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Physiology Y1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

How does blood pressure vary between species?

A

Giraffes and birds have very high arterial blood pressure. Snakes and fish are very low. Thought to be high in birds due to high metabolic need in flight, that avian hearts are 50-100% larger than mammals of the same size, and have stiffer arteries to ensure blood flow to lungs.

These adaptations predispose birds to aortic rupture and haemorrhage.

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2
Q

How do blood pressure and pressure waveform change during circulation?

A

Total peripheral resistance is the sum of resistances of all vessels. TPR causes blood pressure and pressure waveform to decrease from the aorta to the veins, draining to the right atrium.

PWF is independent of flow, being 5x faster than flow.

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3
Q

Which vessel is the main site of resistance and why?

A

The resistance of a single capillary is more than an arteriole but net resistance of capillary network is less than that of the resistance of an arteriole.

So, arteriole is the main site of resistance.

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4
Q

How can resistance be changed to supply different tissues?

A

Skeletal arterioles vasodilate. Kidney and GI tract arterioles vasoconstrict.

TPR is maintained but blood flow through non-critical organs is reduced.

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5
Q

How does exchange occur at the capillaries?

A

Over a concentration gradient.

  • Most substances diffuse via filtration pores and intracellular clefts.
  • Transport of proteins by trancytosis and can involve a specific carrier.
  • Transmigration of leukocytes in diapedesis.
  • Vesicles may fuse to form transient channels.
  • Pinocytosis is endocytosis of fluid.
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6
Q

What features if the venous system allow for venous return?

A

Veins and venules can change compliance/tone. Have splanchnic region venous bed (spleen, liver, small intestine, large intestine) that holds 1/4 of blood volume.

Vessel diameter controlled by ANS sympathetic activity. Constriction increases venous pressure and return.

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7
Q

What can happen if venous return is perturbed and an example of this?

A

When venous valves are damaged, venous pressure increases and vessels distend. Hydrostatic pressures at venule end will increase and exceed oncotic pressure, and there is more filtration.

This can lead to oedema if the lymphatic system cannot drain excess fluid.

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8
Q

What is the function of the lymphatic system?

A

Collects lymph from interstitial fluid and returns it to the heart.

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9
Q

How does the lymphatic system carry out its function?

A
  • One cell thick walls, these cells can be microvalves when internal pressure is greater than the external pressure.
  • Have gaps to fill so fluid, cells and proteins can move.
  • Have secondary valves to open and close during contractions. Endothelial cells in lymphatic vessels mildly contractile.
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10
Q

Describe diastole.

A

Atria are relaxed initially and ventricular pressure is below atrial pressures. This pressure difference causes the AV valve to open and blood to flow into the ventricle. Atria contract at 20% filling, so atrial function is not essential to ventricular pumping, atrial fibrillation does not have a catastrophic effect on the heart, only in exercise.

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11
Q

Describe systole.

A

Ventricles contract when ventricular pressure is greater than atrial pressure. AV valve closes to prevent the backflow of blood. Semilunar valve opens and blood enters the aorta. Ventricle starts to relax when aortic pressure is more than ventricular pressure.

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12
Q

When are the 2 isovolumetric phases in the cardiac cycle?

A

When arterial pressure is greater than ventricular pressure and all valves are closed. Blood volume in the ventricle is constant. Phase ends when ventricular pressure exceeds arterial pressure.

When ventricular pressure is greater than arterial pressure and all valves are closed.

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13
Q

Why is there a dichromatic notch on the aortic pressure waveform?

A

Ventricle relaxes and its pressure falls below aortic pressure. Pressure difference becomes so large that blood starts to recoil back to ventricle. Recoil acts to close semilunar valves and is responsible for notch.

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14
Q

Explain how the cardiac cycle is coordinated by electrical activity.

A
  1. Electrical propagation originates at SAN, shown by a flat line on an ECG.
  2. Signal propagates throughout atria to AVN, where it is delayed for ventricular filling, shown as P wave on an ECG.
  3. Rapid conduction through ventricles via Bundle of His and purkinje fibres ensures coordinated contraction, shown as QRS complex on an ECG.
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15
Q

Describe the ionic mechanism behind cardiac action potential.

