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Cardiopulmonary Renal > Special Circulation > Flashcards

Special Circulation Flashcards

1
Q

What is auto-regulation?

A

Maintain organ blood flow via vascular smooth muscle contraction/relaxation. Specific to brain, kidney, heart. Aldo called Bayless myogenic response/ myogenic response

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2
Q

What is functional sympatholysis?

A

Where local control of blood flow overrides sympathetic activity. Transient vasoconstriction due to increased sympathetic drive (a-receptors), but followed by vasodilation due to locally released metabolites. Important in skeletal, heart and brain

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3
Q

What is hyperemia?

A

Increased blood flow in a tissue or organ. Usually due to local control of blood flow

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4
Q

What is metabolic hyperemia?

A

Increased metabolic activity results in local increases in metabolite concentrations. Metabolites override sympathetic activity (functional sympatholysis). E.g. inhibition of sympathetic mediated vasoconstriction during exercise

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5
Q

Outline sympathetic control of blood flow control

A

Sympathetic

  • post-ganglionic fibers release NE onto target organs
  • adrenal medulla releases NE and E into bloodstream
  • both act on a1 and a2 adrenoreceptors —> vasoconstriction
  • general sympathetic tone provides basal levels of vasoconstriction throughout the circulatory system which contributes to TPR
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6
Q

Outline the impact of parasympathetic influence in blood flow

A

Minor importance

  • post-ganglion fibers release acetylcholine
  • ACh mediates vasodilation-this is important in blood vessels of the penile erectile tissue
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7
Q

What is the problem with coronary circulation ?

A

The coronary circulation receives about 5% of CO at rest, which is considerable given its limited size. O2 extraction from blood is high at about70% at rest. To get more O2 to the h3art blood flow must increase, hence O2 delivery to heart is flow limited

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8
Q

How is coronary blood flow regulated?

A

Local control (metabolic hyperemia)

  • dominant mechanism for regulating coronary blood flow
  • working heart muscle releases vasoactive metabolites (NO, adenosine)

Sympathetic control (less important):

  • brief vasoconstriction via a receptors
  • less important than local control due to functional sympatholysis, I.e. local effects override sympathetic vasoconstriction

Autoregulation

  • still debated, appears to operate largely via local metabolic control
  • No ckear evidence fir myogenic autoregulation
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9
Q

Describe coronary circulation layout

A
  • O2 is supplied by coronary arteries on epicardium
  • heart muscle does not obtain O2 from ventricle /atria lumens
  • absence of inter-coronary vascular or collateral vascular connections means that blockage of an artery leads to ischemia downstream of block
  • some cope for angiogenesis and collaterization within the myocardium to improve blood supply in long-term ischemic areas of cardiac muscle
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10
Q

What are the mechanical effects on coronary blood flow?

A
  • systole= vascular compression
  • diastole= maximal flow
  • pressure differences less in right ventricles
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11
Q

How can tachycardia impact coronary blood flow?

A
  • shorter diastole reduces flow
  • overridden by metabolic (active) hyperemia(vasodilation)
  • oxygen consumption of heart is very high (increased in exercise) relies on oxidative mechanism
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12
Q

Why is metabolic hyperemia important?

A

Most important for increasing coronary blood flow *adenosine

Coronary blood flow and metabolic activity of the heart must be limked

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13
Q

What are the effects of increasing heart rate on coronary blood flow?

A

At high HRs duration of diastole is decreased

This leads to decreased coronary perfusion, build up of vasodilator metabolites- ensuring adequate coronary blood flow

O2 consumption of heart very high (increased in exercise). Relies on oxidative metabolism.

Coronary blood flow a d metabolic activity of heart must be tightly linked

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14
Q

What are the effects of exercise on coronary blood flow?

A

Exercise leads to increased oxygen demand

O2 extraction from blood already high (about 75% at rest )

Increased O2 demand met by increased coronary blood flow

At rest, CBF= 80 ml/100 gm tissue

In exercise= 400

Increased blood flow mediated by metabolic vasodilators (active hyperemia). Response is very rapid

Vasodilators: adenosine, NO, K+, and H+

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15
Q

What is the role of sympathetics in coronary blood flow?

