Week 1 Flashcards

1
Q

What is the function of the CV system?

A

To act as a bulk flow system for transporting stuff around the body, such as:
-oxygen and carbon dioxide.
-nutrients.
-metabolites.
-hormones.
-heat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is the output from the left and right chambers equal?

A

The pumping chambers on the left and right sides of the heart are in series therefore output must be equal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is he significance of vascular beds being arranged in parallel?

A

-all tissues get oxygenated blood.
-allows regional direction of blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the pressure difference of the CV measured?

A

mean arterial pressure - central venous pressure.
affects all tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is flow measured?

A

flow= change in pressure / resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is resistance? Explain the cause of resistance in blood vessels. What is the function of resistance in blood vessels?

A

Resistance is a force that opposes the flow of a fluid. In blood vessels, most of the resistance is due to vessel diameter. As vessel diameter decreases, the resistance increases and blood flow decreases. Selectively redirects flow.
Resistance is used to create blood pressure, the flow of blood and is also a component of cardiac function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the aorta.

A

The aorta are elastic arteries with a wide lumen, thick elastic wall and damp pressure variations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe muscular arteries.

A

Arteries are muscular arteries with a wide lumen, strong, thick non-elastic wall and are a low resistance conduit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe arterioles and their function.

A

Arterioles are resistance vessels with a narrow lumen and thick contractile wall.
They act as ‘taps’, controlling resistance (and therefore flow) to each vascular bed.
They control the regional flow of blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe venules and veins and their function.

A

Venules and veins have a wide lumen and thin distensible walls.
They are capacitance vessels and control the fractional distribution of blood between veins and the rest of the circulation. They act as a low resistance conduit and reservoir.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does Poiseulle’s law state?

A

Blood vessel radius, length and viscosity all influence the resistance to blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is capacitance?

A

Vascular capacitance refers to the degree of active constriction of vessels (mainly veins) which affect return of blood to the heart and thus cardiac output.
Venules form larger veins that serve as the primary capacitance vessels of the body- the site where most of the blood volume is found and where regional blood volume is regulated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List the sequence of events occuring during excitation-contraction coupling in cardiac muscle.

A

Plateau in action potential of myocyte membrane allows influx of calcium, stimulating muscle contraction:
- calcium enters via L-type voltage-gated channels.
-higher intracellular calcium triggers release of more calcium from sarcoplasmic reticulum through ryanodine receptors.
-released calcium attaches to troponin C > tropomyosin moves > actin-myosin cross bridges > contraction.

cross-bridges last as long as calcium occupies troponin.

intracellular calcium is removed, inducing relaxation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the basis of non-pacemaker action potentials.

A

-Resting membrane potential: High resting K+ permeability.
-Initial depolarisation: Increase in Na+ permeability.
-Plateau: Increase in permeability Ca2+ (L-type) and decrease in K+ permeability.
-Repolarisation: Decrease in permeability Ca2+ and increase in permeability K+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the basis of pacemaker action potentials.

A

Some cells have unstable resting membrane potential and act as pacemakers.
-Pacemaker potential (=pre-potential):
- gradual decrease in K+ permeability.
- Early increase in permeability Na+ (NaF).
- Late increase in permeability Ca2+ (T-type).
-Action potential: increase in permeability of Ca2+ (L-type).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the initiation and spread if electrical activity throughout the heart.

A
  • The special conducting system:
    o Sinoatrial node: primary pacemaker cells located in the wall of the right atrium. Rate 60-100bpm. Usually determines normal heart rhythm. 0.5 m/s.
    o Annulus fibrosus: non-conducting, acts as insulator.
    o Atrioventricular node: delay box located at the base of right atrium, near septum. Rate: 40-60bpm. 0.05 m/s.
    o Bundle of his and purkinje fibres: rapid conduction system. Rate 20-40bpm. 5m/s.
  • Ensures coordinated contraction of the heart.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What events in the heart do the P-wave, QRS-complex and T-wave correspond to?

