Chapter 14 Cardiovascular disease
Myocardial cells constitute 75% of the heart mass but only about 25% of the cell number. They are designed to perform two fundamental functions: initiation and conduction of electrical impulses and contraction. Although most myocardial cells are able to perform both these functions, the vast majority are predominantly contractile cells (myocytes) and a small number are specifically designed as electrical cells. The latter, collectively known as the conducting system of the heart, are not nervous tissue but modified myocytes lacking in myofibril components. They have the ability to generate electrical impulses which are then conducted to the myocytes, leading to contraction by a process known as excitation-contraction coupling. The rate of electrical impulse generation and the force of myocardial contraction are modified by numerous factors including autonomic input and stretch.
Three epicardial coronary arteries supply blood to the myocardium, and a more complex network of veins is responsible for drainage. In the face of continuous arterial pressure fluctuations, blood vessels, especially in the cerebral circulation, maintain constant tissue perfusion by a process known as ‘autoregulation’; blood vessel control is, however, complex involving additional local and central mechanisms.
The sinus node is a complex spindle-shaped structure that lies in the lateral and epicardial aspects of the junction between the superior vena cava and the right atrium (Fig. 14.1). Physiologically, it generates impulses automatically by spontaneous depolarization of its membrane at a rate quicker than any other cardiac cell type. It is therefore the natural pacemaker of the heart.
A number of factors are responsible for the spontaneous decay of the sinus node cell membrane potential (‘the pacemaker potential’), the most significant of which is a small influx of sodium ions into the cells. This small sodium current has two components: the background inward current (Ib) and the ‘funny’ (If) current (or pacemaker current) (Fig. 14.2). The term ‘funny’ current denotes ionic flow through channels activated in hyperpolarized cells (−60 mV or greater), unlike other time- and voltage-dependent channels activated by depolarization. The rate of depolarization of the sinus node membrane potential is modulated by autonomic tone (i.e. sympathetic and parasympathetic input), stretch, temperature, hypoxia, blood pH and in response to other hormonal influences (e.g. tri-iodothyronine and serotonin).
Figure 14.2 Myocardial action potentials. Ib, background inward sodium current; If, ‘funny’ current; ICaT, transient (or ‘T’ type) and ICaL, long-lasting (or ‘L’ type) calcium channels; INa, inward sodium current; ITo, transient outward potassium current; IKl, inward rectifier potassium current; IK delayed rectifier potassium current.
Action potentials in the sinus node trigger depolarization of the atrial and subsequently the ventricular myocytes. These cells have a different action potential from that of sinus node cells (Fig. 14.2). Their resting membrane potential is a consequence of a small flow of potassium ions into the cells through open ‘inward rectifier’ channels (IKl); at this stage sodium and calcium channels are closed. The arrival of adjacent action potentials triggers the opening of voltage-gated, fast, self-inactivating sodium channels, resulting in a sharp depolarization spike. This is followed by a partial repolarization of the membrane due to activation of ‘transient outward’ potassium channels.
The plateau phase which follows is unique to myocytes and results from a small, but sustained inward calcium current through L-type calcium channels (ICaL) lasting 200–400 ms. This calcium influx is caused by a combined increase in permeability of the cell, especially the sarcolemmal membranes to calcium (Fig. 14.3). This plateau (or refractory) phase in myocyte action potential prevents early reactivation of the myocytes and directly determines the strength of contraction. The gradual inactivation of the calcium channels activates delayed rectifier potassium channels (IK) repolarizing the membrane. Atrial tissue is activated like a ‘forest fire’, but the activation peters out when the insulating layer between the atrium and the ventricle – the annulus fibrosus – is reached. Controversy exists about whether impulses from the sinoatrial (SA) node travel over specialized conducting ‘pathways’ or over ordinary atrial myocardium.
