Cardiovascular Assessment

and Monitoring
 RELATED ANATOMY AND PHYSIOLOGY
• The cardiovascular system is essentially a transport system
for distributing metabolic requirements to, and collecting
byproducts from, cells throughout the body.
• The heart pumps blood continuously through two separate
circulatory systems: both to the lungs, and all other parts of
the body.
• Structures on the right side of the heart pump blood through
the lungs (the pulmonary circulation) to be oxygenated.
• The left side of the heart pumps oxygenated blood
throughout the remainder of the body (the systemic
circulation).
CARDIAC MACROSTRUCTURE
• The heart is cone-shaped and lies
diagonally in the mediastinum
towards the left side of the chest.
• The adult heart is about the size of
that individual’s fist, weighs around
300 g, and is composed of
chambers and valves that form the
two separate pumps.
• The upper chambers, the atria,
collect blood and act as a primer to
the main pumping chambers, the
ventricles.
• The atria are low-pressure chambers,
they have relatively thin walls and
are relatively compliant.
• The ventricle propels blood against
either pulmonary or systemic
pressure, they are much thicker and
more muscular walls than the atria.
• As pressure is higher in the systemic
circulation, the left ventricle is much
thicker than the right ventricle.
• Dense fibrous connective tissue rings
provide a firm anchorage for
attachments of atrial and ventricular
muscle and valvular tissue.
• One-way blood flow in the system is facilitated by valves.
Valves between the atria and ventricles are composed of
cusps or leaflets sitting in a ring of fibrous tissue and
collagen.
• The cusps are anchored to the papillary muscles by
chordae tendinae so that the cusps are pulled together
and downwards at the onset of ventricular contraction.
• The atrioventricular valves are termed the tricuspid valve
in the right side of the heart and the mitral or bicuspid
valve in the left side of the heart.
• Semilunar valves prevent backflow from the pulmonary
artery (pulmonic valve) and aorta (aortic valve) into the
right and left ventricles.
The heart wall has three distinct layers

• The outer protective known

as the pericardium
• A medial muscular layer or
myocardium
• Inner layer or endocardium
that lines the heart
• The pericardium is a double-walled, firm fibrous sac that
encloses the heart. The two layers of the pericardium are
separated by a fluid-filled cavity, enabling the layers to
slide over each other smoothly as the heart beats.
• The pericardium provides physical protection for the
heart against mechanical force and forms a barrier to
infection and inflammation from the lungs and pleural
space.
• Branches of the vagus nerve, the phrenic nerves and the
sympathetic trunk enervate the pericardium.
• The myocardium forms the bulk of the heart and is composed
primarily of myocytes.

• Myocytes are the contractile cells, and autorhythmic cells, which

create a conduction pathway for electrical impulses.
• Myocytes are cylindrical in shape and able to branch to
interconnect with each other.
• The junctions between myocytes are termed intercalated discs and
contain desmosomes and gap junctions.
• Desmosomes act as anchors to prevent the myocytes from
separating during contraction. Gap junctions contain connexons,
which allow ions to move from one myocyte to the next.
• The movement of ions from cell to cell ensures that the whole
myocardium acts as one unit, termed a functional syncytium.
• The endocardium is composed primarily of
squamous epithelium, which forms a
continuous sheet with the endothelium that
lines all arteries, veins and capillaries.
• The vascular endothelium is the source of
many chemical mediators, including nitric
oxide and the endothelin involved in vessel
regulation.
 Coronary Perfusion
• The heart is perfused by the right and left coronary arteries
that arise from openings in the aorta called the coronary ostia
• The right coronary artery (RCA) branches supply the
atrioventricular node, right atrium and right ventricle, and the
posterior descending branch supplies the lower aspect of the
left ventricle.
• The left coronary artery divides into the left anterior
descending artery (LAD) and the circumflex artery (CX) shortly
after its origin.
• The LAD supplies the interventricular septum and anterior
surface of the left ventricle.
• The CX supplies the lateral and posterior aspects of the left
ventricle.
• The cardiac veins collect venous blood from
the heart.
• Cardiac venous flow is collected into the great
coronary vein and coronary sinus and
ultimately flows into the right atrium.
• Lymph drainage of the heart follows the
conduction tissue and flows into nodes and
into the superior vena cava.
 PHYSIOLOGICAL PRINCIPLES
Mechanical Events of Contraction
• Energy is produced in the myocytes by a large number of mitochondria
contained within the cell.
• The mitochondria produce adenosine triphosphate (ATP), a molecule
that is able to store and release chemical energy.
• Sarcoplasmic reticulum, are used to store calcium ions.
• The myocyte cell membrane (sarcolemma) extends down into the cell to
form a set of transverse tubules (T tubules), which rapidly transmit
external electrical stimuli into the cell.
• Cross-striated muscle fibrils, which contain contractile units, fill up the
myocyte. These fibrils are termed sarcomeres.
• The sarcomere contains two types of protein myofilaments, one thick
(myosin) and one thin (actin, tropomyosin and troponin).
 Electrical events of Depolarisation, Resting
Potential and Action Potential
• Electrical impulses termed action potentials are
transmitted along this pathway and trigger
contraction in myocytes.
• Action potentials represent the inward and outward
flow of negative and positive charged ions across
the cell membrane.
• Cell membrane pumps create concentration
gradients across the cell membrane during diastole
to create a resting electrical potential of −80 mV.
• There are five key phases to the cardiac action
potential:
• 0. depolarisation
• 1. early rapid repolarisation
• 2. plateau phase
• 3. final rapid repolarisation
• 4. resting membrane phase.
• The action potential is created by ion exchange
triggered by an intracellular and extracellular
fluid trans-membrane imbalance.
• There are three ions involved: sodium,
potassium and calcium.
• Normally, extracellular fluid contains
approximately 140 mmol/L sodium and 4
mmol/L potassium. In intracellular fluid these
concentrations are reversed.
Physiological events during a normal action potential:
• At rest cell membranes are more permeable to potassium and consequently.
• potassium moves slowly and passively from intracellular to extracellular fluid;
• rapid ion movement caused by sodium flowing into the cell alters the charge
from −90 mV to +30 mV;
• there follows a brief influx of calcium via the fast channel and then more via
the slower channel to create a plateau, the time of which determines stroke
volume due to its influence on the contractile strength of muscle fibres;
• the third phase occurs when the potassium channel opens, allowing
potassium to leave the cell, to restore the negative charge, causing rapid
repolarisation.
• the final resting phase occurs when slow potassium leakage allows the cell to
increase its negative charge to ensure that it is more negative than
surrounding fluid, before the next depolarisation occurs and the cycle repeats
• Depolarization is initiated in the sino-atrial (SA) node and
spreads rapidly through the atria, then converges on the
atrio-ventricular (AV) node; atrial depolarization normally
takes 0.1 second.
• There is a short delay at the AV node (0.1 sec) before
excitation spreads to the ventricles. This delay is shortened
by sympathetic activity and lengthened by vagal stimulation.
• Ventricular depolarization takes 0.08–0.1 sec, and the last
parts of the heart to be depolarized are the posteriobasal
portion of the left ventricle, the pulmonary conus and the
upper septum.
Cardiac Macrostructure and Conduction

• The conduction
pathway is composed
of the sinoatrial (SA)
node, the
atrioventricular(AV)
node, the bundle of
His, right and left
bundle branches and
Purkinje fibres.
• Pacemaker cells of the sinus and atrioventricular nodes differ, in
that they are more permeable to potassium, so that potassium
easily ‘leaks’ back out of the cells triggering influx of sodium and
calcium back into cells.
• This permits the spontaneous automaticity of pacemaker cells.
• At the myocyte, the action potential is transmitted to the
myofibrils by calcium from the interstitial fluid via channels. During
repolarization (after contraction), the calcium ions are pumped out
of the cell into the interstitial space and into the sarcoplasmic
reticulum and stored.
• Troponin releases its bound calcium, enabling the tropomyosin
complex to block the active sites on actin, and the muscle relaxes.
 CARDIAC OUTPUT
• Cardiac output is the product of heart rate and stroke volume.
• Alteration in either of these will increase or decrease cardiac
output, as will alteration in preload, afterload or contractility.
• In the healthy individual, the most immediate change in
cardiac output is seen when heart rate rises.
• In the critically ill, the ability to raise the heart rate in response
to changing circumstances is limited, and a rising heart rate
may have negative effects on homeostasis, due to decreased
diastolic filling and increased myocardial oxygen demand.
• Preload is the load imposed by the initial fibre length
of the cardiac muscle before contraction (i.e. at the
end of diastole).
• The primary determinant of preload is the amount of
blood filling the ventricle during diastole, and it is
important in determining stroke volume.
• Preload influences the contractility of the ventricles
(the strength of contraction) because of the
relationship between myocardial fibre length and
stretch.
• Preload reduces as a result of large-volume loss
(e.g.mhaemorrhage), venous dilation (e.g. due to
hyperthermia or drugs), tachycardias (e.g. rapid atrial
fibrillation or supraventricular tachycardias), raised
intrathoracic pressures (a complication of IPPV), and raised
intracardiac pressures (e.g. cardiac tamponade).

• Drugs such as vasodilators can cause a decrease in venous

tone and a resulting decrease in preload.