A

Action potential propagates along SAN via gap junctions in intercalated discs. Blocked by annulus fibrosus so must pass AVN. Action potential is determined by ion movement through ion gated channels down ion concentration gradients.

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16
Q

Why is refractory period important?

A

Refractory period lasts longer than in skeletal muscle to give the heart time to relax and fill, preventing tetany.

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17
Q

Describe how the SAN acts as the primary pacemaker.

A

Automaticity of SAN is determined by the rate at which threshold potential is reached.

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18
Q

Define chronotropism.

A

The alteration in the rate of SAN firing is under ANS control.

Sympathetic activity increases heart rate = tachycardia
Parasympathetic activity decreased heart rate = bradycardia

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19
Q

Define dromotropism.

A

The rate of conduction can be altered by ANS.

Sympathetic activity reduces the delay in AVN and increases heart rate.

Parasympathetic activity increases the delay in AVN and decreases heart rate.

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20
Q

What is heterometric autoregulation?

A

An established relationship between end diastolic volume and systolic volume. Moment to moment adjustment to systolic volume based to pre-load/end diastolic volume.
Ensures systolic volume of right and left ventricles are balanced over time. So, outputs from right and left sides of heart can vary over a short period but are maintained over time, preventing congestion.

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21
Q

Define inotropism.

A

An influence of contractility modulated by ANS.

Sympathetic activity = norepinephrine or epinephrine binding to beta 1 adrenergic receptor = increased intracellular calcium ion concentration = more cross bridges = increased contractility.

Parasympathetic fibres do not innervate ventricles so does not affect contractility.

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22
Q

How and why are outputs from the right and left sides of the heart balanced when cardiac output changes?

A
  • Positive inotrophy = increases contractility = increases systolic volume = increases cardiac volume.
  • Increasing heart rate = reduced diastolic filling time = reduced end diastolic and systolic volumes = reduced cardiac output.

Lusitropy is when sympathetic activity causes positive dromotropism and inotropism, causing more contraction and quicker relaxation. Ensures filling time to be suitable and cardiac output to be maintained at high heart rates.

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23
Q

What are 4 challenges of maintaining a stable mean arterial pressure?

A
  • Physiological demand, such as exercise
  • Orthostatic reaction, such as posture change
  • Response to environmental changes
  • Pathological, such as circulatory shock or haemorrhage
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24
Q

When maintaining mean arterial pressure, what is constrained and what is not?

A

Constrained - changes to cardiac output, blood volume, blood velocity

Unconstrained - resistance, as this can help meet demand

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25
Q

Describe resistance juggling.

A

Skeletal muscle arterioles vasodilate, which increases their share of cardiac output. GI tract and kidney arterioles vasoconstrict, which decreases their share of cardiac output.

Venous return increases, allowing cardiac output to arterioles and organs to increase. Increased resistance in other areas maintains TPR and MAP.

26
Q

What dual control is systemic circulation under?

A

Auto intrinsic regulatory control mechanisms and central extrinsic control via ANS.

27
Q

What are baroreceptors and where are they located?

A

Baroreceptors respond to changes in MAP. Located in the aortic arch and the carotid sinus in the carotid artery bifurcation and base of the neck. Both patches are close to the heart so gravity does not distort the response to changes in MAP.

28
Q

Describe extrinsic central regulation of MAP with baroreceptors.

A
  1. Pressure increases and causes elastic arteries to stretch and stimulate baroreceptors.
  2. Signal to baroreceptors in the aortic arch via the aortic nerve and to those in the carotid sinus.
  3. Signals sent to vagus nerve and then to carotid sinus nerve.
  4. Signal is sent to the CVS medullary centre to produce signal outputs mediated by parasympathetic and sympathetic efferent nerves of ANS.
  5. Parasympathetic vagal nerves to SAN, AVN and atria to modulate heart rate and conduction. Sympathetic/cardiac nerve to SAN, AVN, atria and ventricles to modulate heart rate, conduction and contractility.
  6. Sympathetic vasoconstriction fibres innervate smooth muscle vessels and control resistance, affecting venous return and cardiac output.
29
Q

Describe chemical/hormonal control of MAP.

