The Heart

The cardiovascular system is a sealed system which works under pressure to transport blood to respiring tissues via capillaries and to return the blood to the heart

The main functions of the cardiovascular system are rapid nutrient transport, waste removal, hormonal control, temperature regulation and host immune defence.

Myocardium is the thick muscle walls of the heart made up of cardiac muscle cells.

The endocardium is the inner surface of the walls of the heart in contact with the blood.

The epicardium is the inner lining of the pericardium and is continuous with the covering of the heart itself.

The pericardium is a fluid filled membranous sac which the heart is contained within.

Systole is the contractile phase of the cardiac cycle whereas diastole is the phase of relaxation and filling with blood. Alternation between contraction and relaxation produces the differences in pressure which pushes blood into the chambers of the heart and into circulation.

Gap junctions join cardiac muscle cells together, allowing the spread of electrical excitation from one cell to another so that cardiac muscle can function as a whole tissue.

The conducting system is found within the myocardium and is made up of specialised cells which are essential for heart excitation.

In order for the heart to contract, the myocyte plasma membrane is depolarised → sodium channels open → voltage gated calcium channels open → calcium enters cell and calcium released from SR → rise in cytosolic calcium → contraction

The sinoatrial node generates action potentials which travel the walls of the heart causing both atria to contract. The impulses are delayed when they reach the atrioventricular node allowing the atria to fully contract and empty. The AV node sends impulses along the bundle of His and Purkinje fibres to the ventricles so the ventricles contract from the apex up.

The intrinsic conduction system is made up of 2 cell types: fast and slow depolarising pacemaker cells.

Sinoatrial nodal cells have a less polar resting potential as they’re ‘leaky’ meaning ions can enter spontaneously to the point where there’s an action potential meaning the cells are always active and able to generate their own spontaneous activity.

The absolute refractory period of myocytes in around 250 ms.

Cardiac arrythmias occur as a result of random signals from the SAN making it hard to regulate the heartbeat.

Chronotropic control is the control of heart rate. It is mediated by nodal tissues and the central nervous system (influence of sympathetic vs parasympathetic). When action potentials are plotted, the slope of phase 4 depolarisation in SAN cells determine heart rate.

Temperature also affects heartrate which is why heartrate increases when ill with fever.

Stroke volume is the volume of blood pumped per contraction and is normally 70-140ml, only 60% of the end diastolic volume. End diastolic volume is the volume of blood in the ventricle prior to contraction.

The Frank-Starling law of the heart represents the relationship between stroke volume and end-diastolic volume.

Inotropy is the contractile function of the heart.

Sympathetic control of cardiac contractile force and velocity involves noradrenaline and β1 receptors. cAMP activates protein kinase leading to increased calcium concentration from outside the cell and the SR. Calcium binds troponin which enhances actin-myosin interaction and kinases also directly enhances this interaction.

Most receptors in the heart are β1 and muscarinic M2, but β2, α1 and angiotensin II are also found.

arterial blood pressure = cardiac output x total peripheral resistance

Total peripheral vascular resistance is dependent on blood viscosity and arteriolar radius - the higher the radius the lower the resistance.

Blood pressure of a healthy young adult is around 120/80 mmHg.

The arteriolar radius is constricted by sympathetic nerves releasing noradrenaline.

Arteriolar radius is dilated by sympathetic cholinergic nerves, acetylcholine and muscarinic M3 receptors, plasma adrenaline and local controls such as reduced PO2 and increased PCO2, K+ and adenosine.

Immediate regulation of arterial blood pressure is regulated by arterial blood pressure and chemoreceptor reflexes. Long-term regulation of arterial blood pressure is controlled by hormones vasopressin, angiotensin II, aldosterone and atrial natriuretic peptide.

Increase in cardiac output via increased stroke volume and increased heart rate, as well as increased peripheral resistance via increased blood viscosity and decreased arteriolar diameter lead to increased arterial blood pressure.

Drugs for high blood pressure may be β1 antagonists, selective α1 antagonists or ACE inhibitors.