• Preload increases with fluid overload, hypothermia or other

causes of venous constriction, and ventricular failure. Body
position will also affect preload, through its effect on venous
return.
• The volume of blood filling the ventricles is
also affected by atrial contraction: a reduction
in atrial contraction ability, as can occur during
atrial fibrillation, will result in a reduction in
ventricular volume, and a corresponding fall in
stroke volume and cardiac output.
• Afterload is the load imposed on the muscle during
contraction, and translates to systolic myocardial wall tension.
• It is measured during systole, and is inversely related to stroke
volume and therefore cardiac output, but it is not
synonymous with systemic vascular resistance (SVR), as this is
just one factor determining left ventricular afterload.

• Factors that increase afterload include:

– increased ventricular radius
– raised intracavity pressure
– increased aortic impedance
– negative intrathoracic pressure
– increased SVR.
• As afterload rises, the speed of muscle fibre
shortening and external work performed falls, which
can cause a decrease in cardiac output in critically ill
patients.
• Ventricular afterload can be altered to clinically
affect cardiac performance. Reducing afterload will
increase the stroke volume and cardiac output,
while also reducing myocardial oxygen demand.
However, reductions in afterload are associated with
lower blood pressure..
• Contractility is the force of ventricular ejection, or the inherent ability
of the ventricle to perform external work, independent of afterload or
preload.
• It is increased by catecholamines, calcium, relief of ischemia and
digoxin.
• It is decreased by hypoxia, ischemia, and certain drugs such as
thiopentone, β-adrenergic blockers, calcium channel blockers or
sedatives.
• With increased in contractility caused increased stroke volume and
cardiac output.
• Increasing contractility will increase myocardial oxygen demand, which
could have a detrimental effect on patients with limited perfusion.
• Stroke volume is the amount of blood ejected
from each ventricle with each heartbeat. For
an adult, the volume is normally 50–100
mL/beat, and equal amounts are ejected from
the right and left ventricle
The phases of the cardiac cycle are characterized by pressure
changes within each of the heart chambers, resulting in blood
flow from areas of high pressure to areas of lower pressure.

• During late ventricular diastole (rest), pressures are

lowest in the heart and blood returns passively to fill the
atria. This flow also moves into the ventricle through the
open AV valves, producing 70–80% of ventricular filling.
• The pulmonic and aortic valves are closed, preventing
backflow from the pulmonary and systemic systems into
the ventricles.
• Depolarisation of the atria then occurs, sometimes
referred to as atrial kick, stimulating atrial contraction and
completing the remaining 20–30% of ventricular filling.
• During ventricular systole (contraction), the atria relax while
the ventricles depolarise, resulting in ventricular contraction.
• Pressure rises in the ventricles, resulting in the AV valves
closing. When this occurs, all four cardiac valves are closed,
blood volume is constant and contraction occurs
(isovolumetric contraction).
• When the pressure in the ventricles exceeds the pressure in
the major vessels the semilunar valves open.
• This occurs when pressure in the left ventricle reaches
approximately 80 mmHg and in the right ventricle
approximately 27–30 mmHg.
• During the peak ejection phase, pressure in the left ventricle
and aorta reaches approximately 120 mmHg and in the right
ventricle and pulmonary artery approximately 25–28 mmHg.
• During early ventricular diastole, the ventricles repolarize and
ventricular relaxation occurs. The pressure in the ventricles
falls until the pressures in the aorta and pulmonary artery are
higher and blood pushes back against the semilunar valves.
Shutting of these valves prevents backflow into the ventricles,
and pressure in the ventricles declines further.

• During ventricular contraction, the atria have been filling

passively, so the pressure in the atria rises to higher than that
in the ventricles and the AV valves open, allowing blood flow
to the ventricles. Any rise in heart rate will shorten the resting
period, which may impair filling time and coronary artery flow
as these arteries fill during diastole.
The activities of the heart are regulated by two
responsive systems: intrinsic regulation of
contraction, and the autonomic nervous system.

• Intrinsic regulation of contraction responds to

the rate of blood flow into the chambers.
• Ventricular contraction is also intrinsically
influenced by the size of the ventricle and the
thickness of the ventricle wall.
• Autonomic nervous system control and regulation of heart rate.
• Inputs from the autonomic nervous system regulate heart rate changes in
accordance with body needs by stimulating or depressing these
pacemaker cells.
• Cardiac innervation includes sympathetic fibres from branches of T1–T5,
and parasympathetic input via the vagus nerve.
• The heart rate at any moment is a product of the respective inputs of
sympathetic stimuli (which accelerate) and parasympathetic stimuli (which
depress) on heart rate.
• Rises in heart rate can thus be achieved by an increase in sympathetic
tone or by a reduction in parasympathetic tone (vagal inhibition).
• Slowing of the heart rate can be achieved by decreasing sympathetic or
increasing parasympathetic activity.

• Hormonal, biochemical and pharmacological inputs also exert heart rate

influences by their effect on autonomic neural receptors or directly on
pacemaker cells.
 THE VASCULAR SYSTEM
• All vessels in the circulatory system are lined by endothelium, including the
heart.
• The endothelium creates a smooth surface, which reduces friction and also
secretes substances that promote contraction and relaxation of the vascular
smooth muscle.
• Arteries function to transport blood under high pressure and are characterized
by strong elastic walls that allow stretch during systole and high flow. During
diastole, the artery walls recoil so that an adequate perfusion pressure is
maintained.
• Arterioles are the final small branches of the arterial system prior to capillaries,
and have strong muscular walls that can contract (vasoconstrict) to the point of
closure and relax (vasodilate) to change the artery lumen rapidly in response to
tissue needs. The lumen created by the arterioles is the most important source
of resistance to blood flow in the systemic circulation (just under 50%).
• Capillaries function to allow exchange of fluid,
nutrients, electrolytes, hormones and other
substances through highly permeable walls
between the blood plasma and interstitial
fluid.
• Veins collect and transport blood back to the
heart at low pressure and serve as a reservoir
for blood.
 Blood Pressure
• Blood flow is maintained by pulsatile ejection of blood
from the heart and pressure differences between the
blood vessels.
• Blood pressure is measured from the arteries in the
general circulation at the maximum value during systole
and the minimum value occurring during diastole.
• There are three main regulatory mechanisms of blood
pressure control: (a) short-term autonomic control; (b)
medium-term hormonal control; and (c) long-term
renal system control.
 Autonomic control
• The cardiovascular control centre connects with
the hypothalamus to control temperature, the
cerebral cortex and the autonomic system to
control cardiac activity and peripheral vascular
tone.
• Information about blood pressure and resistance is
sensed by neural receptors (baroreceptors) in the
aortic arch and the carotid sinuses, which detect
changes in blood supply to the body and the brain.
 Hormonal control
• Changes in blood pressure are also detected by the adrenal
medulla, which secretes catecholamines as cardiac output
declines.
• The two main catecholamines, norepinephrine (noradrenaline)
and epinephrine (adrenaline), mimic the action of the
sympathetic system.
• Noradrenaline directly stimulates the alpha-adrenergic receptors
of the autonomic system, causing vasoconstriction and raising
blood pressure, while adrenaline has a wider range of effects,
including stimulating β1-adrenergic receptors, resulting in
increased cardiac contractility and heart rate and thereby also
raising blood pressure.
 Renal control
• Renal control of blood pressure in the long-
term occurs via control of blood volume.
Generally, as blood pressure or volume rises,
the kidneys produce more urine; conversely,
as blood pressure or volume falls, the kidneys
produce less urine.
 ASSESSMENT
• It is essential that the critical care nurse conducts a
comprehensive cardiac assessment on a critically ill
patient.
• The nursing assessment aims to both define patient
cardiovascular status as well as to inform
implementation of an appropriate clinical
management plan.
• A thorough cardiac assessment requires the critical
care nurse to be competent in a wide range of
interpersonal, observational, and technical skills.
• A useful guide in taking a specific cardiac history is to use
directed questions to seek information regarding symptom
onset, course, duration, location, precipitating and alleviating
factors.
• Some common cardiovascular disease related symptoms to be
observant for include: chest discomfort or pain, palpitations,
syncope, generalized fatigue, dyspnea, cough, weight gain or
dependent edema.
• Additionally, a health history should be inclusive of known
cardiovascular risk factors, such as hyperlipidemia or
hypertension, and any medications the patient may be taking
including over the counter medications.
• The nurse should take note of the patient’s
general appearance noting whether the patient
is restless, able to lie flat, in pain or distress, is
pale or has decreased level of consciousness.
• Patients with compromised cardiac output will
likely have decreased cerebral perfusion and
may have mental confusion, memory loss or
slowed verbal responses.
• Assessment of any pain should be noted.
Specific physical assessment in relation to
cardiovascular function should be inclusive of:
• vital signs
• respiratory assessment for signs of pulmonary edema (shortness of breath
or basal crepitations)
• assessment of neck vein distension for signs of right sided venous
congestion
• assessment for signs of peripheral edema
• capillary refill time with >3 sec return indicative of sluggish capillary return
• 12-lead ECG for signs of ischemia or cardiac pathology
• appearance and temperature of the skin for signs of peripheral constriction
or dehydration
• core body temperature measurement
• urine output with <0.5 mL/kg/hour a potential indicator of decreased renal
perfusion
 ASSESSMENT OF PULSE
• The radial pulse is distant from the central arteries, it is useful for
gathering information on rate, rhythm and strength.
• Heart rate below 60 beats per minute is defined as ‘bradycardia’ (‘brady’ is
Greek for slow, and ‘kardia’ means heart). A heart rate greater than 100
beats per minute is called ‘tachycardia’ (’tachy’ in Greek meaning swift).
• An important aspect of pulse assessment involves assessment for
regularity.
• Detection of an irregular pulse should trigger further investigation and
prompt ECG assessment for atrial fibrillation, a condition in which atrial
contraction becomes lost due to chaotic electrical activity with variable
ventricular response.
• Assessment of pulse, especially if palpated in the carotid or femoral artery,
can reveal a bounding pulse, that may be indicative of hyper dynamic state
or aortic regurgitation. An alternating strong and weak pulse, known as
pulsus alternans, may be observed in advanced heart failure.
 AUSCULTATION OF HEART SOUNDS

• Auscultation of the heart involves listening to heart

sounds over the pericardial area using a stethoscope.
• When auscultating heart sounds, normally two
sounds are easily audible known as the first (S1) and
second (S2) sounds.
• A useful technique when listening to heart sounds is
to feel the carotid pulse at the same time as
auscultation which will help identify the heart sound
that corresponds with ventricular systole..
• The first heart sound (S1) occurs at the beginning of ventricular systole,
following closure of the intra-cardiac valves (mitral and tricuspid valves). This
heart sound is best heard with the diaphragm of the stethoscope and loudest
directly over the corresponding valves (4th intercostal space [ICS] left of
sternum for tricuspid and 5th ICS left of the mid clavicular line for mitral
valve).