Figure 14.3 The ‘complete’ cardiac cell. (1) Spontaneous depolarization in sinus node cells due to sodium (Na) influx through the ‘funny’ current generates the ‘pacemaker’ potential. (2) This activates other atrial and ventricular myocytes, triggering action potentials and activating L-type calcium (Ca) channels in the surface and transverse tubule membranes (at top and bottom of figure). (3) The resulting Ca influx acts on Ca-induced Ca release channels (RyR2) on the sarcoplasmic reticulum (SR), resulting in release of stored Ca, which acts on actin and myosin fibrils, resulting in contraction. Ca reuptake pumps in the SR, regulated by phospholamban, replenish the stores; various exchange pumps also expel Ca from the cell. (4) Autonomic input has either a positive chronotropic/inotropic effect (β1 receptors) or a negative chronotropic/inotropic effect (muscarinic receptors).
The depolarization continues to conduct slowly through the atrioventricular (AV) node. This is a small, bean-shaped structure that lies beneath the right atrial endocardium within the lower interatrial septum. The AV node continues as the His bundle, which penetrates the annulus fibrosus and conducts the cardiac impulse rapidly towards the ventricle. The His bundle reaches the crest of the interventricular septum and divides into the right bundle branch and the main left bundle branch.
The right bundle branch continues down the right side of the interventricular septum to the apex, from where it radiates and divides to form the Purkinje network, which spreads throughout the subendocardial surface of the right ventricle. The main left bundle branch is a short structure, which fans out into many strands on the left side of the interventricular septum. These strands can be grouped into an anterior superior division (the anterior hemi-bundle) and a posterior inferior division (the posterior hemi-bundle). The anterior hemi-bundle supplies the subendocardial Purkinje network of the anterior and superior surfaces of the left ventricle, and the inferior hemi-bundle supplies the inferior and posterior surfaces. Impulse conduction through the AV node is slow and depends on action potentials largely produced by slow transmembrane calcium flux. In the atria, ventricles and His-Purkinje system, conduction is rapid and is due to action potentials generated by rapid transmembrane sodium diffusion.
Each myocyte, approximately 100 µm long, branches and interdigitates with adjacent cells. An intercalated disc permits electrical conduction to adjacent cells. Myocytes contain bundles of parallel myofibrils. Each myofibril is made up of a series of sarcomeres (Fig. 14.4). A sarcomere (which is the basic unit of contraction) is bound by two transverse Z lines, to each of which is attached a perpendicular filament of the protein actin. The actin filaments from each of the two Z bands overlap with thicker parallel protein filaments known as myosin. Actin and myosin filaments are attached to each other by cross-bridges that contain ATPase, which breaks down adenosine triphosphate (ATP) to provide the energy for contraction.
Two chains of actin molecules form a helical structure, with another molecule, tropomyosin, in the grooves of the actin helix, and a further molecule, troponin, is attached to every seven actin molecules. During cardiac contraction the length of the actin and myosin monofilaments does not change. Rather, the actin filaments slide between the myosin filaments when ATPase splits a high-energy bond of ATP. To supply the ATP, the myocyte (which cannot stop for a rest) has a very high mitochondrial density (35% of the cell volume). As calcium ions bind to troponin C, the activity of troponin I is inhibited, which induces a conformational change in tropomyosin. This event unlocks the active site between actin and myosin, enabling contraction to proceed.
Calcium is made available during the plateau phase of the action potential by calcium ions entering the cell and by being mobilized from the sarcoplasmic reticulum through the ryanodine receptor (RyR2) calcium-release channel. RyR2 activity is regulated by the protein calstabin 2 (see p. 770) and nitric oxide. The force of cardiac muscle contraction (‘inotropic state’) is thus regulated by the influx of calcium ions into the cell through calcium channels (Fig. 14.3). T (transient) calcium channels open when the muscle is more depolarized, whereas L (long-lasting) calcium channels require less depolarization. The extent to which the sarcomere can shorten determines the stroke volume of the ventricle. It is maximally shortened in response to powerful inotropic drugs or severe exercise.
