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 (see Figure 9.2) 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.⁶ 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. When ischaemia occurs, the gap junctions may uncouple, so ions do not move as freely. Uncoupling may also contribute to the poor conduction evidenced on ECG during ischaemia.⁵

FIGURE 9.2 Diagram of an electron micrograph of cardiac muscle showing mitochondria, intercalculated discs, tubules and sarcoplasmic reticulum.⁵

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. It has been theorised that the endocardium may also have this function.^1,⁴

Coronary Perfusion

The heart is perfused by the right and left coronary arteries that arise from openings in the aorta called the coronary ostia (see Figure 9.3). 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. This is the most common distribution of the coronary arteries, but it is not uncommon for the right coronary artery to be small and the CX to supply the inferior wall of the left ventricle. The coronary arteries ultimately branch into a dense network of capillaries to support cardiac myocytes. Anastomoses between branches of the coronary arteries often occur in mature individuals when myocardial hypoxia has been present. These anastomoses are termed collateral arteries, but the contribution to normal cardiac perfusion during occlusion of coronary arteries is unclear.¹

FIGURE 9.3 Location of the coronary arteries.⁵

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. Other organelles in the myocyte, called 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) (see Figure 9.4). The myosin molecules of the thick filaments contain active sites that form bridges with sites of the actin molecules on the thin filaments. These filaments are arranged so that during contraction, bridges form and the thin filaments are pulled into the lattice of the thick filaments. As the filaments are pulled towards the centre of the sarcomere, the degree of contraction is limited by the length of the sarcomere. Starling’s law states that, within physiological limits, the greater the degree of stretch, the greater the force of contraction. The length of the sarcomere is the physiological limit because too great a stretch will disconnect the myosin–actin bridges.

FIGURE 9.4 Actin and myosin filaments and other cross-bridges responsible for cell contraction.⁵

Electrical events of Depolarisation, Resting Potential and Action Potential

Automaticity and rhythmicity are intrinsic properties of all myocardial cells. However, specialised autorhythmic cells in the myocardium generate and conduct impulses in a specific order to create a conduction pathway. This pathway ensures that contraction is coordinated and rhythmical, so that the heart pumps efficiently and continuously. 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 (see Figure 9.5).

FIGURE 9.5 (A) Action potential in a ‘fast response’, non-pacemaker myocyte: phases 0–4, resting membrane potential −80 mV, absolute refractory period (ARP) and relative refractory period (RRP). (B) Action potential in a ‘slow response’, pacemaker myocyte. The upward slope of phase 4, on reaching threshold potential, results in an action potential.⁷

Cell membrane pumps create concentration gradients across the cell membrane during diastole to create a resting electrical potential of −80 mV. Individual fibres are separated by membranes but depolarisation spreads rapidly because of the presence of gap junctions. 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.⁸

The contractile response begins just after the start of depolarisation and lasts about 1.5 times as long as the depolarisation and repolarisation (see Figure 9.6).

FIGURE 9.6 Action potential.⁵

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. The following is a summary of 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.⁶

Cardiac muscle is generally slow to respond to stimuli and has relatively low ATPase activity. Its fibres are dependent on oxidative metabolism and require a continuous supply of oxygen. The length of fibres and the strength of contraction are determined by the degree of diastolic filling in the heart. The force of contraction is enhanced by catecholamines.²

Depolarisation is initiated in the sino-atrial (SA) node and spreads rapidly through the atria, then converges on the atrio-ventricular (AV) node; atrial depolarisation 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 depolarisation takes 0.08–0.1 sec, and the last parts of the heart to be depolarised are the posteriobasal portion of the left ventricle, the pulmonary conus and the upper septum.⁸

The electrical activity of the heart can be detected on the body surface because body fluids are good conductors; the fluctuations in potential that represent the algebraic sum of the action potential of myocardial fibres can be recorded on an electrocardiogram (see later in chapter).

Cardiac Macrostructure and Conduction

The electrical and mechanical processes of the heart differ but are connected. The autorhythmic cells of the cardiac conduction pathway ensure that large portions of the heart receive an action potential rapidly and simultaneously. This ensures that the pumping action of the heart is maximised. 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 (see Figure 9.7). The cells contained in the pathway conduct action potentials extremely rapidly, 3–7 times faster than general myocardial tissue. 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.

FIGURE 9.7 Cardiac conduction system: AV, atrioventricular; RBB, right bundle branch; LBB, left bundle branch.⁵

At the myocyte, the action potential is transmitted to the myofibrils by calcium from the interstitial fluid via channels. During repolarisation (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.

