Flashcards in Lecture 21 - Special Circulations 1 Deck (48):
What causes the 3rd heart sound? 4th Heart Sound?
3rd = TURBULENT FLOW due to rapid filling of the ventricle
4th = trial systole
What is the DETERMINANT of blood flow? The regulator of flow?
Determinant = AORTIC PRESSURE
REGULATOR = Metabolic Activity
Ex; in vtachy the BP begins to drop so the heart is not perfused with blood (not enough flow)
What regulates coronary blood flow? (1 major, 2nd follows)
& changes in arterial resistance
Which ventricle is most influenced by TISSUE PRESSURE? When is the tissue pressure HIGHEST in this ventricle? What occurs to flow during this period?
1. LEFT VENTRICLE
2. Early Systole
3. Flow may actually reverse
When is maximal left coronary flow?
During EARLY DIASTOLE
- when pressure falls to ZERO
(the lateral end pressure is too low during early SYSTOLE, thus coronaries have less flow)
What would happen to coronary flow in the Left Ventricle if diastolic pressure falls below 50mmHg (as in hemorrhage, hypovolemic shock, etc)?
FLOW DECREASED SIGNIFICANTLY
= Left Ventricle becomes ischemic
(right ventricle does not generate a lot of pressure since it has less resistance from pulmonary system --> allows perfusion during both systole & diastole)
What area of the heart has the greatest pressure during diastole? Least?
What significance is this in terms of compression of vessels, under abnormal conditions?
GREATEST = ENDOCARDIUM
LEAST = EPICARDIUM
ENDOCARDIUM IS MOST COMPRESSED & thus most risk of ISCHEMIA & infarction
How is blood flow equal in the endocardium & epicardium if the endocardial vessels are more compressed during diastole?
ENDOCARDIUM compensates by INCREASING VASODILATION in resistance vessels
What abnormal conditions in the heart can generate subendocardial ischemia? How?
GREATER ENDOCARDIAL TISSUE PRESSURE
= reduced coronary blood flow due to greater after load
1. Aortic Stenosis
3. CHF (diastolic pressure is elevated)
If subendocardial ischemia occurred, how would the S-T segment change?
S-T segment would be depressed
- vector produced
If after load is increased (as in aortic stenosis, regurgiation, and CHF) what pressure & volume are increased as a result?
End-DIASTOLIC PRESSURE & End Diastolic VOLUME
- more blood left behind
- endocardium becomes ischemic due to lack of flow
If diastolic pressure falls (as in hypotension & shock), how is endocardial flow affected?
FLOW IS MORE RESTRICTED (than epicardium)
= greater risk for ischemia
What are the following affects on Coronary blood flow:
1. Sympathetic Alpha 1 stimulation
2. B-1 receptors on pacemaker cells
3. B-2 Adrenergic receptors
4. Heart rate maintained constant, what affect is induced (if metabolism constant)
1. Weak Vasoconstriction
2. Beta 1 causes an increase in Contractility & HR, which temporarily decreases flow to certain areas & indirectly increases METABOLIC ACTIVITy
= VASODILATION via B-1
3. B-2 = coronary VASODILATION (but less sensitive to NE stimulation)
4. VAGAL stimulation = vasodilation
What is the function of atropine?
Blocking vagal coronary vasodilation
- suggest acetylcholine effect mediated via release of NO
How does Beta 1 act on pacemaker cells & myocardium? What is the indirect affect on coronaries?
1. Beta 1 - increases HR and contractility (increases after load)
2. Increases metabolic activity and causes VASODILATION
What is the major factor in REGULATION of coronary blood flow? How is this related to flow? (linear/hyperbolic etc)
- FLOW LINEARLY related to METABOLIC activity
What are the major metabolic substrates in the heart? Why does this make the heart a large consumer of O2?
- needs a lot of O2 to break down fatty acids
What limits O2 supply
- O2 consumption increases, flow must increase as well (or ischemia results)
What is different in skeletal & cardiac muscle in terms of O2?
Heart cannot extract more oxygen like skeletal muscle
- if it needs more O2 it increases FLOW (vasodilation)
What is cardiac work?
What can be approximated by Cardiac Work?
Which type of work consumes more O2: pressure or volume work?
1. Cardiac Work = Mean Arterial Pressure x Systolic Stroke VOlume
2. OXYGEN CONSUMPTION
3. PRESSURE work consumes more oxygen (ex: hypertension/aortic stenosis - any after load)
- need to overcome large isometric force to open aortic valve
What are the 3 components that are ALWAYS involved in Oxygen DEMAND?
What is the equation for myocardial oxygen SUPPLY?
What are the 2 main determinants of supply?
Myocardial blood flow X arterial oxygen content
1. Diastolic Perfusion Pressure (pressure perfusing the coronaries)
2. Coronary Vascular Resistance
What is external compression & intrinsic regulation of Coronary Vascular Resistance?
