Cardiovascular System

One cardiac cycle lasts ≈0.8 s at 75 beats/min. Atrial systole takes ≈0.1 s, ventricular systole ≈0.27–0.3 s and ventricular diastole ≈0.5 s.

Ventricular systole. In isovolumetric contraction the AV valves close (first heart sound, S1) and pressure rises with all four valves shut. Then the semilunar valves open and ejection begins.

Ventricular diastole. It starts with isovolumetric relaxation, when the semilunar valves close (S2; the dicrotic notch on the aortic trace). Rapid passive filling follows once the AV valves open, then diastasis. Atrial systole finally adds about the last 20% of filling at rest.

A faster heart rate shortens diastole far more than systole. This reduces both filling time and coronary perfusion time.

Cardiac output (CO) is heart rate (HR) multiplied by stroke volume (SV). Stroke volume is end-diastolic volume minus end-systolic volume, typically 120 − 50 = 70 mL.

Three factors set stroke volume:

Preload. Ventricular filling and end-diastolic fibre length.

Afterload. The wall stress the ventricle must develop to eject, set mainly by aortic pressure and systemic vascular resistance.

Contractility. The inotropic state, independent of loading.

Sympathetic β1 stimulation raises both heart rate (positive chronotropy) and contractility (positive inotropy). Vagal tone slows the SA node. In the steady state, cardiac output must equal venous return.

Within physiological limits, the heart ejects whatever volume returns to it. More diastolic filling stretches the sarcomeres toward their optimal length (≈2.2 µm). It also increases the Ca²⁺ sensitivity of the myofilaments. Both effects raise stroke volume. This intrinsic mechanism matches the outputs of the right and left ventricles beat by beat.

Pacemaker cells (SA and AV nodes) have no stable resting potential. In phase 4 they depolarise slowly from about −60 mV to threshold (≈−40 mV), driven by the funny current (If) and T-type Ca²⁺ current. Their upstroke is carried by L-type Ca²⁺ channels.

Working ventricular myocytes rest at ≈−90 mV. They depolarise rapidly through fast Na⁺ channels and then hold a long plateau carried by L-type Ca²⁺ current. This plateau makes the refractory period long enough to prevent tetanus.

The impulse spreads from the SA node across the atria (P wave). It is delayed ≈0.1 s at the AV node (PR interval), then spreads rapidly through the His–Purkinje system (QRS). Ventricular repolarisation produces the T wave.

Flow = ΔP / R. Poiseuille's law gives R = 8ηL/πr⁴, so halving a vessel's radius increases its resistance sixteenfold. For the systemic circulation, MAP ≈ CO × TPR, and MAP is roughly diastolic pressure plus one-third of the pulse pressure.

Arterial pressure is regulated on three time scales:

Seconds. The baroreceptor reflex.

Minutes to hours. The renin–angiotensin–aldosterone system, ADH and natriuretic peptides.

Days. Renal pressure natriuresis, which sets long-term extracellular fluid volume.

Net fluid flux across a capillary wall is Kf × [(Pc − Pi) − σ(πc − πi)], where P is hydrostatic pressure and π is oncotic pressure.

Typical values are a capillary hydrostatic pressure of ≈30 mmHg at the arteriolar end and ≈10 mmHg at the venular end, an interstitial hydrostatic pressure of about −3 mmHg, a plasma oncotic pressure of ≈28 mmHg and an interstitial oncotic pressure of ≈8 mmHg.

With these values, fluid is filtered at the arteriolar end and partly reabsorbed at the venular end. The small daily excess, a few litres, returns to the blood as lymph. Oedema develops when hydrostatic pressure or permeability rises, oncotic pressure falls or lymphatic drainage fails.

Tissues match blood flow to their needs through three types of mechanism:

Myogenic autoregulation. Arterioles constrict when stretched.

Metabolic vasodilators. Adenosine, CO₂, H⁺, K⁺ and low O₂ dilate arterioles.

Endothelial mediators. Nitric oxide and prostacyclin dilate; endothelin-1 constricts.

Autoregulation keeps flow to the brain, kidney and heart nearly constant over a wide range of perfusion pressures. Pulmonary vessels respond the opposite way. Hypoxia makes them constrict, which diverts blood to well-ventilated alveoli.

Atherosclerotic narrowing of the coronary arteries causes stable angina: exertional chest tightness relieved by rest or glyceryl trinitrate. If a plaque ruptures or erodes and a thrombus forms on it, the result is an acute coronary syndrome: unstable angina, NSTEMI or STEMI. Infarction begins in the subendocardium and spreads outward toward the epicardium.

Localising the culprit artery. ST elevation in V1–V4 indicates an anterior infarct (LAD). ST elevation in II, III and aVF indicates an inferior infarct (usually the RCA). ST elevation in I, aVL, V5 and V6 indicates a lateral infarct (circumflex).

Diagnosis and treatment. Cardiac troponin confirms necrosis. Treatment is urgent reperfusion by primary PCI, together with antiplatelet therapy.

Complications. These include arrhythmias, heart failure and cardiogenic shock, papillary muscle rupture, septal or free-wall rupture, ventricular aneurysm with mural thrombus, and pericarditis.

Heart failure is the inability of the heart to pump enough blood for the body's needs at normal filling pressures. It is classified by ejection fraction: reduced (HFrEF, EF ≤40%), mildly reduced (HFmrEF, 41–49%) and preserved (HFpEF, EF ≥50%).

Left-sided failure causes pulmonary congestion: breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea and basal crackles.

Right-sided failure causes systemic venous congestion: raised JVP, peripheral oedema and hepatomegaly. The commonest cause of right heart failure is left heart failure.

