Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
55 Cards in this Set
- Front
- Back
Why does blood flow oscillate during muscle contractions? (Why is blood flow low during the actual contraction?)
|
when the muscle is actually contracted, it is compressing the blood vessels = lower blood flow. Then the muscle contraction weakens as it is deprived nutrients/oxygen, opening the vessel more
|
|
What happens to muscle capillaries (normally dormant) during exercise?
|
dormant capillaries open up to reduce the distance oxygen must diffuse to get to muscles
|
|
When muscles are being deprived of oxygen (due to high metabolic rate during exercise), what vasomotor effects can occur?
|
vasodilation by adenosine
|
|
Increased sympathetics can have what effect on blood vessel diameter?
|
vasoconstriction by sympathetics decreases vessel diameter
|
|
Sympathetics have what effect on BP?
|
increase BP by vasoconstriction
|
|
During strenuous exercise, where is norepinephrine/epinephrine released from?
|
postsynaptic sympathetic nerves and adrenal medulla
|
|
Norepinephrine binds which receptors?
|
alpha (vasoconstriction)
|
|
Epinephrine binds which receptors?
|
beta adrenergic (slight vasodilation)
|
|
During exercise, there is an increased sympathetic tone that causes systemic vasoconstriction to increase BP. What parts of the body do not exhibit vasoconstriction?
|
brain, heart have poor vasoconstriction innervation. active muscle actually has local vasodilator effects
|
|
How does blood flow to active muscles increase during exercise?
|
heart rate up, vasoconstriction = high BP, reduced flow to non-mucular areas = more flow/volume to active areas
|
|
How do sympathetics increase venous return during exercise?
|
vasoconstriction = higher systemic filling pressure = higher venous return
|
|
When performing full whole body exercise (swimming) vs. only using a few muscles (hammering), in which situation would a person have a higher BP?
|
Using a few muscles. In both situations, sympathetics will vasoconstrict to increase BP, but the active muscle vessels will vasodilate. With whole body exercise, there is more muscle involved, therefore more vessels vasodilate. If we are just hammering, everything vasoconstricts except the arm muscle vessels that vasodilate (and brain/heart vessels of course)
|
|
What benefits do we get from increased blood pressure during exercise?
|
more force to push blood to muscle; stretch vessel walls to help the local vasodilation in some vessels
|
|
Increase in systemic filling pressure during exercise is caused by what?
|
sympathetic vasoconstriction increasing BP
|
|
The 2 components of cardiac output that increase during exercise are systemic filling pressure and lower venous resistance. Why is there lower venous resistance?
|
vasodilation in the active muscle tissue; but constriction everywhere else to increase the systemic filling pressure
|
|
The anterior left ventricle gets its blood supply from which artery?
|
left coronary
|
|
The posterior left ventricle gets its blood supply from which artery?
|
right coronary
|
|
Most coronary blood returns to the right atrium via which structure?
|
coronary sinus
|
|
Coronary flow is what % of total cardiac output?
|
5%
|
|
Coronary blood flow to the left ventricle is highest during (systole or diastole)?
|
diastole! systole is when the flow is highest almost everywhere else in the body, but since the muscle contraction in the left ventricle compresses the vessels during systole, there is minimal blood FLOW during systole
|
|
As the heart begins pumping faster or more vigorously, what happens to the coronary arteries?
|
local vasodilation to supply the myocardium. oxygen demand regulates the vessel dilation/constriction
|
|
When there is a high oxygen demand by cardiac muscle, why/how does adenosine get released?
|
if there is low oxygen, more ATP is degraded to AMP to release adenosine into the tissue. adenosine is a vasodilator
|
|
What direct effect does norepinephrine have on the coronary blood vessels?
|
causes vasoconstriction (the indirect effect is vasodilation as the myocardium pumps faster and has a higher oxygen requirement)
|
|
What indirect effect does norepinephrine have on the coronary blood vessels?
|
vasodilation as the myocardium pumps faster and has a higher oxygen requirement
|
|
What indirect effect does acetylcholine have on the coronary blood vessels?
|
vasoconstriction indirectly since heart rate is slowed down and there is less oxygen demand for the myocardium (the direct effect is vasodilation as in all other vessels)
|
|
There is more (sympathetic or parasympathetic) innervation to the coronary vessels.
|
sympathetics
|
|
Binding of norepinephrine/epinephrine to Alpha receptors in the coronary vessels lead to ...
