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Physiology > Cardiovascular Drugs And Exercise > Flashcards

Cardiovascular Drugs And Exercise Flashcards

1
Q

Compare CO while at rest and while exercising

A

At rest - 5L/min
Exercise - 25L/min

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2
Q

How do you work out CO

A

CO = stroke volume x heart rate

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3
Q

What three factors affect CO?

A

-Sympathetic loading
-Parasympathetic unloading
Hormones
Starling forces

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4
Q

What happens during increased CO?

A

Vasodilation in metabolically active muscle
Metabolites
- K+
- pH
- adenosine
- EDRF - potent vasodilator

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5
Q

What is EDRF?

A

Endothelium derived relaxing factor

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6
Q

What happens to TPR during exercise?

A

It will decrease but remain constant even as intensity continues to increase

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7
Q

How do you calculate BP?

A

BP = CO x TPR

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8
Q

What will happen to BP when CO increases

A

It will decrease as TPR decreases dramatically

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9
Q

What happens during dynamic exercise?

A

Systolic BP increase
diastolic BP may decrease

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10
Q

What happens during static exercise?

A

Systolic BP increases
Diastolic BP also increases
Physical compression of muscle blood vessels increases TPR and therefore Diastolic pressure

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11
Q

What does circulation depend on?

A

Perfusion pressure
Vascular resistance

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12
Q

What does control of vascular resistance depend on?

A

Intrinsic factors
Extrinsic factors

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13
Q

What are intrinsic factors?

A

Auto regulation
- myogenic
- metabolic
- endothelial
Mechanical compression
- cardiac muscle
- skeletal muscle

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14
Q

What are extrinsic factors?

A

Nervous
Hormonal

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15
Q

What is autoregulation?

A

The ability of an organ to maintain blood flow despite changes in perfusion pressure
Occurs in the absence of extrinsic factors

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16
Q

What are the features of coronary blood flow?

A

High basal flow
High basal O2 consumption
High myocardial O2 extraction
High density of myocardial capillaries
O2 transport increases by myoglobin in myocyte

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17
Q

Describe control of coronary blood flow

A

Flow is closely linked to O2 demand
Decreased O2, increased CO2, NO, H+, K+, lactate, PGs, and adenosine cause vasodilation
Sympathetic vasoconstrictor tone also present
Vasodilators dominate
Increased sympathetic activity to sinus node increases HR
Indirectly causes vasodilation due to increased metabolism

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18
Q

What percentage of CO does the heart get?

A

At rest - 5%
Moderate exercise - 5%

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19
Q

What percentage of CO does skeletal muscle get?

A

At rest - 18%
Moderate exercise - >70%

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20
Q

Describe the neurohormonal control scene at skeletal muscle

A

Action of sympathetic nerves and hormones
- alpha adrenoreceptors
- important at rest
- adrenaline
- beta 2 adrenoreceptors
- supports local metabolites during exercise

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21
Q

Describe local metabolic control of skeletal muscle

A

Metabolic vasodilation
-k+, PO4(3-), pH, hypoxia and lactic acid (H+)
Dominates as exercise increases

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22
Q

What areas are splanchnic?

A

GIT
liver
Pancrease
Spleen

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23
Q

What percentage of CO do splanchnic beds get?

A

At rest - 30%
Moderate exercise - 5%

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24
Q

What sort of regulation is there for splanchnic areas?

A

Autoregulation
Nervous control - sympathetic vasoconstrictor nerves
- hypotension or exercise

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25
Q

What CO does pulmonary circulation get

A

Blood flow through lungs
Heavy exercise - 4-7 fold

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26
Q

What is pulmonary circulation characterised by?

A

High compliance
High flow
Low resistance
Low pressure

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27
Q

What control is there over pulmonary circulation?

A

Local gas tension
Hypoxic pulmonary vasoconstriction
Allow perfusion/ventilation matching

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28
Q

What percentage of CO does cutaneous circulation get?

A

At rest - 4-10%
Moderate exercise - <20%

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29
Q

What is non-acral skin?

A

Trunk and upper limbs

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30
Q

What is acral skin?

A

Extremities of hands, feet and ears

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31
Q

What percentage of CO does cerebral blood flow get?

A

At rest - 14%
Moderate exercise - 14%
Only accounts for 2% of body mass though

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32
Q

What control is over cerebral blood flow?

A

Metabolic
- low O2, adenosine, low pH and high CO2 - vasodilation
Myogenic
- protect from changes in BP
- decreased MAP
- cerebral vessels constrict

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33
Q

What are the unique features of cerebral blood flow?

A

Active regions receive increased BP
Blood brain barrier
Brain enclosed in skull
- intracranial pressure influences cerebral perfusion

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34
Q

What effect does intracranial pressure have on blood vessels?

