Cardiology Flashcards
Cardiac cycle: Systole
1. Atrial systole
Beginning of cardiac cycle
Initiated by atrial excitation and follows crest of P wave on ECG
At the end of diastole, atrial contraction forces small blood bolus into LV chamber –> atrial kick
Heart sound: S4
Cardiac cycle: Systole
2. Isovolumic ventricular contraction
Mitral valve closure –> ventricular systole (occurs during QRS complex)
~50ms for ventricle to develop sufficient pressure to force aortic valve open. Myocytes are contracting around a fixed volume of blood until LVP meets and exceeds aortic pressure.
Heart sound: S1
*LV volume (LVEDV) is highest during this phase
Cardiac cycle: Systole
3. Rapid ventricular ejection
Aortic valve opens and blood exits the arterial system at high velocity
Pressure continues to climb even though blood is being ejected because the LV myocytes are still actively contracting
Atrium relaxes and begins to fill
*Highest pressure in LV is reached during this phase
Cardiac cycle: Systole
4. Reduced ventricular ejection
Ejection velocity decreases as ventricular systole nears completion.
Ventricular myocytes begin repolarising, contraction wanes and LVP falls rapidly
Aortic valve closure marks the end of this phase
Cardiac cycle: Diastole
5. Isovolumic ventricular relaxation
Isovolumic relaxation begins as LV contraction ends
Atrium continues to fill with venous blood
Heart sound: S2 (AV valve closure)
Cardiac cycle: Diastole
6. Rapid ventricular filling
LVP drops below L atrial pressure and the mitral valve opens
Rapid passive ventricular filling occurs
Heart sound: opening snap of MV (if stenotic), S3
Cardiac cycle: Diastole
7. Reduced ventricular filling (diastasis)
Cardiac cycle ends with reduced filling
This phase typically disappears when HR increases because cycle length is shortened at the expense of diastole
Arterial pressure continues to fall as blood flows through capillary beds (diastolic pressure of ~80mmHg)
Aortic pressure: Dicrotic notch
Aortic pressure dips briefly immediately following aortic valve closure
Caused by aortic valve bulging backward into LV under the weight of aortic pressure when it closes
Jugular venous pressures: a, c and v waves
a wave: R atrial contraction at the beginning of systole generates a pressure wave that forces blood into R ventricle and also causes the a wave
c wave: ventricular contraction causes ventricular pressure to rise sharply –> AV valve bulges back into atrium –> backward deflection of tricuspid valve generates jugular venous pulse
v wave: during ventricular systole, blood flows from venous system into R atrium and dam against closed TV. Pressure builds as atrium fills = upslope of v wave. Downward slope of v wave corresponds to rapid atrial emptying once TV opens
S3
Low intensity rumbling HS during early diastole
Rapid ventricular filling –> turbulence that makes LV walls reverberate and rumble (can be normal in children)
S4
Associated with atrial contraction - reflects blood being forced into ventricle at high pressure by hypertrophied atrium
Preload
Load that is applied to a myocyte and establishes muscle length before contraction begins
In LV, preload = volume of blood entering the chamber during diastole (EDV)
Afterload
It is the load against which a myocyte must shorten
- Aortic pressure (for LV)/mean arterial pressure (MAP)
- Vascular resistance
3 determinants of stroke volume
Preload, afterload and contractility
Contracility: measure of muscle’s ability to shorten against afterload. Equates with sarcoplasmic free Ca concentration
LV preload is determined by end diastolic pressure. Surrogate markers for EDP are… (2)
Right atrial pressure
Central venous pressure
Frank-Starling Law of the Heart
Stretching the sarcomeres of myocyte increases the amount of force that muscle is able to generate on next beat. Therefore, stroke volume increases with increased blood volume entering the ventricles.
Short-term and long-term adjustments to cardiac output involving preload
Short term: SNS activation vasoconstricts and forces blood out of veins –> ventricle to increase preload –> increased stroke volume –> increased CO
Long term: activation of RAAS leads to fluid retention by kidneys –> sustained increased in circulating blood volume which increases preload –> increased SV –> increased CO