The Heart as A Pump Flashcards

1
Q

The heart

A

Two pumps acting in series

Systemic circulation = High Pressure

Pulmonary circulation = Low pressure

Output of left and right sides over time must be equal

Atria act as “priming pumps” for ventricles - the main pumps are the ventricles

Systole = Contraction and ejection of blood from ventricles

Diastole = Relaxation and filling of ventricles

At rest each ventricle pumps ~ 70 ml blood per beat (= Stroke volume)
At a heart rate of 70 bpm = 4.9 litres blood pumped per minute (i.e. the approximate volume of blood in the body) ~14,000 litre water tank
= 294 litres of blood pumped every hour
= ~7000 litres /day by each ventricle
= ~14,000 litres per day by both ventricles
By 60 years of age the total combined cumulative output of both ventricles is ~300 million litres…i.e. the capacity of this oil tanker!

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2
Q

Heart muscle

A

Specialised form of muscle

Discrete cells but interconnected Atrial electrical muscle

Cells contract in response to action potential in membrane

Action potential causes a rise in Ventricular intracellular calcium muscle
Cardiac action potential relatively long – lasts for durations of a single contraction of heart (~280 ms)

Action potentials are triggered by spread of excitation from cell to cell

Myoblasts connect to form long fibers of muscle fibers so cells are multinucleated - in cardiac muscle - connected by gap junctions between cells - they are electrically coupled - so when 1 AP originates in the SA node, it is able to cross all over the heart and give 1 synchronous beat (via the help of Purkinje fibres)

AP is a long duration in comparison (280ms) - needs this to be the case as this is how long it takes to fully contract the heart (for reference skeletal AP is 3-5ms)

Arrangement of muscle in heart - in a kinda figure of 8 - so when ventricles contract there is a squeezing twisting action to force the blood out of heart

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3
Q

Heart valves

A

4 valves - 2 separating atria from ventricles (Tricuspid (right) and mitral (left)), and 2 separating ventricles form respective blood vessels (output valves) (pulmonary (right) and aortic (left)) - these valves are operated by pressure difference across the two sides of the valve - i.e. the blood flows from high pressure to low pressure so, when the pressure in one chamber drops the valves open and blood flows through

Valve cusps are pushed open to allow blood flow and close together to seal and prevent backflow.

Cusps of mitral and tricuspid valves attach to papillary muscles via chordae tendineae.
Prevents inversion of valves on systole (contraction) (as there is less pressure in the atrium, without the papillary muscles and chordate tendineae, on systole of the ventricles, the blood could go back into the atria

When the aortic valve is closed the mitric valve is open and vice versa

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4
Q

Conduction system

A

Pacemaker cells in sinoatrial node generate an action potential

Activity spreads over atria – atrial systole (contraction)

We don’t want ventricles same time as the atria (want them contraction at then of atrial contraction)

Reaches the atrioventricular node and delayed for ~ 120 ms - allows for atria to complete contraction

From a-v node excitation spreads down septum between ventricles

Next, excitation spreads through ventricular myocardium from inner (endocardial) to outer (epicardial) surface via Purkinje fibers

Ventricle contracts from the apex up forcing blood through outflow valves

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5
Q

Cardiac cycle can be split into 7 phases

A

1) atrial contraction
2) isovolumetric contraction
3) rapid ejection
4) reduced ejection
5) isovolumetirc relaxation
6) rapid filling
7) reduced filling

When we excercise our systole (contraction) stays the same speed (constant) and diastole (relaxation) is the one that increases

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6
Q

Wiggers Diagram

A

Can compare pressure in aorta and ventricles - can see sound we hear with a stethoscope, can align this with electrocardiograph and ventricle volume and time
Usually done for the left side of the heart - could be done with right, would be similar but pressure would be less

Shows the 7 phases of the heart

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7
Q

Phase 1 of cardiac cycle - atrial contraction

A

Atrial pressure rises due to atrial systole. This is called the “A wave”

Atrial contraction accounts for final ~10% of ventricular filling. This value varies with age and exercise

P wave in ECG signifies onset of atrial depolarisation

Mitral/Tricuspid: Open Aortic/Pulmonary: Closed

At the end of Phase 1 ventricular volumes are maximal: termed the End-Diastolic Volume (EDV) (Typically ~120 ml)

Most of the blood flowing into the ventricle is passive - due to the ventricle wall relaxing - therefore pressure decreases therefore blood flows in, last bit of blood gets into ventricles by atrial kick (when atria contracts (gives you final 10% of ventricular blood volume))

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8
Q

Phase 2 of the cardiac cycle - Isovolumetric contraction

A

Mitral valve closes as intraventricular pressure exceeds atrial pressure

Rapid rise in ventricular /pressure as ventricle contracts

Closing of mitral valve causes the “C wave” in the atrial pressure curve

Mitral/Tricuspid: Closed Aortic/Pulmonary: Closed

Isovolumetric since there is no change in ventricular volume (all valves are closed)

QRS complex in ECG signifies onset of ventricular depolarisation.
Closure of the mitral and tricuspid valves results in the first heart sound (S1) (the lub part of lub dub)

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9
Q

Phase 3 - Rapid ejection

A

Ejection begins when the intraventricular pressure exceeds the pressure within the aorta.

