Cardiophysiology Flashcards

(30 cards)

0
Q

In diastole, coronary blood flow is highest in…

A

Left ventricular subendocardial region

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1
Q

In systole, Coronary vascular resistance is highest in…

A

Left ventricular subendocardial region (due to heavy compression—vasodilator build-up)

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2
Q

Resting heart rate is influenced by…

A

Parasympathetic/vagal nerve innervation of the heart, dependent in atropine sensitive cholinergic receptors in SA node.

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3
Q

3 actions of pressor center in baroreceptor reflex consist of…

A

Heart: HR, contractility increase
Resistance vessels: TPR increase
Capacitance vessels: CVP/SV increase

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4
Q

Explain autoregulation of a vascular bed.

A

Local metabolites and VSM myogenic responses to a change in local perfusion pressure. c.f. Lungs, brain

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5
Q

Explain Reactive hyperemia

A

The local effect of metabolites in response to inadequate blood flow relative to local metabolism.

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6
Q

How will leaky aortic valve (aortic insufficiency) affect LV coronary blood flow?

A

During diastole, blood will leak back to LV, increasing preload and increasing the work needed to be done by LV (flow will go up). But work by pressure is MUCH more important.

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7
Q

Direct effects of sympathetic nerves on VSM fibers consist of…

A

Vasoconstriction via alpha adrenoceptors (adrenergic receptors) and vasodilation via beta adrenoceptors. This is NOT autoregulation.

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8
Q

What does Atropine do?

A

Blocks muscarinic (cholinergic) receptors for Ach released by parasympathetic nerves to the heart.

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9
Q

What does Propanolol do?

A

Blocks beta-adrenergic receptors for norepinephrine released by sympathetic nerves to the heart.

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10
Q

What are intrinsic regulations of the heart?

A

Heterometric/starlings law of heart

Homometric/Treppes mechanism

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11
Q

Why does athletes have slow heart rate?

A

Increased vagal tone

Slow intrinsic SA node firing rate

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12
Q

Name humoral factors that lead to vasoconstriction of VSM in resistance vessels.

A
Predominantly NE
HIGH dosage of E
ADH
Angiotensin II
Endothelin
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13
Q

Name humoral factors that lead to vasodilation of VSM in resistance vessels.

A

Histamine
LOW dose of E (via beta adrenergic receptors)
Bradykinin
Endothelium Derived Relaxing Factor (EDRF); NO

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14
Q

Describe chemoreceptor reflex effects.

A

The carotid body detects low O2 and pH. TPR is directly increased as a result, HR more complicated; MAP increased.
Breathing is induced and arousal stimulated during sleep.

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15
Q

Name four mechanisms that aid Venous Return.

A

Muscle pump
Respiratory pump
Cardiac suction
Valves in vein

16
Q

Explain five ways Blood Volume regulation works when discharge rate of low baroreceptor reflex is increased.

A

Decreased renal sympathetic nerve activity-> increased renal filtration pressure
Increased filtration pressure (stretch) also results in Decreased renin release
Decreased ADH
Increased HR by reflex
Blood Volume increase in atria result in Release of Atrial Natriuretic Peptide (ANP)—helps excrete sodium and salt

17
Q

At a capillary level, what three factors will increase in Blood Volume? Think of arterial/venous end pressure.

A

Decreased MAP
Decreased venous end pressure
Increased TPR/arterial end pressure
All these three result in decreased capillary pressure and helps the interstitial fluid to flow in vascular urge

18
Q

Explain autotransfusion.

A

This is the effect to restore BV by increasing sympathetic outflow to precapillary end of VSM in arterioles, decreasing capillary pressure. Interstitial fluid flood in. Hematocrit decreases as a result. Think of one of five BV regulation.

19
Q

Explain blood flow regulation in skin during exercise.

A

As body temperature increases, sympathetic nerves controlling cutaneous blood flow are inhibited, leading to vasodilation and dissipation of heat. Local vasodilator has little effect.

20
Q

In the exercising skeletal muscle, what is the status of sympathetic activity in the arterioles?

A

Although TPR increases as a result of sympathetic controller turned up, local vasodilator override such effects. Vasodilation occurs. Same applies in brain and heart.

21
Q

What initiates sympathetic outflow during the exercise?

A

Efferent reflex of skeletal muscles turn on the central sympathetic command in the brain, I.e. anticipation of exercise.

22
Q

Explain Cushing’s Reflex

A

Brain Swelling (edema) or an intracranial mass increases intracranial pressure->presses brainstem controller->blood pressure increases and HR slows down (BRR turnt down!)

23
Q

Describe the effects of hyperventilation on cerebral blood flow.

A

It lowers CO2 partial pressure in the arteries (hypocapnia) resulting in vasoconstriction of cerebral vessels. Cerebral blood flow decreases.

24
Describe Acute Hypertensive Encephalopathy and two hypotheses for its pathophysiology.
Sustained or sudden increase in MAP to high levels, resulting in vascular cerebral crisis. 1. Vasospasm (Excessive Autoregulation): intense vasoconstriction leading to cerebral ischemia. 2. Forced Vasodilation (Failed Autoregulation): higher capillary pressure forces fluid leak into tissues.
25
What should happen if the breaking point in MAP to maintain a steady flow via Autoregulation were to shift to right? I.e. Be able to Autoregulate at high MAP?
Turn on sympathetic nerve activity.
26
How does standing and walking for a few minutes every hour during prolonged sitting help prevent edema?
Muscle pumps operate to send blood from the dependent venous toward the heart and use the valves in the leg veins to keep venous blood flowing back.
27
What could result in very low blood pressure and a slightly below normal heart rate?
Overdosing with a drug causing blockage of sympathetic actions?
28
How do you explain an increased pulse pressure in toxic shock syndrome?
Decreased TPR due to leaky capillaries -> decreased MAP -> decrease in afterload and end-diastolic pressure. Systolic pressure may go up as a reflex, resulting in an increased pulse pressure.
29
What happens to pulmonary vascular resistance during heavy exercise?
Falls as pulmonary arterial pressure and flow increase as a result of increased need to oxygenate the blood.