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CDL301 > Physiology of the heart > Flashcards

Physiology of the heart Flashcards

1
Q

What is the resting membrane potential of cardiac cells?

A

-70 mV

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2
Q

In what types of tissue is the pacemaker potential found?

A

Nodal and conducting tissue

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3
Q

What are the electrophysiological features of nodal tissue (SA node and AV node)?

A

Slower depolarisation due to slow Ca2+ influx

Gradual upsloping depolarisation (pacemaker activity)

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4
Q

What are the electrophysiological features of conducting tissue (Purkinje fibres)?

A

Rapid depolarisation due to fast Na+ current

Long plateau phase due to Ca2+ influx

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5
Q

What are the electrophysiological features of atria?

A

Rapid depolarisation due to fast Na+ current

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6
Q

What are the electrophysiological features of ventricles?

A

Rapid depolarisation due to fast Na+ current

Long plateau phase due to Ca2+ influx

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7
Q

Describe the process of triggered activity

A

Increased intracellular Ca2+ can trigger a large after-depolarisation which triggers a series of action potentials, resulting in tachyarrhythmias

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8
Q

Describe the process of increased automaticity

A

If the SA node fails, other cardiac tissues such as the AV node or Purkinje fibres can take over and fire at a lower rate as a safety mechanism.
Sometimes, the other pacemakers take over inappropriately, resulting in abnormal ectopic activity

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9
Q

Describe the process of re-entry

A

Under normal conditions, if an impulse has to go around an obstruction, the impulse splits and propagates in both directions and then joins up again when the two impulses meet. Leaves behind refractory tissue so impulses cannot go backwards.

In a damaged heart, a unidirectional conduction block is present. impulse can only go in one particular direction.. by the time the impulse comes around and reaches the damaged tissue, if damaged tissue can conduct retrogradely, it can conduct back up to tissues that are now repolarised. continuous circulation of the impulse can occur, this is a phenomenon known as circus movement. repetitively excites a region of the heart.

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10
Q

What is the length of the AV delay?

A

200ms

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11
Q

1st degree heart block

A

longer PR interval

impulses still reach the ventricles

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12
Q

2nd degree heart block

A

consecutive normal ECGs followed by P wave with no QRS complex

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13
Q

3rd degree heart block

A

atria contract independently of ventricles

ventricles fire at a slower rate

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14
Q

Normal heart rate? (normal sinus rhythm)

A

60-80bpm

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15
Q

What heart rate is classed as sinus bradycardia?

A

Less than 60bpm

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16
Q

Atrial tachycardia

A

Multiple P waves because atria contract quickly

ventricles do not contract at the same speed (because of AV delay)

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17
Q

Ventricular tachycardia

A

wide QRS complex - impulses activating the ventricles take longer as they come from a different part of the heart

18
Q

Atrial fibrillation

A

no p waves
fibrillating waves in the atria hit the AV node and randomly fire the ventricles, resulting in an irregular ventricular response
results in blood clots e.g. atrial thrombus

19
Q

Ventricular fibrillation

A

variable morphology
no clear ventricular rhythm
irregular ventricular response

20
Q

What effect does sympathetic stimulation have on the heart?

A
  1. NA activates B1 adrenoceptors on the myocytes
  2. Activates cAMP
  3. Increases slope of pacemaker potential
  4. Depolarisation takes shorter amount of time to reach threshold so fires AP faster
  5. heart rate increases and automaticity increases
21
Q

What effect does parasympathetic stimulation have on the heart?

A
  1. ACh acts on M2 receptors on the nodal and atrial tissue
  2. Decreases slope of pacemaker potential
  3. Depolarisation takes longer to reach threshold
  4. heart rate decreases and automaticity decreases

ACh released by the vagal nerve acts on M2 receptors on nodal tissue and slows conduction through AV node –> PR interval increases

22
Q

What are the classes of the Vaughan Williams Classification of anti-arrhythmic drugs?

A 
class I = sodium channel blockers 
class II - Beta adrenoceptor antagonists 
class III - drugs prolonging action potential 
class IV - Ca2+ channel blockers
23
Q

What are the effects of digoxin on the heart?

