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ACEM Primary VIVA > VIVA: Physiology - The Heart > Flashcards

VIVA: Physiology - The Heart Flashcards

1
Q

Describe the conducting system of the heart

A

SA node is located at the junction of the SVC and RA
AV node is in the right posterior interatrial septum
Three bundles of atrial fibres connect the SA node to the AV node
AV node is continuous with the bundle of His, which gives off a left bundle branch at the top of the interventricular septum and continues as the right bundle branch
Left bundle branch divides into an anterior fascicle and a posterior fascicle
Branches and fascicles run subendocardially down either side of the septum and come into contact with the Purkinje system
Purkinje fibres spread to all parts of the ventricular myocardium (left side of interventricular septum first, then down septum to apex, up atrioventricular grooves, with spread from endocardial to epicardial surfaces)
Last parts to be depolarised are posterobasal portion of LV, pulmonary conus, and uppermost septum

*SA, SV, RBB and LBB to be at standard

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2
Q

Describe the phases of the cardiac cycle that produce the waves and segments in a normal ECG

A

3 to be standard:
- p wave: atrial depolarisation
- PR segment: AV conduction
- QRS: ventricular depolarisation
- ST segment: plateau portion of ventricular depolarisation
- QT: ventricular action potential
- T wave: ventricular repolarisation
- Note atrial repolarisation buried in QRS complex

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3
Q

How do membrane changes in infarcted myocytes cause ST segment elevation?

A

1 to pass:
- Abnormally rapid repolarisation due to accelerated opening of K+ channels (seconds to few minutes)
- Decreased resting membrane potential due to loss of intracellular K+
- Slow depolarisation of the affected cells compared to surrounding normal cells

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4
Q

Please draw or describe the Frank Starling law as it relates to cardiac muscle

A

Frank Starling law states that the energy of contraction is proportional to initial length of cardiac muscle fibre
EDV acts as a surrogate measure of degree of cardiac muscle stretch
Curve of SV against ventricular EDV

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5
Q

What factors influence the Frank Starling curve?

A

Positive, shifting curve up and to the left:
- Circulating catecholamines
- Inotropes (e.g. caffeine, theophylline, digoxin)
- Sympathetic input

Negative, shifting curve down and to right:
- Acidosis
- Hypercarbia
- Hypoxia
- Vagal/parasympathetic stimulation
- Pharmacological depressants (e.g. quinidine, procainamide, barbiturates)
- Intrinsic depression (with heart failure)

NB The causes of this depression are not fully understood but may reflect down-regulation of B-adrenergic receptors and associated signalling pathways and impaired calcium liberation from the sarcoplasmic reticulum)

*need two positive and two negative factors with correct influence to pass

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6
Q

What two factors determine cardiac output?

A

CO = HR x SV*
SV is related to preload and afterload of the heart and the intrinsic contractility of the myocardial cells
HR is determined by sympathetic vs parasympathetic stimulation

*needed to pass

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7
Q

Draw and describe the action potential of a cardiac pacemaker cell

A
  1. Prepotential initially due to decreased K+ efflux* and increased Na+ influx via “funny channels” (open in response to hyperpolarisation), then completed by Ca2+ influx through Ca2+ T channels
  2. Action potential occurs due to influx of Ca2+ via Ca2+ L channels
  3. Repolarisation is due to K+ efflux (there is no plateau)
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8
Q

Please draw and describe a normal ECG complex

A

p wave: atrial depolarisation
PR interval: AV conduction delay (120-200ms)
QRS: ventricular depolarisation (70-100ms)
ST segment: plateau portion of ventricular depolarisation (~320ms)
QT: duration of ventricular action potential (QTc >440ms in men, >460ms in women, should not be <350ms)
T wave: ventricular repolarisation

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9
Q

What are the common mechanisms that cause abnormalities of cardiac conduction?

A

4 to pass:
- Abnormal pacemakers (e.g. ectopic beats, atrial/ventricular fibrillation)
- Re-entry circuits (e.g. tachyarrhythmias)
- Accessory pathways (e.g. WPW)
- Conduction deficits (e.g. heart block, bundle branch blocks)
- Prolonged repolarisation (e.g. long QTc)
- Electrolyte disturbance (e.g. hypo/hyperK)

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10
Q

What is the effect of sympathetic and parasympathetic stimulation on the pre-potential?

