Professional Documents
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Cardiovascular Assessment
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 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).
• 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.
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
• 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:
• 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:
• 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.
• 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.
• 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