A

Symp. NS activated in exercise

Symp. NS- transient coronary vasoconstriction (via a1) AND inotropic and chronotropic (via B1)

This leads to increased metabolic activity—> increased vasodilator metabolites—> metabolic hyperemia—> increased coronary blood flow

Symp. Effects in exercise increase metabolism of the heart which triggers metabolic hyperemia resulting in a functional sympatholysis

Metabolic hyperemia is far more important in regulating coronary blood flow because there is functional sympatholysis

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16
Q

What are the clinical correlates of coronary blood flow?

A

O2 supply/O2 demand ratio important

O2 supply= CBF x arterial O2 content

O2 demand= myocardial O2 consumption (= CBF x A-VO2 difference)

Decreased O2 supply/ O2 demand=myocardial hypoxia (ischemia)

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17
Q

What are the diseases of coronary circulation ?

A

Coronary vascular reserve

  • difference between max flow via vasodilation and flow at rest
  • Disease decreases coronary reserve as arterioles cannot compensate (by dilation) fir shortened diastole and increased metabolic demand

Coronary blood flow reduction

  • e.g. with coronary atherosclerosis
  • decreased myocardial O2 supply
  • effects: myocardial ischemia, angina pectoris(chest pain)
  • metabolic switch to anaerobic glycolysis, FFA oxidation

Complete flow back

  • rapid nutrient depletion
  • infarcts, necrosis
18
Q

Describe how coronary heat disease leads to ischemic heart disease

A

Leading cause of death in the west
Result in: sudden death(coronary occlusion)

Progressive weakening of the heart, cardiac failure

Cause: atheromatous plaques in coronary vessels

Due to: poor diet, genetic predisposition

19
Q

What are the clinical impact of atheromatous plaque?

A
  1. Leads to progressive narrowing of coronary artery—> insufficient O2 to meet demands—> cardiac ischemia which leads to both angina and myocardial infarction
  2. leads to Protrusion through endothelium—> comes into contact with flowing blood—> platelets aggregate fibrin deposited—> thrombus formed—> occlude coronary artery—> cardiac ischemia
20
Q

What are the symptoms of angina pectoris?

A

Chest and/or l3ft arm pain

21
Q

What is angina pectoris?

A

Triggered when cardiac O2 demand excess supply

  • with exercise and coronary atherosclerosis
  • with cold and stress via increased sympathetic vasoconstriction
  • coronary occlusion: triggered with exercise
  • coronary vasospasm: triggered at rest

Indicates Ann underlying insufficiency of coronary vascular reserve

  • usually due to narrowed coronary arteries e.g. with atherosclerosis
  • ischemic heart muscle releases algogenic (pain generating) substances, e.g. substance P

Pain radiates down left arm because cardiac chemisensitive afferents converge with somatic afferents
-radiating (when pain includes source organ and extends beyond ) versus refferred pain (pain doses not include source organ /area)

22
Q

What is the goal of angina treatment?

A

Decrease oxygen demand, of increase oxygen supply

Increase oxygen with surgery- by pass, stents

Decreased oxygen demand with drugs that decrease prel9ad, decrease HR & contractility

23
Q

What is used to treat angina?

A
  1. Decreased oxygen by decreased work load
    • decreased work load by decreased contractility, decreased preload, and decreased afterload

Anti anginal drugs

Nitroglycerin: venodilation (and arteriolar dilation)

Beta blockers: decreased HR and contractility

Ca channel blockers: decreased contractility, decreased afterload and preload (vasodilation)

24
Q

Describe the metabolic needs of skeletal muscle

A

Has highly variable metabolic needs
, receiving between 18% at rest and 80% during intense exercise of total CO. Tonic, sympathetic mediated vasoconstriction restricts blood flow at rest. High energy demands during exercise are met by increased blood flow due to locally mediated vasodilation

