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Physiology > Cardiovascular Drugs And Exercise > Flashcards

Cardiovascular Drugs And Exercise Flashcards

(85 cards)

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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
What CO does pulmonary circulation get
Blood flow through lungs Heavy exercise - 4-7 fold
26
What is pulmonary circulation characterised by?
High compliance High flow Low resistance Low pressure
27
What control is there over pulmonary circulation?
Local gas tension Hypoxic pulmonary vasoconstriction Allow perfusion/ventilation matching
28
What percentage of CO does cutaneous circulation get?
At rest - 4-10% Moderate exercise - <20%
29
What is non-acral skin?
Trunk and upper limbs
30
What is acral skin?
Extremities of hands, feet and ears
31
What percentage of CO does cerebral blood flow get?
At rest - 14% Moderate exercise - 14% Only accounts for 2% of body mass though
32
What control is over cerebral blood flow?
Metabolic - low O2, adenosine, low pH and high CO2 - vasodilation Myogenic - protect from changes in BP - decreased MAP - cerebral vessels constrict
33
What are the unique features of cerebral blood flow?
Active regions receive increased BP Blood brain barrier Brain enclosed in skull - intracranial pressure influences cerebral perfusion
34
What effect does intracranial pressure have on blood vessels?
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
35
What are the cardiovascular changes when moving from supine to standing?
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
When does fainting occur?
When baroreceptors do not detect the change in BP Cerebral BP continues to fall
37
What should you do if someone faints?
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
What is systemic hypertension?
Systolic BP - >140mmHg Diastolic BP - >90mmHg
39
What are the ratios of primary and secondary hypertension?
Primary - 90-95% Secondary - 5-10%
40
What are the risk factors of hypertension?
Increasing age Obesity Lack of exercise High salt diet Alcohol Smoking Stress Secondary causes
41
What are the treatments of hypertension
Modifications of lifestyle Pharmacological intervention - diuretics - decreases blood volume - thiazides - increases K+ channel activity in VSM, hyperpolarisation increases Ca2+ entry, decreases vascular resistance
42
What are sympatholytics?
Block action of sympathetic nervous system
43
Give two examples of sympatholytics
Guanethidine Trimetaphan
44
How does guanethidine work?
Fill synaptic storage vesicles in preference to NA Block fusion of storage vesicles with neurolema Decreases NA release from sympathetic nerves
45
How does trimetaphan work?
Blocks ganglia in SNS and PNS Nicotinic receptor antagonist
46
Give examples of Adrenergic drugs
Alpha 1 antagonists - prazosin Alpha 2 agonist - clonidine
47
How do alpha 1 antagonists work?
Block postganglionic alpha 1 receptors on VSM Decrease peripheral resistance and venous pressure Decreases low density lipoprotein Increases high density lipoprotein
48
How do alpha 2 agonists work?
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
What do Beta adrenoreceptor Amat agonists do?
Decreases sympathetic drive Decreases HR and CO Decreases renin production Decreases TPR
50
How do calcium channel antagonists work?
Interfere with opening/closing of L-type Ca2+ channels
51
Give examples of both vascular selective and less vascular selective calcium channel anatagonists
Nifedipine (vascular) - little effect on cardiac conduction Verapamil and diltiazem (less vascular) - more prone to cardiac conduction defects
52
Give examples of renin-angiotensin cascade modulators
ACE inhibitors Angiotensin ll antagonists
53
How do ACE inhibitors work?
Decreases Angiotensin ll production Causes vasodilation Reduced sodium retention Decreases breakdown of endogenous Vasodilator, bradykinin
54
How do angiotensin ll antagonists work?
Blocks direct agonist vasoconstrictor effect Blocks indirect presynaptic potentiation of transmitter release
55
How does sodium nitroprusside work?
Given IV for rapid BP decrease in emergencies Effects are short term - minutes Decrease in cGMP activity causes relaxation
56
What is cardio vascular disease (CVD)?
An umbrella term for all diseases of the heart and circulation
57
List the types/causes of heart failure
Coronary artery diseases Valve disease Aneurysm Cardiac arrhythmia Cardiomyopathy Pericarditis
58
What is heart failure?
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
How is the frank starling mechanism affected during heart failure?