A

P-wave = atrial depolarisation
QRS-complex = ventricular depolarisation
T-wave = ventricular repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does the PR interval correspond to and what is the normal range for this?

A

-The time from atrial depolarisation to ventricular depolarisation, mainly due to transmission.
- normal range is 0.12-0.2 s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the duration of the QRS complex correspond to and what is the normal range for this?

A

-The duration of the QRS complex corresponds to the time for the whole of the ventricle to depolarise.
-normally takes about 0.08 s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does the duration of the QT interval correspond to and what is the normal range for this?

A

The time for ventricles to depolarise and repolarise.
-varies with heart rate but normally about 0.42s at 60 bpm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How to measure heart rate from an ECG.

A

For regular heart rhythms, heart rate can easily be estimated using the large squares (0.2s) on an ECG.

Simply identify two consecutive R waves and count the number of large squares between them. By dividing this number into 300 (300 x 0.2 = 60 secs, remember, this number represents 1 minute) we are able to calculate a person’s heart rate.

Or, count the R waves in 30 large squares (= 6 secs) and multiply by 10.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is considered a normal resting heart-rate?

A

60-100 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is considered bradycardia?

A

below 60 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is considered tachycardia?

A

above 100 bpm

25
Q

What is meant by the term STEMI.

A

If there is a pattern lnown as ST-elevation on the ECG, this is called a STEMI, short for ST elevation myocardial infarction.

26
Q

What is meant by the term non-STEMI?

A

If there is elevation of the blood markers suggesting heart damage, but no ST elevation seen on the ECG tracing.

27
Q

Illustrate the sequence of changes in pressure and volume in the chambers of the heart throughout the cardiac cycle.

A
  1. Late diastole- both sets of chambers are relaxed and ventricles fill passively.
  2. Atrial systole- atrial contraction forces a small amount of additional blood into ventricles.
  3. Isovolumic ventricular contraction- the first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. Maximum blood volume in ventricles= end-diastolic volume (EDV).
  4. Ventricular ejection- as ventricular pressure rises and exceeds the pressure in the arteries, the semilunar valves open and blood is ejected.
  5. Isovolumic ventricular relaxation- as ventricles relax, pressure in ventricles falls. Blood flows back into cusps of semilunar valves and snaps them closed. Minimum blood volume in ventricles = end-systolic volume (ESV).
28
Q

Interpret a pressure volume loop.

A
29
Q

Explain the generation of the heart sounds.

A

Heart sounds occur due to turbulence in blood flow caused by:
1st = closure of the AV (mitral and tricuspid) valves.
2nd = closure of the semi-lunar (aortic and pulmonary valves).

3rd= rapid passive filling phase.
4th = active filling phase.

30
Q

What are additional heart sounds called?

A

Murmurs.

31
Q

What causes a systolic murmur?

A

Stenosis of aortic/pulmonary valves or regurgitation through mitral/tricuspid valves.

32
Q

What causes a diastolic murmur?

A

Stenosis of mitral/tricuspid valves or regurgitation through aortic/pulmonary valves.

33
Q

What could a continuous murmur be?

A

patent ductus arteriosus.

34
Q

What are the effects of the sympathetic systems on heart rate?

A

This increases heart rate = tachycardia.

35
Q

What are the effects of the parasympathetic system on heart rate?

A

Vagus nerve releases ACh that acts on muscarinic receptors on the sinoatrial node.
This hyperpolarises cells and decreases the slope of the action potential.
This decreases heart rate = bradycardia.

36
Q

Explain the effects of the sympathetic system on stroke volume.

A

The adrenaline acts on beta-1 receptors in the myocytes.
This increases contractility (an ionotropic effect).
This gives a stronger, but shorter contraction.
This increases stroke volume.

37
Q

does the parasympathetic system impact stroke volume?

