Cardiovascular 1 to 10
List in order, the mechanical phases of the cardiac cycle.
(1) Atrial systole.
(2) Isovolumetric ventricular contraction.
(3) Ventricular ejection.
(4) Isovolumetric ventricular relaxation.
(5) Ventricular filling
Pass criteria: 3 out of 5 to pass
What factors influence myocardial contractility?
Sympathetic stimulation via nerves or circulating catecholamines;
Increased heart rate (small effect);
Drugs such as xanthines, glucagon, cardiac glycosides, adrenergic agents;
Increased myocardial mass (chronic).
Parasympathetic stimulation (small)
Hypercapnoea, hypoxia, acidosis;
Drugs such as calcium channel blockers, beta-blockers, quinidine, barbiturates;
Cardiac failure (intrinsic myocardial depression;
Cardiomyopathy or infarction
Pass criteria:Five of the factors listed with at least two each positively or negatively inotropic to pass this subsection
Describe the cardiac events that relate to the ST interval.
- ST segment represents the plateau (Phase 2) of the AP and the T wave is repolarisation (Phase 3).
- ST segment elevation concave upwards
What are the parameters that define cardiac output?
- Cardiac output (CO) = heart rate (HR) X stroke volume (SV)
What are the factors that influence stroke volume?
- Myocardial contractility
How can cardiac output be measured?
The Fick principle states that the amount of a substance taken up by an organ (or by the whole body) per unit of time is equal to the arterial level of the substance minus the venous level (A-V difference) times the blood flow. The principle can be used to determine cardiac output by measuring the amount of O2 consumed by the body in a given period and dividing this value by the A-V difference across the lungs
Whole body O2 consumption is calculated by collecting expired gas in a spirometer and determining its O2 content, which is then subtracted from the calculated O2 content of inspired gas. The arterial O2 content can be measured in an arterial sample and the mixed venous blood O2 content is obtained from a pulmonary artery catheter
In the indicator dilution method, a known amount of a substance is injected into a vein and the concentration of the indicator in serial samples of arterial blood is determined. The output of the heart is equal to the amount of indicator injected divided by its average concentration in arterial blood after a single circulation through the heart. The cardiac output for that period is calculated and then converted to output per minute
The indicator must, of course, be a substance that stays in the bloodstream during the test and has no harmful or haemodynamic effects. A popular indicator dilution technique is thermodilution, in which the indicator used is cold saline
Draw and explain the action potential in a cardiac pacemaker cell.
Describe the major differences between a cardiac myocyte AP and the pacemaker?
- Resting membrane potential, –90mV rapid depolarisation voltage gated Na (overshoots)
- Phase 1 rapid repolarisation = closure of Na channels.(inner v outer gates)
- Plateau phase 2 voltage gated Ca2+ channels open (slower L type)
- Phase 3 repolarisation Ca2+ ch close
- Phase 4 due to various K+ efflux
- Na fast v Ca dependent,
- Automaticity due to rising prepotential (K+/ Ca+),
- Plateau phase, resting potentials
Draw an ECG trace and, below this, identify the 5 phases of the cardiac (contractile) cycle.
- Atrial systole
- Isovolumetric ventricular contraction
- Ventricular ejection
- Isovolumetric ventricular relaxation
- Ventricular filling
Draw an ECG trace and, below this, demonstrate the left ventricular volume trace.
Please give approximate volume values on the y-axis
- The end-diastolic ventricular volume is approx. 130ml
- The end-systolic ventricular volume is approx. 50ml [thus about 80ml is ejected by each ventricle per contraction, at rest and the ejection fraction (the percent of the EDV that is ejected with each contraction) is about 65%.
Draw the action potential in a cardiac pacemaker cell, and explain the ionic fluxes.
- Prepotential initially due to decrease in efflux K+ then completed by influx Ca2+ through T channels
- AP due to influx Ca2+ via L channels
- Repolarisation due to efflux K, no plateau
How do sympathetic and parasympathetic stimulation change the prepotential.
- Noradrenaline binds to Beta 1 receptor and raises cAMP, resulting in increased opening of L channels and Ca2+ influx.
- Thus increased slope of prepotential and firing rate
- Thus decreased slope of prepotential and firing rate
- ACh binds to M2 receptor and decreases cAMP, resulting in both slowing of Ca channel opening and opening of special K channels (counters decay of K efflux) leading to greater fall in prepotential
Pass Criteria: Must mention thick ascending limb of loop of Henle and reduced resorption of Na and Cl
Draw a normal ECG tracing, showing the durations of the major intervals.
- PR 0.16 , QRS 0.12, QT 0.4
How does the ECG change with hyperkalaemia?
- Initial tall peaked T waves. Intervals normal K 7.0
- Later no atrial activity, QRS broad/slurred
- Ventricular arrhythmias then fibres eventually unexcitable, sine wave appearance
How does it change with hypokalaemia?
- Long PR, ST depression, inverted T
- U wave
Where are Baroreceptors found in the body?
- Stretch receptors in adventitia of vessel walls, major ones found in carotid sinus and aortic arch to monitor arterial side of circulation
- Also “cardiopulmonary receptors” in right and left atria, and pulmonary circulation to monitor venous circulation
- Carotid sinus and aortic arch to pass
What is the effect of vessel wall distension on a baroreceptor?
- Stretch of vessel wall leads to increased baroreceptor discharge, transmitted by afferents in glossopharyngeal and vagus nerves to medulla. (vasomotor centre) This results in release of inhibitory GABA which reduces sympathetic outflow, and excitatory effects on vagal motor neurones. Net effect is:
- Inhibition of tonic discharge of vasoconstrictor nerves
- Excitation of cardiac vagal innervation
- Results in vasodilation, with decrease in BP, HR and CO