25
Q

Contrast blood flow in skeletal muscle in rest and contraction

A

At rest- vasoconstriction

  • rich sympathetic innervation mediated basal vasoconstriction
  • normal TPR & MAP
  • Low concentrations of vasoactive metabolites at rest do notovverrude sympathetic control

During exercise- vasodilation

  • functional sympatholysis: local control (active/reactive hyperemia due to vasoactive metabolites like lactate, K+, adenosine) overrides sympathetic vasoconstriction
  • massive increase in blood flow to muscle (capillary recruitment)
  • TPR & MAP changes depending on static vs dynamic exercise
26
Q

Contrast dynamic and static exercise

A

Phasic, dynamic exercise

  • e.g. running
  • active hyperemia due to metabolites
  • blood flow is not interrupted
  • capillary recruitment—> reduced local resistance
  • sympathetic control maintains global TPR & MAP

Static exercise

  • e.g. weightlifting
  • sustained contractions block blood flow—> increased local resistance & TPR
  • increased TPR abd cardiac output can lead to increased MAP
  • vasodilation after contraction due to ischemia and build-up metabolites
  • reactive or ischemia hyperemia
27
Q

What is intermittent claudication?

A

Pain and cramping in legs during exercise

Caused by peripheral vascular disease due to atheromatous plaques in arteries supplying legs

28
Q

Describe cerebral circulation

A

At rest, the cerebral circulation receives about 15% of CO, a large proportion because the human brain has high O2 consumption abd metabolic needs. Local control dominates, sympathetic innervation is sparse

29
Q

What are the features of cerebral circulation?

A

Critical circulation, maintained at any cost

  • disruption of blood flow for seconds- unconsciousness
  • for minutes- irreversible brain damage, death
  • Circle of Willis: interconnecting arterial vessels safety mechanism fir cerebral perfusion, especially if an artery occluded

Brain requires glucose as energy source

  • ketones can also be metabolized during starvation
  • some cells, e.g. retinal photoreceptors, can only use glucose as they do not have mitochondria

Mechanical effects: increased intracranial pressure—> decreased blood flow

Vasoactive metabolites: CO2, H+ (pH), adenosine

30
Q

Explain autoregulation in cerebral circulation

A

Blood flow remains at constant at pressures 60-180 mmHg

Due to autoregulation (bayliss myogenic response)

Less than 60 mmHg—> decreased perfusion —> confusion, unconsciousness

Chronic high blood pressure shifts autoregulation curve to right, maintaining blood flow at higher pressures

31
Q

What is the impact of PO2 in cerebral circulation ?

A

-Large drop in PO2(hypoxemia) required fir significant increases in blood flow (below 50 from normal 95 mm.Hg)

32
Q

What is the impact of PCO2 in cerebral circulation?

A
  • blood flow sensitive to small changes in PCO2
  • PCO2 alters pH via formation of carbonic acid, sensed by chemoreceptors
  • Increased PCO2 (hypercapnia)—> vasodilation
  • Decreased PCO2 (hypocapnia)—> vasoconstriction
33
Q

What are the key roles of control mechanisms ?

A
  • central perfusion (whole brain):
    • (bayliss) myogenic autoregulation
  • regional changes
  • metabolic hyperemia is dominant control mechanism
  • regional increased in neuronal activity —> increased oxygen demand
  • metabolic hyperemia links blood flow to metabolic demand
  • astrocytes are important in ‘neurovascular coupling’
  • research use: BOLD fMRI infers neuronal activity by measuring local blood oxygen levels

Sympathetic control:

  • minimal effect on cerebral blood flow
  • sparse sympathetic innervation in cerebral arterioles and arteries
34
Q

What is the key determinant if cerebral blood flow?

A

CPP (Cranial perfusion pressure)= MAP - ICP

Not MAP - CVP (central venous pressure) as in other tissues

Not elevated ICP, e.g.m due to TBI( concussion), is very dangerous

35
Q

What increases intracranial pressure?

A

ICP increased by:
-intracranial bleeding

  • cerebral edema
  • tumor
36
Q

What does increase in ICP cause?

