Special Circulation Flashcards
(42 cards)
What is auto-regulation?
Maintain organ blood flow via vascular smooth muscle contraction/relaxation. Specific to brain, kidney, heart. Aldo called Bayless myogenic response/ myogenic response
What is functional sympatholysis?
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
What is hyperemia?
Increased blood flow in a tissue or organ. Usually due to local control of blood flow
What is metabolic hyperemia?
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
Outline sympathetic control of blood flow control
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
Outline the impact of parasympathetic influence in blood flow
Minor importance
- post-ganglion fibers release acetylcholine
- ACh mediates vasodilation-this is important in blood vessels of the penile erectile tissue
What is the problem with coronary circulation ?
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
How is coronary blood flow regulated?
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
Describe coronary circulation layout
- 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
What are the mechanical effects on coronary blood flow?
- systole= vascular compression
- diastole= maximal flow
- pressure differences less in right ventricles
How can tachycardia impact coronary blood flow?
- shorter diastole reduces flow
- overridden by metabolic (active) hyperemia(vasodilation)
- oxygen consumption of heart is very high (increased in exercise) relies on oxidative mechanism
Why is metabolic hyperemia important?
Most important for increasing coronary blood flow *adenosine
Coronary blood flow and metabolic activity of the heart must be limked
What are the effects of increasing heart rate on coronary blood flow?
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
What are the effects of exercise on coronary blood flow?
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+
What is the role of sympathetics in coronary blood flow?
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
What are the clinical correlates of coronary blood flow?
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)
What are the diseases of coronary circulation ?
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
Describe how coronary heat disease leads to ischemic heart disease
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
What are the clinical impact of atheromatous plaque?
- Leads to progressive narrowing of coronary artery—> insufficient O2 to meet demands—> cardiac ischemia which leads to both angina and myocardial infarction
- leads to Protrusion through endothelium—> comes into contact with flowing blood—> platelets aggregate fibrin deposited—> thrombus formed—> occlude coronary artery—> cardiac ischemia
What are the symptoms of angina pectoris?
Chest and/or l3ft arm pain
What is angina pectoris?
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)
What is the goal of angina treatment?
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
What is used to treat angina?
- 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)
Describe the metabolic needs of skeletal muscle
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