The contractile function of an isolated strip of cardiac tissue can be described by the relationship between the velocity of muscle contraction, the load that is moved by the contracting muscle, and the extent to which the muscle is stretched before contracting. As with all other types of muscle, the velocity of contraction of myocardial tissue is reduced by increasing the load against which the tissue must contract. However, in the non-failing heart, pre-stretching of cardiac muscle improves the relationship between the force and velocity of contraction (Fig. 14.5).
Figure 14.5 The Frank–Starling mechanism, showing the effect on ventricular contraction of alteration in filling pressures and outflow impedance in the normal, failing and sympathetically stimulated ventricle.
This phenomenon was described in the intact heart as an increase of stroke volume (ventricular performance) with an enlargement of the diastolic volume (preload), and is known as ‘Starling’s law of the heart’ or the ‘Frank–Starling relationship’. It has been transcribed into more clinically relevant indices. Thus, stroke work (aortic pressure × stroke volume) is increased as ventricular end-diastolic volume is raised. Alternatively, within certain limits, cardiac output rises as pulmonary capillary wedge pressure increases. This clinical relationship is described by the ventricular function curve (Fig. 14.5), which also shows the effect of sympathetic stimulation.
Adrenergic nerves supply atrial and ventricular muscle fibres as well as the conduction system. β1-Receptors predominate in the heart with both epinephrine (adrenaline) and norepinephrine (noradrenaline) having positive inotropic and chronotropic effects. Cholinergic nerves from the vagus supply mainly the SA and AV nodes via M2 muscarinic receptors. The ventricular myocardium is sparsely innervated by the vagus. Under basal conditions, vagal inhibitory effects predominate over the sympathetic excitatory effects, resulting in a slow heart rate.
β1-Adrenergic stimulation enhances Ca2+ flux in the myocyte and thereby strengthens the force of contraction (Fig. 14.3). Binding of catecholamines, e.g. norepinephrine (noradrenaline), to the myocyte β1-adrenergic receptor stimulates membrane-bound adenylate kinases. These enzymes enhance production of cyclic adenosine monophosphate (cAMP) that activates intracellular protein kinases, which in turn phosphorylate cellular proteins, including L-type calcium channels within the cell membrane. β1-Adrenergic stimulation of the myocyte also enhances myocyte relaxation.
The return of calcium from the cytosol to the sarcoplasmic reticulum (SR) is regulated by phospholamban (PL), a low-molecular-weight protein in the SR membrane. In its dephosphorylated state, PL inhibits Ca2+ uptake by the SR ATPase pump (Fig. 14.3). However, β1-adrenergic activation of protein kinase phosphorylates PL, and blunts its inhibitory effect. The subsequently greater uptake of Ca2+ ions by the SR hastens Ca2+ removal from the cytosol and promotes myocyte relaxation.
The cardiac cycle (Fig. 14.6) consists of precisely timed rhythmic electrical and mechanical events that propel blood into the systemic and pulmonary circulations. The first event in the cardiac cycle is atrial depolarization (a P wave on the surface ECG) followed by right atrial and then left atrial contraction. Ventricular activation (the QRS complex on the ECG) follows after a short interval (the PR interval). Left ventricular contraction starts and shortly thereafter right ventricular contraction begins. The increased ventricular pressures exceed the atrial pressures, and close first the mitral and then the tricuspid valves.
Until the aortic and pulmonary valves open, the ventricles contract with no change of volume (isovolumetric contraction). When ventricular pressures rise above the aortic and pulmonary artery pressures, the pulmonary valve and then the aortic valve open and ventricular ejection occurs. As the ventricles begin to relax, their pressures fall below the aortic and pulmonary arterial pressures, and aortic valve closure is followed by pulmonary valve closure. Isovolumetric relaxation then occurs. After the ventricular pressures have fallen below the right atrial and left atrial pressures, the tricuspid and mitral valves open. The cardiac cycle can be graphically depicted as the relationship between the pressure and volume of the ventricle. This is shown in Figure 14.7, which illustrates the changing pressure-volume relationships in response to increased contractility and to exercise.