Neurohormonal activation. Activation of the sympathetic system and RAAS compensates at first but becomes harmful. This is why ACE inhibitors (or ARNI), β-blockers, mineralocorticoid antagonists and SGLT2 inhibitors improve survival in HFrEF. BNP and NT-proBNP are released from stretched ventricles and support the diagnosis.

A stenotic valve fails to open fully. A regurgitant (incompetent) valve fails to close properly.

Aortic stenosis. Ejection systolic murmur in the 2nd right intercostal space, radiating to the carotids.

Mitral regurgitation. Pansystolic murmur at the apex, radiating to the axilla.

Aortic regurgitation. Early diastolic murmur at the left sternal edge, best heard with the patient sitting forward.

Mitral stenosis. Mid-diastolic rumble at the apex with an opening snap.

Rheumatic heart disease is still the leading cause of mitral stenosis worldwide. Calcific degeneration, and congenitally bicuspid valves in younger patients, are the main causes of aortic stenosis.

Atrial fibrillation is the most common sustained arrhythmia. Chaotic atrial activity, often triggered from the pulmonary veins, produces an irregularly irregular pulse with no P waves on the ECG. Blood stagnates in the left atrial appendage and can form thrombus that embolises to the brain. Treatment combines anticoagulation (guided by the CHA₂DS₂-VASc score) with rate or rhythm control.

AV block is graded by severity. In first-degree block the PR interval is longer than 200 ms.

In second-degree Mobitz I (Wenckebach) block, the PR interval lengthens progressively until a beat is dropped. The block is usually in the AV node and benign. In Mobitz II block, beats are dropped suddenly while the PR interval stays constant. The block is below the AV node (infranodal) and often needs a pacemaker.

In third-degree (complete) block, P waves and QRS complexes are fully dissociated and a slow escape rhythm takes over.

Hypertension is defined as sustained office blood pressure ≥140/90 mmHg in European guidelines, or ≥130/80 mmHg in US guidelines.

About 90–95% of cases are primary (essential). Secondary causes include renal parenchymal disease, renal artery stenosis, primary aldosteronism, phaeochromocytoma, Cushing syndrome, coarctation of the aorta and obstructive sleep apnoea.

Hypertension is the leading modifiable risk factor for stroke. It is also a major cause of left ventricular hypertrophy, heart failure, coronary disease, chronic kidney disease, retinopathy and aortic dissection.

Atherosclerosis is a chronic inflammatory disease of the arterial intima.

Plaque formation. It begins with endothelial dysfunction. LDL enters the intima and is oxidised. Monocytes follow, become macrophages and take up lipid to form foam cells (fatty streaks). Smooth muscle cells then migrate in and lay down a fibrous cap over a lipid-rich necrotic core.

Clinical consequences. Plaques that narrow the lumen cause stable ischaemia: angina and claudication. Thin-capped, lipid-rich plaques can rupture and trigger thrombosis: acute coronary syndrome or stroke.

Risk factors. Smoking, hypertension, diabetes, dyslipidaemia, age, male sex and family history.

Abdominal aortic aneurysm. This is aortic dilatation to ≥3 cm, usually below the renal arteries. Risk factors are smoking, male sex, age and family history. Elective repair is usually advised at about 5.5 cm in men (lower thresholds in women), for rapid growth or for symptoms. Rupture presents with back pain, a pulsatile mass and shock.

Aortic dissection. An intimal tear lets blood split the media. Patients have sudden "tearing" pain that radiates to the back, and a difference in pulse or blood pressure between the arms. Stanford type A involves the ascending aorta and needs emergency surgery. Type B involves only the descending aorta and is usually managed medically or endovascularly.

Virchow's triad (stasis, endothelial injury and hypercoagulability) predisposes to thrombus. Most venous thrombi form in the deep veins of the calf and thigh.

Deep vein thrombosis. Proximal (popliteal or femoral) DVT causes a swollen, painful leg and can embolise to the pulmonary arteries.

Pulmonary embolism. It causes pleuritic chest pain, breathlessness, tachycardia and hypoxaemia. A large embolus can cause obstructive shock. Diagnosis combines the Wells score, D-dimer, compression ultrasound and CT pulmonary angiography. Treatment is anticoagulation, with thrombolysis for massive PE.

Congenital heart disease affects about 1% of live births.

Ventricular septal defect (VSD). The most common lesion. Pansystolic murmur at the left sternal edge.

Atrial septal defect (ASD). Fixed splitting of S2.

Patent ductus arteriosus (PDA). Continuous "machine" murmur.

Coarctation of the aorta. Radio-femoral delay, hypertension in the upper limbs and rib notching. It is associated with Turner syndrome and bicuspid aortic valve.

Tetralogy of Fallot. The commonest cyanotic lesion. It combines a VSD, an overriding aorta, right ventricular outflow obstruction and right ventricular hypertrophy.

Untreated left-to-right shunts can cause pulmonary vascular disease. The shunt then reverses and the patient becomes cyanosed (Eisenmenger syndrome).

Anaemia is haemoglobin below the reference range (WHO: <130 g/L in men, <120 g/L in non-pregnant women). It reduces oxygen-carrying capacity, and the heart compensates with a high cardiac output, causing tachycardia and flow murmurs. Anaemia is classified by mean cell volume. Microcytic anaemia is usually due to iron deficiency. Normocytic anaemia follows blood loss, chronic disease or CKD. Macrocytic anaemia is caused by B12 or folate deficiency, among others.

Shock is inadequate tissue perfusion. There are four types: hypovolaemic (haemorrhage or fluid loss), cardiogenic (pump failure), obstructive (tamponade, massive PE or tension pneumothorax) and distributive (sepsis or anaphylaxis).