences. production of high plasma level of renin
● Intermittent/ sustained elevation of systolic or that result the production of angiotensin
diastolic blood pressure and conversion of angiotensin I to
● Major cause of cerebrovascular accident (stroke/ angiotensin II (vasoconstricting
cardiac diseases or renal failure) substance) which may stimulate
● Labile hypertension – a phenomenon when BP can aldosterone result to retention of water
be markedly elevated at one time and normal at salt
another. iv. Vasodepressor ​- decrease
● Isolated systolic hypertension – ↑ in systolic concentration of vasodilating substance
pressure without diastolic elevation. such as prostaglandin or kinins
● May occur in elderly person or in the presence of d. Associated: Advancing age, Obesity, neural
hyperdynamic circulation or aortic insufficiency mechanism,
2. Secondary – elevated BP is related to underlying
Causes of condition such as kidney disease:
Hypertension a. A known cause: chronic renal disease, disease
of adrenal gland, BC pills, preeclampsia,
1. Nonmodifiable
hyperparathyroidism, diet pills, migral
factors – (cannot
medications
change) genetics, b. Increased peripheral resistance mainly
family history, age,
attributed to structural narrowing of arterial
race which may increase venous return, increase
2. Modifiable factors: cardiac preload, and cause diastolic
○ Inactivity
dysfunction
(Low physical fitness - may engage in
exercise)
○ Stress
○ Obesity
○ Alcohol
○ High Sodium Diet
○ Tobacco Use
○ Menopausal Medications
○ Low fiber diet

Types of Hypertension
Secondary Hypertension Causes
1. Chronic kidney disease CLINICAL MANIFESTATIONS
2. Disorders of the adrenal gland (pheochromocytoma or
Cushing syndrome) 1. Headache in occipital area (most common)
3. Pregnancy (preeclampsia) 2. Lightheadedness
4. Medications such as birth control pills, diet pills, some 3. Tinnitus – buzzing in the ears
cold medications, and migraine medications 4. Early morning vertigo
5. Narrowed artery that supplies blood to the kidney 5. Flushed face
(renal artery stenosis) 6. Epistaxis ( doesn’t mean the px w/ HPT may result to
6. Hyperparathyroidism this, depends on stage II or stage III or how high the
pressure is, and response of the body because of too
JNC7 Parameters
much pressure in the capillaries of the nasal area may
result to epistaxis)
7. Altered vision or fainting
8. Nausea and vomiting
9. Oliguria

