Physiology - Cardiac Flashcards
Describe the normal cardiac conduction pathway
- SA node acts as the pacemaker, connected to the AV node by anterior, middle and posterior internodal tracts
- AV node delays passage of impulse from atria to ventricles
- bundle of his connects AV node to right and left bundle branches (anterior and posterior fasicles on the left)
- purkinje fibers conduct impulses from bundle branches
- ventricular muscle conducts impulse from left side of IV septum to right and down the apex then up to AV grooves
What is the normal ECG complex and what does each wave represent
waves:
- p wave = atrial depolarisation
- q wave = normal left to right depolarisation of the IV septum
- r wave = early ventricular depolarisation
- t wave = ventricular repolarisation
intervals:
- pr interval = conduction through the AV node
- qt interval = ventricular depolarisation and repolarisation (from isovolumetric contraction to isovolumetric relaxation)
- st interval = ventricular repolarisation
How does sympathetic and parasympathetic stimulation change the prepotential
sympathetic:
- NA stimulation of beta 1 receptors causes increased Na+/Ca+2 permeability, making the RMP less negative
- this increases the slope of the pre-potential and firing rate
parasympathetic:
- ACh stimulation of M2 receptors causes increased K+ conductance and slows opening of Ca+2 channels
- this causes hyperpolarisation and decreases the slope of the pre-potential and decreases the firing rate
Describe the difference between a ventricular muscle action potential and a pacemaker cell potential
- ventricular muscle has a greater negative RMP (-90 compared to -60)
- ventricular muscle depolarisation is due to Na+ influx, Ca+2 plays no role
- ventricular muscle does not have a prepotential and no automaticity
Why does tetany not occur in cardiac muscle
cardiac muscle contraction lasts 1.5 times as long as the action potential
What mechanisms cause abnormalities of cardiac conduction
- abnormal pacemaker: lead to ectopic beats, pacemaker failure, fibrillation
- re-entry circuits: lead to tachyarrhythmias
- conduction delays: lead to heart block and bundle branch blocks
- prolonged repolarisation: lead to long QTc
- accessory pathways: lead to WPW
- electrolyte disturbance: cause arrhythmia or arrest
What conditions may predispose to increased automaticity
Acquired:
- IHD
- scar tissue from previous heart operation
- electrolyte imbalance
Congenital
- structural heart disease
- channelopathies
Describe how the kidney handles K+
- K+ is filtered at the glomerulus
- most filtered K+ is actively reabsorbed at the proximal tubules
- K+ is then secreted into the fluid by the distal tubules (induced by aldosterone)
What are the ECG findings associated with hypokalaemia
long PR interval
ST depression
T wave inversion
U waves
Explain the electrophysiology causing STE in MI
1) rapid repolarisation of infarcted muscle due to accelerated K+ ch opening, current flow out of infarct (sec-min)
2) decreased resting membrane potential due to loss of intracellular K+, current flow into infarct (min)
3) delayed depolarisation, current flow out of infarct (30 min)
What are the causes and complications of AF
causes:
overall due to multiple re-entry circuits in atria or foci in pulmonary vein
-IHD, valvular disease, HTN, cardiomyopathy, thyrotoxicosis, pulmonary embolism, sepsis, electrolyte disturbance
complications:
- reduction in cardiac output due to loss of atrial kick causing haemodynamic instability
- embolic events such as stroke
Describe how the waveforms of an ECG relate to the cardiac cycle
- atrial systole starts just after the p wave
- ventricular systole starts near the end of the r wave and ends just after the t wave
What are the phases of the cardiac cycle
1) Atrial systole = phase 1
- contraction of atria propels some additional blood into the ventricles
2) Isovolumetric ventricular contraction = phase 2
- mitral valve closes with increase in ventricular pressure without change in muscle length or volume
3) Ventricular ejection = phase 3
- aortic and pulmonary valves open, 70-90ml blood is ejected from each ventricle, 50ml remain in each ventricle
4) Isovolumetric ventricular relaxation = phase 4
- aortic, pulmonary and AV valves are closed
- ends when ventricular pressure falls below atrial pressure and AV valves open and ventricles begin to fill
5) Ventricular filling = phase 5
- mitral and tricuspid valves open, aortic and pulmonary valves are closed
- blood enters ventricles (70% of ventricular filling)
When do the heart sounds occur in the cardiac cycle
- first = lub, closure of AV valve at beginning of ventricular systole
- second = dub, closure of pulmonary and aortic valves at end of ventricular systole
- third = 1/3 of the way through diastole due to rapid ventricular filling
- forth = due to ventricular filling in patients with ventricular hypertrophy, never heard normally
What are the 2 factors that determine cardiac output
Cardiac Output = heart rate X stroke volume
s
troke volume is determined by preload, afterload and contractility
heart rate is determined by sympathetic and parasympathetic stimulation
Draw a graph to demonstrate the Frank Starling Law and what shifts it
up/left: inotropes, circulating catecholamines, sympathetic input, muscle mass
down/right: acidosis, hypercarbia, hypoxia, vagal/parasympathetic stimuli
Demonstrate the relationship between the aortic pressure and the cardiac cycle
Draw an ECG trace with the cardiac cycle
Draw the jugular venous pressure wave, how it relates to the ECG and explain the origins of the fluctuations.
- a wave: contraction of RA
- c wave: upward bulging of tricuspid valve during isovolumetric ventricular contraction
- v wave: relaxation of RA with tricuspid valve is still closed (maximum atrial filling)
Draw the pressure changes in the ventricle during the cardiac cycle
Draw the pressure volume curve and describe the changes in left ventricular volume through the cardiac cycle
atrial systole:
-phase 1 = small amount of increased ventricular filling due to atrial contraction
ventricular systole:
- phase 2 = mitral valve closes, isovolumetric ventricular contraction, ventricular contraction with no volume change
- phase 3 = ventricular ejection, ventricular volume size decreases
diastole:
- phase 4 = isovolumetric ventricular relaxation
- phase 5 = ventricular filling, 70% of ventricular filling occurs
Draw and describe the action potential of a cardiac pacemaker cell
4 = first part of pre-potential = funny current (start of depolarization)
HCN channel (Na+ influx greater than K+ efflux)
2nd part of pre-potential opening of transient T Ca+2 channels (Ca+2 influx) at -50mV
0 = depolarization opening of long L Ca+2 channels (Ca+2 influx) at -40mV
3 = repolarization peak impulse (0mV), K+ ch open (K+efflux), long Ca+2 ch closes hyperpolarization K+ channels close
Draw and describe the action potential of ventricular muscle
0 = initial rapid depolarization, opening of voltage-gated Na+ ch (Na+ influx)
1 = initial rapid repolarization, closure of Na+ ch, opening of K+ ch (K+efflux), drop to 0mV
2 = prolonged plateau (100x longer than deploarisation) opening of L Ca+2 ch (Ca+2 influx), continued K+efflux
3 = final repolarization, closure of Ca+2 ch and slow K+ efflux
4 = resting membrane potential
