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1MB Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

What occurs during the cardiac cycle?

A

A cycle of atrial and ventricular contractions and relaxations and are in the order:
Passive filling, Atrial Contraction, Isovolumetric ventricular contraction, ventricular ejection and isovolumetric ventricular relaxation.

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2
Q

What is involved in passive filling?

A

Pressure in atria and ventricles close to zero.
AV valve open - venous return flows into ventricles.
Aortic pressure ~ 80mmHg - aortic valve is closed.
Pressure is much lower on the right side of the heart.
Causes 80% ventricular filling.

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3
Q

What is involved in atrial contraction?

A

P-Wave in EC - atrial depolarisation.
Atria contract - between P-Wave and QRS.
Atria contraction complete the EDV

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4
Q

What is involved in isovolumetric ventricular contraction?

A

Ventricular contraction starts after the QRS - ventricular depolarisation.
Ventricular pressure rises.
AV valves shut when atrial pressure exceeds ventricular.
First heart sound heard
Aortic valve still shut - no blood entering or exiting - ventricular pressure rises steeply.

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5
Q

What is involved in ventricular ejection?

A

Ventricular pressure exceeds aorta/pulmonary artery pressure.
Artery valves open.
SV ejected by each ventricle leaving behind End Systolic Volume (ESV)
Aortic pressure rises.
T Wave signals ventricular depolarisation.
Ventricles relax - ventricular pressure starts to fall.
Aortic pulmonary valves shut - second heart sound
Produces dicrotic notch in aortic pressure curve due to valve vibration.

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6
Q

What is involved in isovolumetric ventricular relaxation?

A

Closure of aortic/pulmonary valves signals the start.
Ventricles become shut box due to box valves being shut.
Tension decreased around closed volume.
When ventricular pressure falls below atrial pressure AV valves open and starts new cycle.

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7
Q

First Heart Sound (S1)

A

Caused by closure of mitral and tricuspid valves. Beginning of systole

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8
Q

Second Heart Sound (S2)

A

Caused by closure of aortic and pulmonary valves. End of systole and beginning of diastole.

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9
Q

Auscultation Area (Aortic Valve)

A

2nd Intercostal space right of the sternum

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10
Q

Auscultation Area (Pulmonary Valve)

A

2nd Intercostal space left of the sternum

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11
Q

Auscultation Area (Tricuspid Valve)

A

4th intercostal space left of the sternum

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12
Q

Auscultation Area (Mitral Valve)

A

5th intercostal space in the midclavicular line

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13
Q

Use of estimation of jugular venous pressure

A

An indirect estimate of right atrial pressure (central venous pressure).

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14
Q

Elevation of JVP

A

If pressure in the right atrium is elevated and can be a sign of heart failure.

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15
Q

Normal JVP

A

No more than 3cm vertically above the sternal angle.

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16
Q

When does JVP occur?

A

After right atrial pressure

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17
Q

Systolic Arterial Blood Pressure

A

The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts.

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18
Q

Diastolic Arterial Blood Pressure

A

The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes.

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19
Q

Hypertension

A

Defined as:
clinical blood pressure of 140/90mmHg
day time average of 135/85mmHg

20
Q

Pulse Pressure

A

Difference between systolic and diastolic blood pressures.

21
Q

Mean Arterial Blood Pressure

A

The average arterial blood pressure during a single cardiac cycle which involves contraction and relaxation of the heart.

22
Q

Pressure Gradient Equation

A

MAP - Central Venous Pressure (CVP)

23
Q

Mean Arterial Blood Pressure Equations

A 
[(2xdiastolic) + systolic] / 3
or
diastolic blood pressure + 1/3 pulse pressure
or
CO x SVR
or
SV x HR x SVR
24
Q

Required MAP

A

At least 60 mmHg is needed to perfuse the coronary arteries, brain and the kidneys.

25
Q

Stroke Volume

A

Volume of blood pumped by each ventricle of the heart per heart beat

26
Q

Cardiac Output

A

Volume of blood pumped by each ventricle of the heart per minute

27
Q

Systemic Vascular Resistance

A

The sum of resistance of all vasculature in the systemic circulation

28
Q

Major resistance vessels

A

Arterioles

29
Q

Baroreceptor Reflex

A

Negative feedback acts to minimise any disturbance to controlled variable.