• The second heart sound (S2) occurs at the beginning of diastole, following
closure of the aortic and pulmonary valves and can be best heard over these
valves (2nd ICS to the right and left of the sternum respectively). It is
important to remember that both S1 and S2 result from events occurring in
both left and right sides of the heart.

• While normally left sided heart sounds are loudest and occur slightly before
right sided events, careful listening during inspiration and expiration may
result in left and right events being heard separately. This is known as
physiological splitting of heart sounds, a normal physiological event.
• In assessment of the critically ill patient, extra heart sounds, labelled S3
and S4, may be heard during times of extra ventricular filling or fluid
overload.
• Often referred to as ‘gallops’, these extra heart sounds are accentuated
during episodes of tachycardia.
• S3, ventricular gallop, occurs during diastole in the presence of fluid
overload. Considered physiological in children or young people, due to
rapid diastolic filling, S3 may be considered pathological when due to
reduced ventricular compliance and associated increased atrial pressures.
• S4 is a late diastolic sound and may be heard shortly before S1. Occurs
when ventricular compliance is reduced secondary to aortic or pulmonary
stenosis, mitral regurgitation, systemic hypertension, advanced age or
ischemic heart disease.
• The critical care nurse auscultating the heart should also
listen for a potential pericardial rub. This ‘rubbing’ or
‘scratching’ sound is secondary to pericardial inflammation
and/or fluid accumulation in the pericardial space.

• To differentiate pericardiac rub from pulmonary rub, if

possible the patient should be instructed to hold their
breath for a short duration as pericardial rub will continue
to be audible in the absence of breathing, heard over the
3rd ICS to the left of the mid sternum.
• CONTINUOUS CARDIAC MONITORING
• In the case of the critically ill patient, there are two
main forms of cardiac monitoring, both of which are
used to generate essential data: continuous cardiac
monitoring, and the 12-lead ECG.
• Continuous cardiac monitoring allows for rapid
assessment and constant evaluation with, when
required, the instantaneous production of paper
recordings for more detailed assessment or
documentation into patient records.
• It is now common practice for five leads to be used
for continuous cardiac monitoring, as this allows a
choice of seven views.
• The five electrodes are placed as follows:
– right and left arm electrodes: placed on each shoulder;
– right and left leg electrodes: placed on the hips or level
with the lowest ribs on the chest;
– V-lead views can be monitored: for V1 place the
electrode at the 4th ICS, right of the sternum; for V6
place the electrode at the 5th ICS, left mid-axillary line.
• The 12-lead ECG consists of six limb leads and
six chest leads.
• Placement should be:
– I = negative electrode in right arm and positive
electrode in left arm
– II = negative electrode in right arm and positive
electrode in left leg
– III = negative electrode in left arm and positive
electrodes in left leg
• These three leads views the heart at different angles:
• Lead aVR produces a negative reflection because the electrical
activity moves away from the lead.

• Lead aVL produces a positive deflection because the electrical

activity moves towards the lead. Lead aVL views the electrical
activity from the lateral wall.

• Lead aVF also produces a positive deflection on the ECG

because the electrical activity flows toward this lead. It views
the electrical activity from the inferior wall.
• The six unipolar chest leads (precordial leads) are
designated V1–6 and examine electrical activity along a
horizontal plane from the right ventricle, septum, left
ventricle and the left atrium.
• They are positioned in the following way:
– V1 = 4th ICS, to the right of the patient’s sternum
– V2 = 4th ICS, to the left of the patient’s sternum
– V3 = equidistant between V2 and V4
– V4 = 5th ICS on the midclavicular line
– V5 = 5th ICS, anterior axillary line
– V6 = 5th ICS on the midaxilla line
 Key Components of the ECG

• Key components of the cardiac electrical activity are termed PQRST.

• The P wave represents electrical activity caused by spread of impulses

from the SA node across the atria and appears upright in lead II. Inverted
P waves indicate atrial depolarization from a site other than the SA node.
Normal P wave duration is considered less than 0.12 sec.
• The P–R interval reflects the total time taken for the atrial impulse to
travel through the atria and AV node. It is measured from the start of the
P wave to the beginning of the QRS complex, but is lengthened by AV
block or some drugs. Normal P–R interval is 0.12–0.2 sec.
• The QRS complex is measured from the start of the Q wave to the end of
the S wave and represents the time taken for ventricular depolarization.
Normal QRS duration is 0.08–0.12 sec.
• The Q–T interval is the time taken from ventricular stimulation to
recovery. It is measured from the beginning of the QRS to the end of the T
wave. Normally, this ranges from 0.35 to 0.45 sec, but shortens as heart
rate increases. It should be less than 50% of the preceding cycle length.
• The T wave reflects repolarization of the ventricles. A peaked T wave
indicates hyperkalemia, myocardial infarction (MI) or ischemia, while a
flattened T wave usually indicates hypokalemia. An inverted T wave
occurs following an MI, or ventricular hypertrophy. Normal T wave is 0.16
sec. The height of the T wave should be less than 5 mm in all limb leads,
and less than 10 mm in the precordial leads.
• The ST segment is measured from the J point (junction of the S wave and
ST segment) to the start of the T wave. It is usually isoelectric in nature,
and elevation or depression indicates some abnormality in the onset of
recovery of the ventricular muscle, usually due to myocardial injury.
• The U wave is a small positive wave sometimes seen following the T wave.
 ECG Interpretation
• Interpretation of a 12-lead ECG is an experiential skill, requiring consistent
exposure and practice.
• Calculate the heart rate
• One way is to count the R waves on a 6 sec strip and multiply by 10 to calculate the
rate (the top of the ECG paper is usually marked at 3 sec intervals).
• Use an ECG ruler if one is available.
• Check R-R intervals (rhythm):
• Are the rhythms regular?
• To assess regularity: mark the duration of two neighbouring R waves (R-R interval)
on a plain piece of paper, move this paper to check other R-R intervals on the ECG
strip. R-R intervals should be uniform in a normal ECG which means the patient has
a regular ECG rhythm.
• Locate P waves (check atrial activity):
• Observe for the presence or absence of P waves. Check regularity and shape. Is the
P wave positive?
• The relationship between P waves and QRS complexes: is there a P wave preceding
every QRS complex?
• What is the duration of the P wave?
• Measure P-R interval (check AV node activity):
• l What is the duration of the P-R interval?
• Measure QRS duration (check ventricular activity):
• Is the ventricular electrical activity normal? Is the QRS complex too wide or
narrow? Check the presence of Q wave. If present, is it normal or pathological?

• Note other clues:

• Observe whether the isoelectric line is present between the S and T waves.
• Examine the T wave to see whether it is positive, negative, or flat. Is it less than
0.16 sec?
• Examine the duration of the Q-T interval: is it too long?
• Observe for any extra complexes and note their rate and shape, and whether
they have the same or differentmorphology.
 HAEMODYNAMIC MONITORING
• The reasons for hemodynamic monitoring are
generally threefold:
1. to establish a precise health-related diagnosis
2. to determine appropriate therapy
3. to monitor the response to that therapy.
 Hemodynamic monitoring can be non-
invasive or invasive:
• Non-invasive monitoring does not require any device to be inserted into the
body and therefore does not breach the skin. Directly measured non-invasive
variables include body temperature, heart rate, blood pressure, respiratory
rate and urine output, while other processed forms can be generated by the
ECG, arterial and venous Doppler's, transcutaneous pulse oximetry (using an
external probe on a digit such as the finger or on the ear), and expired carbon
monoxide monitors.

