P: cardiac cycle Flashcards
Semilunar valves
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.
Sinoatrial node
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
Atrial systole
- 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.
Ventricular systole
- 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.
Ventricular diastole
- 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
Tachycardia
- 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.
Pressure changes: ACV wave
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.
Atrial fibrillation
- Arrhythmia causing uncoordinated contractions of atrial fibres
- No P waves on ECG
- Irregular fluctuations: f waves
- AV node activation is irregular: ventricular contractions irregular.
Normal interval between successive ventricular contractions
0.35-0.95 sec (0.8sec)
Aortic pressure curve
- 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
Heart sound 1
- 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.
Heart sound 2
- 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)
Phonocardiography
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.
Left ventricle pressure-volume loop
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.
Preload
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
Afterload
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
Contractility
- 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.
Diastolic pressure curve
pressure generated by progressively larger end diastolic volumes immediately before ventricular contraction occurs.
Systolic pressure curve
systolic pressure achieved during ventricular contraction with increasing EDV.
Frank-Starling law: higher EDV = higher systolic pressure.
Stroke work output
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.
When heart pumps larger quantities of blood:
- 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.
Ventricular fibrillation
- 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
Ventricular fibrillation: Re-entry can occur as a consequence of:
- 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.
Defibrillator
stops fibrillation by simultaneously placing entire myocardium into a refractory state. Autorhythmic cells in heart regain pacemaker control.