This causes the aortic valve to open

Blood continues to flow into the atria from their respective venous inputs

Atrial pressure initially decreases as the atrial base is pulled downward as ventricle contracts. This is called the “X descent”

Rapid decrease in ventricular volume as blood is ejected into aorta

Mitral/Tricuspid: Closed Aortic/Pulmonary: Open

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10
Q

Phase 4 - reduced ejection

A

Repolarisation of ventricle leads to a decline in tension and rate of ejection begins to fall

Atrial pressure gradually rises due to the continued venous return from the lungs - called the V wave

Ventricular repolaristion depicted by T wave of ECG

Mitral/Tricuspid: Closed EDV Aortic/Pulmonary: Open

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11
Q

Phase 5 Isovolumetric relaxation

A

When intraventricular pressure falls below aortic pressure, there is a brief backflow of blood which causes the aortic valve to close

“Dicrotic notch” in aortic pressure curve caused by valve closure

Although rapid decline in ventricular pressure, volume remains constant since all valves are closed. Hence isovolumetric relaxation

Mitral/Tricuspid: Closed Aortic/Pulmonary: Closed
End systolic Volume (ESV)
EDV-ESV = Stroke volume ESV (Typically ~70-80ml)

Closure of the aortic and pulmonary valves results in the second heart sound (S2).

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12
Q

Phase 6 - rapid filling

A

Fall in atrial pressure that occurs after opening of mitral valve is called the Y-descent

When the intraventricular pressure falls below atrial pressure, the mitral valve opens and rapid ventricular filling begins

Ventricular filling normally silent - however, third heart sound (s3) sometimes present.

S3 heart sound is normal in children but can be sign of pathology in adults

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13
Q

Phase 7 reduced filling

A

Rate of filling slows down as ventricle reaches its inherent relaxed volume.

Further filling is driven by venous pressure - At rest ventricles are ~90% full by the end of phase 7

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14
Q

Abnormal valve function

A

Valve doesn’t open enough —> obstruction to blood flow when valve would normally be open —> Stenosis

Valve doesn’t close all the way —> Back leakage when valve should be close —> regurgitation

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15
Q

Aortic valve stenosis

A

Causes:
Degenerative (senile calcification/fibrosis)

Congenital (bicuspid form of valve)

Chronic rheumatic fever –inflammation- commissural fusion

So less blood is able to get through the valve, which leads to increased left ventricle pressure —> LV hypertrophy, and it can lead to left sided heart failure —> angina (blood supply to heart not enough)

Microangiopathic haemolytic anaemia - lack of RBC and Hb, - blood is forced through a restricted valve, therefore there is stress on the RBC causing lysis, —> MHA

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16
Q

Aortic valve regurgitation

A

Causes:
Aortic root dilation (leaflets pulled apart)

Vlavular damage (endocarditis rheumatic fever)

Blood flows back into LV during diastole, which leads to an Increase in stroke volume

Systolic pressure increases

Diastolic pressure decreases

Bounding pulse (head bobbing, Quinke’s sign(beds of nails flush with the beat of the pulse))

LV hypertrophy

17
Q

Mitral valve regurgitation

A

Chordae tendineae & papillary muscle normally prevent prolapse in systole

Myxomatous degeneration can weaken tissue leading to prolapse

Other causes:
Damage to papillary muscle after heart attack

Left sided heart failure leads to LV dilation which can stretch the valve

Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation - leaving a gap when “closed”

As some blood leaks back into LA, this increases preload as more blood enters LV in subsequent cycles, can cause LV hypertrophy

18
Q

Mitral valve stenosis

A

Main cause = Rheumatic fever (99% cases)

Commissural fusion fo valve leaflets - therefore don’t open as widely

Harder for blood to flow from LA—> LV

Therefore increased LA pressure leads to LA dilation, which can cause fibrillation of the atria which could lead to a thrombus forming.

Also the dilation could cause some compression fo the oesophagus to occur leading to dysphagia (swallowing difficulties)

This increased LA pressure could also cause pulmonary oedema and pulmonary hypertension (increased pressure), which could lead to RV hypertrophy