MANAGEMENT

1. Lifestyle modifications
a. Diet and
exercise
(Lifestyle
modification)
b. Limit alcohol and
● Join national committee tobacco use
● Classification of BP c. Reduce stress
● JNC8 parameters, there are changes factor = teach patients how to reduce stress
(feedback, meditation, relaxation).
AMERICAN HEART ASSOCIATION (AHA) 2018 d. Sodium restricted diet
e. DASH DIET = dietary approach to stop HPT
(low sodium, high potassium and high calcium)
f. Health teach = use of ketchup (high sodium
BP Systolic BP Diastolic (mm
content), limit or stoppage of alcohol content
Classification (mm Hg) Hg)
and cigarettes
g. Control weight of the patient.
h. Engage regular exercise
Normal 120 - 129 80 - 84 2. Drug therapy
a. Thiazides – promotes excretion of Na, Cl, and
water
Elevated 130 - 139 85 -89 ■ Cause photosensitivity
■ Sunscreen
■ Hypokalemia
■ Eat banana
Stage 1 HTN 140 – 159 90 – 99
b. Aldosterone blocking diuretics (Aldactone) –
inhibits reabsorption of Na, Cl, while retaining K
in the distal loop of Henle
Stage 2 HTN 160 - 179 100 - 109 ■ Potassium sparing diuretics
c. Furosemide (Lasix) – inhibits reabsorption of
Na, Cl in the ascending loop of Henle.
Stage 3 >​180 > 110 ■ Predictable
d. Calcium channel blockers - anti diuretic effect
■ Reduce peripheral vascular resistance
■ Decrease blood pressure, relax vascular
Isolated >​ 140 < 90 smooth muscle, cause vasodilation
■ Nifedipine
 e. Adrenergic blocking agents - blocks
sympathetic activity at beta or alpha receptor
sites
f. Angiotensin converting enzyme (ACE) Inhibitor
- suppress the renin-angiotensin mechanism
(ex. capotet)
■ Reduces arterial pressure and venous
pressure
■ Lowers bp by decreasing vascular
resistance
■ Cause dry cough = elevations of
bradykinin levels
g. Anti-hypertensive drugs
■ Do not stop abruptly stop
antihypertensive drugs, may cause
rebound hypertension
■ Rebound HTN= difficult to control
■ Goal: Decrease peripheral resistance of
the blood volume, strength and rate of
contraction
■ Beta blockers: metoprolol
Diagnostic Test to Consider​:
● CHECK: BUN + creatinine, proteinuria (urinalysis)
= check kidneys
● Endocrine: Thyroid stimulating hormone
(Hyperthyroidism, Hyperparathyroidism)
● Cholesterol, FBS (Fasting blood sugar) =
associated with the development of hypertension
● Check electrolytes: K. Na, Ca
● Chest x-ray and ECG
● Heart​: cause HF, Left ventricular hypertrophy
because of increase workload that may result to
myocardial hypertrophy = may experience angina,
HF, ventricular hypertrophy, and eventually may
result to ischemia
● Brain: decrease flow of blood to the brain because
of peripheral vasoconstriction, reduce O2 supply,
transient ischemic attack or TIA (thrombosis,
aneurysm, hemorrhage = alter mobility, paralysis,
memory, speech).
● Eyes​: decrease blood flow, increase pressure in the
arterioles, causes retinal vascular sclerosis and
visceral disturbances (presence of spots), if it's not
controlled, result to blindness
● Peripheral Vascular​: blood pressure in the
arterioles, causes gangrene may result = pain upon
walking
● Renal​: Decrease in the perfusion of blood flow to the
kidney, cause secretion of the renin (convert
angiotensin I and angiotensin II) = increase bp and
may experience proteinuria and polyuria, activation
of your RAAS, sodium and water absorption will
occur, O2 supply is also reduced, kidney capabilities
are reduced (Azotemia may happen).
COMPLICATIONS OF HTN
1. Hypertension crisis – severely and abrupt/ sudden
elevated BP of > 180 mm Hg (systolic)
○ Hypertensive emergency – direct damage to
one or more organs are as a result of ↑ BP
(affect kidney, heart, eyes, brain function etc.).
Px is non compliance of medications and
asymptomatic (severe headaches/ dizziness)
○ Hypertension urgency - ↑ BP but there is no
evidence of impending or target organ damage
2. .Aortic aneurysm
○ 3.5 C’s -CAD, Cerebrovascular disease,
Chronic renal disease, CHF and Cardiac arrest
 COMPLICATION OF HYPERTENSION “THE 5 C’s”
● CORONARY ARTERY DISEASE – Can lead to
narrowing of blood vessels making them more likely
to block from blood clots.
○ Weakens the wall.
● CHRONIC RENAL FAILURE – Constant high blood
pressure can damage small blood vessels in the
kidneys, making it not to function properly.
● CONGESTIVE HEART FAILURE – Pumping blood
against the higher in the vessels causes the heart
muscles to thicken
● CARDIAC ARREST – high blood pressure can cause
CAD, damaged arteries cannot deliver enough
oxygen to other parts of the body eventually leading
to heart attack
● CEREBROVASCULAR ACCIDENT – Hypertension
leads to atherosclerosis and hardening of the large
arteries, This, in turn, can lead to blockage of small
blood vessels in the brain
VALVULAR DISORDERS
Inflammatory and Valvular Heart Disease
AORTIC ANEURYSM
Basic Classification
1. True aneurysm – 3 layers (intima, media,
2. False aneurysm or pseudoaneurysm – complete
● Result of localized weakness and stretching of the
arterial walls
● Unknown cause but of atherosclerosis (theory)
● Atherosclerotic plaque deposit beneath the intima
(inner layer of the arterial wall).
● Plaque formation = cause degenerative changes in
the media leading to loss of elasticity, weakening and
even dilation of the aorta
● Types:
○ Thoracic Aneurysm = Abnormal bulging of the
portion of the aorta, hardening of the arteries
common in male; 40 to 70 years of age.
○ Abdominal Aortic Aneurysm = “Triple A”,
prevalent in the elderly; enlarged area in the
aorta.
○ Peripheral = located commonly popliteal,
femoral, carotid, occurs in the legs behind the
knee along the joint.
○ Aortic aneurysm = occurs in the major artery
from the hearts because of the constant stress
in the wall and absence of penetrating vaso
vasorum in the medial layer.
adventitia) wall of artery forms the aneurysm
(asterosclerotic, syphilitic, congenital and
ventricular aneurysm) which follow transmural MI
and subdivided into:
○ Fusiform
○ Saccular
tear of all three arterial coats
○ results in bleeding that fills the
surrounding tissues producing a pulsatile
hematoma.
○ Collection of blood that leaks out
completely of the artery or vein but is
confined next to the vessel by the
surrounding tissues.
○ False aneurysm may be the result from
trauma, infection or after peripheral artery
bypass graft surgery at the site of the
graft-to-artery anastomosis.
 Categories of True Aneurysm Risk factors