A

Sympathetic:
- Noradrenaline binds to B1 receptors and increases cAMP -> opening of L-type channels and Ca2+ influx
- Results in increased slope of prepotential* and increased firing rate

Parasympathetic:
- Acetylcholine binds to M2 receptors and decreases cAMP -> slowing of Ca2+ channel opening and opening of special K+ channels (to counter the decay of K+ efflux)
- Results in greater fall in prepotential, decreased slope of prepotential* and decreased firing rate

*needed to pass

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11
Q

By what mechanisms can tachyarrhythmias be generated?

A
  • Increased automaticity* (e.g. AT, VT)
  • Accessory pathways (e.g. WPW)
  • Re-entry loops (e.g. VT)
  • Early afterdepolarisation (e.g. TdP)
  • Delayed afterdepolarisation (e.g. digoxin toxicity)

*needed to pass + one other

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12
Q

What conditions may predispose to increased automaticity?

A

1 to pass:
- IHD
- Previous repair of congenital heart disease (scar tissue)
- Structural heart disease
- Channelopathies (congenital or acquired)
- Electrolyte imbalances (K+, Mg2+, Ca2+)
- Sympathomimetic agents
- Infiltrative cardiac diseases

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13
Q

The patient is hypotensive and this ECG is performed. What rhythm does it show?

A

Broad complex regular tachycardia consistent with VT
Rate approx 180bpm

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14
Q

What are the abnormalities on the ECG? What is the likely diagnosis?

A

Widespread peaked T waves*
Mild tachycardia
Some inverted T waves
ST elevation

Suggestive of hyperkalaemia*

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15
Q

What are the ECG changes in hyperkalaemia?

A

3/6 to pass:
- Peaked T waves (repolarisation abnormality)
- QRS widening / bizarre QRS (conduction abnormality)
- P wave flattening and loss of P waves (progressive atrial paralysis)
- Sinusoidal ECG
- Ventricular arrhythmias
- Asystole

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16
Q

Describe the way the kidney handles K+

A
  • K+ is filtered at the glomerulus
  • Most filtered K+ is actively reabsorbed at the proximal tubules*
  • K+ is then passively secreted into the fluid at the distal tubules* with reabsorption of Na+ (rate of secretion proportion to distal tubular fluid flow)
  • In a healthy person, the amount of K+ secreted = K+ intake and K+ balance is maintained
  • Normally, >93% of K+ is reabsorbed by the kidneys
  • K+ secretion and excretion alter depending on serum K+ and H+

*needed to pass

17
Q

Please describe the interpret the significant abnormalities in this ECG

A

Sinus rhythm
Rate ~100bpm
Normal axis
ST elevation (STEMI)* in inferior leads*
ST depression and inverted T waves in I, aVL, V2 and V3 (reciprocal changes)

18
Q

Explain the electrophysiological changes that cause the ST segment elevation seen in a myocardial infarction

A

2/3 to pass:
1. Abnormally rapid repolarisation of infarcted muscle due to accelerated opening of K+ channels:
- Current flow out of infarct (normal region negative relative to infarct)
- Occurs within seconds of infarction and lasts a few minutes
2. Decreased resting membrane potential due to loss of intracellular K+:
- Begins in first few minutes secondary to process above
- Current flow into infarct during diastole (ECG configured to record as ST elevation)
3. Slowed depolarisation of affected cells compared with normal cells:
- Occurs at 30mins into infarct process
- Current flow out of infarct

19
Q

Describe the phases of the cardiac cycle and the associated left ventricular pressure changes

A
  1. Atrial systole*:
    - Atria contract
    - Bloods flows into left and right ventricles via open AV valves (mitral and tricuspid)
  2. Isovolumetric ventricular contraction:
    - AV valves close, and pulmonary and aortic valves remain closed
    - Ventricles contract without a change in volume, causing a sharp rise in pressure*
  3. Ventricular ejection*:
    - Aortic valve opens when pressure in LV exceeds the aortic pressure (~80mmHg)
    - Stroke volume is ejected, with LV pressure peaking at 120mmHg before dropping back down
  4. Isovolumetric relaxation:
    - End of ventricular systole and beginning of diastole
    - Aortic valve closes once LV pressure falls below 80mmHg, and AV valves remain closed
    - Rapid pressure drop with no change in volume
  5. Ventricular filling:
    - AV valves open once the ventricular pressure falls below atrial pressures*
    - Blood flows into ventricles from atria

*needed to pass + changes in LV pressure

20
Q

When does the aortic valve open and shut?