The coronary arterial system (Fig. 14.8) consists of the right and left coronary arteries. These arteries branch from the aorta, arising immediately above two cusps of the aortic valve. These arteries are unique in that they fill during diastole, when not occluded by valve cusps and when not squeezed by myocardial contraction. The right coronary artery arises from the right coronary sinus and courses through the right side of the AV groove, giving off vessels that supply the right atrium and the right ventricle. The vessel usually continues as the posterior descending coronary artery, which runs in the posterior interventricular groove and supplies the posterior part of the interventricular septum and the posterior left ventricular wall.
Figure 14.8 (a) Diagram of the normal coronary arterial anatomy. (b) Angiogram of non-dominant right coronary system. (c) Angiogram of dominant left coronary system from the same patient. Right anterior oblique projection.
Within 2.5 cm of its origin from the left coronary sinus, the left main coronary divides into the left anterior descending artery and the circumflex artery. The left anterior descending artery runs in the anterior interventricular groove and supplies the anterior septum and the anterior left ventricular wall. The left circumflex artery travels along the left AV groove and gives off branches to the left atrium and the left ventricle (marginal branches).
The sinus node and the AV node are supplied by the right coronary artery in about 60% and 90% of people, respectively. Therefore, disease in this artery may cause sinus bradycardia and AV nodal block. The majority of the left ventricle is supplied by the left coronary artery and disease in this vessel can cause significant myocardial dysfunction.
Some blood from the capillary beds in the wall of the heart drains directly into the cavities of the heart by tiny veins, but the majority returns by veins which accompany the arteries, to empty into the right atrium via the coronary sinus. An extensive lymphatic system drains into vessels that travel along the coronary vessels and then into the thoracic duct.
In functional terms, the tunica intima with the vascular endothelium and the smooth-muscle-cell-containing tunica media are the main constituents of blood vessels. These two structures are closely interlinked by a variety of mechanisms to regulate vascular tone. The central control of blood vessels is achieved via the neuroendocrine system. Sympathetic vasoconstrictor and parasympathetic vasodilator nerves regulate vascular tone in response to daily activity. Where neural control is impaired, or in various pathological states, e.g. haemorrhage, endocrine control of blood vessels mediated through epinephrine (adrenaline), angiotensin and vasopressin takes over.
At a local level, tissue perfusion is maintained automatically and by the effect of various factors synthesized and/or released in the immediate vicinity. In the face of fluctuating arterial pressures, blood vessels vasoconstrict independently of nervous input when blood pressure drops and vice versa. This process of autoregulation is a consequence of:
The vascular endothelium is a cardiovascular endocrine organ, which occupies a strategic interface between blood and other tissues. It produces various compounds (e.g. nitric oxide (NO), prostacyclin (PGI2), endothelin, endothelial-derived hyperpolarizing factor (ERHF), adhesion molecules, vascular endothelial growth factor (VEGF)) and has enzymes located on the surface controlling the levels of circulating compounds such as angiotensin, bradykinin and serotonin. It has many regulatory roles:
Nitric oxide is a diffusible gas with a very short half-life, produced in endothelial cells from the amino acid L-arginine via the action of the enzyme NO synthase (NOS), which is controlled by cytoplasmic calcium/calmodulin (Fig. 14.9). It is produced in response to various stimuli (Table 14.1), triggering vascular smooth muscle relaxation through activation of guanylate cyclase, leading to an increase in the intracellular levels of cyclic 3,5-guanine monophosphate (cGMP). Its cardiovascular effects protect against atherosclerosis, high blood pressure, heart failure and thrombosis. NO is also the neurotransmitter in various ‘nitrergic’ nerves in the central and peripheral nervous systems and may play a role in the central regulation of vascular tone. The class of drugs used to treat erectile dysfunction, the phosphodiesterase (PDE5) inhibitors, prevent the breakdown of cGMP and promote vasodilatation.
