P: cardiac cycle Flashcards

1
Q

Semilunar valves

A

At origin of pulmonary artery + aorta. Open during ventricular contraction and allow blood to flow only from ventricles into arteries. Closure of semilunar valves generates 2nd heart sound.

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2
Q

Sinoatrial node

A

location: right atrium near opening of superior vena cava.
Spontaneous depolarizations here pass into surrounding myocardial cells + generate contraction:
1. Atrial myocardial cells
2. Pause (fibrous layer)
Ventricular myocardial cells

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3
Q

Atrial systole

A
  • At t=0 sec, both atria and ventricles are in diastole
    • Atrial pressure > ventricular pressure, AV valves open and semilunar valves are closed –> ventricles become 80% filled.
    • Wave of depolarization spreads through both atria (P wave)
      Pressure in atria increases, remaining 20% blood flows into ventricles.
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4
Q

Ventricular systole

A
  • T=100msec, depolarization wave spreads into ventricles QRS wave
  • Ventricle pressure > atrial pressure, so AV valves closed
  • Ventricular contraction strength + pressure increases
  • Below 80mmHg, left ventricular pressure is not strong enough to open SL valves into aorta
  • Below 8mmHg, right ventricular pressure is not strong enough to open SL valves into pulmonary artery
  • Isovolumetric contraction.
  • Atrial pressure increases slightly as upward pressure of ventricles causes AV valves to bulge into atria.
  • At t=130msec, pressure LV> aorta + pressure RV> pressure pulmonary artery so both SL valves open.
  • Total volume of blood ejected = stroke volume.
  • End systolic volume = residual blood remaining in ventricles.
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5
Q

Ventricular diastole

A
  • T=300msec, repolarization of ventricles begins (T wave)
  • T=350 msec, LV pressure < aortic pressure, RV pressure < pulmonary artery pressure, backflow closes SL valves and generates 2nd heart sounds.
  • Atrial pressure increasing (filling)
  • Short period of backflow prior to closing of aortic valve
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6
Q

Tachycardia

A
  • Diastasis is shortened + contribution of atrial contraction is significant
  • Intense exercise: ventricular contraction can begin during rapid filling, contribution of atrial contraction is more important. There is a reduction in stroke volume.
  • Syncope (fainting) can result if inadequate ventricular filling occurs.
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7
Q

Pressure changes: ACV wave

A

A: rise in pressure caused by atrial contraction. Pressure increases by 4-mm Hg in RA and by 7-8mm Hg in left atrium.
C: Increasing ventricular pressure causes bulging of AV valves into atria.
V: Rise in pressure associated with atrial filling.

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8
Q

Atrial fibrillation

A
  • Arrhythmia causing uncoordinated contractions of atrial fibres
  • No P waves on ECG
  • Irregular fluctuations: f waves
  • AV node activation is irregular: ventricular contractions irregular.
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9
Q

Normal interval between successive ventricular contractions

A

0.35-0.95 sec (0.8sec)

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10
Q

Aortic pressure curve

A
  • Ejection of blood from left ventricle into arteries increases pressure to -120mm Hg
  • Immediately before closure of aortic valve, short period of backflow into ventricle - causing incisura/ dicrotic notch
  • Pressure in aorta decreases slowly throughout diastole as elastic recoil pushes blood continually to peripheral vessels
  • Before ventricle contracts again, aortic pressure falls to -80mm Hg
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11
Q

Heart sound 1

A
  • Upon systole, sudden backflow of blood against AV valves causes their closure
  • Bulges into atria until chordae tendineae abruptly stop back bulging.
  • Tautness of valves/ chordae tendineae causes blood to bounce forward again into each ventricle
  • Vibration of valves + turbulent blood transmitted to ventricular walls & surrounding blood vessels
  • Loudest + longest (0.14 sec) heart sound.
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12
Q

Heart sound 2

A
  • Upon diastole, SL valves close + bulge back into ventricles
  • Elastic stretch recoils blood back into arteries
  • Reverberation of blood between the walls of arterial walls and valves and between valves and ventricular walls
  • Duration (0.11 sec)
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13
Q

Phonocardiography

A

detection of 2 further heart sounds with a microphone.

S3: caused by inrushing blood from atria during middle 1/3 of diastole. Typically only heard in younger individuals –> heard in older individuals can be a sign of a heart murmur

S4: Inflow of blood into ventricles following atrial contraction.

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14
Q

Left ventricle pressure-volume loop

A

A: opening of mitral valve + beginning of filling
A-B: pressure falls as diastole progresses, blood volume increasing
B-C: pressure and volume increase as filling progresses, small increase in pressure before C (atrial contraction)
C: mitral valve closes, EDV (end diastolic volume).
C-D: systole begins, isovolumetric contraction.
D: aortic valve opens (80mmHg)
D-E: pressure rises (120mmHg), volume falls, rapid ejection
E-F: pressure + volume fall, reduced ejection
D-F: stroke volume
F: aortic valve closes, ESV
A-F: Diastole begins, isovolumetric relaxation.

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15
Q

Preload

A

degree of tension on the muscle when it begins to contract. Magnitude of EDV and corresponding end diastolic pressure. Point C on pressure-volume loop

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16
Q

Afterload

A

force against which the muscle is acting.
Blood pressure in aorta which the ventricle must exceed to open the aortic semilunar valve to eject blood
Aortic blood pressure - point D on pressure-volume loop

17
Q

Contractility

A
  • Strength of contraction at a given preload + afterload
  • Slope of ventricular pressure curve gives an index of contractility (A)
  • Drugs such as adrenaline can increase contractility (B)
  • Cardiac failure reduces contractility ©
  • Maximum dP/dt is an index of contractility.
18
Q

Diastolic pressure curve

A

pressure generated by progressively larger end diastolic volumes immediately before ventricular contraction occurs.

19
Q

Systolic pressure curve

A

systolic pressure achieved during ventricular contraction with increasing EDV.
Frank-Starling law: higher EDV = higher systolic pressure.

20
Q

Stroke work output

A

physical work done by ventricle to eject stroke volume.
Energy heart converts to work during each heartbeat used mainly to move blood from low-pressure veins to high-pressure arteries.

21
Q

When heart pumps larger quantities of blood:

A
  • Area (EW) becomes larger
  • Extends to right as ventricle fills with more blood during diastole
  • Extends upwards as ventricle contracts with greater pressure
  • Extends left due to reduced end systolic volume resulting from enhanced contractility.
22
Q

Ventricular fibrillation

A
  • Normal depolarization waves spreads rapidly to all myocardial cells
  • All cells become simultaneously refractory - impulse fades
  • Re-entry occurs if cells become excitable again
  • Same impulse generates second wave of depolarization
23
Q

Ventricular fibrillation: Re-entry can occur as a consequence of:

A
  • Increase tissue mass causing long pathway for impulses
  • Decreased rate of conduction caused by: blockage of Purkinje system, ischemia of muscle, high blood potassium levels
  • Shortened refractory period in response to various drugs.

During re-entry, some fibres still refractory, some fully excitable and others can conduct impulses at slow rates –> abnormal patterns of cardiac contraction that ignore pace-setting effects of sinus node.

24
Q

Defibrillator

A

stops fibrillation by simultaneously placing entire myocardium into a refractory state. Autorhythmic cells in heart regain pacemaker control.