A

Aortic valve opens once LV pressure exceeds aortic pressure at 80mmHg marking the end of isovolumetric contraction

Closes once pressure drops below 80mmHg again during isovolumetric relaxation

21
Q

Describe the pressure and volume changes in the left ventricle during systole

A

1 point from each phase with adequate description:
1. Isovolumetric contraction:
- EDV 130ml in LV
- Intraventricular pressure rises sharply until LV pressure exceeds aortic pressure (80mmHg)
2. Ejection / outflow phase:
- Aortic valve opens and ventricular ejection begins
- Peak pressure in LV is 120mmHg
- SV is 70-90ml
- Strength of ventricular contraction diminishes to a point where intraventricular pressure < aortic pressure, leading to closure of aortic valve
3. Isovolumetric relaxation:
- Relaxation of ventricular muscle leads to rapid fall in intraventricular pressure
- End systolic volume is 40-60ml

22
Q

What are the causes of reduced end diastolic volume?

A

Decreased venous return*:
- Decreased blood volume
- Venous pooling (decreased skeletal muscle pump)
- Decreased venous tone
- Gravity / upright posture

Decreased ventricular filling*:
- Increased intrathoracic or intrapericardial pressure (e.g. tamponade)
- Decreased ventricular compliance (diastolic dysfunction)
- Tachycardia (decreased filling time)
- Loss of atrial contraction (e.g. AF)
- Valve stenosis (mitral or tricuspid)

*3 examples needed to pass with 1 from each category

23
Q

Draw and label the pressure volume curve of the left ventricle

A

a to b: isovolumetric contraction
b to c: ventricular systole
c to d: isovolumetric relaxation
d to a: ventricular filling

24
Q

What is cardiac output?

A

Output of the heart per unit time
CO = HR x SV

25
Q

What methods can be used to measure cardiac output?

A

2 to pass:
- Direct Fick method
- Indicator (or thermal) dilution
- Doppler ultrasound techniques

Fick principle:
- Amount of substance taken up by organ per unit time = (arterial - venous concentration) x blood flow
- Can use O2 for the heart
- LV output = O2 consumption (ml/min) / (arterial - venous pO2 in ml/L)

Indicator dilution:
- Substance injected IV and serial sampling in arterial blood is performed
- Concentrations are log plotted and extrapolated to find the circulation time
- Indicator must not be lost from circulation

26
Q

Following administration of antivenom for a snakebit, a 60yo man is noted to be hypotensive. What causes of decreased cardiac output could be causing this man’s hypotension?

A
  1. Variation in heart rate due to induction of arrhythmias or heart block
  2. Reduced preload (venodilation with reduced venous return due to anaphylaxis)
  3. Increased afterload (not likely in this case)
  4. Reduced contractility (e.g. due to ischaemia, venom, drugs)
27
Q

Describe the major differences between a ventricular muscle action potential and a pacemaker action potential

A
  • Greater negative RMP
  • Fast depolarisation via Na+ channels, vs slower Ca2+ dependent depolarisation
  • No prepotential and no automaticity
  • Plateau potential
28
Q

Draw and label a diagram of the jugular venous pressure wave. Explain the origin of the fluctuations in this wave.

A
  1. A wave:
    - Due to atrial systole (some blood regurgitates into great veins when atria contract)
  2. C wave:
    - Bulging of tricuspid valve into atria during isovolumetric contraction
  3. x descent:
    - Increased atrial volume consequent upon tricuspid valve ring being pulled distally during ventricular emptying
  4. V wave:
    - Rise in atrial pressure before tricuspid valve opening during diastole
  5. y descent:
    - Due to emptying of atrium after the tricuspid valve opens during diastole
28
Q

What ECG changes are seen in hypokalaemia?

A
  • U waves
  • Increased P wave amplitude, PR prolongation
  • ST depression
  • T wave inversion
  • Apparent prolonged QT due to fusion of T and U waves (QU prolongation)
  • Supraventricular/ventricular ectopics -> supraventricular tachyarrhythmias -> ventricular arrhythmias
29
Q

How does the ECG relate to the jugular venous pressure wave?

A
30
Q

What are the determinants of myocardial oxygen consumption?

A

2/3 to pass:
- Heart rate
- Wall tension
- Myocardial contractility

31
Q

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

A

2/3 to pass:
- Rate and stroke volume
- Adrenaline and sympathetic discharge
- Venous return

32
Q

What are the physical laws involved?

A

1/2 to pass:
- Starling
- La Place (P = 2T/R)

33
Q

How does decreasing a patient’s heart rate improve symptoms of angina?

A
  • Decreases myocardial O2 demand
  • Increased time for coronary circulation (occurs in diastole)
34
Q

What is stroke volume in a normal adult at rest?

A

70-90ml

ACEM Primary VIVA (45 decks)

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