• Invasive monitoring requires the vascular system to be cannulated and

pressure or flow within the circulation interpreted. Invasive hemodynamic
monitoring technology includes:
• systemic arterial pressure monitoring
• central venous pressure
• pulmonary artery pressure
• cardiac output (thermodilution).
 PRINCIPLES OF HAEMODYNAMIC
MONITORING
• Haemodynamic Accuracy
• Accuracy of the value obtained from hemodynamic
monitoring is essential, as it directly affects the patient’s
condition.
• Electronic equipment for this purpose has four
components:
1. an invasive catheter attached to high-pressure tubing
2. a transducer to detect physiological activity
3. a flush system
4. a recording device, incorporating an amplifier to increase the
size of the signal, to display information.
• Data Trends
• The ability to trend data via a monitor or a
clinical information system is essential for
critical care practice.
• The data trends can be used to assess the
progression of a patient’s clinical condition
and monitor the patient’s response to
treatment.
• Haemodynamic Monitoring Standards
• The standards require that patient monitoring include
circulation, respiration and oxygenation, with the
following essential equipment available for every patient:
an ECG that facilitates continual cardiac monitoring; a
mechanical ventilator, pulse oximeter; and other
equipment available where necessary to measure intra-
arterial and pulmonary pressures, cardiac output,
inspiratory pressure and airway flow, intracranial
pressures and expired carbon dioxide.
 BLOOD PRESSURE MONITORING
• Non-invasive Blood Pressure Monitoring
• Non-invasive blood pressure (NIBP) monitoring requires the use of a
manual or electronic sphygmomanometer.
• Oscillation in the pressure generated by alterations in arterial flow is
captured either through auscultation or automatic sensing.
• On auscultation, a number of Korotkoff sounds can be heard as the cuff
pressure is released:
• a sharp thud that is heard when the patient’s systolic pressure is reached
• a soft tapping, intermittent in nature
• a loud tapping, intermittent in nature
• a low, muffled noise that is continuous in nature and is heard when the
diastolic pressure is reached; as the cuff pressure diminishes further, the
sound disappears.
• Invasive Intra-arterial Pressure Monitoring

• Arterial pressure recording is indicated when precise and continuous

monitoring is required, especially in periods of fluid volume, cardiac output
and blood pressure instability.
• An arterial catheter is commonly placed in the radial artery, although other
sites can be accessed, including the brachial, femoral, dorsalis pedis and
axillary arteries.
• The radial artery is the most common site, as the ulnar artery provides
additional supply to extremities if the radial artery becomes compromised.
• Complications of arterial pressure monitoring include:
• infection
• arterial thrombosis
• distal ischemia
• lair embolism
• accidental disconnection (the insertion sites should be always visible)
• l accidental drug administration through the arterial catheter; all arterial lines and connections

should be clearly identified as such (e.g. marked with red stickers or have red bungs).
• Preload is the filling pressure in the ventricles
at the end of diastole.
• Preload in the right ventricle is generally
measured as CVP and left ventricular preload
can be measured as the pulmonarym capillary
wedge pressure (PCWP).
INVASIVE CARDIOVASCULAR MONITORING

• Central venous pressure monitoring

• Central venous catheters are inserted to facilitate
the monitoring of central venous pressure;
facilitating the administration of large amounts of IV
fluid or blood; providing long-term access for fluids,
drugs, specimen collection; and/or parenteral
feeding.
• The two commonly used sites in critically ill patients
are the subclavian and the internal jugular veins.
• Pulmonary artery pressure (PAP) monitoring
• Pulmonary artery catherization facilitates assessment of filling
pressure of the left ventricle through the pulmonary artery
wedge (occlusion) pressure.
• By using a thermodilution pulmonary artery catheter (PAC),
cardiac output and other hemodynamic measurements can also
be calculated.
• PAP monitoring is a diagnostic tool that can assist in
determination of the nature of a hemodynamic problem and
improve diagnostic accuracy. In addition to measuring PA
pressures, PAC may also be used for accessing blood for
assessment of mixed-venous oxygenation levels.
• Pulmonary capillary wedge pressure (PCWP)
monitoring
• PCWP, or pulmonary artery occlusion pressure
(PAOP), is measured when the pulmonary artery
catheter balloon is inflated with no more than 1–1.5
mL air. The inflated balloon isolates the distal
measuring lumen from the pulmonary arterial
pressures, and measures pressures in the capillaries
of the pulmonary venous system, and indirectly the
left atrial pressure.
• Afterload is the pressure that the ventricle
produces to overcome the resistance to ejection
generated in the systematic or pulmonary
circulation by the arteries and arterioles.
• It is calculated by cardiac output studies: left
heart afterload is reflected as systemic vascular
resistance (SVR), and right heart afterload is
reflected as pulmonary vascular resistance (PVR).
• Systemic and pulmonary vascular resistance

• Systemic vascular resistance (SVR) is a measure of resistance or

impediment of the systemic vascular bed to blood flow. An elevated
SVR can be caused by vasoconstrictors, hypovolemia or late septic
shock. A lowered SVR can be caused by early septic shock, vasodilators,
morphine, nitrates or hypercarbia.
• Pulmonary vascular resistance (PVR) is a measure of resistance or the
impediment of the pulmonary vascular bed to blood flow. An elevated
PVR (‘pulmonary hypertension’) is caused by pulmonary vascular
disease, pulmonary embolism, pulmonary vasculitis or hypoxia. A
lowered PVR is caused by medications such as calcium channel
blockers, aminophylline or isoproterenol, or by the delivery of O2.
 DIAGNOSTICS
• ECHOCARDIOGRAPHY
• Echocardiography (shortened to ECHO) is often
used in critical care to assess patients’
cardiovascular conditions such as heart failure,
hypertensive heart disease, valve disease, and
pericardial disease in critically ill patients. It
adopts a technique of detecting the echoes
produced by a heart from a beam of very high
frequency sound – the ultrasound.
• BLOOD TESTS
• Full Blood Count
• The full blood count (FBC) assesses the status of three major
cells that are formed in the bone marrow: red blood cells
(RBC), white blood cells (WBC) and platelets.
• Electrolytes
• The assessment of electrolyte levels in critically ill patients is
important in diagnosing the patient’s condition. Electrolyte
imbalances, such as potassium and calcium level changes,
can cause cardiovascular abnormalities such as arrhythmias.
• Cardiac Enzymes
• Recent studies have revealed that cardiac
troponin levels are elevated in critically ill
septic patients who do not have evidence of
MI.
• CHEST X-RAY
• Chest X-ray is the oldest non-invasive way to
visualize the images of the heart and blood
vessels, and is one of the most commonly
taken diagnostic procedures in critical care.
• Cardiac Chest X-ray Interpretation
• 1. First the heart size needs to be checked to see if the size of
the heart is appropriate. The cardiac silhouette should be no
more than 50% of the diameter of the thorax, this is called the
cardiothoracic ratio. The position of the heart should be 1/3 of
heart shadow to the right of the vertebrae and 2/3 of the
shadow to the left of the vertebra.
• 2. The shape of the heart should be inspected next on the film
once the size of the heart was inspected. The border is formed
by: the right atrial shadow as the right convex cardiac border;
the superior vena cava as the superior border; and the left
ventricle as the left heart border and cardiac apex.
• 3. The next step should move to the superior border
to identify the aortic arch and the pulmonary
arteries. The aortic arch is called the knob. The
pulmonary arteries and the branches radiate
outward from the. The hilum in the mediasternal
region is formed by the pulmonary arteries and the
main stem bronchi shadows on the film.
• The focus of this step is to check for prominence of
vessels in this region, as this suggests vascular
abnormalities.
• Chest X-ray in Diagnosing Cardiac Conditions
• Patients with chronic heart failure show
cardiomegaly, Kerby B lines or pulmonary
edema. Cardiomegaly is the enlarged heart on
the X-ray film.
• Kerby B lines on the X-ray film is the result of
pulmonary congestion and fluid accumulation
in the interstitium.
• A widened mediastinum and abnormal aortic contour may
indicate aortic dissection.
• Subtle abnormalities in the hilar region may indicate
pulmonary hypertension (PAH).
• A decrease in pulmonary vascular markings and prominent
main and hilar pulmonary arterial shadows in the lung
fields on the chest film are classic signs of pulmonary
hypertension.
• In pericardial disease, the chest X-ray often appears normal
unless the accumulated fluid in the pericardial space is over
250 mL.
• Cardiac Computed Tomography
• Cardiac computed tomography (cardiac CT) is a
recent development in diagnosing cardiac
conditions such as suspected coronary heart
disease, and in the evaluation of coronary
artery bypass grafts. It provides a method to
visualize the anatomical structure of the heart
and coronary arteries reliably and accurately in
patients.
• Magnetic Resonance Imaging
• Magnetic resonance imaging (MRI) is a non-
invasive method that can provide cardiac-
specific biochemical information such as tissue
integrity, cardiac aneurysms, ejection fraction,
and cardiac output.
• MRI is considered an accurate method to
predict the presence of significant coronary
artery disease.
• Nuclear Medicine Cardiac Studies
• The purpose of radionuclide imaging is to assess the
perfusion status of cardiac muscle.
• When lowered perfusion in cardiac muscle is
identified this may indicate heart muscle damage.
Radionuclide imaging is often used in patients who
have been diagnosed with a myocardial infarction and
further investigation is required to determine if
interventions such as cardiac stent or coronary artery
bypass surgery are likely to benefit the patient.
Nursing Care of Patients Undergoing Cardiac CT,
MRI and Nuclear Medicine Studies
• For the critical care nurse, preparation of patients for these
examinations is important because the patients often need to be
transported to the radiology or nuclear medicine departments.
Important considerations include:
• Patient’s allergy profile in relation to imaging contrast needs to
be evaluated before the requests are made.
• These tests all require the patient to lie still for certain periods of
time, therefore sedation may be required during the procedure.
• Appropriate equipment, such as non-metal equipment, needs to
be organized beforehand if the patient is having an MRI study.
Cardiovascular Alterations and Management