A

not really as doesn’t innervate the heart muscle

38
Q

What does starling’s law state?

A

The energy of contraction is proportional to the initial length of the cardiac muscle fibre.

39
Q

What is preload? what is it affected by?

A

How full the ventricle is before contracting (i.e., the EDV).
This is affected by the state of contraction of venules/veins (capacitance vessels).
INCREASED VENOUS RETURN > INCREASED EDV > INCREASED SV.
DECREASED VENOUS RETURN > DECREASED EDV > DECREASED SV.

40
Q

What is afterload? what is it affected by?

A

The load against which the muscle tries to contract - how difficult is it for the heart to pump out the blood (i.e., the TPR).
Affected by the state of contraction of the arterioles.

TPR increases > aortic pressure increases > ventricle works harder to push open aortic valve > less energy left to eject blood > decreased SV.

41
Q

How is cardiac output determined?

A

CO = SV X HR

42
Q

Describe the affect of exercise on cardiac output.

A
  • HR increases via decreased vagal tone and increased sympathetic tone.
  • Contractility increases via increased sympathetic tone, alters ionotropic state, and shortens systole.
  • Venous returns increase via venoconstriction and skeletal/respiratory pumps that maintain preload.
  • TPR falls due to arteriolar dilation in muscle, skin, and heart rate, reducing afterload.
  • CO increase 4-6 times.
43
Q

del

A

del

44
Q

del

A

del

45
Q

del

A

del

46
Q

Bulk flow results in the loss of?

A

3L of fluid per day which is drained by the lymphatic system.

47
Q

What is oedema?

A

The accumulation of excess fluid.

48
Q

What are some causes of oedema?

A

o Raised CVP e.g., due to ventricular failure.
o Lymphatic obstruction e.g., due to filariasis, surgery.
o Hypoproteinemia e.g., due to nephrotic syndrome, liver failure and malnutrition.
o Increased capillary permeability due to inflammation e.g., rheumatism.

49
Q

What are the four types of local controls of blood flow and MAP?

A
  1. active (metabolic) hyperaemia.
  2. pressure (flow) autoregulation.
  3. reactive hyperaemia.
  4. Injury response.
50
Q

Describe active hyperaemia.

A

 ^ in metabolic activity causes ^ concentration of metabolites.
 causes arteriolar dilation.
 ^ flow to wash out metabolites.
 An adaptation to match blood supply to the metabolic needs of that tissue.

51
Q

Describe pressure (flow) autoregulation.

A

 ^ MAP causes decreased flow.
 Metabolites accumulate.
 Arterioles dilate and flow is restored to normal.
 An adaptation to ensure that a tissue maintains its blood supply despite changes in MAP.

52
Q

Describe reactive hyperaemia.

A

o Trigger is occlusion of blood supply:
 This causes a subsequent increase in blood flow.
 An extreme version of pressure autoregulation.

53
Q

Explain the basis of the injury response.

A
  • The injury response causes the release of histamine that causes arteriolar dilation which increases blood flow and permeability. This aids in the delivery of blood-born leucocytes etc. to the injured area.
54
Q

del

A

del

55
Q

del

A

del

56
Q

Give features of the coronary circulation.

A

o Blood supply is interrupted by systole.
o But still must cope with increased demand during exercise.
o Shows excellent active hyperaemia.
o Expresses many beta-2 receptors.
o These swamp any sympathetic arteriolar constriction.

57
Q

Give features of the cerebral circulation.

A

o Needs to be kept stable.
o Shows excellent pressure autoregulation.

58
Q

give a unique feature of the pulmonary circulation

A

o Decreased oxygen causes arteriolar constriction.
o i.e., the opposite response to most tissues.
o Ensures that blood is directed to best-ventilated parts of the lungs (shunt).

59
Q

Give features of the renal circulation.

A

o Main job is filtration.
o Filtration rate kept relatively constant during normal fluctuations in MAP.
o Due to excellent pressure autoregulation.