A

Increased pressure can compress blood vessels which reduces cerebral blood flow
E.G
- increased brain volume = oedema
- increased CSF = hydrocephalus
- increased cerebral blood volume = blockage in venous drainage or vasodilation

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35
Q

What are the cardiovascular changes when moving from supine to standing?

A

Initial venous pooling
Reduces venous return
Reduction in SV/CO
reduction in arterial BP
Detected by barorecptors
Increases HR
Causes arterial vasoconstriction
Increases TPR
Vasoconstriction restores venous return
Arterial BP quickly restored

36
Q

When does fainting occur?

A

When baroreceptors do not detect the change in BP
Cerebral BP continues to fall

37
Q

What should you do if someone faints?

A

Lie them down horizontally
Raise legs to restore cerebral blood flow
Turn head to side
Loosen tight clothing
Apply cold moist towels to face and neck

38
Q

What is systemic hypertension?

A

Systolic BP - >140mmHg
Diastolic BP - >90mmHg

39
Q

What are the ratios of primary and secondary hypertension?

A

Primary - 90-95%
Secondary - 5-10%

40
Q

What are the risk factors of hypertension?

A

Increasing age
Obesity
Lack of exercise
High salt diet
Alcohol
Smoking
Stress
Secondary causes

41
Q

What are the treatments of hypertension

A

Modifications of lifestyle
Pharmacological intervention
- diuretics - decreases blood volume
- thiazides - increases K+ channel activity in VSM, hyperpolarisation increases Ca2+ entry, decreases vascular resistance

42
Q

What are sympatholytics?

A

Block action of sympathetic nervous system

43
Q

Give two examples of sympatholytics

A

Guanethidine
Trimetaphan

44
Q

How does guanethidine work?

A

Fill synaptic storage vesicles in preference to NA
Block fusion of storage vesicles with neurolema
Decreases NA release from sympathetic nerves

45
Q

How does trimetaphan work?

A

Blocks ganglia in SNS and PNS
Nicotinic receptor antagonist

46
Q

Give examples of Adrenergic drugs

A

Alpha 1 antagonists - prazosin
Alpha 2 agonist - clonidine

47
Q

How do alpha 1 antagonists work?

A

Block postganglionic alpha 1 receptors on VSM
Decrease peripheral resistance and venous pressure
Decreases low density lipoprotein
Increases high density lipoprotein

48
Q

How do alpha 2 agonists work?

A

CNS action
- decreases presynaptic inhibition of NA release in vasomotor pathways
- decreases sympathetic drive

Peripheral action
- inhibition of releases of NA from postganglionic nerves
- decreases vasoconstriction

49
Q

What do Beta adrenoreceptor Amat agonists do?

A

Decreases sympathetic drive
Decreases HR and CO
Decreases renin production
Decreases TPR

50
Q

How do calcium channel antagonists work?

A

Interfere with opening/closing of L-type Ca2+ channels

51
Q

Give examples of both vascular selective and less vascular selective calcium channel anatagonists

A

Nifedipine (vascular)
- little effect on cardiac conduction
Verapamil and diltiazem (less vascular)
- more prone to cardiac conduction defects

52
Q

Give examples of renin-angiotensin cascade modulators

A

ACE inhibitors
Angiotensin ll antagonists

53
Q

How do ACE inhibitors work?

A

Decreases Angiotensin ll production
Causes vasodilation
Reduced sodium retention
Decreases breakdown of endogenous
Vasodilator, bradykinin

54
Q

How do angiotensin ll antagonists work?

A

Blocks direct agonist vasoconstrictor effect
Blocks indirect presynaptic potentiation of transmitter release

55
Q

How does sodium nitroprusside work?

A

Given IV for rapid BP decrease in emergencies
Effects are short term - minutes
Decrease in cGMP activity causes relaxation

56
Q

What is cardio vascular disease (CVD)?

A

An umbrella term for all diseases of the heart and circulation

57
Q

List the types/causes of heart failure

A

Coronary artery diseases
Valve disease
Aneurysm
Cardiac arrhythmia
Cardiomyopathy
Pericarditis

58
Q

What is heart failure?

A

A complex syndrome that can result from any structural of functional cardiac disorder that impairs the ability of the heart to function as a pump to support circulation

59
Q

How is the frank starling mechanism affected during heart failure?

A

It fails to the point heart muscle contraction becomes less efficient even though the heart is filled with blood

60
Q

What are the symptoms of heart failure?

A

Dyspnoea
Fatigue
Exercise intolerance
Palpitations
Swelling

61
Q

What are the clinical signs of heart failure?

A

Tachycardia
Elevated jugular venous pressure
Displaced apex beat
Basal lung crepitations
Oedema, ascites

62
Q

What are the pathophysiological changes during heart failure?