1. External compression = strong contraction of LV will squeeze coronaries (more difficult to get O2 & flow)
- local metabolites
- endothelial factors
What is the function of beta blockers?
DOWN!!! = decrease oxygen consumption (demand)
- this way, the limited supply can meet the demand
TRUE OR FALSE: Excessive O2 demand is a primary cause of ischemia?
- excessive O2 is not the primary cause EVER
What does ischemia result from?
- ischemia results from an imbalance between oxygen supply & demand
= RELATIVE lack of flow
When can COLLATERAL vessels begin to grow enough to restore adequate blood supply?
during GRADUAL obstruction of coronary artery
(collateral vessels are insufficient for SUDDEN infarction)
What is the concept of CORONARY STEAL? (important)
DURING exercise: increase in flow to one region of the heart can cause a decrease in flow to the ischemic region
-exercise/vasodilation agent, the normal region vasodilates. The ischemic region is already maximally dilated,...
- thus the normal region has a lower arterial resistance and MORE BLOOD FLOW --> "steals" flow from the ischemic region creating even MORE ISCHEMIA in the damaged area
If there is an arterosclreotic plaque, under which conditions does Coronary Steal begin?
- under resting conditions, the normal region has normal arteriolar resistance & is vasoconstricted
(this is reversed during exercise = vasodilation)
What are the following clinical manifestations of?
1. Exercise Induced Ischemia
2. Stress- Testing w/ Adenosine
3. Peripheral Arterial Disease
- exercise = changes in BP
Stress test w/ adenosine = vasodilation (see on EKG if heart is becoming more stressed/ischemic)
What is Peripheral Arterial Disease? What is this due to?
Claudication—pain, weakness, numbness, or cramping in muscles when walking or using the affected muscles that is relieved by resting those muscles.
This is due to the increased oxygen demand in muscles with use in the setting of inadequate blood flow.
TX: bypass th block (temp)
- ppl w/ coronary disease usually have PAD (and vice versa)
20% of cardiac output goes where? Why?
- about 40% of body mass
Blood flow to skeletal muscle is low under resting state conditions. True or False?
- How does this change with exercise?
- with exercise, flow can increase 20 times
Depends on the type of muscle:
tonic (back muscles)= more flow
phasic (biceps) = less flow
Exercising changes which pressure? Systolic or Diastolic? Why?
- skeletal muscle flow is very low under resting conditions
- exercise keeps diastolic pressure LOW (vasodilates)
- exercise decreases TPR & increases compliance of vessels
How is Metabolic Control exerted in Skeletal Muscle?
Because skeletal muscle has a large flow reserve during rest, how does this affect vascular tone?
What dominates vascular tone during resting state of skeletal muscle?
1. ACTIVE HYPEREMIA
- increased blood flow to metabolically active tissues
2. INCREASED vascular tone (mix of constriction & dilation)
3. VASOCONSTRICTOR influences
-during muscle contraction --> vasodilators to increase O2 delivery
What are the 3 mechanical factors that influence skeletal muscle contraction?
1. Arterial circulation
2. Venous Circulation
3. Neurohormonal Control
Although sympathetic activity is increased during exercise, what happens to vascular resistance in metabolically active tissue?
What alternates during exercise (in terms of arterial circulation)?
Extravascular Compression (via tissue pressure)
(increases w/ metabolic regulation)
When isometric tensions reach 70 or higher, what happens to blood flow?
- cannot be sustained long since vascular resistance INCREASES & cardiac output rises,
= increase in arterial pressure
What are the 3 important mechanisms regulation Venous Circulation?
1. Muscle COntraction "pumps
- assisted by Valves w/ unidirectional flow
2. Respiratory Pump
inspiration = negative pressure in thorax, positive in abdomen
= thoracic veins distended & abdominal compressed
= INCREASED VENOUS RETURN
3. Sympathetic VENOCONSTRICTION
How does expiration affect venous return?
DECREASES venous return
- increases thoracic pressure & decreases abdominal
- thoracic vessels collapse & abdominal vessels distend
What is the affect of sympathetic venoconstriction on venous return? (how is capacitance changed)
- increased return by REDUCING venous capacitance
What is the primary neurohumoral control of skeletal muscle?
What is the function of the following & which receptors do they act on, and when are they elicited:
2. Sympathetic Cholinergics
1. NE - alpha 1 receptor = vasoconstriction
2. S. Cholinergics - muscarinic receptors on endothelial cells = NO & VASODILATION
*Activated during exercise
low = vasodilation; Beta 2
High = vasoconstriction; alpha 1
What are the changes elicited in vascular tone under Low & High concentrations of epinephrine? What receptors are activated in these cases?
Low = VASODILATION
- via Beta -2
HIGH = Vasoconstriction
- via Alpha 1
What are two sympathetic mechanisms that increase flow in skeletal muscle?
1. Sympathetic Cholinergics
2. Shear stress causing No release w/ increase to flow to further vasodilate
What is the affect of administering an alpha antagonist? (vasoconstriction or vasodilation) Is this passive or active?