CBL CVS

The patient's heart rate is high. Describe the action potential in the SAN. What ion channels open/close during the depolarisation/repolarisation?

Phase 0: depolarisation - Ca influx through L type channels Phase 3: repolarisation - K efflux Phase 4: slow depolarisation - HCN channels activated by repolarisation - Na influx K efflux Ca influx Steeper slope of phase 4 -> faster heart rate Adrenaline + beta1 receptor-> increase cAMP -> increase HCN -> faster depolarisation -> increase HR

Would the high heart rate have any effect on the coronary circulation? Explain your reasoning.

Activation of sympathetic nerves -> vasodilation-> increased coronary flow Myocardial oxygen demand increases as HR increases Coronary vasculature collapses during systole -> shortened diastole -> decreased blood flow

Would you expect to see a prolonged clotting time in a patient receiving anti-platelet drugs? Explain your reasoning.

Anti-platelet drugs: agent which decreases platelet aggregation and inhibit thrombus formation Lack of thrombin -> prolonged clotting time

Draw and describe the surface anatomy of the chest in relation to the heart and the relevant auscultation points. Where would you hear the murmur of aortic stenosis.

Aortic valve: 2nd ICS RSE Pulmonary valve: 2nd ICS LSE Mitral valve: 5th ICS midclavicular line Tricuspid valve: 4th ICS LSE Aortic stenosis causes significant turbulence to blood flow during contraction of L ventricle resulting in a diamond shaped murmur. Best heard in 2nd ICS RSE

Describe how the atrial and ventricular pressure changes as a result of birth, after the lungs fill with air.

At first breath, the lungs inflate and there is a fall in pulmonary vascular resistance, increasing the pressure in the left atrium. Increase in prostaglandins due to an increase in O2, causes foramen ovale to close.

Draw and label the normal cardiac cycle

Atrial systole Isovolumetric ventricular contraction Ventricular ejection Isovolumetric ventricular relaxation Ventricular filling

What adrenergic receptors play a role in the regulation of heart rate, myocardial contractility and arterial blood pressure?

B1 adrenoreceptor - in excitation of cardiac muscle - activated by adrenaline and noradrenaline - increase HR, contractility and rate of myocyte relaxation B2 - in blood vessels - inhibition - similar to B1 A1 - excitation in myocytes - increase contractility, vasoconstriction A2 - vasodilation

Given that the patient's heart rate is high, how does this affect the preload, ejection fraction and stroke volume?

CO = SV x HR SV = EDV - ESV EF = SV/EDV x 100 Preload: reduced Ejection fraction: reduced, or could stay the same Stroke volume: reduced

Draw and explain the location of the heart valves within the annulus fibrosis. Describe the similarities and differences between the AV and semilunar valves.

Each ring ring of the annulus fibrosis surrounds a valve. AV valves: between atria and ventricles, variable number of cusps, secured to chordae tendinae and papillary muscles Aortic & Pulmonary valves: major arteries, 3 cusps

Describe the foetal circulation.

Heart begins as a basic cylindrical heart tube and develops in utero Three shunts: ductus arteriosus, ductus venosus, foremen ovale Oxygen is obtained through the placenta via diffusion Pulmonary circulation is bypassed using the forament ovale and ductus arteriosus. Pressure is higher in the right atrium so flows down the pressure gradient from R to L atrium Feral haemoglobin has a higher affinity for oxygen than adult Hb due to reduced ability to interact with 2,3-BPG.

Why might aortic stenosis cause chest pain and dizziness? Why do these problems only present during exertion in this patient?

Increased pressure in L ventricle -> ventricular hypertrophy -> impaired filling -> myocardial ischaemia -> angina L ventricular failure -> symptoms of pulmonary oedema -> shortness of breath, fatigue and palpitations Exertion-> increase HR bp and CO -> increase symptoms Causes relaxation of blood vessels -> bp drops -> dizziness

In the management of ischaemic heart disease patients almost invariably prescribed antiplatelet drugs. Describe what platelets are and how they are activated in a healthy person.

Platelets: disc shaped cell structure made of fragments of megakaryocytes present in the blood Activation 1. Platelets formed and circulate 2. Prostacyclin normally prevents formation of platelet plug by inhibiting exercise 3. Thromboxane triggers growth and activation of platelets 4. Granule contents secreted from platelets 5. Thromboxane A2 is produced by activated platelets, which activates other platelets 6. Activated platelets change in shape 7. Platelets clump/bind, forming a platelet plug. Binding is done through receptors such as fibrinogen. 8. Blood coagulation 9. Blood clotting proteins circulate and are converted to active proteolytic enzymes 10. Conversion of prothrombin to thrombin. Thrombin converts fibrinogen to fibrin. Causes clot to form.

Describe which coronary artery supplies the various territories of myocardium. Which artery is likely to supply the SAN?

SAN branch of the right coronary artery supplies the SAN in 60% of cases. Left Coronary Artery: left atrium, and most of left ventricle. 2/3 of IV septum. AVN and bundle. SAN in 40% cases. Right Coronary Artery: right atrium and most of right ventricle. 1/3 of IV septum. SAN in 60% of cases. Left coronary artery divides into circumflex and anterior interventricular descending artery. Right coronary artery divides into right marginal and posterior descending artery.