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Principles III Anesthesia > Test 1 > Flashcards

Test 1 Flashcards

1
Q

What is the formula for CPP?

A

CPP= DBP-LVEDP

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2
Q

If you have a BP of 95/50, HR 80, and LVEDP of 9….. What is the CPP?

A

50-9= 41mmHg

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3
Q

What ion is responsible for the negative action potential, or phase 4 in the myocardial action potential?

A

K+

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4
Q

Describe what happens in phase 0 of the myocardial action potential.

A

Na+ rushes into the cell causing depolarization.

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5
Q

During phase 1 of the myocardial action potential, K+ and Cl- move out of the cell in response to the inward movement of Na+. What causes the prolonged depolarization in phase 2?

A

Ca+ moving into the cell…. Prolonged the contraction. It is moving out of the sarcoplasmic reticulum.

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6
Q

Does K+ move into or out of the cell during phase 3 of the myocardial action potential?

A

Moves into the cell to repolarize to the negative resting membrane potential.

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7
Q

What drugs increase inotropic effects of the heart by increasing the concentration of Ca++ in myocardial cytosol?

A

Milrinone, digoxin, and epinephrine.

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8
Q

What type of patient is Milrinone typically used for?

A

Heart failure. Increases heart contractility and is a phosphodiasterase 3 inhibitor. Phosphodiasterase breakdown cAMP which contracts the heart.

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9
Q

What effect does Milrinone have on after load?

A

It vasodilates vessels which help to alleviate increased pressures (afterload) on the heart.

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10
Q

What effect does digoxin have on the conduction system of the heart and ultimately chronotropy?

A

Treats pts with afib, aflutter with RVR. Slows conduction in AV node, which increases the refractory period and reduces ventricular rate.

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11
Q

What is the MOA of digoxin?

A

Decreases the Na+ concentration gradient and subsequent Ca+ outflow, which increases Ca+ concentrations in the cells.

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12
Q

What drugs increase the chance of digoxin toxicity due to increased plasma levels?

A

Quinidine, verapamil, and amiodarone

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13
Q

What effect does epinephrine have on the airway and on arterioles?

A

High levels cause smooth muscle relaxation in airways but contraction of smooth muscle that lines most arterioles.

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14
Q

What is the MOA for CCBs and during what phase of the myocardial action potential do they work?

A

Provides negative chronotropic effects on nodal tissue during phase 4 (non-dihydropyrodines) by disrupting movement of calcium through calcium channels.

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15
Q

Non-Dihydropyrodines are used for what purpose?

A

decreases blood pressure and used to decrease HR to prevent cerebral vasospasm. blocks V6CCs in cardiac muscle leading to reduction in muscle contraction. Less contraction of vascular smooth muscle and therefore increase in arterial diameter= vasodilation

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16
Q

What makes up your BP?

A

CO and peripheral vascular resistance

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17
Q

What are beta blockers sometimes used as an adjunct to CCBs?

A

when BP decreases there can be a sympathetic reflex increase in HR and contractility….. which a beta blocker will help control.

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18
Q

What is the allen test and what is it used for?

A

indicative of ulnar artery patency and flow. Have the patient make a fist for 30 seconds, occlude radial and ulnar arteries, open hand (which is now blanched) and release ulnar…. color should return within 7 seconds.

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19
Q

What is clinical presentation of hyperkalemia?

A

peaked T waves; increase in extracellular K+ result in depolarization of membrane potential of cells

20
Q

What is a temporary treatment for hyperkalemia?

A

10-15 units IV insulin, 50ml 50% dextrose… shifts K+ ions into cells

21
Q

An occlusion of right coronary artery may show ischemia in which leads?

A

II, III, aVF

22
Q

What leads will ST segment changes occur if there is an acute anterior wall MI?

A

V3 and V4

23
Q

What is a known risk factor with pulmonary artery catheterization?

A

pulmonary artery rupture

24
Q

What is the effect of HR on coronary blood flow?

A

coronary blood flow is increased with slow HR

25
Q

LVEDP is closely associated with what pressure?

A

pulmonary capillary wedge pressure

26
Q

If no other variables are changed, a reduction in preload will do what to stroke volume?

A

decrease SV

27
Q

What is a normal EF % and how is the number derived?

A

60-65%…. less than 40% indicates severe cardiac disease. It is the blood ejected in each beat divided by end diastolic volume

28
Q

If volume is constant, increase intraventricular pressure causes an ———– in tension of individual cells of ventricular muscle.

A

increase

29
Q

What is the equation for SV?

A

SV=EDV-ESV

30
Q

If MAP increases, what effect does it have on SVR??

A

SVR does not change in response to MAP increase.

31
Q

How do you calculate MAP?

A

(2 x DBP) + SBP/ 3 normal is 70-110 MAP is considered to be perfusion pressure seen by organs

32
Q

What is the calculation for pulse pressure?

A

SP-DP

33
Q

What is LaPlace’s Law as it relates to the vessel?

A

The > the vessel radius, the > the wall tension required to withstand a given internal fluid pressure. The higher the pressure difference, the more tension there will be.

34
Q

What affects stroke volume??

A

venous return controls EDV and thus SV and CO; venous return is dependent on blood volume, venous pressure, vasoconstriction caused by SNS, and pressure drop during inhalation.

35
Q

What is Frank Starling Law as it relates to the heart?

A

> the stretch (preload)= the > contraction

36
Q

What is afterload?

A

it is related to the pressure the ventricle must generate in order to eject blood into the aorta. Changes in afterload affect ability of ventricle to eject blood and thereby alter ESV and SV

37
Q

During a change of rate with depolarization, acetylcholine ______ K+ current and _______ rate of spontaneous depolarization.

A

increases; slows; cardiac myocyte has negative membrane potential at rest. Depolarization rate and duration of action potential in pacemaker cells are affected by ANS activity. AcH binds to Mu 2 receptors and opens K+ channels, this K+ efflux hyperpolarizes the cell, so it takes longer to reach phase 4 threshold.

38
Q

What are the 3 reasons jugular vein cannulation is preferred on the right side??

A

1) dome of right lung and pleura is lower than left 2) straighter line to the atrium 3) the large thoracic duct is not endangered

39
Q

What law talks the relationship b/w LV end diastolic muscle length and LV muscle function?

A

Frank Starling Law

40
Q

What type of patients is SVV NOT useful for?

A

AFIB; stroke volume variance….. % b\w maximal and minimal stroke volumes divided by the average of minimum and maximum over a floating period of 30 seconds; <15 normal

41
Q

How do you calculate SVR?

A

SVR= 80 x (MAP-RAP) divided by CO

42
Q

MAP= 50, HR=90, PA pressure 20/5, CVP=5, PCWP=5, ESV=35, EDV=65. What is SVR?

A

1,333 dyne sec/cm

43
Q

What is the formula for CaO2? CvO2? (content)

A

CaO2= (Hg x 1.36 x SaO2) + (PaO2 x 0.003) normal is 17-20 ml/dl; replaces “a” with “v” for the other formula. normal CvO2 is 12-15 ml/dl

44
Q

What is the CaO2 if Hg=12, SaO2=100%, PaO2=175mmHg?

A

CaO2= (12 x 1.36 x 100) + (175 x 0.003)

45
Q

What is coronary perfusion pressure (CPP)?

A

A part of normal blood pressure that is specifically responsible for coronary blood flow… Important during Cardiac arrest for achieving ROSC.

Principles III Anesthesia (4 decks)

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