Cardio Physiology Flashcards
Action Potential of Ventricular Myocyte
Prolonged period of depolarisation forming a plateu. This allows for prolonged contraction of myocyte to efficiently eject blood. Mechanisms behind long action potential are:
- Fast opening Na+ channels
- Slow calcium channels
- Decrease in membrane permeability for K+
Phase 0 = depolarisation, phase 1 = early fast repolarisation, phase 2 = plateu phase, phase 3 = late repolarisation, phase 4 = return to resting potential
Excitation Contraction Coupling of Myocardial Cells
Action potential spreads to internal cardiac muscle via T tubule systems. Acts on membrane of longitudinal sarcoplasmic tubules causing release of calcium into muscle sarcoplasm from sarcoplasmic reticulum.
Calcium ions then diffuse into the myofibruls and catalyse the chemical reaction that promotes sliding of actin and mysoin filaments.
Pacemaker Cells of the Heart
Sinoatrial nodes have cells that are quickest to depolarise.
Self-excitation of sinus nodal fibres due to:
- SAN fibres have naturally leaky membranes to sodium, open sodium channels
- The high concentration of sodium in the ECF outside the nodal fibres
Conducting System of Heart
Conduction system made up of specialised cardiac cells, not nerves. Sinoatrial node - internode pathways - atrioventricular node - atrioventricular bundle - left bundle banch - right bundle branch - purkinje network - ventricular myocardium.
Abnormal Conditions in Condusting System
In abnormal conditions, other parts of the heart can exhibit intrinsic rhythmical excitation in the same way the SAN does.In the absence of stimulation from the Atria, the AVN will discharge at an intrinsic rhythmical rate slower than that of the SAN. The purkinje fibres if not stimulated by the AVN will discharge at an even slower rate.
Sympathetic Control of Cardiac Function
Sympathetic stimulation distributed to all parts of the heart. Increases cardiac output by increasing heart rate and increasing the force of ventricular contraction. Increases the heart rate by:
- Increasing the rate of SAN discharge
- Increasing rate of conduction
- Increasing level of excitability
Noreadrenaline binds to B-adrenoreceptors leading to an increase in permeability of Na and Ca, meaning cells self excite quicker. Also increase Ca into cell, raising plateau and shortening action potential. Higher plateu, quicker the K+ channels reopen.
Parasympathetic Stimulation
Nerves distribute mainly to the SAN and AVN and also to atrial myocardium.
Slows heart rate by
- decreasing rate of SAN discharge
- decreasing rate of conduction at the AVN
- decreasing excitability of AVN
- anti-sympathetic effects on atrial cells
Release of acetylcholine at ending of vagus nerve. Acts on muscarinic receptors resulting in increased permeability of the cell membranes to potassium and rapid leakage of potassium. This results in increased negativity making cells much less excitable
Imbalance of Potassium in Heart
Hyperkalaemia causes:
- cardiac dilation
- reduced heart rate
- flaccidity
- block AV conduction
- ECG changes - tall t waves, QRS prolonged
- atrial paralysis
Hypokalemia
- ECG changes - prolongation of PR interval, t wave inversion in precordial leads
- increased HR
Imbalance of Calcium in the Heart
Hypercalcaemia causes:
- Spastic contraction because of the effect of Ca2= in intiating myocardial contraction
- Short QT interval, widened T wave
- Increased heart rate
Hypocalcaemia causes:
- Flaccidity
- QT prolongation on ECG
- Arrythmias
- Decreased HR
ECG Waveforms
P - atrial depolarisation
Q - early ventricular depolarisation
R - Ventricular depolarisation
S - Late ventricular depolarisation
T - Ventricular repolarisation
Cardiac Vectors in ECGS
If the action potential / cardiac vector is moving towards the positive electrode in the lead the deflection on the ECG trace is positive and vice versa.
Pressure-Volume Changes in Left Side during Cardiac Cycle
At the beginning of systole, the ventricular volume remains unchanged giving isometric contraction until pressure rises enough to open aortic valve. Increased ventricular pressure causes rapid ejection of blood but as systole ends pressure in the aorta increases and pressure in the left ventricle decreases so the rate of ejection flows. At the point when aortic pressure exceeds left ventricular pressure and there is slight backflow of blood to close the aortic valve. This is the beginning of vetricular diastole.
In diastole the left ventricle relaxes and so pressure falls to near left atrial pressure but no filling occurs initially because the mitral and aortic valves are shut. This phase is called isovolumetric relaxation. When ventricular pressure falls below atrial pressure the mitral valve opens. Initially there is rapid ventricular filling followed by reduced ventricular filling later in diastole. At the end of diastole, atria contract to complete filling the ventricle. This is atrial systole.
Hypertrophy of the Heart
Increased workload will increase volume of blood in heart, making muscle bigger.
Concentric hypertrophy is the thickening if atrial muscle can occur during stenosis.
Eccentric hypertrophy is the thickening of muscle and greater ventricular volume to accommodate for regurgitating blood.
Open/Closing of AV Valves
AV valves are closed during systole and open during diastole
Semilunar valves are open during systole and closed during diastole
Heart Sounds
S4 = ejection of blood from atria during atrial contraction
S1 = closure of AV valves
S2 = closure of semilunar valves
S3 = rapid ventricular filling
S3 and S4 can only be heard in large animals.
Sounds that can be heard on the left side include pulmonary valve, aortic valve, left AV valves. Sounds heard on right side are right atrioventricular valve.
Murmurs
Murmur is an additional noise, arrythmia is an abnormal rhythm. Regurgitation occurs when the valves are closed, stenosis occurs when the valves are open.
Fluid Movement Across Capillaries
Sum of capillary pressure and plasma oncotic pressure determines movement of water. Abnormal forces may lead to oedema.