A
  • collapse veins

- decreases effective CPP reduces blood flow

37
Q

Describe pulmonary circulation

A

All of CO enters the pulmonary circulation. Local control of blood flow is most important, sympathetic control least important. Mechanical effects due to lung inflation also play a role

Differences to other circulations

  • low pressure (8- 20 mmHg at rest)
  • low resistance to flow
  • receives 100% cardiac output (CO), from right ventricle

Hypoxia causes local vasoconstriction in the lungs

  • purpose of lungs is to oxygenate blood
  • blood flow is optimized to alveolar regions rich in oxygen by reducing flow to poorly oxygenated alveoli
  • vasoconstriction around oxygen-poor alveoli via O2 sensing K+ channels (Euler-Liljestrand mechanism)

Vasoactive metabolites also cause vasoconstriction in hypoxic alveoli

38
Q

Summarize cutaneous circulation

A

Skin has a relatively constant, low metabolic rate, receiving about 4% of CO at rest (1-60% with extreme cold/heat). Oxygen needs are easily met by low blood flow, increased blood flow is most important for temperature regulation

39
Q

How is cutaneous circulation controlled?

A 
Sympathetic control (most important):
-Arteriovenous (AV) anastomoses are bypass vessels between cutaneous arteries, and veins, Innervated by adrenergic sympathetic fibers
  • vasodilation of AV shunts allows blood to enter venous plexuses without having to pass through the skin surface capillaries, thus reducing heat loss
  • key for temperature control
  • flow through AV shunts can range from 0 to 1 L/min, severely reducing TPR and MAP

Local control (weak):

  • temperature
  • weak reactive hyperemia
  • weak autoregulation
40
Q

Explain cutaneous thermoregulation

A

Normothermic conditions
-low skin blood flow (about 5% of cardiac output)

During cold stress

  • increased sympathetic vasoconstrictor activity (cutaneous vessels )
  • reduced skin blood flow improves thermal insulation

During heat stress

  • increased sympathet8c cholinergic vasodilator activity
  • increased skin blood flow, can reach 60% of CO!
  • allows more heat dissipation as high skin blood flow delivers heat to the skin surface
  • cutaneous pooling out of blood due to heat exposure without sufficient acclimatization can reduce MAP dangerously
    • can induce syncope (fainting) and ischemic damage in O2^- sensitive organs like intestines
41
Q

Explain skin blood flow responses to cold stress and heat stress in nonglabrous skin

A
  • under nonthermic conditions, skin blood flow is relatively low (approx. 5% of cardiac output ) and skin vessels receive relatively minor neural inputs from active vasoconstrictor and vasodilator nerves
  • During cold stress, reductions of skin and internal temperatures lead to reflex increases in sympathetic nonadrenergic vasoconstrictor nerve activity. Increased vasoconstrictor system tone reduces skin blood flow, th7s increasing thermal insulation and conserving body heat.
  • During heat stress, increasing skin and internal temperatures lead to reflex increases in sympathetic cholinergic sudomotor activity. Increased activity of the vasodilator system leads to potentially dramatic increases in skin blood flow that can reach 60% of cardiac output. High skin blood flow delivers heat to the skin surface where it is removed to the environment primarily through evaporation of sweat
42
Q

Summarize neural controls of thermoregulation effectors in human skin

A
  • thermoregulation reflexes are mediated by the afferent inputs 9f internal and skin temperature
  • These afferent inputs are integrated in the preoptic anterior hypothalamus and spinal cord areas of the central nervous system
  • Efferent control of blood vessels and sweat glands in glabrous skin is mediated by nomadrenergic vasoconstrictor nerves and cholinergic sudomotor nerves, respectively
  • In nonglaborous skin regions, efferent control of blood vessels is effected through a system of dual sympathetic innervation, nor adrenergic active vasoconstrictor nerves and cholinergic active vasodilator nerves
  • Sweat glands also receive cholinergic sympathetic innervation; however, whether cholinergic sudomotor nerves are one and the same is not known

Cardiopulmonary Renal (35 decks)

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