Cardiovasulcar physiology notes PDF

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22.PHYSIOLOGY OF THE HEARTi. Blood pressure in the pulmonary circuit is approx. 28/8 mmHg. ii. Blood pressure in the systemic circuit is approx. 120/80 mmHg.2. HEART VALVES AND CIRCULATION OF BLOODThe valves of the heart open and close in response to pressure changes as the heart contracts and relax...

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22.11.18

PHYSIOLOGY OF THE HEART

i.

Blood pressure in the pulmonary circuit is approx. 28/8 mmHg.

ii.

Blood pressure in the systemic circuit is approx. 120/80 mmHg.

2. HEART VALVES AND CIRCULATION OF BLOOD The valves of the heart open and close in response to pressure changes as the heart contracts and relaxes A. Bicuspid and tricuspid i.

Right and left atrioventricular valves

ii.

Prevent back flow from the ventricles into the atria

B. Pulmonary and aortic i.

Right and left semilunar valves

ii.

Prevent backflow from the arteries into the ventricles

3. CARDIAC CYCLE - 1 Systole A. Contraction i.

Atrial systole

ii. Ventricular systole Diastole B. Relaxation i.

Atrial diastole

ii. Ventricular diastole Cardiac cycle C. Systole + diastole

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4. CARDIAC CYCLE - 2 A. Atrial contraction: blood is pushed into ventricles

B.

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Isovolumetric contraction: ventricles contract but pressure is insufficient to open semilunar valves

C.

Ventricular ejection: ventricles continue to contract, pressure increases, semilunar valves open

D.

Isovolumetric relaxation: atria fill passively, pressure insufficient to open AV valves

E.

Ventricular filling: as atrial pressure increases, AV valves open

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5. CARDIAC CYCLE - 3 i.

At a heart rate of 75bpm, each whole cardiac cycle lasts 0.8 seconds.

ii.

The whole heart is in diastole for 0.4 seconds, atrial systole lasts 0.1 seconds and ventricular systole lasts 0.3 seconds

iii.

The heart is physically capable of beating at more than 200bpm, however the volume of blood pumped by the heart starts to decrease above this rate – why?

iv.

Reason being the cardiac cycle at 200bpm would last 0.3 seconds, with the time available for atrial filling, about 0.2 seconds which is not enough.

6. CONDUCTION IN THE HEART – CARDIAC MUSCLE Intercalated discs link muscle cells together and contain desmosomes and gap junctions Desmosomes hold the muscle cells together tightly Gap junctions allow passage of action potentials from one cell to the next, very quickly – allows the cardiac muscle to function together as a syncytium

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i.

The specialised cells of the SAN produce electrical impulses at a rate of 100 per minute.

ii.

The impulse spread rapidly throughout the atrial muscle, causing a wave of contrition.

iii.

There is a slight delay as the impulse passes through the AVN (this is the only place the impulse can pass from atria to ventricles).

iv.

The impulses pass rapidly down the bundle branches and upwards through the Purkinje fibres, followed by a wave of ventricular contraction.

7. CARDIAC PACEMAKERS

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i.

The cells of the SAN depolarise over time, with movement at ions causing the resting membrane potential to gradually decrease (pacemaker potential).

ii.

Once the membrane potential exceeds a threshold, an action potential is triggered.

iii.

This happens automatically every 0.8 seconds (approx..) at rest

iv.

The cells of the AVN do the same, but more slowly; the result of this is that an action potential is triggered in the AVN cells before they depolarise enough to trigger their own.

v.

Although the SAN generates its own action potentials, it can be influenced by sympathetic and parasympathetic nerves to do this faster or more slowly.

8. PACEMAKER POTENTIALS i.

At a membrane potential of about -60mV, ‘funny channels’ open in the SAN cell membrane

ii.

Sodium enters the cell through the ‘funny channels’, taking a positive charge into the cell

iii.

The inside of the cell becomes less negative in relation to the outside

iv.

A type of voltage – gated calcium channels open, and calcium enters the cell slowly

v.

The cell continues to depolarise gradually (pacemaker potential)

vi.

When the threshold is reached, another type of voltage-gated calcium channel opens, and calcium enters the cell rapidly

vii.

this results in rapid depolarisation – the cardiac action potential.

9. EFFECTS OF AUTONOMIC NS ON PACEMAKER CELLS A. Parasympathetic NS (slows heart rate) i.

Decreases rate of influx of Na+ through the funny channels, and slow Ca2+ influx

ii.

This means it takes longer for the pacemaker potential to reach the threshold for an action potential

B.

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Sympathetic NS (increases heart rate) i.

Increases rate of influx of Na+ and Ca2+

ii.

This means that pacemaker potentials develop quickly, so cardiac action potentials happen more quickly.

10.

CARDIAC ACTION POTENTIAL

11.

CONDUCTION AND ECG As action potentials travel through the heart muscle, they produce electrical currents that can be detected using electrodes on the body surface.

A. The trace varies depending on: i.

The direction of travel

ii.

Whether the cells are depolarising or repolarising

iii. The size of the change in potential The ECG is an electrical trace resulting from action potentials in all the heart muscle fibres. A 12-lead ECG actually consists of 6 electrodes, and the potential between each lead and each other lead (total 12 possible) gives a characteristic shape.

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B. Electrical events

Ventri cles Atria

12.

HEART SOUNDS

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i.

There are actually 4 heart sounds, but only 2 are loud enough to be heard.

ii.

First heart sound (LUBB) – turbulence caused by closure of the AV valves (happens when the ventricles contract)

iii.

