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Cardiology > Cardio physiology > Flashcards

Cardio physiology Flashcards

1
Q

Under what BP is shock?

A

<90mmHg

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2
Q

What do alpha adrenoreceptors do?

A

Vascular smooth muscle has alpha adrenoreceptors.

Here sympathetic nerves can release NA and cause vessel constriction.

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3
Q

Hypertension BP definition

A

BP >140/90

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4
Q

Normal pulse pressure, what is decreased and increased pulse pressure?

A

normal- 30-50mmHg

decreased- <30mmHg

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5
Q

What are complications of atherosclerosis

A

coronary arteries- stable angina or MI

carotid- embolisation leads to TIA or stroke

peripheral arterial disease (intermittent claudication), gangrene

renal artery stenosis

aneurysms (abdominal aortic, popliteal, carotid, femoral)

iliac, femoral and mesenteric arteries can be affected by atherosclerosis too

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6
Q

Important risk factors for coronary heart disease

A

Smoking
High BP
Dyslipidaemia (abnormal lipid levels- I.E. high LDL)
Diabetes

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7
Q

Draw an action potential in a neuron and label the ion changes.

A

Simple version is an upstroke (depolarisation) due to Na+ influx and a downstroke (repolarisation) due to K+ efflux.

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8
Q

Explain where the Na+ and K+ ions are during the resting membrane potential in a neuron, how they move across the membrane and how this movement effects membrane potential

A

At baseline (the resting potential)- Na+ is outside the cell and K+ is inside the cell. The inside of the cell is more negatively charged and the outside is more positively charged. The resting membrane potential is -70mV.

Na+ channels open and Na+ ions move into the cell. K+ channels open and K+ moves out of the cell.

Na+ moving in depolarises the membrane. K+ moving out repolarises it.

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9
Q

Draw an action potential from the SA node and label the movement of ions

A

1) Pacemaker potential
I(f)- funny current- slow Na+ influx
Ca++ influx
Decrease in K+ efflux

2) Rapid upstroke
Ca++ rapid influx (L type Ca channels)

3) Rapid downstroke
K+ efflux
Ca++ channel closure

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10
Q

Is the AV node the only point of electrical contact between the atria and ventricles?

True or false?

A

True.

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11
Q

Why does the AV node delay signal transmission?

A

To allow the atria to contract before the ventricles.

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12
Q

Do the bundles of His and the Purkinje fibres allow the rapid conduction of signals from the AV node to and through the ventricles?

A

Yes.

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13
Q

Draw the action potentials in a contractile cardiac myocyte and explain the ion changes

A

Phase:
0) Rapid Na+ influx
1) Some K+ influx, closure of Na+ channels
2) Ca++ influx- plateau phase
3) K+ influx, Ca++ channel closure
4) Back to resting membrane potential

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14
Q

What causes the PR interval on an ECG?

A

AV nodal delay.

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15
Q

What occurs during the ST segment?

A

Ventricular systole

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16
Q

What do sympathetic nerves do to the heart and what receptor do they use?

A

Sympathetic innervation:
-increases rate of firing from SA node
-decreases AV node delay
-increases contractility

it innervates the SA node, AV node and the myocardium through Beta 1 adrenoreceptors. NA is the neurotransmitter.

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17
Q

What do parasympathetic nerves do to the heart and what receptor do they use?

A

Resting vagal tone (slows intrinsic hr from 100 to 70bpm when resting).

The vagus supplies the SA node and the AV node- it decreases SA firing and increases AV delay.

The receptor is the M2 Muscarinic receptors.

The neurotransmitter is acetylcholine.

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18
Q

How does a cardiac action potential cause muscle contraction (systole)?

A

During the plateau phase of a cardiac myocyte action potential- there is Ca++ release into the cell.

The sarcoplasmic reticulum releases calcium into the myofibrils (strands of actin and myosin which) which are what make up cardiac muscle fibres (cells).

The calcium release allows myosin to bind to actin and then to pull along it (causing muscle contraction and systole).

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19
Q

What is stroke volume?

A

The volume of blood pumped out by the LV in each heart beat.

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20
Q

What is the Frank Starling law?

A

The more the ventricle is filled during diastole (EDV), the more is ejected in systole (SV).

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21
Q

What can increase EDV?

A

Increased venous return.

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22
Q

What happens if increased after load becomes chronic (eg high BP)

A

Ventricle hypertrophies.

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23
Q

Events during the cardiac cycle

A

Passive filling
Atrial contraction
Isovolumetric ventricular contraction
Ventricular ejection
Isovolumetric ventricular relaxation

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24
Q

What is the JVP an estimate of?

A

Right atrial pressure (‘central venous pressure’)

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25
Q

How is the JVP measured?

A

Lie the patient back at a 45 degree angle, look for the pulsation of the internal jugular vein between the 2 heads of the SCM, hepatojugular reflex can be used to check if it is the IJV, then measure the height to the sternal angle. A normal JVP is = or <3cm.