Figure 14.9 Nitric oxide (NO): the stimulus for production and function of NO. Various stimuli lead to the production of NO via cytoplasmic calcium/calmodulin. NO triggers smooth muscle relaxation via the activation of guanyl cyclase. ROC, receptor-operated Ca2+ channel; SAC, stretch-activated Ca2+ channel; IP3, inositol triphosphate; ER, endoplasmic reticulum; GTP, guanine triphosphate; cGMP, cyclic guanine monophosphate.
Endothelial-derived hyperpolarizing factor
von Willebrand factor
P, L, E selectins
Vascular endothelial growth factor (VEGF)
ICAM, intracellular adhesion molecule; VCAM, vascular cell adhesion molecule, PECAM, platelet/endothelial cell adhesion molecule; TNF, tumour necrosis factor; IL, interleukin.
Endothelin is a 21-amino-acid peptide that counteracts the effects of NO. Its production is inhibited by shear stress, i.e. the stress exerted on the vessel wall by the flowing blood, and it causes profound vasoconstriction and vascular smooth muscle hypertrophy. It is thought to play a role in the genesis of hypertension and atheroma.
Angiotensin-converting enzyme located on the endothelial cell membrane converts circulating angiotensin I (synthesized by the action of renin on angiotensinogen) to angiotensin II which has vasoconstrictor properties and leads to aldosterone release (Fig. 12.5). Aldosterone promotes sodium absorption from the kidney and together with the angiotensin-induced vasoconstriction provides haemodynamic stability.
Other factors which influence vasomotor tone include histamine (released by mast cells), bradykinin (synthesized from kininogen by the action of coagulation factor XIIa) and serotonin released by platelets.
PGI2, produced from arachidonic acid in the endothelial cell membrane by the action of the enzyme cyclo-oxygenase, inhibits platelet aggregation. Low-dose aspirin prevents activation of the cyclo-oxygenase pathway in platelets but only to a degree that does not affect PGI2 synthesis, unlike higher doses. Other antithrombotic agents such as clopidogrel (ADP receptor antagonist) and glycoprotein IIb/IIIa inhibitors achieve their effects by acting directly on platelet receptors. The antithrombotic effect of PGI2 is aided by NO, affecting platelets via activation of guanylate cyclase. The endothelial cell membrane also produces other anticoagulant molecules such as thrombomodulin, heparin sulphate and various fibrinolytic factors. Clinically used, fast-acting, heparin preparations are identical to this naturally occurring molecule.
In addition to their ability to prevent clotting, endothelial cells also aid thrombosis. They are responsible for the production of von Willebrand factor through a unique organelle called the Weibel–Palade body, which not only acts as a carrier for factor VIII but also promotes platelet adhesion by binding to exposed collagen (p. 414).
In response to various inflammatory mediators, the vascular endothelium expresses various so-called ‘adhesion molecules’ which promote leucocyte attraction, adhesion and infiltration into the blood vessel wall (Chapter 3).
The endothelial cells are also responsible for the development of new blood vessels (‘angiogenesis’) in the placenta, wound healing, tissue repair and tumour growth. This process is facilitated by VEGF.
The severity of cardiac symptoms or fatigue is classified according to the New York Heart Association (NYHA) grading of cardiac status (see Table 14.19). The differential diagnosis of chest pain is given in Table 14.2.
Ischaemic heart disease (infarction or angina)
Coronary artery spasm
Mitral valve prolapse
Bornholm disease (epidemic myalgia)
Oesophageal disease (see Box 6.3)
Costochondritis (Tietze disease)
Trauma (soft tissue, rib)
Left ventricular failure causes dyspnoea due to oedema of the pulmonary interstitium and alveoli. This makes the lungs stiff (less compliant), thus increasing the respiratory effort required to ventilate the lungs. Tachypnoea (increased respiratory rate) is often present owing to stimulation of pulmonary stretch receptors.