It fails to the point heart muscle contraction becomes less efficient even though the heart is filled with blood
60
What are the symptoms of heart failure?
Dyspnoea Fatigue Exercise intolerance Palpitations Swelling
61
What are the clinical signs of heart failure?
Tachycardia Elevated jugular venous pressure Displaced apex beat Basal lung crepitations Oedema, ascites
62
What are the pathophysiological changes during heart failure?
Reduced left ventricle ejection fraction Fluid retention increased right atrial pressure Reduced venous return
63
How many classifications of heart failure are there?
Four
64
What happens to the stroke volume during heart failure?
Decreased inotropic properties Decreased ESPVR = Decreased stroke volume
65
What happens during myocardial adaptation?
Loss of myocardium decreases CO decreased arterial pressure causes barorecptor activation Which causes increased ADH secretion This raises blood volume Increased venous return
66
What happens during neurohumoral activation?
Sympathetic nervous system activation Increases sympathetic innervation Increases HR and contractility Which increases CO Which which causes vasoconstriction And increases venous return
67
What happens to renal blood flow during heart failure?
RAAS activation Angiotensin ll AT1R Vasoconstriction Aldosterone - sodium/water retention Increased blood volume
68
What are strategies for improving pump function in heart failure?
Preload reduction After load reduction Action potential modulator Increasing myocardial contractility
69
How does preload reduction work?
Remove sodium and water Decreases peripheral oedema, pulmonary congestion l, dyspnoea and syncope Diuretics ACE inhibitors Angiotensin receptor blockers Mineralocorticoid receptor anatagonists
70
How does afterload reduction work?
Decreases end diastolic volume Which decreases ventricular dilatation Hydralazine nitrates ACE inhibitors Beta antagonists Alpha 1 antagonists Alpha 2 agonists
71
How does action potential modulation work?
Decrease pacemaker depolarisation slope Which decreases HR reduction Which stabilises electrical activity And reduces abnormal electrical function Anti-arrhythmics HCN channel inhibitors
72
How does increasing myocardial contractility work?
Maintains stroke volume Digoxin Ivabradine Beta 1 agonist
73
How do diuretic help with preload reduction?
Promote renal excretion of sodium and water by blocking reabsorption of sodium and chlorine - decreases ventricular filling filling pressure - decreases peripheral oedema
74
What are the mechanisms of action for k sparing diuretics?
Mineralocorticoid receptor anatagonists Inhibit action of aldosterone Epithelial sodium channel anatagonists reduce sodium reabsorption in collecting duct Reduced renal excretion of potassium
75
What are the side effects of using diuretics?
Electrolyte disturbances Metabolic alkalosis Utica acid retention - gout Hyperkalaemia Dehydration Hypotension, syncope Renal impairment
76
What are the mechanisms of action for ACE inhibitors?
Inhibition of ACE Prevents the convergence of angio l to angio ll Decreased systemic vascular resistance Decreased venous pressure Increased cardiac output
77
What are the side effects of ACE inhibitors?
Dry cough Increased bradykinin levels in lungs
78
What are the mechanisms of action for beta blockers?
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
What are venodilators?
Short and long acting nitrates Arteriolar vasodilators - reduce after load and increase CO Venodilators - decrease preload, decrease venous pressure means decreased LVEDP
80
What are the mechanisms of action for action potential modulation?
Inhibition of If channel Decreased pacemaker depolarisation slope Decreased HR, more time for filling Increased efficiency
81
What are the side effects of action potential modulation?
Can cause bradycardia or AV block Unhelpful for patients with AF
82
Give examples of anti-arrhythmic drugs
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
How do you increase contractility?
Positive inotropes For short term support of myocardial function in patients with acute heart failure when maximal drug therapy has failed
84
What are the mechanisms of action for positive inotropes?
Anatagonist of cardiomyocyte Na+/K+ ATPase = increased intracellular sodium Inhibition of Na+/Ca2+ exchanger Increased intracellular calcium mean increased force of contraction
85
How do you work out the ejection fraction?
EF = SV / EDV

Physiology (9 decks)

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