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Cardiac > Apex- Cardiac Pathyophys > Flashcards

Apex- Cardiac Pathyophys Flashcards

1
Q

Which surgical procedure presents the HIGHEST risk of CV morbidity and mortality for the patient with CAD?

A. ORIF femur fracture
B. VATS
C. Open AAA repair
D. Carotid endarterectomy

A

C.

High risk procedures = emergency surgery (esp in elderly), open aortic surgery, peripheral vascular surgery, long surgical procedures with significant volume shifts and/or blood loss

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2
Q

If a patient had a recent MI, the risk of re-infarction is greatest within ________ days/weeks of the orginal event

A

30 days

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3
Q

How long should elective surgery be delayed for after an MI?

A

4-6 weeks

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4
Q

5 patient risk factors that increase risk for cardiac event during surgery

which one confers the greatest risk of periop MI?

A
  • ischemic heart disease
  • CHF
  • cerebrovascular disease
  • DM
  • Creat > 2mg/dL

unstable angina = greatest risk

unstable angina → new-onset angina (<2 months), increasings sx (intensity, freq, duration), duration exceeding 30 minutes, sx responding less to medical therapy

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5
Q

Risk of perioperative MI in the general population is ~ ____ %

A

0.3%

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6
Q

If the patient has ahd a previous MI, than the perioperative risk of reinfarction is:
- if > 6 months ago →
- if 3-6 months ago →
- if < 3 months ago →

A
  • if > 6 months ago → 6 %
  • if 3-6 months ago → 15%
  • if < 3 months ago → 30%

remember as <3 months ago = 30%, then half it, and half it again

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7
Q

NYHA heart failure classification for someone with symptoms with less than normal activity but no symptoms at rest

A

3

compared to sx with normal activity + no sx at rest = 2

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8
Q

Which NYHA heart failure classification requires referral to a cardiologist prior to GA

A

Class 3 - symptoms with less than normal activity (none at rest)

or

Class 4 - symptoms with minimal activity or even at rest

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9
Q

T/F- NYHA heartfailure class 4 patients to undergo MAC anesthesia can proceed without a cardiac referrel as long as the preoperative evaluation reveals stable cardiac disease

A

True

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10
Q

When should a patient be referred to a cardiologist before surgery?

A

NYHA classification of 3 or 4 who is scheduled for high- or intermediate-risk surgery

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11
Q

factors that reduce myocardial o2 supply (4)

A
  1. tachycardia
  2. hypoxemia
  3. anemia
  4. left shift in oxyhemoglobin curve
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12
Q

Factors that increase myocardial o2 demand (7)

A

SNS stimulation : increased HR and BP
Increased preload/wall tension
Increased afterload
Increased contractility

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13
Q

Myocardial injury and infarction injure the sarcolemma. Disruption of the sarcolemma allows for what to happen?

A

intracellular proteins (CK-MB, troponin-I, tropinin-T) to enter systemic circulation

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14
Q

What lead is best for monitoring dysrhythmias?

A

Lead II

it also can identify inferior wall ischemia (II = inferior ischemia)

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15
Q

Most MIs occur within ______ hours after surgery

A

48

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16
Q

Treatment of intraoperative myocardial ischemia should focus on itnerventions that do what?

A

make the heart slower, smaller, and better perfused

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17
Q

Which leads are best for detecting LV ischemia intraoperatively?

AKA: ST changes

A

V3, V4, V5

*classic teaching says V5 is best (anterior axillary line 5th ICS)
*newer data says V3 & V4 may be superior to V5
*if need to choose- choose V4 - midclavicular line 5th ICS

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18
Q

The combination of what 3 leads has an ischemic detection rate of up to 96%?

A

II, V4, V5

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19
Q

Do most MI’s occur intraop or postop?

A

postop - within 48 hrs of surgery

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20
Q
A

Myocardial ischemia & advanced age

Curve A demonstrates a greater rise in pressure at a given volume → decreased compliance → myocardial ischemia and advanced age

Curve C demonstrates increased compliance → aortic insuffiency and dilated cardiomyopathy

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21
Q

If the patient has diastolic dysfunction, CVP and PAOP will (overestimate/underestimate ventricular filling pressures)

A

overestimate

pts with diastolic dysfuction require higher filling pressures to prime the ventricle

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22
Q

What describes the ventricular filling pressure that results from a given end-diastolic volume?

A

Diastolic compliance

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23
Q

Decreased diastolic compliance shifts the curve (up/down) and (left/right)

What does t his mean?

A

up and left

Theres a higher end diastolic PRESSURE for a given volume

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24
Q

Increased diastolic compliance shifts the curve (up/down) and (left/right)

what does this mean?