A

Hormones and neurotransmitters released by adrenal medulla nerves.

  • Norepinephrine and epinephrine are released by sympathetic activity.
  • Acetylcholine released by parasympathetic activity.
30
Q

Give the ligand, locations and effects of the adrenergic receptors.

A

Norepinephrine and epinephrine:

  • Alpha-1, on all arterioles, vasoconstriction
  • Alpha-2, abdominal veins, venoconstriction
  • Beta-1, heart, increase cardiac output
  • Beta-2, coronary and skeletal muscle arterioles, increase blood flow
31
Q

Give the ligand, locations and effects of the cholinergic receptors.

A

Acetylcholine.

  • M2, atria SAN and AVN, decreases cardiac output
  • M3, coronary and skeletal muscle arterioles, vasodilation
32
Q

Describe what happens when MAP decreases.

A

Decreased signal from baroreceptors to medullary CVS centre > parasympathetic activity decreases and sympathetic activity increases > heart rate and stroke volume increase as contractility increases > arterioles vasoconstrict to increase TPR, venoconstriction increases stroke volume and heart rate

33
Q

Describe what happens when MAP increases.

A

Increased signal from baroreceptors to medullary CVS centre > parasympathetic activity increases and sympathetic activity decreases > heart rate and cardiac output decrease due to decreased contractility > less vasoconstriction and venoconstriction > TPR decreases

34
Q

Name the 5 sets of routine tests to assess cardiovascular function in animals.

A 
Peripheral blood flow
State of hydration 
Palpation of arterial pulse
Auscultation of heart 
Jugular pulse/distension = venous pressure
35
Q

What does peripheral blood flow indicate and how is it measured?

A

How fast blood gets around the system and capillary refill time.

  • Colour of mucous membranes - gums, corner of eye
  • Cyanoses - bluish colour due to deoxyhaemoglobin, cold extremities
36
Q

What does state of hydration indicate and how is it measured?

A

Not enough water in peripheral tissue means there is not enough water in the CVS system.

  • Find relatively loose skin and test skin tending: skin creeps back down over 10 seconds if dehydrated.
  • Loss of urine vs input (hard to measure)
  • Mucous membranes are moist if there is too much water in the system
37
Q

What does palpation of arterial pulse indicate and how is it measured?

A
  • Heart rate for detecting irregularities
  • Pulse to detect strong or weak stroke volume
  • Full or impaired pulse
  • Pulse strength affected by stroke volume, TPR and elasticity
38
Q

What does auscultation of of the heart indicate and how is it measured?

A

There are 2 periods of noise due to turbulence when AV, aortic and pulmonary valves close. Used to determine strength of contraction, size of heart and heart sound issue (leakage, murmur, stenosis).

39
Q

What does jugular pulse/distension/venous pressure indicate and how is it measured?

A

Not normally done but can be in some species, such as horses. Venous pressure reflects degree of filling in jugular vein.

If jugular vein can be seen when standing up, suggests damming of blood on the right hand side, suggesting occlusion and congestion.

40
Q

What do ECGs measure?

A

Electrical activity of whole heart

41
Q

Give what each part of an ECG trace represents.

A

P wave = atrial depolarisation

QRS complex = ventricular depolarisation

T wave = repolarisation of ventricles

42
Q

What is respiratory sinus arrhythmia?

A

A physiological phenomenon where RR interval, that reflects heart rate, varies during breathing cycle.

43
Q

Name 1 example of an arrhythmia.

A

AV block

44
Q

What is 1st degree AV block?

A

Defects in conduction between atria and ventricles causes a delay in AVN. This leads to a prolonged PQ interval.

