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 = sodium influx
- t wave = ventricular repolarisation
intervals:
- pr interval = reflexes conduction through the AV node
- st interval = ventricular repolarisation
- qt interval = ventricular depolarisation and 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
IHD
scar tissue from previous heart operation
structural heart disease
channelopathies
electrolyte imbalance
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
What is the stroke volume in a normal adult at rest
70-90ml
What is the definition of ejection fraction
the percentage of end diastolic ventricular volume ejected with each stroke, normally 65%
What is cardiac preload and what factors effect it
- the degree to which ventricles are stretched prior to contracting, equivalent to end diastolic volume
- increases force of contraction by the frank starling law
determined by: blood volume, venous return, sympathetic tone, venous compression (muscle pump)
What methods can be used to measure cardiac output
- ficks principle: output from LV = oxygen consumption / AO2-VO2
- indicator dilution method = flow = amount of indicator injected / concentration of indicator in arterial blood
What are causes of decreased cardiac output
arrhythmia
reduced preload (venodilation, volume loss)
increased afterload
reduced contractility (ischaemia)
What are the determinants of myocardial oxygen consumption
heart rate
myocardial contractility
wall tension
What are the changes in cardiac function with exercise and how are these mediated
- oxygen extraction can increase by 100%
- cardiac output can increase by 700%: mostly by increased HR from adrenaline and sympathetic discharge
- systolic blood pressure increases, diastolic blood pressure decreases: by sympathetic discharge
- stroke volume can increase by less than 200%: contributed by increased venous return
What physical laws are involved in the alteration of cardiac function in exercise
Starling Law = determines the energy of contraction
energy of contraction is proportional to initial fiber length
Leplace Law = determines left ventricular wall stress
wall stress is directly proportional to LV pressure and radius and indirectly proportional to wall thickness
What factors influence contractility
hypoxia
drugs (inotropes)
pH
sympathetic tone
hypercapnea
myocardial damage
What factors reduce cardiac contractility
- metabolic abnormalities = hypoxia, severe acidosis, hypercarbia
- reduced sympathetic tone or increased parasympathetic tone
- blockade of circulating catecholamines
- myocardial disease
- pharmacological depressants = antiarrhythmics, calcium channel blockers
- intrinsic depression in heart failure
- hypothermia
How do changes in myocardial contractility alter the relationship between end diastolic volume and stroke volume
- frank starling law describes that the energy of contraction is proportional to initial muscle fiber length
- the frank starling curve shows the relationship between stroke volume and preload
- increasing myocardial contractility (inotropes) shifts the curve up and to the left
- decreasing myocardial contractility shifts the curve down and to the right
How does decreasing a persons heart rate improve the symptoms of angina
- decreasing HR causes a decrease in myocardial oxygen demand
- at a slower HR, there is more time for the coronary circulation (normally occurs during diastole)
What effect does increasing preload and afterload have on myocardial oxygen demand
- increasing both will cause an increase in myocardial oxygen demand
- pressure work produces a greater increase in oxygen consumption than does volume work
- changes in afterload have a greater effect than changes in preload
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 = due to atrial systole -c wave = due to increased atrial pressure by bulging of tricuspid valve during isovolumetric ventricular contraction -v wave = mirrors the rise in atrial pressure against a closed tricuspid valve
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
Times of each segment of ECG
- PR = 0.12-0.2 seconds, atrial depolarisation and conduction through AV node
- QRS = 0.08-0.12 seconds, ventricular depolarisation and atrial repolarisation
- QT = 0.4-0.43 seconds, ventricular depolarisation and repolarisation
- ST = 0.32 seconds, ventricular repolarisation