• CORONARY HEART DISEASE

• Coronary heart disease (CHD) is the term used to
describe the effects of a reduction or complete
obstruction of blood flow through the coronary arteries
due to narrowing from atherosclerosis and/or thrombus.
• The commonest manifestations of CHD are chest pain
due to angina, acute coronary syndrome (ACS, a term
used to collectively describe acute myocardial infarction
[AMI] and unstable angina) and sudden death.
• CHD may also cause arrhythmias and heart failure.
• MYOCARDIAL ISCHAEMIA
• When coronary blood flow is insufficient to meet myocardial
tissue demand for oxygen, myocardial ischemia occurs.
• Critical restriction to blood flow occurs when the diameter of
the lumen of the blood vessel is reduced by more than half.
• Coronary blood flow is also determined by perfusion
pressure, which can be adversely affected by abnormalities
in blood flow (valvular disease), vessel wall (coronary spasm)
and the blood (anemia, polycythemia).
• Myocardial oxygen demand is influenced by heart rate,
strength of myocardial contraction and left ventricular wall
tension.
• ANGINA
• Angina is the commonest manifestation of CHD and is
the term used to describe the symptoms of discomfort
that occur during myocardial ischemia.
• The classic angina pattern consists of retrosternal
constricting pain/discomfort, which may radiate to the
arms, throat, jaw, teeth, back or epigastrium.
• Associated symptoms often include shortness of
breath, nausea, vomiting, sweating, palpitations and
weakness.
 UNSTABLE ANGINA AND ACUTE MYOCARDIAL
INFARCTION
• Unstable angina and AMI form a continuum on the basis of
reduction in coronary blood flow and subsequent damage
to myocardial cells.
• Unstable angina may indicate transient ischemia, whereas
AMI indicates myocardial tissue death.
• ACS results from the rupture or erosion of an
atherosclerotic plaque, leading to release of
vasoconstrictor substances and potentially triggering
coagulation activity.
• Formation of thrombi results in intermittent and/or
prolonged obstruction of the coronary artery.
• MYOCARDIAL INFARCTION
• Myocardial infarction (MI) occurs when blood flow to the
myocardium is severely impaired for more than 20
minutes as myocardial cell necrosis begins.
• Coronary artery thrombus arising from an atherosclerotic
plaque is found in the majority of patients dying of AMI.
• Cellular death begins in the subendocardial layer and
progresses through the full muscle thickness, so that by 2
hours with total occlusion a full ‘transmural’ infarction
will result.
The location and impact of the infarction will depend on which coronary
artery has been obstructed:

• Left anterior descending (LAD) affects the function of the left ventricle
and interventricular septum, including ventricular conduction tissue.
• Patients with anteroseptal MI are at high risk of heart failure, cardiogenic
shock and mortality due to pump deficits.
• Circumflex (CX) affects the left ventricle lateral and posterior walls and
the SA node in 50% of people. The impact on pump efficiency of lateral
and posterior wall necrosis is not as severe as anteroseptal infarcts,
although patients are at more risk of arrhythmias.
• Right coronary artery (RCA) affects the inferior wall of the left ventricle
and the right ventricle, as well as the AV node in most patients and the SA
node in 50% of people. There is potentially severe impact on ventricular
function if both the inferior wall and the right ventricle are affected, as
well as a high risk of arrhythmias due to SA and AV node involvement.
• Clinical Features
• Patients with AMI most often present with chest pain.
• This pain is described as central crushing retrosternal pain, which
lasts longer than 20 minutes and is not relieved by nitrate therapy.
• The pain may radiate to the neck, jaw, back and shoulders and is
often accompanied by ‘feelings of impending doom’, sweating and
pallor.
• Nausea is often associated with the pain, due to vagal nerve
stimulation. Depending on the size and location of the AMI,
patients may also present as sudden death and with varying
degrees of syncope and heart failure.
Patient Assessment and Diagnostic Features
• A key feature of assessment of the patient
with chest pain is the use of protocols and
guidelines to promote rapid assessment so
that revascularization procedures such as
thrombolysis and percutaneous coronary
intervention (PCI) can be implemented as soon
as possible.
• Physical examination

• Physical appearance varies and depends on the impact of pain, size and
location of the infarction in the individual.
• Heart rate and blood pressure may be raised due to anxiety.
• Impaired left ventricular function may result in dyspnea, tachycardia,
hypotension, pallor, sweating, nausea and vomiting.
• Impaired right ventricular function may be indicated by jugular vein
distension and peripheral edema.
• Abnormalities in heart sounds may be present, including a muffled and
diminished first heart sound due to decreased contractility. A fourth
heart sound is common, whereas a third heart sound is uncommon.
• Many patients develop a pericardial rub after about 48–72 hours due to
an inflammatory response to the damaged myocardium.
• Electrocardiographic examination
• Patients with chest discomfort should be assessed by
an appropriately qualified person and have an ECG
recorded within 5 minutes of arrival at a healthcare
facility to determine the presence and extent of
myocardial ischemia, the risk of adverse events and
to provide a baseline for subsequent changes.
• Most importantly, the ECG is essential to determine
whether emergency reperfusion is required, and is
recommended as the sole test for selecting patients
for PCI or thrombolysis.
• On acute presentation, myocardial injury
(infarction) is most commonly associated with
ST segment elevation on the ECG, although this
is not universal.
• A typical pattern of ECG changes over time
(evolution of the ST segments, Q wave
development and T wave inversion) are often
seen (described below), but these changes too
are not universal.
• Typical ECG evolution pattern
• The initial ECG features of myocardial infarction are
ST segment elevation with tall T-waves recorded in
leads overlying the area of damaged myocardium.
• These changes gradually change, or evolve, over
time, with ST segments returning to baseline
(within hours), while Q waves develop (hours to
days) and T waves become inverted (days to weeks).
• Given the expected time course for evolution, it is
possible to approximate how recently infarction has
occurred, which is essential in determining
management:

• acute (or hyperacute): there is ST elevation but Q waves or T

inversion have not yet developed (see Figure 10.5).
• recent: Q waves have developed. ST segment elevation may still
be present. Evolution is underway. The infarction is more than 24
hours old.
• old (fully evolved): Q waves and T inversion are present. ST
segments are no longer elevated. Infarction occurred anything
from a few days to years ago.
• Biochemical markers
• Intracellular cardiac enzymes enter the blood
as ischemic cells die, and elevated levels are
used to confirm myocardial infarction and
estimate the extent of cell death. The cardiac
troponins T and I (cTnT and cTnI) have been
found to be both sensitive and specific
measures of cardiac muscle damage.
 Coronary angiography and left
heart catheterisation

• Coronary angiography gives a detailed record of coronary

artery anatomy and pathophysiology.
• Specially designed catheters are advanced with the
assistance of a guide wire into the ascending aorta via the
femoral or brachial arteries and maneuvered into the
ostium of each coronary artery.
• Contrast media is then injected and images are taken from
several views to provide detailed information on the
extent, site and severity of coronary artery lesions and the
blood flow into each artery.
• Exercise test
• Exercise testing with ECG monitoring forms
part of the diagnostic screen for patients
suspected of stable angina. The Bruce protocol
is used most often and considered positive for
CHD if there is 1 mm or more of reversible ST
segment depression.
• Chest radiography
• An initial chest X-ray film is useful to exclude
other causes of chest pain, such as
pneumonia, pneumothorax and aortic
aneurysm, and to assess whether heart failure
and/or pulmonary congestion are present.
 Collaborative Management of Angina and
Acute Coronary Syndrome
• The management of stable angina patients is aimed at:
• (a) secondary prevention of cardiac events;
• (b) symptom control with medication;
• (c) revascularization; and
• (d)brehabilitation
• Treatment of acute coronary syndrome aims at rapid
diagnosis and prompt re-establishment of flow
through the occluded artery to ensure myocardial
perfusion and reduce size of infarction. In addition,
treatment aims to:
• minimize the area of myocardial ischemia by increasing coronary
perfusion and decreasing myocardial workload
• maximize oxygen delivery to tissues
• control pain and sympathetic stimulation
• counter detrimental effects of reperfusion
• preserve ventricular function
• reduce morbidity and mortality.
• Reperfusion therapy
• Reperfusion therapy includes coronary angioplasty, ideally with
stent and thrombolytic therapy (also termed fibrinolysis).
• Patients fast-tracked for reperfusion therapy have one or more
of the following indications:
• (a) ischemic or infarction symptoms for longer than 20 minutes;
• (b) onset of symptoms within 12 hours;
• (c) ECG changes (ST elevation of 1 mm in contiguous limb leads,
ST elevation of 2 mm in contiguous chest leads; left bundle
branch block).
• Thrombolytic therapy
• Thrombolytic therapy has been demonstrated
to show a significant reduction in mortality in
the high-risk group.
• The greatest reduction in mortality occurs if
the reperfusion occurs within the first ‘golden’
• hour of presentation.
• Coronary angioplasty
• Coronary angioplasty (PTCA) procedures are being used about
twice as frequently as coronary artery bypass graft surgery,
• In this procedure, a catheter is introduced by the brachial or
femoral artery into the coronary arteries and advanced into
the area of occlusion or stenosis under the guidance of
imagery and specifically designed catheters.
• A balloon attached to the end of the catheter is then inflated
to widen the lumen of the artery by stretching the vessel wall,
rupturing the atheromatous plaque and cracking the intima
and media of the artery.
• Nursing management of patients post-PTCA includes care of the puncture
site to prevent bleeding and detect arterial changes (including clot and
aneurysm).
• The sheath used to aid insertion and maintain access is usually maintained
for 1–2 hours post procedure for emergency access.