1. Saccular – outpouching on one side of an artery. 1. Age of the patient (>65)

Looks like a berry 2. Elevated BP
when they occur 3. Hypertension history
on the arteries of 4. Smoking (Abdominal Aneurysm high risk)
the blood vessel 5. Hypercholesterolemia
and frequently 6. Atherosclerosis (susceptible to aortic aneurysm)
arise on the 7. Peripheral vascular disease
ascending and
Clinical Manifestations
descending
thoracic aorta 1. Chest pain – common (px with thoracic aneurysm
2. Fusiform - balloon on all sides (Circumferential because of the location, in the ascending aorta and
arterial dilation). All of the sides are affected, filled the aortic arch that can sometimes produce forceness
with necrotic debris and thrombus. Ca may because of laryngeal nerve, chest pain may radiate to
infiltrate the area, sac may dilate because of the neck to back and shoulder)
weakened media layer 2. Dysphagia – compression of the esophagus
3. Aortic Dissection - “​dissecting aneurysm​”, theory (common in thoracic aneurysm)
and degeneration of the 3. Pulsatile mass in the periumbilical area slightly to the
medial layer allows the left of the midline during PE (abdominal aortic
blood to separate the aneurysm) - do not do deep palpation
arterial intimal layer from 4. Bruits audible with a stethoscope
the adventitial layer , 5. Abdominal or back pain – result from compression of
cause is unknown but nearby anatomic structures. (Abdominal aortic
exposure to hypertension is susceptible to this, aneurysm)
causing the degeneration and necrosis. ○ Blue toe syndrome = mattling of the feet and
Pregnancy (increased blood volume and hormonal toe of the patient. (common with Triple A)
changes and hypertension that leads to
degeneration) , traumatic dissection (direct injury Diagnostic Studies
due to procedure or even in arteriography)
1. CXR
CLASSIFICATION OF ANEURYSM 2. ECG – to r/o evidence of MI
3. Echocardiography
4. Ultrasound
5. CT scan
6. Angiography – mapping of the aortic system by
contrast image

