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ACEM Part 1 > Physiology - Cardiac > Flashcards

Physiology - Cardiac Flashcards

1
Q

Describe the normal cardiac conduction pathway

A
  • 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
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2
Q

What is the normal ECG complex and what does each wave represent

A

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

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3
Q

How does sympathetic and parasympathetic stimulation change the prepotential

A

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

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4
Q

Describe the difference between a ventricular muscle action potential and a pacemaker cell potential

A
  • 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
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5
Q

Why does tetany not occur in cardiac muscle

A

cardiac muscle contraction lasts 1.5 times as long as the action potential

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6
Q

What mechanisms cause abnormalities of cardiac conduction

A
  • 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
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7
Q

What conditions may predispose to increased automaticity

A

IHD
scar tissue from previous heart operation
structural heart disease
channelopathies
electrolyte imbalance

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8
Q

Describe how the kidney handles K+

A
  • 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)
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9
Q

What are the ECG findings associated with hypokalaemia

A

long PR interval
ST depression
T wave inversion
U waves

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10
Q

Explain the electrophysiology causing STE in MI

A

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)

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11
Q

What are the causes and complications of AF

A

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

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12
Q

Describe how the waveforms of an ECG relate to the cardiac cycle

A
  • 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
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13
Q

What are the phases of the cardiac cycle

A

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)

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14
Q

When do the heart sounds occur in the cardiac cycle

A
  • 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
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15
Q

What are the 2 factors that determine cardiac output

A

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

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16
Q

What is the stroke volume in a normal adult at rest

A

70-90ml

17
Q

What is the definition of ejection fraction

A

the percentage of end diastolic ventricular volume ejected with each stroke, normally 65%

18
Q

What is cardiac preload and what factors effect it

A
  • 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)

19
Q

What methods can be used to measure cardiac output

A
  • ficks principle: output from LV = oxygen consumption / AO2-VO2
  • indicator dilution method = flow = amount of indicator injected / concentration of indicator in arterial blood
20
Q

What are causes of decreased cardiac output

A

arrhythmia
reduced preload (venodilation, volume loss)
increased afterload
reduced contractility (ischaemia)

21
Q

What are the determinants of myocardial oxygen consumption

A

heart rate
myocardial contractility
wall tension

22
Q

What are the changes in cardiac function with exercise and how are these mediated

A
  • 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
23
Q

What physical laws are involved in the alteration of cardiac function in exercise

A

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

24
Q

What factors influence contractility

A

hypoxia
drugs (inotropes)
pH
sympathetic tone
hypercapnea
myocardial damage

25
Q

What factors reduce cardiac contractility

A
  • 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
26
Q

How do changes in myocardial contractility alter the relationship between end diastolic volume and stroke volume

A
  • 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
27
Q

How does decreasing a persons heart rate improve the symptoms of angina

A
  • 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)
28
Q

What effect does increasing preload and afterload have on myocardial oxygen demand

A
  • 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
29
Q

Draw a graph to demonstrate the Frank Starling Law and what shifts it

A

up/left: inotropes, circulating catecholamines, sympathetic input, muscle mass

down/right: acidosis, hypercarbia, hypoxia, vagal/parasympathetic stimuli

30
Q

Demonstrate the relationship between the aortic pressure and the cardiac cycle

A
31
Q

Draw an ECG trace with the cardiac cycle

A
32
Q

Draw the jugular venous pressure wave, how it relates to the ECG and explain the origins of the fluctuations

A

-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

33
Q

Draw the pressure changes in the ventricle during the cardiac cycle

A
34
Q

Draw the pressure volume curve and describe the changes in left ventricular volume through the cardiac cycle

A

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
35
Q

Draw and describe the action potential of a cardiac pacemaker cell

A

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

36
Q

Draw and describe the action potential of ventricular muscle

A

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

37
Q

Times of each segment of ECG

A
  • 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

ACEM Part 1 (38 decks)

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