• Care is as follows:
• Observations. Observe access site for hemorrhage and hematoma, assess
perfusion to the lower limb, including color, warmth and pulses. This
monitoring needs to be done often in the first few hours, when
complications are most likely to occur.
• ECG monitoring. This includes 12-lead ECG on return and ongoing ECG
monitoring and chest pain assessment to detect reocclusion. Patients need
to be requested to inform nursing staff of any chest pain or discomfort.
• Vital signs. These are recorded every 15 minutes for the first hour, half-
hourly for one hour, and then hourly according to the patient’s condition.
• Removal of sheath. This is usually performed by medical or specially trained nursing
staff.
• Achievement of hemostasis. Use either application of pressure for at least 5
minutes or vascular sealing.
• Pressure application can be by a manual compression device (such as Femostop,
RADI Medical Systems, Uppsala, Sweden) and less often digital, to maintain a
pressure of about 20 mmHg.
• Vascular sealing uses a device such as the Angioseal12345Vascular Closure Device
(St Jude Medical Inc, St Paul, MN). This includes a collagen plug and a small
biodegradable plate inside the artery, which is held in place by a small suture,
tamping tube and small spring on the exterior. The tension spring is removed and
the suture trimmed half an hour after application. This enables the patient to
mobilize and reduces nursing time.30
• Assess International Normalised Ratio (INR), prothrombin (PT) and partial
thromboplastin time (PTT), as bleeding is more likely to occur if anticoagulants are
above the therapeutic range. Weight-adjusted heparin (100 units/kg) is usually
used during PTCA to prevent thrombus formation, and glycoprotein IIb/IIIa
inhibitors such as abciximab may be used to prevent platelet aggregation and
thrombus formation for patients at high risk of occlusion.
• Bed rest (2–6 hours) is used to discourage the patient from moving the
joint of the insertion site to prevent clot displacement and hematoma
formation. Initially the patient should lie relatively flat if femoral artery
access has been used, then progress to sitting. The period of rest has
been demonstrated to be safely reduced to 1 hour in low-risk patients
(normotensive and normal platelet count).
• Pain relief is used primarily to promote comfort for patients who find
bed rest to cause pain and discomfort.
• Urine output. Adequate urine output is essential as radiographic IV
contrast is cleared by the kidneys, so it is vital that nurses ensure good
hydration and monitor initial urine output.
• Oral antiplatelet drugs, such as clopidogrel or ticlopidine, may be given
prior to the procedure to prevent later reocclusion in the stent. Usually
patients will be discharged on this medication to continue for up to 3
months while endothelium lines the stent/injured area. Unless
contraindicated, all patients will take aspirin for the rest of their lives.
• Nursing management of ACS and MI
• The nursing role in patients with ACS and MI
includes reducing myocardial workload and
maximizing cardiac output, provision of
treatments, careful monitoring to determine the
effects of treatment and detect complications,
rapid treatment of complications, comfort and
pain control, psychosocial support and teaching
and discharge planning.
• Reduction of myocardial workload includes ensuring the patient has
bed rest, providing support with activities and limiting stress.
• A calm, caring manner during nursing care is essential to lower patient
and family stress levels. Individual evaluation of the patient and the
family is necessary to determine the most appropriate management of
visiting.
• ECG monitoring (preferably including ST monitoring) and evaluation of
heart rate, shortness of breath, chest discomfort and blood pressure
are essential to determine ischemia, treatment effects, myocardial
workload and complications. This monitoring should occur hourly
during the acute phase, reducing as the patient recovers.
• Provision of oxygen by mask or nasal cannulae in the first 6 hours is
standard practice to raise SaO2 levels in the myocardium, although
there is no evidence of patient benefit if heart failure is not present.
Oxygen saturation levels should be routinely assessed concomitantly.
• Symptom relief should be provided, including analgesia
for pain. Analgesia management should be conducted
by nurses because of their continued contact and thus
more accurate assessment and treatment of pain.t is
essential to treat pain, not only for the distress it
causes patients but also because pain causes
stimulation of the sympathetic nervous system (SNS).
• SNS responses include elevated heart rate and
potential for arrhythmias, peripheral vasoconstriction
and increased myocardial contractility and, therefore,
an overall increase in myocardial oxygen demand.
• Nursing care for thrombolysis
• Patients receiving thrombolytics require
constant observation, regular non-invasive
blood pressure measurement for hypotension,
and monitoring for allergic reactions to
streptokinase.
• Continuous ECG monitoring for arrhythmias
and ST segment changes is essential.
• Independent Practice Emotional responses and patient
and family support
• ACS or AMI is usually accompanied by feelings of acute
anxiety and fear, as most patients are aware of the
significant threat posed to their
• Anxiety is a common response to the stress of an acute
cardiac event and leads to important physiological and
psychological
• . Therefore, staff working in emergency and coronary care
should employ strategies to reduce a patient’s anxiety.
Increasing a patient’s sense of control, calm and confidence in care
reduces the patient’s sense of vulnerability, whether it is realistic or
not.This can be achieved by:

• providing order and predictability in routines, allowing the patient to

make choices, providing information and explanations, and including
the patient in decision making
• using a calm, confident approach communicating with patients and
families, while reducing conversation demands as excessive
conversation by patients may unnecessarily raise heart rate.
• restricting the number and type of visitors in the acute phase is
customary, but many patients feel safer if a family member is present
• provision of comprehensive information to families, with more
concise information in understandable language for patients.
 HEART FAILURE
• In normal circumstances, the heart is a very effective, efficient pump with
reserve mechanisms available to allow output to meet changing
demands.
• These mechanisms include (a) increasing heart rate to increase total
cardiac output, (b) dilation to create muscle stretch and more effective
contraction, (c) hypertrophy of myocytes over time to generate more
force, and (d) increasing stroke volume by increasing venous return and
increased contractility.

• Heart failure is a complex clinical condition that is characterized by an

underlying structural abnormality or dysfunction that results in the
inability of the ventricle to fill with or eject blood.
• The condition is also known as congestive cardiac failure or Chronic heart
failure (CHF) describes the long-term inability of the heart to meet
metabolic demands.
• The causes of heart failure can be categorised
according to (a) myocardial disease, (b)
arrhythmias, (c) valve disease, (d) pericardial
disease and (e) congenital heart disease
• Myocardial disease may be caused by myocardial infarction and
fibrosis from prolonged ischemic heart disease which accounts for
approximately two-thirds of systolic heart failure causing systolic
dysfunction and a reduced ejection fraction.
• Arrhythmias, including both brady- and tachyarrhythmias, may
cause heart failure due to changes in filling time affecting preload
and resultant cardiac output.
• Heart failure patients are also at high risk of sudden cardiac death
due to ventricular fibrillation or tachycardia.
• Valvular disease causing heart failure usually involves valves on the
left side of the heart (mitral and/or aortic valves).
• Aortic stenosis results in an increase in afterload and ventricular
hypertrophy develops with reduced diastolic compliance resulting in
a reduced ejection fraction.
• Mitral stenosis is usually due to rheumatic heart disease.
There are several terms used to describe the pathology and signs and
symptoms of heart failure. These include:

• Backward failure: refers to the systemic and pulmonary congestion that occurs
as a result of failure of the ventricle to expel its volume.
• Forward failure: is due to an inadequate cardiac output and leads to decrease
in vital organ perfusion.
• Acute heart failure: includes the initial hospitalization for the diagnosis of heart
failure and exacerbations of chronic heart failure.
• Chronic heart failure: develops over time as a result of the inability of
compensatory mechanisms to maintain an adequate cardiac output to meet
metabolic demands.
• Systolic heart failure: refers to the inability of the ventricle to contract
adequately during systole resulting in a reduced ejection fraction and an
increased end-diastolic volume. This is the most common form of heart failure.
• Diastolic heart failure (or heart failure with preserved systolic function
[HFSF]): indicates normal systolic function with a normal ejection fraction
but impaired relaxation so there is a resistance to filling with increased
filling pressures. Diastolic dysfunction usually occurs in conjunction with
systolic dysfunction and is more common in the elderly.
• Low cardiac output syndrome: this occurs in response to hypovolemia
and/or hypertension. Severe vasoconstriction further reduces the cardiac
output.
• High cardiac output syndrome is the result of an increase in metabolic
demands causing a decrease in SVR leading to an increase in stroke
volume and cardiac output. Burns and sepsis are the main causes.
• Left sided heart failure: occurs when there is a reduced left ventricular
stroke volume resulting in accumulation of blood in the pulmonary
system.
• Right sided heart failure: is the congestion of blood in the systemic system
due to the inability of the right ventricle to expel its blood volume.
 PATIENT ASSESSMENT, DIAGNOSTIC PROCEDURES AND
CLASSIFICATION

Cardiac Assessment:
• Pulse rate and rhythm: The pulse rate is generally elevated due to
a low cardiac output. However, if the patient is prescribed beta-
adrenergic blocking agents and/or angiotensin converting
enzyme (ACE) inhibitors, the pulse rate may be low.
• Palpation of the precordium and apical impulse: This may be
displaced laterally and downward to the left due to an increased
heart size.
• Auscultation of a third heart sound (S3 gallop): This occurs due to
a low ejection fraction and diastolic dysfunction. A fourth heart
sound may also be present due to a decrease in ventricular
compliance.
• Assessment of jugular venous pressure (JVP): This is to estimate
the degree of venous volume. If raised it reflects hypervolemia,
right ventricular failure, and reduced right ventricular
compliance. It can also be raised in the presence of tricuspid
valve disease. The hepatojugular reflex is also assessed by
pressing on the liver and observing an increase in JVP. This
results in an increase in blood flow to the right atrium.