Management

1. Risk factor modification

a. Diet – sodium restriction
b. Use of Anti-hypertensive drugs
■ Does Not cure aneurysm but controls HTN
c. Monitor the size of aneurysm every 6 months
2. Hemodynamic monitoring
3. Pain management
a. Morphine Sulfate
Etiology of Aortic Aneurysm
4. Surgery - repairs the artery by closing/ application of
1. Unknown a synthetic patch drop over the arterial defect.
2. Atherosclerosis – plaques formation cause a. open - suturing
degenerative changes in the middle layer of the b. Endovascular aortic repair - newest alternative
arterial wall procedure (EVAR)
3. Genetic predisposition (hereditary)
4. Congenital
5. Mechanical, traumatic, infection (syphilis that may
affect arterial wall) – least common
 ENDOVASCULAR AORTIC REPAIR ○ Postoperative care

INFECTIVE
ENDOCARDITIS

● An infection of the inner

layer (endocardium) of the
heart. It may affects the
cardiac valves (normal
heart is resistant to
infection because bacteria
do not adhere easily
because of constant blood
flow)– mitral and tricuspid
valves
● Bacterial endocarditis
● Mouth, spread through
● Fixation of the ruptured abdominal aortic aneurysm
the bloodstream
(5.5 cm or 2 inches)
● Repair is done by resecting the vessel and sewing the Predisposing Factors
bypass graft in place
1. Aging – degenerative heart disease (invasive
● Become a mainstay of therapy for treating an
testing)
infrarenal abdominal aortic aneurysm and involves the
2. Intravenous drug abuse (Tricuspid valve; Cocaine
transluminal placement and attachment of a sutureless
aortic graft (Stent graft) prosthesis across an Abuse)
3. Structural heart or valves defect – increase
aneurysm
● Performed under a local or regional anesthesia number of platelet and fibrins in the endothelium
a. Etiology:​ presence of microorganism in
● May be performed if the patient's abdominal aorta or
the body; Streptococcus and
iliac arteries are not extremely tortuous, small, calcified
or filled with thrombi Staphylococcus, portal of entry (UTI,
catheter, etc.)
● Complication includes bleeding, hematoma, wound
infection, distal ischemia or embolization; dissection or
perforation of the aorta; graft thrombosis or infection,
graft migration, proximal or distal graft leaks, bowel
ischemia.
● MANAGEMENT:
○ Px must lie supine for 6 hrs
○ HOB may be elevated (45 degrees after 2 hrs)
○ Bedpan
○ Vital signs and doppler assessment (peripheral
pulses are performed every 15 mins)
○ Check access site (femoral artery)
○ Assess for bleeding, pulsation, swelling, pain,
and hematoma formation
○ Temperature should be monitored every 4 hours
○ Check for any signs of postimplantation
syndrome (begins usually 24 hours of stent graft
placement; sy&sx: spontaneous occurring fever,
leukocytosis, and occasionally transient
thrombocytopenia.
○ Notified of persistent coughing, sneezing,
vomiting, or systolic blood pressure >180mm Hg
○ IV infusion may be continued until the px can
drink normally
○ 6 hours after the procedure, the px may roll from
side to side and may be able to ambulate with
assistance to the bathroom
 4. Echocardiography - evaluate for diagnosis
5. Chest X-Ray – detect the presence of an enlarged
heart
6. ECG – shows 1​st​ or 2​nd​-Degree block
7. CRP - detect presence of inflammation and infection

Management

1. Antibiotic includes prophylaxis (Specific cardiac

condition)
a. Ceftriaxone (Rocephin) – streptococcus
b. Vancomycin (Vanocin) – staphylococcus
2. Antipyretic for fever
3. Rest (bed rest)
4. Anti-embolic stocking – prevents thrombus formation
(Applied early in the morning)
5. Restrict normal activity 4 – 6 weeks
6. Surgery – repair or replacement for severe valvular
damage (replacement is needed)