A

Reduced left ventricle ejection fraction
Fluid retention
increased right atrial pressure
Reduced venous return

63
Q

How many classifications of heart failure are there?

A

Four

64
Q

What happens to the stroke volume during heart failure?

A

Decreased inotropic properties
Decreased ESPVR
= Decreased stroke volume

65
Q

What happens during myocardial adaptation?

A

Loss of myocardium decreases CO
decreased arterial pressure causes barorecptor activation
Which causes increased ADH secretion
This raises blood volume
Increased venous return

66
Q

What happens during neurohumoral activation?

A

Sympathetic nervous system activation
Increases sympathetic innervation
Increases HR and contractility
Which increases CO
Which which causes vasoconstriction
And increases venous return

67
Q

What happens to renal blood flow during heart failure?

A

RAAS activation
Angiotensin ll
AT1R
Vasoconstriction
Aldosterone
- sodium/water retention
Increased blood volume

68
Q

What are strategies for improving pump function in heart failure?

A

Preload reduction
After load reduction
Action potential modulator
Increasing myocardial contractility

69
Q

How does preload reduction work?

A

Remove sodium and water
Decreases peripheral oedema, pulmonary congestion l, dyspnoea and syncope
Diuretics
ACE inhibitors
Angiotensin receptor blockers
Mineralocorticoid receptor anatagonists

70
Q

How does afterload reduction work?

A

Decreases end diastolic volume
Which decreases ventricular dilatation
Hydralazine
nitrates
ACE inhibitors
Beta antagonists
Alpha 1 antagonists
Alpha 2 agonists

71
Q

How does action potential modulation work?

A

Decrease pacemaker depolarisation slope
Which decreases HR reduction
Which stabilises electrical activity
And reduces abnormal electrical function
Anti-arrhythmics
HCN channel inhibitors

72
Q

How does increasing myocardial contractility work?

A

Maintains stroke volume
Digoxin
Ivabradine
Beta 1 agonist

73
Q

How do diuretic help with preload reduction?

A

Promote renal excretion of sodium and water by blocking reabsorption of sodium and chlorine
- decreases ventricular filling filling pressure
- decreases peripheral oedema

74
Q

What are the mechanisms of action for k sparing diuretics?

A

Mineralocorticoid receptor anatagonists
Inhibit action of aldosterone
Epithelial sodium channel anatagonists reduce sodium reabsorption in collecting duct
Reduced renal excretion of potassium

75
Q

What are the side effects of using diuretics?

A

Electrolyte disturbances
Metabolic alkalosis
Utica acid retention - gout
Hyperkalaemia
Dehydration
Hypotension, syncope
Renal impairment

76
Q

What are the mechanisms of action for ACE inhibitors?

A

Inhibition of ACE
Prevents the convergence of angio l to angio ll
Decreased systemic vascular resistance
Decreased venous pressure
Increased cardiac output

77
Q

What are the side effects of ACE inhibitors?

A

Dry cough
Increased bradykinin levels in lungs

78
Q

What are the mechanisms of action for beta blockers?

A

Inhibition if beta 1 and beta 2 adrenoreceptors
Reduced production of cAMP
Decreased HR, decreased force of contraction but increased relaxation of the heart
Decreased renin from kidney, decreased water retention
Increased vasodilation of peripheral arterioles, decreased diastolic BP

79
Q

What are venodilators?

A

Short and long acting nitrates
Arteriolar vasodilators - reduce after load and increase CO
Venodilators - decrease preload, decrease venous pressure means decreased LVEDP

80
Q

What are the mechanisms of action for action potential modulation?

A

Inhibition of If channel
Decreased pacemaker depolarisation slope
Decreased HR, more time for filling
Increased efficiency

81
Q

What are the side effects of action potential modulation?

A

Can cause bradycardia or AV block
Unhelpful for patients with AF

82
Q

Give examples of anti-arrhythmic drugs

A

Class lll - K+ channel blockers
- prolong AP and refractors period
- no effect on sodium channels
- normal conduction velocity

Class iv- L-type calcium channel blockers
- decreased conduction velocity through AV node
- mean decreased plateau phase of cardiac AP and decreased contractility

83
Q

How do you increase contractility?

A

Positive inotropes
For short term support of myocardial function in patients with acute heart failure when maximal drug therapy has failed

84
Q

What are the mechanisms of action for positive inotropes?

A

Anatagonist of cardiomyocyte Na+/K+ ATPase = increased intracellular sodium
Inhibition of Na+/Ca2+ exchanger
Increased intracellular calcium mean increased force of contraction

85
Q

How do you work out the ejection fraction?

A

EF = SV / EDV

Physiology (9 decks)

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