Second heart sound (DUPP) – turbulence caused by semilunar valves closing (when the ventricles stop contracting)

13.

CARDIAC VOLUMES SV = EDV - ESV i.

End diastolic volume (EDV) – volume of blood in the ventricles at the end of diastole: approx. 130ml at rest

ii.

End systolic volumes (ESV) – volume of blood in the ventricles at the end of systole: approx. 60ml at rest

iii.

Stroke volume (SV) amount of blood ejected from the ventricles in one beat

iv.

ESV gives an indication of the extend of emptying of the ventricles (NB ventricular hypertrophy, congestive heart failure)

v.

EDV gives an indication of how much the heart is filling (NB very low BP, high heart rate)

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14.

CARDIAC OUTPUT Cardiac output = stroke volume x heart rate

Mild exercise: Typical SV (100ml) x Typical HR (100bpm). Cardiac output = 10L/min Moderate exercise: Typical SV (1030ml) x Typical HR (150bpm). Cardiac output = 19.5L/min

15.

NEURAL FACTORS AFFECTING THE HEART A. Nervous system i.

Resting HR is about 70bpm (reduced from about 100bpm by ‘vagal tone’)

ii.

The sympathetic NS increases both heart rate and contractility

iii.

The parasympathetic NS decreases heart rate but has little effect on contractility

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OTHER FACTORS: A. Age iv. B.

New-born babies have a HR of around 120bps, which declines with age. Sex

i. C.

Adult females often have higher resting HR than males Physical fitness

i. D.

Physical fitness decreases resting HR, especially in endurance-trained people Body temperature

i.

Increased body temperature increases heart rate

ii.

Decreased body temperature decreases both heart rate and contractility.

16.

REGULATION OF STROKE VOLUME A. Preload (the extent of stretch of the heart muscle) i. ii. B.

The more the heart is filled with blood, the more the muscle is stretched Venous return is increased during physical activity due to the skeletal muscle pump Afterload (the pressure against which the heart needs to pump, to expel blood)

i.

The higher the arterial pressure, the lower the stroke volume

ii.

If the artery walls are stiff e.g. due to aging, then they stretch less when blood is pumped into them, increasing pressure and afterload

C. 13

Contractility (the ability of the muscle to produce a force)

i.

The more forcefully the muscle contracts, the more blood is expelled.

ii.

Inotropic agents such a s adrenalin, and the influence of the sympathetic nervous system increase contractility

17.

ELASTIC TISSUE i.

Elastic tissue in blood vessel walls is stretched when blood is pushed into the vessels

ii.

The elasticity ‘absorbs’ the pressure, preventing a very sharp rise in pressure in the vessel (which would happen if the vessel wall was less elastic)

iii.

Between heart beats, the elastic tissue recoils, putting continuous pressure on the blood inside the vessels and thus continuous blood flow

iv.

Without the elastic recoil, pressure would fall dramatically between beats, as would blood flow

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A. Vasoconstriction v.

Contraction of smooth muscle in the vessel walls, also precapillary sphincters in arterioles

vi.

Causes narrowing of the diameter of the blood vessel

vii.

Caused by sympathetic nerve activity and the hormone angiotensin 2

viii.

Increases the resistance of blood vessels to blood flow

B.

Vasodilation i.

Relaxation of smooth muscle in the vessel walls, also precapillary sphincters in arterioles

ii.

Causes widening of the diameter of the blood vessel

iii.

Caused by withdrawal of sympathetic nerve activity and locally released chemicals e.g. nitrous oxide and lactic acid

iv.

Decreases the resistance of blood vessels to blood flow

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18.

19.

CAPILLARY EXCHANGE i.

Blood flows through capillaries under pressure

ii.

This causes plasma to filter through the walls into the interstitial fluid

iii.

Large molecules cannot filter through, so remain in the capillary

iv.

The plasma concentration increases, and water is reabsorbed by osmosis

v.

The remaining filtered fluid osmoses into the lymph vessels and is returned to the blood

WHAT HAPPENS TO CAPILLARY EXCHANGE IF THE BLOOD PRESSURE IS HIGH? i.

The hydrostatic force (pressure) causing fluid to leave the capillaries is greater than the osmotic pressure attracting it back into the capillaries

ii.

The rate of filtration is faster than the lymph vessels can accommodate (lymph flow is very slow as it is not under pressure)

iii.

Fluid builds up in the interstitial space - oedema

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20.

HYPERTENSION

21.

FACTORS CONTRIBUTING TO HYPERTENSION Blood pressure = cardiac output x total peripheral resistance A. Anything that increases cardiac output or total peripheral resistance will increase blood pressure i.

Increased blood volume

ii.

Increased heart rate

iii.

Increased TPR

iv.

Fluid retention e.g. due to high NaCl (salt consumption or hyperaldosteronism)

v.

Kidney conditions that result in fluid retention

vi.

Atherosclerosis causing narrowed blood vessels

22.

EFFECTS OF HYPERTENSION ON THE BODY i.

Stroke due to brain haemorrhage

ii.

Damage to capillaries in the eye, eyesight damage

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iii.

Oedema

iv.

Left ventricular atrophy (heart muscle becomes enlarged and stiffened) resulting in reduced pumping ability of the heart – heart failure

v.

Damage to kidney blood vessels – renal failure

vi.

Injury to artery walls precipitating atherosclerosis

23.

EFFECT OF INCREASING SYSTOLIC BP ON RISK OF STROKE

24.

EFFECT OF INCREASING SYSTOLIC BP ON INCIDENCE OF CARDIOVASCULAR DISEASE (INCLUDING ATHEROSCLEROSIS)

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