MAJOR TYPES OF VALVULAR HEART DISEASE

Clinical Manifestations 1. Stenosis – heart valve leaflets fused together, opening

narrow, stiff, unable to open or close properly
1. Fever and chills – 90% a. Scar of the valves from endocarditis or infarction
2. Fatigue and weakness b. Constriction of the valve
(malaise, anorexia) c. Cannot fully open or close (Funnel like/ rigid)
3. splinter hemorrhage – d. Calcium deposits - impedes the forward flow,
occur in nail bed of the blood decreasing cardiac output (lesser blood
vascular (block and lack of ejection), impaired ventricular feeling
longitudinal) 2. Regurgitation – improper or incomplete or incompetent
4. Petechiae – fragmentation closure of heart valves, resulting in back flow of blood
and microembolization of a. Common cause: Deformity of valve cusps caused
vegetative lesions (also by vegetative lesions caused by the bacterial
common in conjunctiva, endocarditis
buccal mucosa) b. Do not close completely = Too loose
5. Osler’s nodes – painful, c. Cause: Scarring/ tearing of MI or cardiac dilation
tender, red pea-size d. Contraction = backflow where it just left
lesion found in the e. Heart enlarges = streched valve
fingertips or toes f. Excess blood volume behind
6. Janeway’s lesion – flat, painless, small red spots
found on the palms and soles
7. Roth’s spot – hemorrhagic retinal lesion through MITRAL STENOSIS
examinations
8. Murmur - noted 80% of the cases ( cardiac vault is ● Thickening and
shortening
affected)
9. Splenomegaly - embolization to the spleen result in between the
the sharp LUQ pain commissures
10. Embolization to the brain (40%) - causes neurologic (junctional
problem (hemiplegia, ataxia, aphasia), change in the areas) of the
leaflets that
level of consciousness
obstruct the
Diagnostic Studies flow of blood
from the left
1. Blood culture – primary tool
atrium into the left ventricle.
2. Leukocytosis around 11,000 unit/ liter
● Cause: Rheumatic endocarditis
3. Erythrocyte sedimentation rate (ESR) - > 30 mm/hour
● Narrowing of the cardiac valve
because the presence of infection
● Reduced CO
● affectleft atrium, because of the pressure and dilation,
may cause atrial hypertrophy
● Pulmorary hypertension
● Problem: inflow of the left ventricle
● Group A hemolytic Streptococcus
● Look like a funnel

Clinical Manifestations

1. Dyspnea sometimes accompanied by hemoptysis

(reduced lung compliance because increase pressure
caused transudation of lung fluid in interstitium)
2. Palpitations – from atrial fibrillation and fatigue (prone
to form blood clots)
3. Chest pain - ↓ CO
4. Seizures (from emboli because of stagnation of blood
in the left atrium)
5. Hepatomegaly
Nicole: Slide 111 onwards.
6. Peripheral edema (Back up pressures not only to the
LA but also affect RV)
MANAGEMENT
7. Crackles - because problem of gas exchange,
pulmonary congestion and hypertension 1. Sodium restriction
8. Cyanosis 2. Oral diuretics – Relieve pulmonary congestion
3. Digitalis and anti-arrhythmic drugs – AF
4. Antibiotic – AHA guidelines do not recommend
PATHOPHYSIOLOGY infective endocarditis prophylaxis for most
patients with rheumatic heart disease. Some
doctors prescribe prophylactic antibiotics before
dental procedures. However, the maintenance of
optimal oral health care remains an important
component of an overall healthcare program
5. Anticoagulant – Prevent and treat emboli
6. Beta blockers – Control long-term use of oral
beta blockers, ↓ HR, ↑ tolerance to exercise
7. Percutaneous Transluminal Balloon Valvuloplasty
– Open narrowed cardiac valves, contraindicated
in px with left atrial thrombus or left ventricular
thrombus, beneficial to px with no complications
or additional conditions
8. Surgery – Mitral Commissurotomy – Surgical
incision of a commissure, relieve constriction
9. Avoid strenuous exercise or activity – Prevent ↑
HR
Digitalis – Slows HR → prevents atrial fibrillation, 5. Digitalis
administers IV 6. ACE inhibitors