Orthopnoea refers to breathlessness on lying flat. Blood is redistributed from the legs to the torso, leading to an increase in central and pulmonary blood volume. The patient uses an increasing number of pillows to sleep.
Paroxysmal nocturnal dyspnoea (PND) is when a patient is woken from sleep fighting for breath. It is due to the same mechanisms as orthopnoea. However, as sensory awareness is reduced whilst asleep, the pulmonary oedema can become quite severe before the patient is awoken.
Central sleep apnoea syndrome (CSAS). If hypopnoea occurs rather than apnoea, the phenomenon is termed ‘periodic breathing’, but the two variations are known together as CSAS. This occurs due to malfunctioning of the respiratory centre in the brain, caused by poor cardiac output with concurrent cerebrovascular disease. The symptoms of CSAS, such as daytime somnolence and fatigue, are similar to those of obstructive sleep apnoea syndrome (OSAS, p. 818) and there is considerable overlap with the symptoms of heart failure. CSAS is believed to lead to myocardial hypertrophy and fibrosis, deterioration in cardiac function and complex arrhythmias, including non-sustained ventricular tachycardia, hypertension and stroke. Patients with CSAS have a worse prognosis compared to similar patients without CSAS.
These represent an increased awareness of the normal heart beat or the sensation of slow, rapid or irregular heart rhythms. The most common arrhythmias felt as palpitations are premature ectopic beats and paroxysmal tachycardias. A useful trick is to ask patients to tap out the rate and rhythm of their palpitations, as the different arrhythmias have different characteristics:
Premature beats (ectopics) are felt by the patient as a pause followed by a forceful beat. This is because premature beats are usually followed by a pause before the next normal beat, as the heart resets itself. The next beat is more forceful as the heart has had a longer diastolic period and therefore is filled with more blood before this beat.
Bradycardias (p. 702) may be appreciated as slow, regular, heavy or forceful beats. Most often, however, they are simply not sensed. All palpitations can be graded by the NYHA cardiac status (see Table 14.19).
A vasovagal attack is a simple faint and is the most common cause of syncope. The mechanism begins with peripheral vasodilatation and venous pooling of blood, leading to a reduction in the amount of blood returned to the heart. The near-empty heart responds by contracting vigorously, which in turn stimulates mechanoreceptors (stretch receptors) in the inferoposterior wall of the left ventricle. These in turn trigger reflexes via the central nervous system, which act to reduce ventricular stretch (i.e. further vasodilatation and sometimes profound bradycardia), but this causes a drop in blood pressure and therefore syncope. These episodes are usually associated with a prodrome of dizziness, nausea, sweating, tinnitus, yawning and a sinking feeling. Recovery occurs within a few seconds, especially if the patient lies down.
Postural (orthostatic) hypotension is a drop in systolic blood pressure of 20 mmHg or more on standing from a sitting or lying position. Usually, reflex vasoconstriction prevents a drop in pressure but if this is absent or the patient is fluid depleted or on vasodilating or diuretic drugs, hypotension occurs.
Postprandial hypotension is a drop in systolic blood pressure of ≥20 mmHg or the systolic blood pressure drops from above 100 mmHg to under 90 mmHg within 2 hours of eating. The mechanism is unknown but may be due to pooling of blood in the splanchnic vessels. In normal subjects, this elicits a homeostatic response via activation of baroreceptors and the sympathetic system, peripheral vasoconstriction and an increase in cardiac output.
Obstructive. The obstructive cardiac causes listed in Table 14.3 all lead to syncope due to restriction of blood flow from the heart into the rest of the circulation, or between the different chambers of the heart.
Arrhythmias. Stokes–Adams attacks (p. 700) are a sudden loss of consciousness unrelated to posture and due to intermittent high-grade AV block, profound bradycardia or ventricular standstill. The patient falls to the ground without warning, is pale and deeply unconscious. The pulse is usually very slow or absent. After a few seconds the patient flushes brightly and recovers consciousness as the pulse quickens. Often there are no sequelae, but patients may injure themselves during falls. Occasionally a generalized convulsion may occur if the period of cerebral hypoxia is prolonged, leading to a misdiagnosis of epilepsy.