The cardiac conduction system and the mechanical efficiency of the heart as a pump are directly connected. Disruption to conduction may not prevent myocardial contraction but may result in poor coordination and lower pump efficiency. Interruption to flow through the coronary arteries may alter depolarisation. Disrupted conduction from the SA to the AV node may allow another area in the conduction system to become the new dominant pacemaker and alter cardiac output. Although the autonomic nervous system influences cardiac function, the heart is able to function without neural control. Rhythmical myocardial contraction will continue because automaticity and rhythmicity are intrinsic to the myocardium.

Cardiac Output

Determinants of Cardiac Output

Cardiac performance is altered by numerous homeostatic mechanisms. Cardiac output is regulated in response to stress or disease, and changes in any of the factors that determine cardiac output will result in changes to cardiac output (see Figure 9.8). 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. However, 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.

FIGURE 9.8 Determinants of cardiac function and oxygen delivery.⁹

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 as indicated in Figure 9.8, 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. However, a threshold is reached when fibres become overstretched, and force of contraction and resultant stroke volume will fall.

Preload reduces as a result of large-volume loss (e.g. haemorrhage), 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). Some 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.

Preload of the left side of the heart, assessed at the end of filling of the left ventricle from the left atrium using the pulmonary capillary wedge pressure (PCWP), is assumed for clinical purposes to reflect left ventricular end-diastolic volume (LVEDV). Due to the non-linear relationship between volume and pressure,¹⁰ caution must, however, be taken when interpreting these values, as rises in LVEDP may indicate pathology other than increased preload. Preload of the right side of the heart is indirectly assessed at the end of filling of the right ventricle from the right atrium through central venous pressure (CVP) monitoring.

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. Afterload of the right side of the heart is assessed during the ejection of blood from the right ventricle into the pulmonary artery. This volume is indirectly assessed by calculating pulmonary vascular resistance. 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, and this limits the extent to which afterload can be manipulated.

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 difficult to measure clinically. It is increased by catecholamines, calcium, relief of ischaemia and digoxin. It is decreased by hypoxia, ischaemia, and certain drugs such as thiopentone, β-adrenergic blockers, calcium channel blockers or sedatives. Such changes affect cardiac performance, with increases in contractility causing 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.

Cardiac output is dependent on a series of mechanical events in the cardiac cycle (see Figure 9.9). As normal average heart rate is maintained at approximately 70 beats/min the average phases of the cardiac cycle are completed in less than a second (0.8 sec). Electrical stimulation of myocardial contraction ensures that the four chambers of the heart contract in sequence. This allows the atria to act as primer pumps for the ventricles, while the ventricles are the major pumps that provide the impetus for blood through the pulmonary and systemic vascular systems. The phases of the cardiac cycle are characterised by pressure changes within each of the heart chambers, resulting in blood flow from areas of high pressure to areas of lower pressure.

FIGURE 9.9 The cardiac cycle.⁵

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 repolarise 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.¹

Regulation of Cardiac Output

The heart is a very effective pump and is able to adapt to meet the metabolic needs of the body. 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. Blood flow into the heart depends on venous return from systemic and pulmonic veins and varies according to tissue metabolism, total blood volume and vasodilation. Venous return contributes to end-diastolic volume (preload) and pressure, which are both directly related to the force of contraction in the next ventricular systole. The intrinsic capacity of the heart to respond to changes in end-diastolic pressure can be represented by a number of length–tension curves and the Frank-Starling mechanism (see Figure 9.10). According to this mechanism, within limits, the more stretch on the cardiac muscle fibre before contraction, the greater the strength of contraction. The ability to increase strength of contraction in response to increased stretch is because there is an optimal range of cross-bridges that can be created between actin and myosin in the myocyte. Under this range, when venous return is poor, fewer cross-bridges can be created. Above this range, when heart failure is present, the cross-bridges can become partially disengaged, contraction is poor, and higher filling pressures are needed to achieve adequate contractile force.

FIGURE 9.10 The Frank-Starling curve. As left ventricular end-diastolic pressure increases, so does ventricular stroke work.⁵

Ventricular contraction is also intrinsically influenced by the size of the ventricle and the thickness of the ventricle wall. This mechanism is described by Laplace’s law, which states that the amount of tension generated in the wall of the ventricle required to produce intraventricular pressure depends on the size (radius and wall thickness) of the ventricle.¹ As a result, in heart failure, when ventricular thinning and dilation is present, more tension or contractile force is required to create intraventricular pressure and therefore cardiac output.

The heart’s ability to pump effectively is also influenced by the pressure that is required to generate above end diastolic pressure to eject blood during systole. This additional pressure is usually determined by how much resistance is present in the pulmonary artery and aorta, and is in turn influenced by the peripheral vasculature. This systemic vascular resistance, causing resistance to flow known and measured as afterload, is in relation to the left ventricle and is influenced by vascular tone and disease.

