Dla Before Lecture 10: Special Circulation Flashcards
How are the following regulated?
1) Coronary
2) Cutaneous
3) Skeletal
4) Cerebral
5) Pulmonary
Metabolic Demand:
1) Coronary
2) Cerebral –> Brain
- Unaffected by parasympathetics and sympathetics
3) Skeletal
4) Pulmonary (Hypoxia-vasocon)
-Can change how much blood flow by how much is needed, metabolites do that (skeletal, heart, brain)
Thermoregulation
1) Cutaneous
How Autonomic control effects the blood flow
Sympathetics:
- NE Released
- Activate A1 and A2 –> Vasocon.
Parasympathetic:
- Ach Released
- Vasodil.
Coronary Circulation
Factors that affect it
- Receives 5% CO at rest
- O2 to heart depends on flow (Direct relationship)
Factors that effect O2 –> heart:
1) Local control (metabolic hyperemia)
- Release NO and adenosine –.> Vasodilation, increase blood vessels diameter –> increase blood flow
2) Sympathetics
- Vasoconstriction–> decrease flow, overpowered by metabolics
What supplies heart O2?
-Coronary arteries on epicardium
Problem/blockage= ischemia
Systole and diastole affect on Coronary blood flow?
Increase:
-Diastole
Decrease:
1) Systole
2) Sympathetics
3) Tachycardia -> Increase HR -> decreases diastole –>Vasocon.
4) Exercise (increase O2 demand) –>Vasoconstricts
(All overridden by vasodilation metabolics)
Oxygen demand calc
O2 demand = myocardial O2 consumption
Myocardial O2 consumption= Coronary Blood flow X Area-VO2 difference
Pathology:
(Decrease O2/O2 demand = ischemia)
Effects of Disease on Coronary circulation
-Disease decreases coronary reserve as arterioles cannot compensate (by dilation) for shortened diastole and increased metabolic demand
(Ex: Atherosclerosis
-Reduces blood flow to mycardial tissue = restricting O2 supply)
Symps:
1) Myocardial ischemia –> can lead to necrosis (complete flow block)
2) Angina Pectoris (chest pain)
Coronary artery disease –> ischemic heart disease (IHD)
Cause:
-Atheromatous plaques in coronary vessels (Diet, genes)
Results:
1) Sudden death (coronary occlusion)
2) Progressive weakening of heart (Cardiac failure)
Angina Pectoris
-Indicates an underlying insufficiency of coronary vascular reserve
Sym:
-Chest/left arm pain (Triggered when cardiac O2 demand exceeds supply)
(Somatic afferents cause pain to radiate down left arm)
Treatment:
1) Nitroglycerin
- cause vasodilation
2) Beta blockers
- Decrease HR and contractility
Skeletal muscle circulation at rest and during exercise
At rest:
-Vasoconstriction
During exercise:
-Vasodilation –> reduction in TPR
Phasic and static exercise and skeletal muscle circulation
1) Phasic –> Running
- Active hyperemia
- blood flow is not interrupted
- capillary recruitment → reduced local resistance
- sympathetic control maintains global TPR and MAP
2) Static –> Weightlifting
- Reactive or ischemic hyperemia
- sustained contractions block blood flow → increased local resistance & TPR
- increased TPR and cardiac output can lead to increased MAP
- vasodilation after contraction due to ischemia and build-up of metabolites
Intermittent Claudation
-Disease of skeletal muscle blood flow
Sym:
-Pain/cramping in leg during exercise
Cause:
-Peripheral vascular disease –> from atheromatous plaques in arteries supplying legs
Cerebral Circulation
-Maintained at all costs
-Circle of Willis –> Collateral blood flow for artery obstructions/cerebral perfusion
(aneurysms common)
- Brain requires glucose for energy
- Increase intracranial pressure, decreases blood flow
- Also has adenosine metabolites
Hypertension patient
- Messed up Cerebral circulation
- Chronic high perfusion pressures
- Shifting auto-regulatory curve of blood flow and perfusion pressure to the right –> maintains blood flow at high blood pressure
CO2 & O2 in Cerebral Circulation
• PO2
- Large drop in PO2
(hypoxemia) required for significant increases in blood flow
• PCO2
↑ PCO2 (hypercapnia) →
vasodilation
↓ PCO2 (hypocapnia) → vasoconstriction