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MRCS > Cardio physiology > Flashcards

Cardio physiology Flashcards

1
Q

Mechanism of contraction in cardiac myocytes

A

Myocytes contain myofibrils

Myofibrils are made up of sarcomeres

Sarcomeres contain thin actin filaments and thick myosin filaments

In the absence of calcium –> troponin/tropomyosin complexes block cross-bridging

Calcium binds troponin –> allows cross-bridging and contraction

ATP required to detach myosin and actin

Myocytes have two systems of intracellular
membranes:
■ T-tubules
■ sarcoplasmic reticulum.

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2
Q

Cardiac action potential cycle

A

Phase 0

  • Rapid increase in sodium permability
  • Rapid depolarisation

Phase I

  • Rapid repolarisation
  • Rapid decrease in sodium permeability
  • Small increase in potassium permability

Phase 2

  • Slow repolarisation
  • Plateu effect due to influx of Ca2+
  • Plateau lasts about 200 ms.

Phase 3

  • Rapid repolarisation
  • Increase in potassium permability
  • Inactivated Ca2+ influx

Phase 4
-Resting membrane potential,
for ventricular muscle -90mV
-SA node and conduction system do not have resting potential, continual rhythmic firing

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3
Q

Action potential: Phase 0

A

Na fast gates open, increase Na permability

Na fast influx

Cell becomes most positive it can be away form resting potential –> depolarisation

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4
Q

Action potential: Phase 1

A

Na permability reduces, fast Na gates closed

Rapid repolarisation begins, electrical potential moves more negatively away from positive Na peak

Small increase in K permeability

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5
Q

Action potential: Phase 2

A

Slow repolarisation – plateau effect due to inward
movement of calcium

Plateau lasts about 200 ms.

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6
Q

Action potential: Phase 3

A

Rapid repolarisation – increase in potassium permeability

Inactivation of slow inward Ca++ channels

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7
Q

Action potential: Phase 4

A

The resting membrane potential of the ventricular

muscle is about −90 mV

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8
Q

Location of AV node

A

Atrioventricular node

Located in atrioventricular fibrous ring on the right side of atrial septum

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9
Q

Vagal stimulation to heart

A

Vagal innervation to the SA node

Increased activity slows firing of SA node

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10
Q

Phases of the cardiac cycle

A

Phase I: Isovolumetric contraction

Phase II: Ejection

Phase III: Diastolic relaxation

Phase IV: Filling phase of diastole

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11
Q

Phase I: cardiac cycle

A

Isovolumetric contraction

Atroventricular valve closes

Aortic and pulmonary valves closed

Volume remains constant but pressure dramatically increases as ventricles contract

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12
Q

Phase IIa: cardiac cycle

A

Ejection

Pressure in ventricles exceeds that in the aorta and pulmonary artery

Aortic and pulmonary valves open, blood ejected from ventricle

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13
Q

Phase IIb: cardiac cycle

A

Ejection - equal pressures

Aortic and pulmonary artery pressures now equal to that of the ventricles - flow reduces

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14
Q

Phase III: cardiac cycle

A

Diastolic relaxation

Isovolumetric relaxation, volume in ventricles remains the same and the resting ventricular pressure forms as pulmonary and aortic valves close

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15
Q

Phase IVa: cardiac cycle

A

Passive filling during diastole

Atrioventricular valve opens

Low atrial pressure due to suction effect of ventricle

Rapid ventricular filling

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16
Q

Phase IVb: cardiac cycle

A

Decline in rate of filling as atrial volume increases

Atria now full, flow rate reduced

85% of final diastolic ventricular volume reached

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17
Q

Phase IVc: cardiac cycle

A

Atrial contraction

SA node depolarises

Atrial muscle contracts

Provides an additional 15% to ventricles (at-rest)
At higher HR and stroke volumes this is significantly more
–> Failure of atrial contraction therefore at higher heart
rates, e.g. fast atrial fibrillation (AF); exercise may be life-threatening.

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18
Q

Normal right atrial pressures

A

0-4 mmHg

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19
Q

Normal right ventricular pressure

A

25 / 0-4 mmHg

20
Q

Normal left atrial pressures

A

0-10 mmHg

21
Q

Normal left ventricular pressures

A

120 / 0-10 mmHg

22
Q

Third heart sound

A

Rapid ventricular filling

23
Q

Fourth heart sound

A

Atria contracting against a stiff ventricle

LVH or HF

24
Q

a-wave JVP

A

First peak: Atrial contraction

Absent in AF

Cannon waves in complete HB as atria contract against a closed tricuspid valve

Giant waves in pulmonary hypertension, tricuspid and pulmonary stenosis

25
Q

c-wave JVP

A

Small peak on approach to x-descent

This is tricuspid valve bulging during isovolumetric contraction of ventricles

Timed with carotid artery pulse wave

26
Q

x-descent JVP

A

First valley

Due to tricuspid valve moving down during ventricular
systole.