Autonomic nervous system control and regulation of heart rate

Although the pacemaker cells of the heart are capable of intrinsic rhythm generation (automaticity), 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.¹⁰ 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). Conversely, slowing of the heart rate can be achieved by decreasing sympathetic or increasing parasympathetic activity.⁴

Hormonal, biochemical and pharmacological inputs also exert heart rate influences by their effect on autonomic neural receptors or directly on pacemaker cells. In mimicking the effects of direct nervous inputs, these influences may be described as sympathomimetic or parasympathomimetic. Sympathomimetic stimulation (e.g. through the use of isoprenaline) achieves the same cardiac endpoints as direct sympathetic activity, increasing the heart rate, while sympathetic antagonism (e.g. beta-blockade therapy) slows the heart through receptor inhibition. By contrast, parasympathomimetic agonist activity slows the heart rate, while parasympathetic antagonism (e.g. via administration of atropine sulphate) raises the heart rate by causing parasympathetic receptor blockade.⁴

The Vascular System

The vascular system is specialised according to the different tissue it supplies, but the general functions and characteristics are similar. 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 characterised 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 (see Figure 9.11). Just before the capillary beds are precapillary sphincters, bands of smooth muscle that adjust flow in the capillaries. Venules collect blood from the capillaries to veins. Excess tissue fluid is collected by the lymphatic system. Lymphatic veins have a similar structure to the cardiovascular system veins described below, with lymph returning to this system at the right side of the heart.

FIGURE 9.11 The structure of arteries, veins and capillaries.³

Veins collect and transport blood back to the heart at low pressure and serve as a reservoir for blood. Therefore, veins are numerous and have thinner, less muscular walls, which can dilate to store extra blood (up to 64% of total blood volume at any time). Some veins, particularly in the lower limbs, contain valves to prevent backflow and ensure one-way flow to the heart. Venous return is promoted during standing and moving by the muscles of the legs compressing the deep veins, promoting blood flow towards the heart.^1,⁴

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. The focus of the cardiovascular assessment varies according to the setting, clinical presentation and treatments commenced, if any. However, the main priority should be to determine whether the patient is haemodynamically stable or requiring initiation or adjustment of supportive treatments.

A thorough cardiac assessment requires the critical care nurse to be competent in a wide range of interpersonal, observational, and technical skills. A cardiac assessment should be performed as part of a comprehensive patient assessment and should consider the following elements.

It is important to create a health history, if not already obtained. This history should aim to elicit a description of the present illness and chief complaint. 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, generalised fatigue, dyspnoea, cough, weight gain or dependent oedema. Chest pain, discomfort or tightness should be initially considered indicative of cardiac ischaemia until proven otherwise by further examination and diagnostic assessment. Additionally, a health history should be inclusive of known cardiovascular risk factors, such as hyperlipidaemia or hypertension, and any medications the patient may be taking including over the counter medications.

Prior to inspecting or palpating the patient, 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. Additionally, assessment of any pain should be noted.

Specific physical assessment in relation to cardiovascular function should be inclusive of:

Assessment of Pulse

In the critical care environment, the heart rate can be observed from a cardiac monitor; however, this does not give qualitative information about the arterial pulse. Routinely performed as part of most patient assessments, information gathered from pulse assessment can give useful cues and direct further assessments. Although 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. In addition to rate and rhythm, assessment of pulse, especially if palpated in the carotid or femoral artery, can reveal a bounding pulse, that may be indicative of hyperdynamic 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. While challenging to achieve competence in, cardiac auscultation is an important part of cardiac physical examination and relies on sound understanding of cardiac anatomy, cardiac cycle and physiologically associated sounds. For accurate auscultation, experience in assessment of normal sounds is critical and can only be obtained through constant practice. 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.

Practice tip

When learning to interpret heart sounds, feel the carotid pulse at the same time as auscultation which will help identify the heart sound that corresponds with ventricular systole (S1).

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 triscupid and 5th ICS left of the midclavicular line for mitral valve). Following closure of these two valves, ventricular contraction and ejection occurs and a carotid pulse may be palpated at the same time that S1 is audible.

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.

A guide to placement of stethoscope when listening to heart sounds is presented in Table 9.1.

TABLE 9.1 Guide to placement of stethoscope when listening to heart sounds

Stethescope placement		Auditable region of heart
2nd intercostal space	right of sternum	aortic valve
2nd intercostal space	left of sternum	pulmonary valve
4th intercostal space	left side of sternum	tricuspid valve
5th intercostal space	midclavicular line	mitral valve

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. As S3 occurs early in diastole, it will be heard and associated more closely with S2.