A

Causes increase in intracellular Ca2+:
Increases vagal tone by accentuating vagus nerve, slowing heart rate
Slows conduction of AV node
Increases ectopic activity (because of increase in intracellular Ca2+)
Increases force of contraction (because of increase in intracellular Ca2+)

24
Q

How is digoxin used in atrial fibrillation?

A

Blocks AV node to slow ventricular response

25
Q

How is digoxin used in severe heart failure?

A

Slows the heart rate and increases the force of contraction

26
Q

What is the danger of drugs which prolong AP?

A

Prolonging AP causes QT prolongation

triggers arrhythmias such as polymorphic ventricular tachycardia - can be lethal

27
Q

What are the adverse effects of amiodarone?

A
  • interstitial pneumonitis (in the lungs)
  • abnormal liver function
  • hyperthyroidism or hypothyroidism
  • sun sensitivity
  • slate grey skin discolouration
  • corneal microdeposits
  • optic neuropathy
28
Q

What is the effect of amiodarone on warfarin?

A

Warfarin is an anticoagulant which is attached to proteins while it is carried around the bloodstream
The part of warfarin in the plasma is active and causes anti-coagulation
Amiodarone displaces warfarin from the proteins, causing the patient to become over-coagulated

29
Q

What is the equation for cardiac output?

A

cardiac output = heart rate x stroke volume

30
Q

Define stroke volume (ml)

A

Volume of blood ejected each time the heart contracts

31
Q

Define ejection fraction

A

% volume of blood ejected with each cardiac contraction

32
Q

What is preload?

A

Filling pressure

33
Q

What is venous return?

A

Blood volume coming back to the heart

34
Q

What is afterload?

A

Resistance to ejection in the circulation

35
Q

Describe the role of calcium in the cardiac AP

A

As the AP is conducted, a small amount of Ca2+ moves into the cells through L type Ca2+ channels but this is not enough to trigger a contraction
Ca2+ binds to ryanodine receptors on the membrane of the SR to cause release of Ca2+ from SR into the cell
Ca2+ binds to troponin, causing contraction

36
Q

Describe how calcium causes cardiac muscle contraction

A
  1. myosin binding sites on actin are covered by troponin and tropomyosin so there is no interaction between actin and myosin
  2. Ca2+ attaches to troponin and reveals myosin binding sites. ATP is hydrolysed when myosin head is unattached.
  3. ADP and phosphate are bound to myosin as myosin head attaches to actin
  4. ADP and phosphate release causes head to change position and actin filament to move - contraction
  5. binding of ATP causes myosin head to return to resting position
37
Q

Describe the structure of cardiac muscle and why it is important

A

cross-branching between muscle cells are important for:
fast electrical impulse transmission across the heart
mechanical contraction - muscle cells contract together so heart contracts as one functional unit

38
Q

How do changes in venous return affect how the heart contracts?

A

increased venous return results in an increase in end-diastolic pressure which increases stroke volume/cardiac output

39
Q

What changes in contractility and afterload result in heart failure?

A

Decrease in contractility - a large increase in pre-load is needed to increase cardiac output
Increase in afterload - heart ejects blood into high pressure + high resistance circulation. Will need to fill heart more to obtain required cardiac output.

40
Q

Describe an experiment showing the effect of sympathetic NS on heart contraction

A

Infusion with a vehicle fluid - end diastolic pressure increases with an increase in stroke volume/cardiac output/stroke work
Infusion with a NA infused fluid - for a smaller change in end diastolic pressure there is a larger change in stroke volume/cardiac output

41
Q

What are the features of heart failure patients?

A

Decreased contractility
Increased afterload
Operate on higher LVEDP to obtain more cardiac output

42
Q

How can digoxin and diuretics be used to treat heart failure?

A

Digoxin is positively ionotropic, causing an increase in intrinsic contractility, increasing cardiac output
Then diuretics can lower pre-load without resulting in low cardiac output to treat pulmonary congestion

CDL301 (2 decks)

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