|
vasoconstriction
|
|
Binding of norepinephrine/epinephrine to Beta receptors in the coronary vessels lead to ...
|
vasodilation
|
|
Epicardial coronary vessels have more (alpha or beta) receptors?
|
alpha receptors (constrictor) are more likely in epicardial vessels
|
|
Intramuscular coronary vessels have more (alpha or beta) receptors?
|
beta receptors (dilators) are more likely in intramuscular cardial vessels
|
|
What direct effect does norepinephrine have on the coronary blood vessels?
|
causes vasoconstriction (the indirect effect is vasodilation as the myocardium pumps faster and has a higher oxygen requirement)
|
|
What indirect effect does norepinephrine have on the coronary blood vessels?
|
vasodilation as the myocardium pumps faster and has a higher oxygen requirement
|
|
What indirect effect does acetylcholine have on the coronary blood vessels?
|
vasoconstriction indirectly since heart rate is slowed down and there is less oxygen demand for the myocardium (the direct effect is vasodilation as in all other vessels)
|
|
There is more (sympathetic or parasympathetic) innervation to the coronary vessels.
|
sympathetics
|
|
Binding of norepinephrine/epinephrine to Alpha receptors in the coronary vessels lead to ...
|
vasoconstriction
|
|
Binding of norepinephrine/epinephrine to Beta receptors in the coronary vessels lead to ...
|
vasodilation
|
|
Epicardial coronary vessels have more (alpha or beta) receptors?
|
alpha receptors (constrictor) are more likely in epicardial vessels
|
|
Intramuscular coronary vessels have more (alpha or beta) receptors?
|
beta receptors (dilators) are more likely in intramuscular cardial vessels
|
|
Under normal, resting conditions, cardiac muscle uses what for energy instead of carbohydrates?
|
fatty acids
|
|
When the heart is under ischemic conditions, what is the most likely cause of the pain?
|
build up of lactic acid as the myocardial cells resort to glycolysis for ATP (under low oxygen supply during ischemia)
|
|
As a coronary occlusion develops, what live-saving mechanism occurs in the coronary circulation?
|
small anastomoses dilate and develop to prevent ischemia
|
|
What is a myocardial infarction?
|
the cardiac muscle has such little blood flow that it cannot function
|
|
Why does infarcted myocardium appear blue?
|
extreme vasodilation= stagnant blood. since it is stagnant, it is fully deoxygenated as the ischemic myocardium is using all the oxygen from what little blood is available
|
|
Which area is most likely to first be affected by myocardial infarction? (subendocardial or epicardial vessels)
|
subendocardial vessels are first affected by ischemia since they are almost completely compressed (no blood flow) during systole anyways. This gives the vessels even less time to perfuse the area
|
|
What is systolic stretch?
|
after an infarct or ischemia, myocardium loses contractility and is forced outward during systole instead of contracting. this dissipates the contractile force of the entire ventricle
|
|
After myocardial infarction, why does venous blood dam in the veins?
|
MI = low cardiac output = lower pressure in renal arteries = less fluid removed from system = more fluid retention = congestion in veins (potential pulmonary edema)
|
|
Why is ventricular fibrillation common after infarction? 4 reasons
|
high extracellular potassium, injury current, high sympathetics, dilated ventricle (longer conduction time)
|
|
Why can an injured area rupture after infarction?
|
systolic stretch (bulging of weak/non-contracting myocardium during systole) gets more and more intense
|
|
What is cardiac tamponade?
|
collecting of blood in the pericardium instead of the right atrium (now decreased cardiac output and compression of heart)
|
|
Within a few months after an infarction, why is cardiac output an function back to normal even if some myocardial cells have died?
|
remaining cells hypertrophy to compensate
|
|
After an infarction, why do we want a patient to have bed rest?
|
if the patient is active, they will vasodilate the main coronary vessels. after an infarction, the patient is relying on the collateral circulation. vasodilation of the main coronaries will take blood away from these essential anastomoses
|
|
What is "coronary steal syndrome"?
|
after an infarct, if a patient is overly active, their coronary vessels will dilate. this pulls blood away from anastomoses that are essential after an infarct
|
|
What is angina pectoris?
|
chest pain on exertion due to coronary constriction
|
|
Why does nitroglycerin help angina?
|
vasodilator (becomes nitric oxide)
|
|
What class of drug is propanolol? How does it work?
|
Beta-blocker; blocks sympathetic beta adrenergic receptors = prevents excitement of the heart = keeps oxygen demand low for the heart
|