• Blood pressure: Lying and standing blood pressure are measured

to assess postural hypotension due to a low cardiac output and
also the prescribing of beta adrenergic blocking agents and ACE
inhibitors.
• Peripheries: Look for the presence of cyanosis which may be due to
vasoconstriction. Assess the fingers for clubbing which indicates long-term
cyanosis usually as a consequence of congenital heart disease. Also assess
the patient for ankle edema. Peripheral edema up to the midcalves indicates
a moderate amount of excess fluid and the patient may require a bolus dose
of diuretic medication.

• Pulmonary assessment includes chest auscultation for inspiratory crepitations

that do not clear with coughing.
• They are initially heard in the bases but as congestion increases they become
diffuse.
• General assessment of the patient includes daily weighing, looking for signs
of cachexia (usually associated with severe chronic heart failure), anaemia
and dizziness.
 Diagnostic Tests
• Trans-thoracic echocardiography is the most useful investigation to
confirm diagnosis. This is the gold standard diagnostic test for heart
failure. This test is vital, as it can distinguish systolic dysfunction (left
ventricular ejection fraction [LVEF] <40%) from diastolic dysfunction, and
therefore help determine treatment.
• Assessment of cardiac function can also be done by invasive techniques
(e.g. coronary angiography) and nuclear cardiology tests (e.g. gated
radionuclide angiocardiography).
• ECG should be done as an initial investigation. Most common
abnormalities include ST-T wave changes,left bundle branch block, left
anterior hemiblock, left hypertrophy, atrial fibrillation and sinus
tachycardia.
• chest X-ray for cardiomegaly and pulmonary markings including
evidence of interstitial edema: perihilar pulmonary vessels, small basal
pleural effusion obscuring the costophrenic angles, Kerley B line
(indicating raised left atrial pressure).

• Full blood count for anaemia and mild thrombocytopenia.

• Urea, creatinine and electrolytes for dilutional hyponatraemia,

hypokalaemia, hyperkalaemia, low magnesium, and glomerular
filtration rate.

• Liver function tests for elevated levels of AST, ALT, LDH and serum
bilirubin.
• Thyroid fun
• ction tests particularly in patients with no history of coronary artery
disease and who develop atrial fibrillation.
• Urinalysis for specific gravity and proteinuria.

• Myocardial ischemia and viability need to be assessed in

patients with heart failure and coronary artery disease.
These can be assessed by a stress ECG, stress
echocardiography or a stress nuclear study. Coronary
angiography is useful to determine the contribution of
coronary artery disease in these patients.

• Natriuretic peptides includes plasma ANP and B-type

natriuretic peptide (BNP).
• Endomyocardial biopsy should be conducted if there is a
suspicion of cardiomyopathy.
• NURSING MANAGEMENT
• Treatment of CHF is lifelong and multifactorial,
requiring a well-coordinated, multidisciplinary
approach. The goals of heart failure treatment
are to identify and eliminate the precipitating
cause, promote optimal cardiac function,
enhance patient comfort by relieving signs and
symptoms, and help the patient and family
cope with any lifestyle changes.
• Lifestyle Modification and Self-care Management
• Patient education is the key to self-management and must include
family members to be effective. Patient education should include
information on the following:
• The disease process. This involves discussing what heart failure is,
signs and symptoms and why they occur, and strategies to improve
their symptoms
• Lifestyle changes
• Medications and side effects
• Self-monitoring and acute symptoms
• The importance of adherence to their medications and management
plan.
 CARDIOMYOPATHY
• Primary disorders of the myocardium in which
there are systolic, diastolic or combined
abnormalities.
 DILATED CARDIOMYOPATHY
• Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy
and is characterized by ventricular and atrial dilation and systolic
dysfunction.
• All four chambers become enlarged which is not in proportion to the degree
of hypertrophy.
• It presents as heart failure of variable severity, sometimes complicated by
thromboembolism, at least partly due to atrial fibrillation, which is common.
• Conduction abnormalities are common in DCM further exacerbating AV
dyssynchrony and left ventricular dysfunction.
• DCM is the most common cause of sudden cardiac death due to ventricular
arrhythmias.
• Idiopathic DCM is the most common cause of heart failure in young people.
• Etiology of DCM includes coronary heart disease, myocarditis, cardiotoxins,
genetics and alcohol.
• Diagnosis
• Many of the features of DCM are non-specific.
• Heart Failure is present with typical symptoms of dyspnea, fatigue,
peripheral edema and cardiomegaly.
• S3 and S4 heart sounds may be present on auscultation.
• Atrial and ventricular arrhythmias are common, particularly atrial
fibrillation, ventricular tachycardia, ventricular fibrillation and torsades
de pointes.
• Left bundle branch block (LBBB) is often present, which worsens systolic
performance and shortens survival, especially when the QRS is markedly
prolonged.
• Echocardiography demonstrates the defining abnormalities and may be
useful in revealing atrial thrombus.
• Endocardial biopsy is undertaken to differentiate from myocarditis or
rarer causes of cardiomyopathy.
• Management
• Treatment for DCM is similar to that of heart failure and includes
beta-adrenergic blocker therapy, ACEIs, diuretics and
antiarrhythmic therapy .
• The use of cardiac resynchronization therapy (CRT) has produced
significant clinical improvements and is recommended for DCM
patients with NYHA functional class III–IV, optimal medical
therapy, LVEF ≤35%, and sinus rhythm with QRS greater than 120
msec.
• Cardiac transplantation is considered when standard therapies
fail to influence clinical progression and left ventricular assist
devices and ICDs may be used as a bridge to transplantation.
 HYPERTROPHIC CARDIOMYOPATHY

• A genetic abnormality that gives rise to

inappropriate hypertrophy especially in the
intraventricular septum with preserved or
hyperdynamic systolic function.
• The main abnormality with HCM is diastolic
rather than systolic as in DCM.
• Diagnosis

• Echocardiography will confirm the presence and pattern of hypertrophy

and the presence (or absence) of an outflow tract gradient.
• Examination findings include cardiomegaly and pulmonary congestion.
• An S4 heart sound is common, and the ECG shows left ventricular
hypertrophy and often ventricular arrhythmias.
• When the obstructive form (HOCM) is present, a systolic murmur, mitral
regurgitation murmur and deep narrow Q waves on ECG, may be
present.
• The majority of patients are asymptomatic and when they present to
hospital it will be in severe symptoms of dyspnea, angina and syncope.
• Angina is the result of an imbalance between oxygen supply and demand
due to the increased myocardial mass and not due to atherosclerosis.
• Management

• Treatment for HCM is aimed at the prevention of sudden cardiac death and
pharmacotherapy to increase diastolic filling and to reduce the LVOTO.
• Pharmacotherapy includes beta-adrenergic blocker or calcium channel blocker
therapy, as these decrease contractility and lessen outflow tract obstruction.
• Care is necessary with medication selection, as vasodilation may worsen
obstruction, causing hemodynamics to suffer.
• For severely symptomatic patients or those worsening despite maximal drug
treatment, surgical myectomy to reduce the size of the septum and lessen
obstruction may be necessary and can result in a marked improvement of
symptoms.
• Septal ablation with alcohol injected into the first septal branch of the left
anterior descending artery is a less invasive alternative, a procedure that is
usually undertaken with pacemaker insertion as AV block is produced.
• Although surgical myectomy remains the gold standard, both treatments provide
effective symptom relief and improvement in heart failure severity
 RESTRICTIVE CARDIOMYOPATHY
• Restrictive cardiomyopathies (RCMs) limit
diastolic distensibility or compliance of the
ventricles.
• The stiff ventricular walls feature diastolic
dysfunction and there is impaired ventricular
filling. Infiltrates into the interstitium and the
replacement of normal myocardium with
abnormal tissue hamper this.
• Diagnosis