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26
Q

Causes of an elevated JVP

A

raised right atrial pressure which can be caused by:
Heart failure
Tricuspid regurgitation (endocarditis or rheumatic heart disease)
Pulmonary hypertension

27
Q

How is BP measured?

A

When the BP cuff is inflated between systolic and diastolic pressure, it creates turbulence in the artery [whenever the pressure in the artery exceeds the cuff pressure]. This turbulence can be heard with a stethoscope. The sounds are called korotkoff sounds. The first sound is systolic pressure, the last sound is diastolic pressure.

28
Q

What is roughly right atrial pressure?

A

Close to 0 mmHg.

29
Q

The pressure gradient which drives blood flow around systemic circulation is between…?

A

The Aorta and Right atrium.

Using terminology-
Mean arterial pressure (MAP) - central venous pressure (CVP).

30
Q

What is another name for the right atrial pressure?

A

Central venous pressure

31
Q

What is Mean arterial pressure (MAP)?

A

The mean arterial pressure over a cardiac cycle.

32
Q

How is MAP calculated?

A

(2 x diastole + systole)/3

Diastole is twice as long as systole.

33
Q

What is the normal range for MAP?

A

70 - 105mmHg

If someone’s BP is 120/80 their MAP is 93.3 mmHg.

34
Q

What is the minimum MAP needed to perfuse the vital organs (coronary arteries, brain, kidneys)?

A

At least 60mmHg

35
Q

What is Cardiac Output?

A

Volume of blood pumped out by each ventricle per minute

36
Q

Relationship between Blood Pressure, Cardiac Output and Systemic Vascular Resistance

A

Blood pressure = Cardiac Output X Systemic Vascular Resistance (the total resistance of blood vessels).

So if you modify CO or vascular resistance you can increase BP.

Systemic vascular resistance aka total peripheral resistance.

37
Q

How is blood pressure regulated moment-to-moment?

A

Baroreceptor reflex.

Reflex summary:
-changes in BP sensed- by baroreceptors (carotid sinus, aortic arch)
-Sensory information carried by vagus and CN IX
-Control cente: in medulla
-Effectors: increasing/decreasing sympathetic and parasympathetic tone to heart and vessels (hr, contractility, systemic resistance)

Moment-to-moment control helps prevent postural drops.

38
Q

Why do baroreceptors only respond to acute changes in BP?

A

For longer term sustained changes, the baroreceptor firing rate becomes ‘used to it’. They re set to the new set point.

For example if high BP is sustained, baroreceptor firing decreases (lower firing indicates lower BP).

39
Q

Taking a 70kg young male, what volume of water would the separate fluid compartments hold?

A

60% of body weight is water.

2/3rds of water is intracellular water
1/3rd is extracellular water (plasma volume + interstitial volume)

70kg
60% = 42kg
2/3rds = 28kg
1/3rd = 14kg (extracellular fluid)

~1/5th = 3kg plasma volume
~4/5ths= 14kg interstitial tissue fluid

40
Q

How is plasma volume controlled?

A

Through controlling water and Na+.

Hormones are the effectors which control water and Na+.

41
Q

Which hormones regulate plasma volume?

A

1) RAAS (renin-angiontensin-aldosterone system)
2) Natriuretic Peptides
3) ADH (anti-diuretic hormone)/ aka Arginine Vasopressin

42
Q

How does the RAAS system work and what does it do?

A

Renin is released from the kidneys in response to low BP. (Kidneys sense low BP.)

Renin converts angiotensinogen to angiotensin I. (Angiotensinogen is released from the liver).

Angiotension I is converted to Angiotensin II in the lungs by the ACE.

Angiotensin II has the effects of:
1) Vasoconstriction
2) Increasing ADH release from pituitary (ADH increases renal water reabsorption)
3) Increasing thirst
4) Causing aldosterone release from the adrenal cortex. Aldosterone causes renal Na+ and water reabsorption.

Overall this causes raised plasma volume and BP.

43
Q

**Juxtaglomerular apparatus **

Roughly draw a nephron.

Draw a cross section of the the juxtaglomerular apparatus

What is the juxtaglomerular apparatus and what does it do?

[Note: ‘Juxta’ meaning next to].

A

See pic.

Rough nephron drawing:
Include: glomerulus, bowman capsule, proximal convoluted tubule, loop of henle, distal convoluted tubule, collecting duct, glomerular artery, glomerular vein

Cross section of juxtaglomerular apparatus:
Include: Macula densa in distal convuluted tubule (sense Na+ in tubules), granular cells (secrete renin), mesangial cells- extra glomerular and glomerular (kinda like packing peanuts).

What is it + Job: It it the part of a nephron/kidney which senses the BP/plasma volume and changes how much water and Na the kidneys keep/excrete.
BP too low= secrete renin
BP too high= don’t secrete renin

44
Q

What factors stimulate renin release from the juxtaglomerular apparatus?

A

1) Decreased renal artery BP (low systemic BP)
2) Low Na+ concentration in the renal tubules
3) Sympathetic renal innervation

45
Q

Where are natriuretic peptides released from and in response to what?

A

The heart and brain.

