Cardiac Cycle Flashcards
What are two main phases of a heart beat
Diastole-ventricular relaxation,ventricles fill with blood. Lasts 2/3 of each beat
Systole-ventricular contraction ,ventricles generate pressure then eject into arteries. Lasts 1/3 of each beat
- What is end-diastolic volume?
The maximum volume of blood in heart just before ventricles start to contract (at max relaxation of heart)
What is end systolic volume
Amount of blood in heart after contraction completed- residual blood left in heart
Stroke volume
Voume of blood expelled by the heart in any one cardiac cycle
End-diastolic volume - End-systolic volume = Stroke volume
typical stroke volume in a resting 70 Kg man is 70ml
What is ejection fraction?
The fraction of end diastolic volume that is ejected by heart- gives indication of heart function
How is ejection fraction calculated and what is it’s normal range?
Stroke volume/End-diastolic volume) x 100 = Ejection fraction
Normal: 52-72%
What would be the ejection fraction range in a patient with heart failure
30-35%
7 steps of cardiac cycle
Atrial systole
Isovolumetric contraction
Rapid ejection
Slow ejection
Isovolumetric relaxation
Rapid passive filling
Slow passive filling aka diastasis
Atrial systole
- Ventricle already almost full from passive filling driven by pressure gradient
-
Atria contract to ‘top up’ volume of blood in the ventricle
P wave
S4 may be heard but abnormal due to forceful contraction of atria to overcome stiff or hypertrophic ventricle
Isovolumetric contraction
- This is the interval where both the AV valves and semi-lunar valves are closed, with the SL valves about to open
- Due to this, the contraction of ventricles with no volume change occurs
- Ventricular pressure increases to aortic pressure
QRS complex
First lub sound S1 due to closure of atrioventricular valve
Rapid ejection
- As ventricles contract, ventricular pressure exceeds pressure in aorta and pulmonary arteries → semilunar valves open, blood pumped out due to pressure gradient and ventricular volume decreases
- Opening of aortic and pulmonary valves marks start of phase
Aortic pressure increases
No sound made
Slow ejection
- This phase marks end of systole
- Blood flow from ventricles decreases and ventricular volume decreases more slowly
- Reduced pressure gradient from ventricles into arteries so semilunar valves begin to close
T wave
Isovolumetric relaxation
- Semilunar valves shut but AV valves remain closed until ventricular pressure drops below atrial pressure
- Atrial pressure continues to rise
Dichrotic notch caused by rebound pressure
2nd heart sound dub S2 due to semilunar valve closing
What is the rate of pressure decline in the ventricles here determined by and what is this rate called?
The rate of relaxation of the muscle fibres
Relaxation regulated largely by the Ca2+ ATPases in the SR membrane
Lusitropy (rate of muscle relaxation)
Rapid passive filling
Once intraventricular pressure drops below atrial pressure, AV valves open and atrial blood flows rapidly into ventricles
Isoelectric (flat) on ecg
Abnormal S3 due to severe hypertension or. Mitral incompetent
Slow passive filling aka diastasis
- Ventricular volume fills more slowly
- Ventricles are able to fill considerably without atrial contraction
- After this phase cardiac phase restarts with atrial contraction to top up filling of ventricle
What are the similarities and differences in blood pressure and volume between left and right ventricles?
- left ventricle pumps blood at a higher pressure than right ventricle
- However, right ventricle ejects same volume of blood as left, just into a lower pressure circuit
- Patterns of pressure change are identical in both
- What is the difference between the pulmonary and systemic circuit?
Pulmonary circulation moves blood between the heart and the lungs
Systemic circulation moves blood between the heart and the rest of the body
Typical systemic pressure is 120/80
Typical pulmonary pressure is 25/5
What is the pulmonary capillary wedge pressure an indirect measure of?
Left atrial pressure
Why would a pulmonary capillary wedge pressure be measured clinically?
Gives an idea of the severity of left ventricular failure and mitral valve stenosis
Both of which are caused by an increase in the left atrial pressure → this increase pulmonary oedema which can be life threatening
Pulmonary artery pressure shows clear diastolic and systolic pressures
Explain the pressure volume loop
- We start with A, end-diastolic volume
- Isovolumetric contraction occurs, causing increase in pressure but not volume change since no valves opened
- We then encounter aortic pressure, B, causing aortic valve to open
- Blood goes from ventricle to aorta so ventricular volume will decrease
- This leads to end-systolic volume, C after pressure goes up then drops slightly due to rapid then slow ejection
- Then we get isovolumetric relaxation- no change in ventricle volume but drop in ventricle pressure, D
- We then gradually fill heart again with blood to reach end-diastolic volume and cycle repeats
Preload on pressure volume loop
Blood filling the ventricles during diastole is determines preload that stretches the resting ventricular muscle
Larger amount of blood returning to heart → increased preload → increased stretch of ventricular muscle → increased force produced
What is afterload on the pressure volume loop?
The blood pressures in great vessels (aorta and pulmonary artery) represent the afterload
If afterload increases, there’s less shortening of muscle fibres → less able to expel blood from ventricles
- What is the End-systolic pressure volume relationship (ESPVR)? (i.e. what does it show?)
Maximum pressure that can be developed by ventricle at any given volume
How does the stroke volume and the appearance of the pressure volume loop change (horizontally and vertically) when we increase preload?
Increases in preload result in increased stroke volume- this is Frank-Starling relationship
loop gets wider horizontally
How does the stroke volume and the appearance of the pressure volume loop change when we increase afterload
decreased stroke volume because the amount of shortening of muscle fibres that occurs decreases
loop gets thinner horizontally and taller vertically
What are untie for cardiac output
L/min
Cardiac output formula
Cardiac output (L/min)= heart rate (bpm) x stroke volume (L)
- Which 3 factors influence stroke volume?
-
Preload
Afterload
Contractility
What is the definition of contractility?
Contractile capability (strength of contraction) of heart
- What is it increased by?Sympathetic stimulation
- What is the extrinsic mechanism?Changes Ca2+ delivery to myofilaments
How does the steepness of the ESPVR line change with increases and decreases in contractility?
When more calcium delivered to myofilaments (more sympathetic activity) and so more contractility, we get a steeper ESPVR and vice versa
How does the End-Diastolic Volume change during exercise,
Increases
Due to increased venous return and respiratory pumps
How does the End-Systolic volume change during exercise and what causes this?
Decreases
Sympathetic activation of the myocytes increases ventricular contractility
How does the increase in arterial pressure during exercise affect the afterload?
Increases it
Why doesn’t the increase in afterload, reduce the End-Systolic Volume?
This effect is offset by the large increase in contractility
- How is the Stroke Volume affected during exercise?
Increased End-Diastolic Volume and decreased End-Systolic Volume which leads to an increased Stroke Volume
heart rate increases to an extremely high rate, how is the End-Diastolic Volume affected?
Decreases because the diastolic filling time can be reduced