• Clinically there is heart failure (increase in JVP, dyspnoea, S3 and S4 heart

sounds, and oedema), particularly right ventricular, and infiltration of the
conduction system may cause conduction defects and heart block.
• Low-voltage ECGs are commonly seen.
• Patients commonly present with decreased exercise tolerance due to the
impaired ability to increase heart rate and cardiac output because of
reduced ventricular filling.
• Restrictive cardiomyopathy must be distinguished from constrictive
pericarditis (which it may closely resemble), as pericarditis may be easily
managed.
• If echocardiography demonstrates a restrictive pattern then a myocardial
biopsy may be undertaken to determine its etiology, especially in the case of
systemic infiltrative disease
• Management
• There is no treatment for RCM so the aim of
therapy is to relieve symptoms. This includes
diuretics, corticosteroids and pacing. The use
of nitrates should be done with caution as the
filling defect can be worsened by decreased
venous return or hypovolaemia. Generally,
prognosis is poor with many dying within 1–2
years of diagnosis.
 HYPERTENSIVE EMERGENCIES
• Acute, uncontrolled hypertension is often divided into two
categories: hypertensive emergencies and hypertensive
urgencies.
• In hypertensive emergencies blood pressure needs to be reduced
within one hour to prevent end-organ damage, such as
hypertensive encephalopathy, papilledema or aortic dissection.
• Immediate blood pressure reduction with IV agents under critical
care monitoring is needed.
• By contrast, hypertensive urgencies are those in which end-organ
damage is not occurring, and although prompt management is
required, this can be approached more gradually with oral
antihypertensive agents under close supervision, without
necessarily requiring admission to a critical care unit.
• Diagnosis
• A thorough history is taken, including any hypertension
management, known renal or cerebrovascular disease, eclampsia
in previous pregnancies if gravid, or use of stimulants or illicit
drugs such as cocaine.
• Patient assessment should include evidence of end-organ damage,
such as back pain (aortic dissection), neurological damage:
headache, altered consciousness, confusion, visual loss, stupor or
seizure activity (encephalopathy); cardiac damage: chest pain, ST
segment changes, cardiac enlargement, or the development of
heart failure or pulmonary edema; and renal damage: oliguria and
azotaemia.
• Serum urea, creatinine, electrolytes, urinalysis, ECG and chest X-
ray should be performed.
• Management
• More severe, or malignant, hypertension may cause retinal
hemorrhage or papilledema, and emergency treatment
should immediately be instituted.
• There is a need for rapid treatment of severe hypertension
include intracranial bleeding, acute myocardial infarction,
pheochromocytoma, recovery from cardiac surgery, and
bleeding from vascular procedure sites.
• Hypertensive emergencies in pregnancy threaten both the
mother and the fetus.
• The aim of treatment is to acutely lower the blood pressure,
but neither too quickly nor too dramatically.
• Recommendations vary, but an initial aim of 150/110–
160/100 mmHg within 2–6 hours, or a 25% reduction in mean
arterial pressure within 2 hours.
• Continuous direct arterial pressure monitoring should be in place during
treatment.
• Intravenous sodium nitroprusside, a rapidly acting arterial and venous
dilator, is most frequently used, at doses of 0.25–10 μg/kg/ min.97
Weaning of nitroprusside is undertaken after the later introduction of oral
antihypertensives.
• Care is required to avoid hypotension during treatment, as well as
rebound hypertension as nitroprusside is withdrawn.
• Rapidly acting beta-adrenergic blocking agents with short half-lives such
as IV esmolol may be used at doses of 50– 100 μg/kg/min (or higher) in
patients without standard contraindications to beta-adrenergic blockers
(asthma, heart failure).
• Glyceryl trinitrate infusions at 10–100 μg/ min or higher are used for
combined venous and arterial dilation, especially if there is angina.
• Intravenous furosemide may be introduced during the acute phase.
• After intravenous therapies have been established and progress towards
target pressures is made, oral agents are introduced. These include oral
beta-adrenergic blockers, calcium channel blockers, ACE inhibitors and
diuretics.
 CARDIOGENIC SHOCK
• Cardiogenic shock manifests as circulatory failure from cardiac
dysfunction,and is reflected in a low cardiac output (CI <2.1
L/min/m2), hypotension (SBP <90 mmHg) and severe pulmonary
congestion, high central vascular filling pressures (CVP; PAOP >18
mmHg).
• Cardiogenic shock is commonly associated with AMI and manifests
when 40% or more of the left ventricle is ischemic.
• It is also related to mechanical disorders (e.g. acute cardiac valvular
dysfunction or septal defects), deteriorating cardiomyopathies or
congestive cardiac failure, trauma and obstruction or inhibition of
left ventricular ejection (referred to as obstructive shock e.g.
pulmonary emboli, dissecting aneurysm, tamponade)
 CLINICAL MANIFESTATIONS
The clinical features of cardiogenic shock are reflective of congestive cardiac
failure, although with greater severity:

• low cardiac output and hypotension

• poor peripheral perfusion: pale, cool, clammy peripheries
• oliguria
• altered mentation, restlessness and anxiety
• tachycardia and arrhythmias
• pulmonary congestion with widespread inspiratory crackles and
hypoxemia (perhaps with frank pulmonary edema)
• dyspnoea and tachypnea
• respiratory alkalosis (hyperventilation) or acidosis (respiratory fatigue)
• lactic acidosis
• distended neck veins, elevated jugular venous pressure.
 NURSING PRACTICE

• Treatment of cardiogenic shock includes

hemodynamic management, respiratory and
cardiovascular support, biochemical
stabilization and reversal or correction of the
underlying cause. This complex presentation
requires a coordinated approach to the
multiple aspects of care of a patient with
cardiogenic shock.
• Independent Practice
• A rapid response to impending deterioration
associated with cardiogenic shock includes
repeated assessment and measures to
optimise oxygen supply and demand.
Assessment
Frequent, thorough assessment of the patient’s status is essential,
focusing on:

• 1. identification of patients at risk of clinical deterioration;

• 2. assessment of the severity of shock and identification of organ or
system dysfunction;
• 3. assessment of the impact of treatment; and
• 4. identification of complications of treatment.

• Assessment follows a systematic approach and is conducted as often

as indicated by the patient’s condition, centering on the
cardiovascular system, as well as related systems that cardiac
function influences, including respiratory, renal, neurological and
integumentary.
• Optimizing oxygen supply and demand

• As cardiogenic shock is associated with an imbalance of

oxygen supply and demand throughout the body,
measures to optimize this balance by increasing oxygen
supply and decreasing demand are essential. Strategies to
increase oxygen supply include:
– positioning the patient upright to promote optimum ventilation
by reducing venous return and lessening pulmonary edema
(but may contribute to worsening hypotension)
– administering oxygen, continuous positive airway pressure
(CPAP) and bi-level positive airway pressure (BiPAP) support as
required
Strategies to reduce oxygen demand include:
• limiting physical activity
• implementing measures to reduce patient anxiety,
including communication, explanation and analgesic
and sedative medications (avoiding those that are
cardio-depressive) where appropriate
• ensuring that visiting practices are appropriate for the
patient (which may require facilitating lengthy visits by
a loved one, limiting visiting time, or being selective
with the visitors who remain with the patient).
• Collaborative Management
• Typical treatment regimens require preload
reduction, augmentation of contractility with
intravenous inotropes and afterload
manipulation.
• Preload management
• Preload reduction relieves pulmonary
congestion, reduces myocardial workload and
improves contractility, which is in part impaired
by overstretched ventricles.
• Careful assessment of patient fluid status is
necessary prior to either the administration of
small aliquots of fluid to enhance deteriorating
myocardial function or enhanced diuresis to
reduce circulating blood volume.
Measures to reduce preload include:

• lsitting a patient up with their legs either hanging over the

side of the bed or in a dependent position
• IV diuretics (frusemide)68 given usually as intermittent
boluses or if necessary as a continuous infusion
• venodilation (glyceryl trinitrate infusions at 10–200 μg/min
titrated to blood pressure)69
• continuous haemofiltration (might be considered to rapidly
reduce circulating volume)
• continuous positive airway pressure (indicated for
pulmonary relief, with the additional benefit of reducing
venous return).
• Inotropic therapy
• Intravenous positive inotropes promote
myocardial contractility to improve cardiac
output and blood pressure.
• Afterload control
• Specific management of afterload, independent of contractility,
is sometimes necessary, although caution is needed as the
maintenance of blood pressure often provides little scope for
further afterload reduction.
• Arteriodilators such as sodium nitroprusside reduce afterload
and increase cardiac output, although with limitations due to
hypotension.
• The introduction of oral angiotensin-converting enzyme (ACE)
inhibitors as soon as possible after stabilization of the patient
with infarct-related cardiogenic shock is strongly recommended.
 Adjunctive therapies
• Intra-aortic balloon pumping
• Low cardiac output, pulmonary congestion, reduced MAP, and
myocardial ischaemia from cardiogenic shock may all be
improved by the introduction of intra-aortic balloon pump (IABP)
therapy.
• Balloon inflation during diastole raises MAP and promotes
coronary and systemic blood flow, while balloon deflation in
advance of systole reduces afterload.
• This afterload reduction improves cardiac output and reduces left
ventricular systolic pressure, lessening the oxygen demands of
the ischemic ventricle by reducing the necessary contractile force
of the left ventricle.
• Respiratory support
• Oxygen is administered for hypoxemia, but responses may be limited as
the primary gas exchange defect is an intrapulmonary shunt.
• Non-invasive ventilatory approaches may be sufficient, but a wary eye
for the need to intubate and mechanically ventilate should be
maintained in the acute phase of treatment.
• CPAP at conventional levels of 5–15 cmH2O is well established as a
support for the spontaneously breathing patient with pulmonary
edema.
• CPAP improves hypoxemia, lessens WOB, reduces left ventricular
afterload and provides additional benefit by impeding venous return,
an effect that may lessen pulmonary congestion. These benefits are
weighed against the potential for hypotension.
• Endotracheal intubation and ventilation
should be undertaken when neither CPAP nor
BiPAP result in improvement, or when the
patient continues to deteriorate or tire.
• Biochemical normalisation
Frequent biochemistry measurement is necessary to
detect and monitor the following aspects of care:
• arterial blood gases to identify the adequacy of
ventilation and oxygenation and the presence of
metabolic acidosis
• lactic acid measurement to assess the level of shock
and changes in patient response to treatment
• hypokalaemia or hypomagnesaemia due to aggressive
diuretic use
• hyperkalaemia due to severe acidosis, especially in the
presence of renal failure
• hyperglycemia due to the stress response to
acute illness, and in response to
sympathomimetic administration
• bicarbonate levels decline due to pH buffering,
but replacement therapy is not routinely
undertaken unless the arterial pH is life-
threatening
• urea and creatinine to detect the onset of acute
renal failure due to renal hypoperfusion.