Moya A, Sutton R, Ammirati F et al. Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS). Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009; 30(21):2631–2671.
Fatigue may be a symptom of inadequate systemic perfusion in heart failure. It is due to poor sleep, a direct side-effect of medication, particularly beta-blockers, electrolyte imbalance due to diuretic therapy and as a systemic manifestation of infection such as endocarditis.
Cyanosis is a dusky blue discoloration of the skin (particularly at the extremities) or of the mucous membranes when the capillary oxygen saturation is less than 85%. Central cyanosis (p. 799) is seen with shunting of deoxygenated venous blood into the systemic circulation, as in the presence of a right-to-left heart shunt. Peripheral cyanosis is seen in the hands and feet, which are cold. It occurs in conditions associated with peripheral vasoconstriction and stasis of blood in the extremities leading to increased peripheral oxygen extraction. Such conditions include congestive heart failure, circulatory shock, exposure to cold temperatures and abnormalities of the peripheral circulation, e.g. Raynaud’s, p. 788.
Premature beats occur as occasional or repeated irregularities superimposed on a regular pulse rhythm. Similarly, intermittent heart block is revealed by occasional beats dropped from an otherwise regular rhythm.
Atrial fibrillation produces an irregularly irregular pulse. This irregular pattern persists when the pulse quickens in response to exercise, in contrast to pulse irregularity due to ectopic beats, which usually disappears on exercise.
Carotid pulsations are not normally apparent on inspection of the neck but may be visible (Corrigan’s sign) in conditions associated with a large-volume pulse, including high output states (such as thyrotoxicosis, anaemia or fever) and in aortic regurgitation.
A ‘collapsing’ or ‘water hammer’ pulse (Fig. 14.10) is a large-volume pulse characterized by a short duration with a brisk rise and fall. This is best appreciated by palpating the radial artery with the palmer aspect of four fingers while elevating the patient’s arm above the level of the heart. A collapsing pulse is characteristic of aortic valvular regurgitation or a persistent ductus arteriosus.
Alternating pulse (pulsus alternans). This is characterized by regular alternate beats that are weak and strong. It is a feature of severe myocardial failure and is due to the prolonged recovery time of damaged myocardium; it indicates a very poor prognosis. It is easily noticed when taking the blood pressure because the systolic pressure may vary from beat to beat by as much as 50 mmHg (Fig. 14.10).
Pulsus bisferiens (Fig. 14.10). This is a pulse that is found in hypertrophic cardiomyopathy and in mixed aortic valve disease (regurgitation combined with stenosis). The first systolic wave is the ‘percussion’ wave produced by the transmission of the left ventricular pressure in early systole. The second peak is the ‘tidal’ wave caused by recoil of the vascular bed. This normally happens in diastole (the dicrotic wave), but when the left ventricle empties slowly or is obstructed from emptying completely, the tidal wave occurs in late systole. The result is a palpable double pulse.
Paradoxical pulse. Paradoxical pulse is a misnomer, as it is actually an exaggeration of the normal pattern. In normal subjects, the systolic pressure and the pulse pressure (the difference between the systolic and diastolic blood pressures) fall during inspiration. The normal fall of systolic pressure is <10 mmHg, and this can be measured using a sphygmomanometer. It is due to increased pulmonary intravascular volume during inspiration. In severe airflow limitation (especially severe asthma) there is an increased negative intrathoracic pressure on inspiration which enhances the normal fall in blood pressure. In patients with cardiac tamponade, the fluid in the pericardium increases the intrapericardial pressure, thereby impeding diastolic filling of the heart. The normal inspiratory increase in venous return to the right ventricle is at the expense of the left ventricle, as both ventricles are confined by the accumulated pericardial fluid within the pericardial space. Paradox can occur through a similar mechanism in constrictive pericarditis but is less common.