Cardiac function

part 1, lecture 2 *INCOMPLETE*

What are the phases of the cardiac cycle?

atrial systole

isovolumetric contraction

ventricular ejection

isovolumetric relaxation

late diastole

phase 1 - Atrial systole

last 20% of filling occurs when the atria contract

additional flow of blood called the atrial kick or boost

small backflow into venae cavae as no one-way valves - used to diagnose high right atrial blood pressure.

phase 2 - Isovolumetric contraction

ventricular contraction with no change in ventricular volume

spiral bands of ventricular muscle contract and squeeze blood upwards

blood pushes on underside of AV valves and forces them closed

AV and semilunar valves are closed, therefore blood has nowhere to go

pressure builds up quickly without changing ventricular volume

phase 3 - ventricular ejection

contraction of ventricles creates enough pressure to open semi-lunar valves

blood ejected into arteries

pressure generated by ventricles is driving force for blood flow

high pressure blood forced into arteries displaces the low pressure blood that fills them and pushes it further into the vessels

phase 4 - isovolumetric relaxation

ventricles begin to relax, leading to a rapid fall in ventricular pressure

ventricular pressure falls below aortic pressure

small volume of blood flows backwards and closes aortic valve —→ brief rise in arterial pressure (dicrotic notch)

phase 5 - late diastole

both chambers are relaxed

ventricle begins to fill with blood passively before atrial systole & start of another cycle

What is occurring during the 2 sounds that make up the heartbeat?

“lub” - closure of AV valves

“dub” - closure of semi-lunar valves

Abnormal sounds heard during auscultation of the heart.

gallops - third sound is heard

clicking - abnormal movement of the valves

whoosh - murmurs caused by valvular incompetance

EMG

burst of electrical activity measured when a muscle is contracted.

ECG

small changes in potential detected between different locations on the skin

potentials caused by the spread of electrical currents through underlying structures.

3 main waves on an ECG

P wave - atrial depolarisation

QRS complex - ventricular depolarisation

T wave - ventricular repolarisation

*NB - atrial repolarisation masked by QRS complex and therefore not represented

What is the R-R interval an accurate measurement of?

heart rate

What is a long Q-T interval indicative of?

long Q-T syndrome - channelopathies where there are mutations in myocardial Na⁺ & K⁺ channels

can sometimes occur because of drug side-effects

aortic stenosis

reduction in valve orifice area for left ventricle when opened

high outflow resistance

large pressure gradient across aortic valve during ejection

peak systolic pressure in ventricle greatly increased

increase in cardiac afterload, decrease in stroke volume, increase in cardiac muscle mass

risk of heart faliure

end diastolic volume

volume of blood in the heart at the end of the cardiac filling phase

end systolic volume

volume of blood left in the heart at the end of the ejection phase

Describe experiment 1 (increased preload and the Starling law) done by Starling.

1. peripheral resistance (therefore afterload) and heart rate were kept constant. Cardiac filling pressure (therefore preload) was increased.

2. cardiac output increased under these conditions

3. Increased cardiac output must be due to increased stroke volume as heart rate was kept constant

4. left ventricular and aortic pressures increased - greater amount of blood ejected against the same resistance.

5. increased filling pressure lead to ventricular stretch to accommodate for the increased end diastolic volume.

6. stimulates intrinsic property to increase the force of contraction in response to elongation/stretch

“energy of contraction is a function of the length of the muscle fibre” - Starling law of the Heart

TL;DR - put more blood in, get more blood out so heart volume remains the same.

Describe experiment 2 (increased afterload and the Starling law) done by Starling.

1. Heart rate and filling pressures are kept constant

2. peripheral resistance (therefore afterload) is increased. Heart finds it harder to force blood through the system.

3. increase in aortic & left ventricular pressures

4. increase in end systolic volume as less complete emptying of the heart

5. initial fall in stroke volume & cardiac output as pumping against an increased resistance

6. increased afterload promotes increase in end diastolic volume - ventricle walls stretched more

7. cardiac output increased by Frank-Starling mechanism

*NB - biphasic response: 1st a small decrease in cardiac output then a recovery of cardiac output

The Anrep effect

Autoregulation method where myocardial contractility increases with afterload

Sustained myocardial stretch activates Na⁺/H⁺ exchangers

Na⁺ enters the sarcolemma

Na⁺ gradient reduces

Na⁺/Ca²⁺ exchanger that exploits this gradient stops working as effectively

Ca²⁺ accumulates inside the sarcolemma and taken up by sarcoplasmic reticulum SERCA pumps as a result

CICR from sarcoplasmic reticulum increased upon stimulation of cardiac myocyte by action potential

increase in force of contraction

increase stroke volume & cardiac output to try to maintain tissue perfusion.