30
Q

Normal Baroreceptor Reflex from Lying to Standing

A

Venous return to the heart decreases - effect of gravity
MAP very transiently decreases
Reduces firing rate of baroreceptors
Vagal tone to the heart decreases and sympathetic tone to the heart increases.
Increases heart rate and stroke volume
Sympathetic constrictor tone increases, increasing SVR
Sympathetic constrictor tone to the veins increases the venous return to the heart and stroke volume
results in rapid correction of the transient fall in MAP.
Increases HR, SV and SVR

31
Q

Postural Hypotension

A

Results from failure of baroreceptors to gravitational shifts in blood when moving from horizontal to vertical position.

32
Q

Risk Factors for Postural Hypotension

A 
Age Related
Medications
Certain Diseases
Reduced intravascular volume
Prolonged bed rest
33
Q

Symptoms of Postural Hypotension

A 
Lightheadedness
Dizziness
Blurred Vision
Faintness
Falls
34
Q

Diagnosis of Postural Hypotension

A

A positive result is indicated by a drop within 3 minutes of standing from lying position:
- in systolic blood pressure of at least 20mmHg with or without symptoms
or
- a drop in diastolic blood pressure of at least 10 mmHg with symptoms

35
Q

Why do baroreceptors only respond to acute changes?

A

Baroreceptors reset and will only fire again if there is an acute change in MAP above the new higher steady state level.

36
Q

How is blood pressure regulated?

A

By Baroreceptors response to stretch and regulation of the extracellular fluid volume.

37
Q

Calculation for total body fluid?

A

Total Body Fluid = Intracellular Fluid + Extracellular Fluid - 1/3rd of the total

38
Q

Calculation for Extracellular Volume

A

Extracellular fluid = plasma volume + interstitial fluid volume

39
Q

How does ECFV regulate MAP?

A

If plasma volume decreases, compensatory mechanisms shifts fluid from the interstitial compartment to the plasma compartment. Plasma volume and hence steady state blood volume and MAP would be regulated if ECFV is regulated.

40
Q

2 Main Factors affect extracellular fluid volume

A

Water excess or deficit

Na+ excess or deficit

41
Q

How do Hormones affect MAP?

A

Hormones act as effectors to regulate the extracellular fluid volume (including plasma volume) by regulating the water and salt balance in our bodies. Healthy people stay in a stable water and salt balance where water input = water output.

42
Q

Components of RAAS and their role

A

Renin - released from the kidneys, stimulates formation of angiotensin I in the blood from angiotensin which is produced in the liver.
Angiotensin I is converted to angiotensin II by angiotensin converting enzyme - ACE mainly produced by pulmonary vascular endothelium.
Angiotensin II stimulates the release of aldosterone from adrenal complex and causes systemic vasoconstriction which increases SVR also stimulates thirst and ADH release.
Aldosterone - a steroid hormone acts on the kidneys to increase sodium and water retention - therefore increases plasma volume.

43
Q

How is RAAS regulated?

A

By mechanisms that stimulate Renin release from the juxtaglomerular apparatus in the kidney. These are:

  • Renal artery hypotension caused by systemic hypotension (decreases BP)
  • Stimulation of renal sympathetic nerves
  • Decreased Na+ in renal tubular fluid sensed by macula densa (specialised cells of kidneys tubules)
44
Q

What are natriuretic Peptides?

A

peptide hormones synthesised by the heart(also brain and other organs) released in response to cardiac distension or neurohormonal stimuli.

45
Q

Role of natriuretic peptides?

A

They cause excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure.
Decrease renin release - decreases blood pressure
Acts as a vasodilator - decreasing SVR and blood pressure
Provide a counter - regulatory system for the RAAS

46
Q

Two types of natriuretic peptides synthesised by the heart

A

Atrial natriuretic peptides (ANP)

Brain-type Natriuretic peptide (BNP)

47
Q

Atrial Natriuretic Peptides

A

28 amino acid peptide, synthesised and stored by atrial muscle cells released in response to atrial distension (Hypervolemic states)

1MB Cardiovascular (4 decks)

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