Chapter 14 Cardiovascular disease
Essential anatomy, physiology and embryology of the heart
The conduction system of the heart
The cellular basis of myocardial contraction – excitation-contraction coupling
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.
Blood vessel control and functions of the vascular endothelium
The Bayliss myogenic response – the ability of blood vessels to constrict when distended
The vasodilator washout effect – the vasoconstriction triggered by a decrease in the concentration of tissue metabolites.
Vasomotor control
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.
Table 14.1 Some of the products and functions of the vascular endothelium
Endothelial product | Function(s) | Stimulus |
---|---|---|
Nitric oxide | ||
Prostacyclin (PGI2) | ||
Prostanoids | ||
Endothelin | ||
Endothelial-derived hyperpolarizing factor | ||
Angiotensin-converting enzyme | ||
von Willebrand factor | ||
Adhesion molecules |
|
|
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.
PGI2 is synergistic to NO and also plays a role in the local regulation of vasomotor tone.
Symptoms of heart disease
The following symptoms occur with heart disease:
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.
Table 14.2 Differential diagnosis of chest pain
Central | Lateral/peripheral |
---|---|
Cardiac | Pulmonary |
Ischaemic heart disease (infarction or angina) | Infarction |
Coronary artery spasm | Pneumonia |
Pericarditis/myocarditis | Pneumothorax |
Mitral valve prolapse | Lung cancer |
Aortic aneurysm/dissection | Mesothelioma |
Non-cardiac | Non-pulmonary |
Pulmonary embolism | Bornholm disease (epidemic myalgia) |
Oesophageal disease (see Box 6.3) | Herpes zoster |
Mediastinitis | Trauma (ribs/muscular) |
Costochondritis (Tietze disease) |
|
Trauma (soft tissue, rib) |
|
Central chest pain
Retrosternal heavy or gripping sensation with radiation to the left arm or neck that is provoked by exertion and eased with rest or nitrates – angina (p. 729)
Similar pain at rest – acute coronary syndrome (p. 734)
Severe tearing chest pain radiating through to the back – aortic dissection (p. 787)
Sharp central chest pain that is worse with movement or respiration but relieved with sitting forward – pericarditis pain (p. 774)
Sharp stabbing left submammary pain associated with anxiety – Da Costa’s syndrome.
Palpitations
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.
Paroxysmal tachycardias (see p. 698) are felt as a sudden racing heart 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).
Syncope
Table 14.3 Cardiovascular causes of syncope
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.
Micturition syncope refers to loss of consciousness whilst passing urine.
Carotid sinus syncope occurs when there is an exaggerated vagal response to carotid sinus stimulation, provoked by wearing a tight collar, looking upwards or turning the head.
FURTHER READING
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.
Examination of the cardiovascular system
General examination
Clubbing (p. 799) is seen in congenital cyanotic heart disease, particularly Fallot’s tetralogy and also in 10% of patients with subacute infective endocarditis.
Splinter haemorrhages. These small, subungual linear haemorrhages are frequently due to trauma, but are also seen in infective 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.
The arterial pulse
Rhythm
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.
Character of pulse
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.
A small-volume pulse is seen in cardiac failure, shock and obstructive valvular or vascular disease. It may also be present during tachyarrhythmias.
A plateau pulse is small in volume and slow in rising to a peak due to aortic stenosis (Fig. 14.10).
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).
Bigeminal pulse (pulsus bigeminus). This is due to a premature ectopic beat following every sinus beat. The rhythm is not regular (Fig. 14.10) because every weak pulse is premature.
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.
Dicrotic pulse (Fig. 14.10) results from an accentuated dicrotic wave. It occurs in sepsis, hypovolaemic shock and after aortic valve replacement.
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.
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