27
Q

v-waveJVP

A

Second peak

Rise in atrial pressure as atria fills prior to opening of tricuspid valve

28
Q

y-descent JVP

A

Second valley

Tricuspid valve opens and blood enters ventricle causing pressure in atria to drop

29
Q

JVP waveforms

A

ACX VY

At
CX

Vascular

Yunit

30
Q

Coronary flow is lowest…

A

During isovolumetric contraction - Phase I

Compression of the intramyocardial arteries

Conditions resulting in low diastolic BP or increased
intramyocardial tension during diastole (e.g. an
increased end diastolic pressure) may compromise
coronary blood flow

31
Q

Tissue with least coronary flow

A

Subendocardial muscle where the tension is highest

32
Q

Coronary flow is highest…

A

Diastole when there is an adequate diastolic BP

Increased when there is adequate time between beats - i.e. at slower HRs

33
Q

Factors increasing afterload

A

Raised aortic pressure

Aortic valve stenosis

Ventricular cavity size, great volume, requires greater tension to achieve same pressure (Laplace’s law)

34
Q

Techniques to measure cardiac output

A

Thermodilution

Dye test

Doppler USS

35
Q

Definition of MAP

A

= diastolic blood pressure + 1/3 of pulse pressure

36
Q

Factors increasing diastolic blood pressure

A

Total peripheral resistance

Arterial compliance (distensibility - stores elastic energy that means diastolic BP higher)

Heart rate

37
Q

Factors increasing the systolic blood pressure

A

Stroke volume

Ejection velocity (without an increase in stroke volume)

Diastolic pressure of the preceding pulse

Arterial rigidity (arteriosclerosis)

38
Q

Definition of systematic vascular resistance

A

SVR = MAP - mean right atrial pressure / CO

Resistance to flow of blood through arterioles.

By constricting and dilating, arterioles control the
blood flow to capillaries according to local needs.

39
Q

PAOP

A

~ Left atrial pressure
Normally 6-12 mmHg

> 15 –> pulmonary oedema

Flotation balloon catheter is passed through the
right heart into the pulmonary artery

The major advantage of the catheter is that it can
be used to measure CO

40
Q

Adrenaline

A

Alpha + Beta

Inotrope
Chronotrope
Vasopressor

β2-effect at low doses causes vasodilatation in
skeletal muscle, lowering SVR.

α-vasoconstrictor effect at higher doses increases SVR and myocardial oxygen demands, with adverse
effect on cardiac output

41
Q

Noradrenaline

A

α-effect.

Vasopressor

Indicated in septic shock when hypotension due to
peripheral vasodilatation persists despite adequate
volume replacement

42
Q

Isoprenaline

A

Exclusively β-effect

Ionotrope
Chronotrope

Vasodilatation in skeletal muscle; therefore reduces
SVR

Tachycardia limits clinical use

Used to increase rate in heart block while awaiting pacing

43
Q

Dopamine

A 
Low dose causes vessel dilataion of:
Renal
Cerebral
Coronary 
Splanchnic

via D1 and D2 receptors and β1 receptors, resulting in increased cardiac contractility and heart rate

High dose stimulates α-receptors, causing vasoconstriction

44
Q

Dobutamine

A

β1 β2

Inotrope
Vasodilator

β1 effect increases heart rate and force of contraction

Mild β2 effect causes vasodilatation

First choice inotrope in cardiogenic shock due to
left ventricular dysfunction.

Dobutamine and low-dose dopamine in conjunction
used in cardiogenic shock to increase BP via increased cardiac contractility and urinary output (UO; via increased renal perfusion)

45
Q

Dopexamine

A

β2 and D receptors.

Inotrope, chronotrope.

Peripheral vasodilatation, increased splanchnic blood flow and increased renal perfusion (increased UO)

46
Q

Vasodilator therapies

A

Nitrates
-Vendilatation reducing pre-load

Nitroprusside

  • Arterial vasodilator with short t1/2-
  • Infusion

Hydralazine

  • Arterial vasodilator
  • Reduces afterload
47
Q

Phosphodiesterase inhibitors

A

Prevent breakdown of cyclic AMP by phosphodiesterase III

Inotropic and vasodilator
-little chronotropic

Increased myocardial contractility (increased CO)
with reduced PAOP and SVR

No significant rise in heart rate or myocardial oxygen
consumption

MRCS (24 decks)

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