S4 is a late diastolic sound and may be heard shortly before S1. S4 occurs when ventricular compliance is reduced secondary to aortic or pulmonary stenosis, mitral regurgitation, systemic hypertension, advanced age or ischaemic heart disease. Patients with severe ventricular dysfunction may have both S3 and S4 audible, although when coupled with tachycardia, these may be difficult to differentiate and will require specialist assessment.

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. Detection of pericardial rub warrants further investigation by ultrasound.

Practice tip

To differentiate pericardial rub from pulmonary rub, ask the patient to hold their breath for a short duration as pericardial rub will continue to be audible in the absence of breathing and pleural rub will not be audible while the patient is not breathing.

In addition to pericardial rub, murmurs may also be audible. Murmurs are generally classified and characterised by location with the most common murmurs associated with the mitral or aortic valves due to either stenosis or regurgitation at these locations. Murmurs are best thought of as turbulent flow or vibrations associated with the corresponding valve and can be of variable pitch. Specialist cardiac referral is indicated upon detection of cardiac murmurs to differentiate pathological murmurs as seen during valvular dysfunction or myocardial infarction from innocent systolic ‘high flow’ murmurs detected in children or adolescents as a result of vigorous ventricular contraction. Murmurs may be classified using the Levine scale,¹² seen in Table 9.2.

TABLE 9.2 Classification of heart murmurs using the Levine scale ¹²

Grade 1	low intensity and difficult to hear
Grade 2	low intensity, but audible with a stethoscope but no palpable thrill
Grade 3	medium intensity and easily heard with a stethoscope
Grade 4	loud and audible and with palpable thrill
Grade 5	very loud but cannot be heard outside the praecordium and with palpable thrill
Grade 6	audible with the stethoscope away from the chest

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.

Internationally, a minimum standard for an ICU requires availability of facilities for cardiovascular monitoring.¹³ 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. In addition, practice standards for electrocardiographic monitoring in hospital settings have been established.¹⁴

It is now common practice for five leads to be used for continuous cardiac monitoring,⁵ as this allows a choice of seven views. The five electrodes are placed as follows:¹⁵

• 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 monitoring lead of choice is determined by the patient’s clinical situation.¹⁵ Generally, two views are better than one. V1 lead is best to view ventricular activity and differentiate right and left bundle branch blocks; therefore, one of the channels on the bedside monitor should display a V lead, preferably V1, and the other display lead II or III for optimal detection of arrhythmias. When the primary purpose of monitoring is to detect ischaemic changes leads III and V3 usually present the optimal combination.¹⁴

The skin must be carefully prepared before electrodes are attached, as contact is required with the body surface and poor contact will lead to inaccurate or unreadable recordings, causing interference or noise. Patients who are sweaty need particular attention, and it may be necessary to shave the areas where the electrodes are to be placed in very hairy people.

12-lead ECG

The Dutch physiologist Einthoven was one of the first to represent heart electrical conduction as two charged electrodes, one positive and one negative.¹⁶ The body can be likened to a triangle, with the heart at its centre, and this has been called Einthoven’s triangle. Cardiac electrical activity can be captured by placing electrodes on both arms and on the left leg. When these electrodes are connected to a common terminal with an indifferent electrode that stays near zero, an electrical potential is obtained. Depolarisation moving towards an active electrode produces positive deflection.

The 12-lead ECG consists of six limb leads and six chest leads. The limb leads examine electrical activity along a vertical plane. The standard bipolar limb leads (I, II, III) record differences in potential between two limbs by using two limb electrodes as positive and negative poles (see Figure 9.12):¹⁷ Leads I, II, and III all produce positive deflections on the ECG because the electrical current flows from left to the right and from upwards to downwards. 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

FIGURE 9.12 Einthoven triangle formed by standard limb leads.¹⁷

The three unipolar limb leads (aVR, aVL, aVF) record activity of the heart’s frontal plane. Each of these unipolar leads have only one positive electrode (the limb electrode such as left arm, right arm and left leg), with the centre of the Einthoven’s triangle acting as the negative electrode. The waveforms of these leads are usually very small therefore they are augmented by the ECG machine to increase the size of the potentials on the ECG strip.¹⁷ 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 aVR does not provide a specific view of the heart.

• 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 (see Figure 9.13):

• 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

FIGURE 9.13 Position of chest leads.¹⁷

Amplitude (voltage) in the ECG is measured by a series of horizontal lines on the ECG (see Figure 9.14). Each line is 1 mm apart and represents 0.1 mV. Amplitude reflects the wave’s electrical force and has no relation to the muscle strength of ventricular contraction.⁸ Duration of activity within the ECG is measured by a series of vertical lines also 1 mm apart (see Figure 9.14). The time interval between each line is 0.04 sec. Every 5th line is printed in bold, producing large squares. Each represents 0.5 mV (vertically) and 0.2 sec (horizontally).