MITRAL REGURGITATION VALVULOPLASTY PROCEDURES

Backflow of blood from the left ventricle into the left atrium Annuloplasty​ – Repair of the valve annulus
during systole

Etiology:

1. Inflammatory and infective – Rheumatic heart

disease and endocarditis
2. Degenerative changes or calcification of the
mitral annulus – MVP
3. Process that dilates the papillary muscles or the
chordae tendineae – Left ventricular hypertrophy,
MI
4. Congenital defects - Systemic lupus
erythematosus, cardiomyopathy

Chordoplasty – Repair of the chordae tendineae,

involves the mitral valve

MITRAL VALVE PROLAPSE – MVP

● One or both mitral valve cusps buckle back into

the left atrium during ventricular systole –
Displacement of the thickened mitral valve leaflet
● Structural abnormalities of the mitral valve reflex

Etiology:

1. Unknown
2. Familial incidence – First degree relatives,
CLINICAL MANIFESTATIONS echocardiogram
3. Excess collagen tissue in the valve leaflets
1. Systolic murmur
2. Cool, clammy extremities
4. Elongated chordae tendineae – Causes the
buckle back of leaflets
3. Dyspnea
4. Palpitations – First symptom 5. Infective endocarditis
5. Fatigue
6. Cough from pulmonary congestion
7. Shortness of breath on exertion

DIAGNOSTIC STUDIES

1. ECG
2. 2-D Echo

MANAGEMENT

1. Restrict physical activities

2. Reducing sodium intake
3. Diuretics
4. Nitrates
 Etiology:

1. Congenital leaflet malformation

2. Inflammatory changes rheumatic endocarditis –
Stiffening of the valve
3. Cusp calcification

CLINICAL MANIFESTATIONS

1. Murmur – Very common, best heard at the apex,

accentuated by standing and Valsalva maneuver
which ↓ venous return
2. Palpitations
3. Light-headedness
4. Dizziness
5. Chest pain – Px does not respond to nitrates,
responds to beta blockers or calcium channel CLINICAL MANIFESTATIONS
blockers
6. Activity intolerance Similar to mitral stenosis, difference is the affected valve
7. Syncope
1. Angina pectoris
8. Dyspnea
2. Syncope
9. Surgery – Valve replacement – Depends on the
3. Heart failure
condition
4. Pulmonary edema
10. Health teaching
5. Narrow pulse pressure
● Practice oral hygiene
● Avoid sharp objects in the oral cavity 6. Dyspnea on exertion – Encourage bedrest, give
● Avoid OTC medications that contain antibiotics
alcohol or caffeine
Digitalis and diuretics – Not effective in mitral stenosis, for
Aspirin – Prevent blood clots px with left ventricular failure

Beta blockers – Relieve palpitations and chest pain Beta blocker – Induce left ventricular failure

AORTIC STENOSIS AORTIC REGURGITATION

Narrowing of the orifice that obstructs the flow of blood ● Flow of blood back into the left ventricle from the
from the left ventricle and the aorta during systole aorta during diastole
 ● There is a leak in the aortic valve 6. Austin-flint murmur – A low frequency diastolic
● 25% regurgitation ↓ diastolic blood pressure, ↑ murmur at the cardiac apex
pulse pressure, assessment reveals bulging
radial pulse MANAGEMENT

Etiology: 1. Diet – Low sodium to avoid volume overload for

asymptomatic px
1. Inflammatory lesions that deform the leaflets of 2. Activity – Avoid physical exertions and
the aortic valve competitive sports
2. Trauma – Congenital anomalies, rheumatic 3. Medications – Calcium channel blockers, ACE
endocarditis inhibitors
3. Congenital abnormality 4. Prosthetic valve replacement
4. Rheumatic conditions ● For childbearing age women to avoid
potential complications from long-term
anticoagulants
● Perform before left ventricular failure
occurs
● ​Lasts for 7-15 years

Different types of mechanical valve:

● Tissue valve – Autograft – Px pulmonic

valve and portion of pulmonary artery as
aortic valve
● Bioprosthesis – 4 seal
● Pig valve
● Equine – Horse

5. Homograft – Anagram
● Human valve
● From tissue donations for aortic and
pulmonic valve replacement
● Lasts for 10-15 years

Porcine Heterograft Valve​ –Carpenter Edwards

MECHANICAL VALVE REPLACEMENT

CLINICAL MANIFESTATIONS
Bileaflet​ – St. Jude
1. Weakness
2. Severe dyspnea
3. Hypotension
4. Palpitations – Can cause dysrhythmia
5. Corrigan’s pulse – Forceful and sudden collapse
of pulse
● Very common in px with aortic ● More durable than tissue prosthetic valve
regurgitation
● For younger patients with endocarditis
● Sometimes called as water hammer
● Can cause thromboembolism
pulse
 ● Requires long-term use of anticoagulant Palpation

Caged Ball Valve​ – Starr Edwards ❖ Temperature – Bilateral

❖ Pulses – Note the rhythm, amplitude and
symmetry of pulses
➢ Bilateral
➢ Except in carotid pulse –
Stimulates carotid sinus
❖ Allen’s Test – Assess patency of radial
and ulnar arteries
➢ Before ABG
❖ Homan’s sign – Compress the
PERIPHERAL VASCULAR DISEASE gastrocnemius muscle of the calf for
tenderness

Auscultation ​– Assess for bruits

DIAGNOSTIC EVALUATION

● Doppler Ultrasonography – Detects blood flow

● Ankle Brachial Index – Compares blood pressure
in the upper and lower limbs
● Exercise Test
● Duplex Ultrasonography – Px with deep vein
thrombosis

PERIPHERAL ARTERIAL OCCLUSIVE DISORDERS

ASSESSMENT ● Affects men and involvement of the upper

extremities
● Health History – Intermittent claudication
● Hallmark symptom is intermittent claudication

Intermittent claudication – Symptom that describes

muscle pain on mild exertion in the calf muscle, which
occurs during exercise, and is relieved by short rest

● Physical examination

Inspection

❖ Capillary refill – Less than 3 seconds

➢ < 3 seconds – Diminish blood
flow
❖ ​Edema – Press skin for 5 seconds
➢ Pitting edema​ – + Indentation
➢ Grading scale ● Distal occlusion – Common in elderly and px with
❖ Elevation pallor – Reddish-blue diabetes
discoloration of the extremities, occurs ● Extremities are cold and pale when in an
within 20 seconds-2 minutes after elevated position
extremities are placed in elevated
position Peripheral Vascular Disease – Commonly affects elderly
➢ Rubor – Redness, means there and px with diabetes, there is disturbance in flow to
is damage to the arteries peripheral vessels, leads to ischemia and excessive
❖ Clubbing fingers – Due to prolong lack of accumulation of fluid which causes venous and lymphatic
oxygen stasis
❖ Trendelenburg’s Test – Indicates
weakness in the hip
Cellular anaerobic metabolism – Build-up of lactic acid
and pyruvic acid waste products

● Clinical manifestations – Muscle atrophy, bruit,

diminish or absent peripheral pulse
● Lack of treatment and intervention leads to
changes in skin and nails, gangrene, and
ulceration
● Palpation – Bilateral

MANAGEMENT

● Exercise
● Do not apply heat in px with arterial insufficiency
● Medications – Pentoxifylline (Trental), cilostazol
● Surgery – Endarterectomy, bypass graft

