Cardiac physiology

Question 1

What are inward rectifier channels?

Answer 1

VR K channels, K leaves; cardiac contractile cells

Question 2

What causes the plateau in a cardiac contractile AP graph?

Answer 2

Slow open of VR Ca++ channels. Inward rectifier K channels CLOSE. Puts repolarization on pause. At the end, they are closed and inactivated.

Question 3

Drop down of repolarization is caused by?

Answer 3

delayed rectifier cells (2nd population) and re-opening of inward rectifier (1st population)

Question 4

What protects from cardiac tetany?

Answer 4

Contraction and relaxation is almost completely encompassed by the plateau of the AP wave, inactivated until relaxation is almost over

Question 5

Increase of Ca++ into cell does what?

Answer 5

Increase the strength of contraction?

Question 6

PSNS and SNS affect what part of the conductive system of the heart?

Answer 6

The pre-potential, how long it takes to reach threshold

also under the influence of funny circuit channels

Question 7

The autonomic innervation of the heart, do Beta 1s affect the pre-potential?

Answer 7

probably not, since they are located at the myocardium. The mechanism of pre-potential occurs at the conductive cells. M2 receptors slow HR, but have no real effect on stroke volume. That is because they work at the level of timing in the intrinsic conductive cell, not contractile cell dealing with Ca++ entry (beta 1)

Question 8

What three issues can be addressed by an EKG?

Answer 8

conduction pathway abnormal?
heart enlarged?
region of myocardial damage?

Question 9

larger P waves than normal

Answer 9

more deflection or more period of time from start to end of P wave

Question 10

enlarged R wave

Answer 10

enlarged ventricles

Question 11

enlarged Q

Answer 11

MI, heart attack

Question 12

flattened T wave

Answer 12

ventricles not getting enough O2, coronary artery ischemia

Question 13

baseline is depressed

Answer 13

indicative of ischemia

Question 14

P–QR segment longer

Answer 14

myocardial damage to atrial tissue

Question 15

baseline raised

Answer 15

MI, heart attack

Question 16

S–T too long

Answer 16

damage to conduction system in heart/ventricles

Question 17

What is a pathological example of bradycardia?

Answer 17

arteriosclerosis in the carotid arteries, the baroreceptors here think the pressure is too high so they tell medulla oblongata to decrease HR

Question 18

Chemical metabolic signals occur at capillary beds. What intrinsic control would low O2, hi H+, HI CO2, and hi K+ initiate?

Answer 18

stimulate endothelial cells at capillary wall to release NO, a vasodilator that increases blood flow (turns on the tap)

Question 19

Chemical metabolic signals occur at capillary beds. Whta intrinsic control would low CO2,hi O2, low H+, and low K+ initiate?

Answer 19

endothelial cells would produce endothelians - vasoconstrictors that decrease BF

Question 20

On the arterial side of a capillary bed, there is a net +10 mmHg out. On the venous side, there is a net -8mmHg in. What accounts for the remaining 2 mmHg?

Answer 20

Lymphatics

On arterial side, hydrostatic pressure is predominant. On venous side, osmotic gradient is predominant.

Question 21

What is a pathology associated with losing osmotic pressure?

Answer 21

protein deficiency - bloated bellies and starvation

Question 22

What is the patholgy of elephantiasis?

Answer 22

lymph ducts are blocked, and the seeping plasma fluid is not recollected and remains in the interstitium

Question 23

What are the known causes of secondary hypertension?

Answer 23

Renal hypertension

Pheochromocytoma

Question 24

Renal hypertension

Answer 24

atherosclerosis of renal artery decreases blood flow, and therefore decreases the blood pressure AT the nephron. The granular cells/juxtaglomerular cells, which are specialized smooth muscle cells around the afferent arteriole, secrete renin. Renin then, in turn, activates angiotensin II, which is a powerful systemic vasoconstrictor. High blood pressure ensues.

Question 25

Pheochromocytoma

Answer 25

chromaffin cells that make up the adrenal medulla, tumor of the adrenal medulla produce an xs of Epinephrine which increases Cardiac output and therefore blood pressure

Question 26

What are the pharmacological steps taken to reduce HBP?

Answer 26

1. Diuretics, decrease blood volume 2. Start a Beta blocker, tenormin/lopressor (beta 1 specific nd do not block the vasodilation of coronary arteries) 3. ACE inhibitors - blocks formation of angiotensin II, VASOTECH, ZESTRIL OR Angiotensis receptor blocker, COZAAR, DIOVAN 4. Ca++ channel blockers - prevent entry of Ca++ from the glycocalyx, decrease the strength of contraction, PROCARIDA, CARDIZEM, NORVASC 5. alpha 1 blocker, this is last resort because you could lower BP too much and cause shock

Question 27

afterload

Answer 27

back pressure exerted by arterial BP, what keeps the semilunar valves closed

Question 28

When would you give a pateint digitalis/digoxin?

Answer 28

congestive heart failure

Question 29

What is digitalis/digoxin mechanism of action?

Answer 29

shuts down Na+/K+ pumps, so that a Na gradient is not set up across the membrane. Without the gradient, Ca++ stays inside the myocardial contractile cell. This is because Ca++ usually leaves the cell via antiport with Na.