45
Q

What is 2nd degree AV block?

A

Can occur due to overstimulation of parasympathetic nervous system, causing action potentials to not move through AVN due to dromotropism.

46
Q

What is 3rd degree AV block?

A

Action potential from SAN does not transmit at all and some ventricular cardiac conduction cells become ectopic. These cells can pace heart due to pacemaker potential but heart rate is slower and QRS width is much longer.

47
Q

How can blood pressure be measured?

A

In surgery with a fluid filled catheter inserted into vein or using a sphygmomanometer measuring sound generated by turbulence in vessel constriction by a cuff. This blood pressure = systolic blood pressure, when pressure drops enough as blood is allowed back through vessel and sound is heard. When pressure drops enough so sound cannot be heard, laminar flow = diastolic blood pressure.

48
Q

How can cardiac output be measured?

A

Fick Principle - gold standard. Invasive and requires cardiac catheterisation. Sample taken from artery, right ventricle or pulmonary trunk. CO = oxygen uptaken by lungs is divided by difference between arterial and venous contents.

Thermodilution - heart catheterised and unknown mass of cold saline injected in right atrium or right ventricle. Distal thermistor records the temperature of saline in pulmonary trunk or artery. CO = injected temperature divided by area under temperature-time graph. (Greater CO = dilute faster = area smaller)

49
Q

Define circulatory shock.

A

A state of inadequate organ perfusion. Cells do not get enough oxygen delivered to them to sustain aerobic respiration.

50
Q

What causes low volume circulatory shock/hypovolaemia?

A

Decreased pressure causes decreased hydrostatic pressure. Oncotic pressure is fairly constant, so decreased hydrostatic pressure affects transcapillary exchange. Decreased blood volume causes decreased MAP and CO, and so decreased filtration and perfusion.

51
Q

What is the response to low volume circulatory shock/hypovolaemia?

A

Auto-regulated intrinsic vasodilation. Reduces hydrostatic pressure further in a positive feedback system.

52
Q

What causes distributive circulatory shock that is initially normovolaemic?

A

Anaphylaxis, sepsis, neurological injury

53
Q

What is the effect of distributive circulatory shock?

A

Loss of muscle tone of arteries or inflammation and dilation of vessels. Causes decreased TPR, CO, MAP and perfusion.

54
Q

What is the response to distributive circulatory shock?

A

If triggered by anaphylaxis or sepsis, histamine is released. There is vasodilation and promoted vessel permeability, causes increased fluid extravasation and decreased TPR, MAP, CO and perfusion.

Reduces sympathetic drive, causing reduced vascular tone. Extravasation prevents diffusion, causing hypoxia and anaerobic respiration.

55
Q

What causes cardiogenic circulatory shock?

A

Myocardial infarction, heart failure, arrhythmia.

Potentially hypervolaemic

56
Q

What causes obstructive circulatory shock?

A

Cardiac tamponade, aortic stenosis, pulmonary embolism

Potentially hypervolaemic

57
Q

What is the effects of cardiogenic and obstructive circulatory shocks?

A

Decreased MAP, CO and venous return. Kidneys retain fluid fully, causing decreased hydrostatic pressure and decreased filtration and perfusion. Leads to hypoxia, anaerobic respiration and lactate build up.

58
Q

What happens in response to cardiogenic and obstructive circulatory shocks?

A

Increased vasodilation causes further decreased hydrostatic pressure and increased capillary permeability.

59
Q

What is the effect of the positive feedback system in circulatory shock?

A

Decreased cardiac output causes tissue hypoxia and increased vasodilation and permeability. This leads to increased extravasation and decreased venous return. Lactic acid build up causes multiple organ damage if acidosis is severe.

60
Q

What is the difference between reversible and irreversible circulatory shock?

A

Reversible - if CVS function normalises when cause is removed.

Irreversible - removal of original cause is not enough to stabilise CVS function. When positive feedback system causes pathophysiological state where vessel and organ damage is too great to support recovery.

Physiology Y1 (12 decks)

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