In the heart in response to cardiac distension (EG in heart failure).

46
Q

What do natriuretic peptides do?

A

Help decrease the BP. By:

1) Are vasodilators.
2) Cause renal excretion of Na+ and water.
3) Decreases renin secretion.

47
Q

Why do natriuretic peptides and the RAAS system hormones work in opposition?

A

Natriuretic peptides work to decrease BP. (eg released by cardiac distension.)

RAAS hormones work to increase BP. (eg released by juxtaglomerular apparatus in response to low BP.)

48
Q

1) What are the 2 types of natriuretic peptides?

2) What natriuretic peptide scan be used in suspected Heart Failure?

A

ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide).

ANP is released by atria in response to atrial distension.

BNP is released by the ventricles. It was first found to be secreted by the brain.

2) Serum BNP and serum NT-pro-BNP. (N terminal piece of Pro BNP is a part of pro BNP which is the precursor to BNP).

49
Q

Where is ADH made and stored?

A

ADH is made in the hypothalamus and stored in the posterior pituitary.

50
Q

What factors stimulate ADH secretion?

A

1) Low plasma volume
2) Main driver- Increased serum osmolality

[serum osmolality is monitored by osmoreceptors in the brain close to the hypothalamus.]

51
Q

What does ADH do?

A

1) Vasoconstricts (small effect in healthy people, becomes important in shock)

2) Increases renal water reabsorption. (Not Na+ reabsorption, corrects raised serum osmolality, concentrates urine.)

Increases BP.

52
Q

List 4 mechanisms which correct low blood pressure.

A

1) Baroreceptor reflex
2) RAAS system
3) Vasoconstriction also means renal artery vasoconstriction, this decreases urine out put (conserves BP) and releases EPO which increases red blood cell production.
4) Low capillary pressure causes less fluid shifting from intravascular space to interstitial tissue space.

53
Q

What are the effectors in controlling vascular resistance?

A

Vascular smooth muscle.

Total systemic resistance can be changed by vasoconstriction government or dilating the arterioles (main resistance vessels).

54
Q

What mechanisms control vasoconstriction?

A

Vascular smooth muscles are controlled by:

INTRINSIC CONTROL
Tissues control their own blood supply. [over rides extrinsic control.]
1) metabolic hyperaemia (eg raised pCO2, decreased pO2)
2) humoral agents- histamine, bradykinin, Nitric Oxide/serotonin, thromboxin A2, Leukotrienes
3) Temperature
4) Myogenic response to stretch

EXTRINSIC CONTROL
Nerves:
1) Baroreceptor reflex
- sympathetic innervation to arteries

Hormones:
1) Adrenaline from adrenal medulla
2) Angiotensin II
3) ADH (vasopressin)

55
Q

How does adrenaline affect the body? (Based on the receptors it acts on)

A

Acting on Alpha receptors- causes vasoconstriction
Acting on Beta 2 receptors- causes vasodilation

Alpha receptors can be found on blood vessels in the skin, gut and kidneys.

Beta 2 receptors can be found in arteries in the bronchi, cardiac muscle and skeletal muscle.

This combination helps redirect blood during exercise.

56
Q

How do sympathetic nerves cause vasoconstriction?

A

Neurotransmitter: Noradrenaline
Receptors: alpha adrenergic receptors
Effector: Vascular smooth muscle

57
Q

What is intrinsic control of vascular smooth muscles?

A

Tissues/organs match their blood flow to their metabolic need.

‘Metabolic hyperaemia’

58
Q

What metabolic factors cause intrinsic control of vascular smooth muscles to cause vasodilation?

A

Metabolic hyperaemia is caused by:

-Decreased local PO2
-Increased local PCO2
-Increased local H+ (decreased pH)
-Increased extracellular K+ (due to repolarisation in muscles*)
-Adenosine release from ATP

*skeletal and cardiac have same action potential

59
Q

What humeral agents cause local vasodilation?

A

Nitric Oxide
Histamine
Bradykinin

These are often released in response to inflammation or tissue damage

Nitric Oxide is continually released by the endothelium

60
Q

What humoural agents cause vasoconstriction?

A

Serotonin
Thromboxane A2
Leukotrienes
Endothelin

61
Q

What is the myogenic response to stretch in blood vessels?

A

Intrinsic control of vasodilation.

If MAP rises in a vessel, this causes the blood vessel to constrict to limit flow.

If MAP decreases, vessel dilates to increase flow.

This is important in the kidneys and the brain to keep constant.

62
Q

What factors increase venous return?

A

Increased venomotor tone
Increased blood volume
Increased skeletal muscle pump activity
Increased respiratory pump activity

^ >venous return= >EDV = >Stroke volume.

^respiratory pump- inspiration causes decreases in thoracic pressure and increased abdominal pressure= raised pressure gradient.

63
Q

What is the use fo having a circulation/ why do we have blood vessels and a pump?

A

1) oxygen delivery and waste (CO2) pick up
2) Transporting other nutrients (eg glucose)
3) Hormones
4) Immune recognition and defence

Cardiology (5 decks)

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