Pentoxifylline – ↑ erythrocyte flexibility, ↓ fibrinogen, has

antiplatelet effect

Cilostazol – Vasodilator, inhibit platelet aggregation,

contraindicated in px with congestive heart failure

Endarterectomy – Surgical incision in the artery to

remove atheromatous obstruction
Distal to proximal

Bypass Graft – Reroute the blood flow around the

BUERGER’S DISEASE
stenosis
● Tobacco smoke stains on male patient's fingers
THROMBOANGITIS OBLITERANS – Buerger’s
suggest diagnosis of thromboangiitis obliterans –
Disease
Buerger’s Disease
● A condition in which the small arteries and
● Patient presented with small, painful ulcers on
tips of thumb and ring finger
arterioles constrict in response to various stimuli
● Affects the medium-sized arteries, veins and
nerves of the upper and lower extremities – Only
affects hands and feet
● Large arteries – Not involved, very rare
● Cause is unknown – Theories related to smoking,
familial tendency, autoimmune
● More common in younger men ages 25-40
 ➢ Postoperative – ↑ BP without
bleeding
❖ A
​ rterial bypass graft

STEPS OF BUERGER ALLEN EXERCISE

1. Elevate feet on padded chair or board for ½ to 3

minutes
2. Sit in a relaxed position while each food is flexed
and extended then pronated and supinated for 3
minutes. The feet should become entirely pink. If
the feet are blue or painful, elevate them and
relax as necessary
3. Lie quietly for 5 minutes, keeping legs warm with
CLINICAL MANIFESTATIONS
blanket
4. Pharmacologic therapy
1. Redness along the lines of the veins and arteries
2. Spasm of the digital arteries that result to pallor
3. Diminished sensation
4. Paresthesia – Sensation of tickling, tingling,
burning or numbness
5. Skin is shiny and thin
6. Nails are thickened and malformed

Intermittent claudication – Calf pain during activities

❖ P​allor
❖ ​P​ulses decreased

❖ ​P​erishing cold
❖ ​P​ain

❖ ​P​aresthesia

❖ ​P​aralysis

No diagnostic studies

MANAGEMENT

1. Smoking cessation
2. Keep extremities warm
3. Managing stress
4. Keeping affected extremities in a dependent
position
5. Regular exercise
6. Wound care
7. Buerger’s Allen exercise – Promote circulation
and establish collateral circulation
8. Calcium channel blockers to ↓ the blood viscosity RAYNAUD’S PHENOMENON
and ↑ RBC flexibility to improve peripheral blood
flow to relief symptoms ● A spasm of arteries causing blanching of ​fingers
9. Surgery – Depends on the condition and toes​ and affects young women ages 15-40
❖ A
​ mputation – If px has gangrene ● Vasospasm induce color changes – Fingers,
❖ Sympathectomy – If there is interruption toes, ears, nose
of SNS input to the affected vessels ● Also known as white-red disease
● Unknown cause
 ❖ Emerge hands in warm water to reduce
spasms
6. Measures to avoid injury to the hands
7. Vasodilators
❖ Calcium channel blockers such as
nifedipine – Relax smooth muscles,
reduce vasospastic attack
❖ Alpha blockers such as minipress –
Counter norepinephrine
8. Surgery – Sympathectomy – For advance cases

THEORIES OF RAYNAUD’S PHENOMENON

A. Vasospasm occurs secondary to SNS stimulation

B. Abnormalities in the endothelium -
Endothelium-derived vasoactive substance
C. Other contributing factors: Occupation related
trauma and pressure on the fingertips
D. Exposing to heavy metals

PRECIPITATING FACTORS

1. Exposure to cold
2. Emotional upset
3. Caffeine intake
4. Tobacco use

Buerger’s Disease – Strong relationship to smoking

Raynaud’s Phenomenon – Response to cold and stress

CLINICAL MANIFESTATIONS

1. Sensory changes – Numbness, stiffness,

decreased sensation and aching pain
2. Thickened fingertips and nails become brittle
3. Pallor
4. Skin becomes bluish
5. Hyperemia
6. Ulcerations and gangrene – Serious
complications

Hyperemia​ – Is an excess of blood in blood vessels

MANAGEMENT

1. Loose, warm clothing

2. Avoid extreme temperature
3. Smoking cessation
4. Avoid caffeine and drugs with vasoconstrictive
effects
5. Stress reduction management