A

down and right

there is a LOWER end-diastolic PRESSURE for a given EDV

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25
Q

What do elevated filling pressures put patients at a higher risk for?

A

Pulmonary edema

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26
Q

What are 2 conditions that dilate the heart and cause increased diastolic compliance (lower pressure for a given volume)

A

Dilated cardiomyopathy
Chronic aortic insufficency

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27
Q

What are PAOP and CVP indirect measurements of?

A

Volume

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28
Q

Identify a compensatory mechanism in the patient with CHF:

A. decreased brain natriuretic peptide
B. Decreased LVEDP
C. Increased renal blood flow
D. Increased sympathetic tone

A

D. Increased sympathetic tone

To maintain BP, pts with CHF rely on elevated levels of circulating catecholamines (increased SNS tone)
*anesthetic techniques that reduce SNS tone can preceiptate CV collapse - ex) a standard propofol induction dose is not a good idea bc it decreases SNS tone while simultaneously reducing myocardial contractility. Propofol should be slowly titrated at a much lower dose

CHF reduces renal blood flow which is the primary mechanism that activates RAAS
Atrial dilation from CHF increases release of natriuretic peptides

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29
Q

Identify a compensatory mechanism in the patient with CHF:

A. decreased brain natriuretic peptide
B. Decreased LVEDP
C. Increased renal blood flow
D. Increased sympathetic tone

A

D. Increased sympathetic tone

To maintain BP, pts with CHF rely on elevated levels of circulating catecholamines (increased SNS tone)
*anesthetic techniques that reduce SNS tone can preceiptate CV collapse - ex) a standard propofol induction dose is not a good idea bc it decreases SNS tone while simultaneously reducing myocardial contractility. Propofol should be slowly titrated at a much lower dose

CHF reduces renal blood flow which is the primary mechanism that activates RAAS
Atrial dilation from CHF increases release of natriuretic peptides

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30
Q

Most common cause of right heart failure

A

left heart failure

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31
Q

3 ways to treat RV failure

A
  1. Reverse causes of increased PVR (hypoxia, hypothermia, hypercarbia, acidosis, high PEEP, nitrous oxide)
  2. Inotropes → milrinone, dobutamine
  3. Pulmonary vasodilators → inhaled nitric oxide or sildenafil (PDE-5 inhibitor)
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32
Q

Pathophysiolgoic complications r/t chronic systemic HTN include all of the following EXCEPT:

A. LVH
B. increased myocardial o2 concsumption
C. dysrhythmias
D. Decreased diastolic filling time

A

D. Decreased diastolic filling time

diastolic filling time is determined by the HR, not BP

Systemic HTN increases afterload. The LV must generate a higher amount of wall tension to open the aortic valve → to compensate for this increased afterload: heart undergoes concentric hypertrophy → increased MVO2 → thicker heart = reduced compliance = diastolic dysfunction (decreased lusitropy)

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33
Q

T/F- systemic HTN is almost always caused by an increased SVR

A

True

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34
Q

SBP &/OR DBP ranges for
Normal, Elevated, Stage 1, 2, and 3 HTN

A

Normal → <120 & <80
Elevated → 120-129 & <80
Stage 1 HTN → 130-139 or 80-89
Stage 2 HTN → > 140 or > 90
Stage 3 HTN → >180 and/or >120

Stage 3 HTN = hypertensive crisis

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35
Q

primary vs secondary HTN

A

primary → no identifiable cause (95%)
secondary → + identifiable cause (5%)

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36
Q

Normal cerebral autoregulation occurs at a CPP between what and what?

A

CPP 50-150

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37
Q

Why is it important to adequately hydrate the chronically hypertensive patient prior to anesthetic induction?

A

Bc hypertensive patients are volume contracted (even more so if they are on a diuretic)

→ agents that cause myocardial depression and vasodilation will unmask a volume contracted state and these patients will have an exaggerated hypotensive response to anesthetic induction

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38
Q

why shouldn’t a betablocker be started on the day of surgery in a patient who is normally not on a betablocker?

A

Studies have shown it increases the risk of hypotension, vradycardia, stroke, and death.

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39
Q

Why shouldnt peeps take their ACE/ARBs prior to surgery?

A

It can produce vasoplegia under anesthesia

*refractory hypotension

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40
Q

ACEi/ARB induced vasoplegia that is unresponsvie to conventional first-line therapies (vasopressors and fluids) should be treated with what? (3)

A
  1. vasopressin
  2. terlipressin
  3. methylene blue (nitric oxide antagonist)
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41
Q

How does methylene blue tx refractory hypotension?

A

it inhibits nitric oxide (substance released from the lining of the vessels that results in vasodilation)

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42
Q

@ what systolic/diastolic BP should elective surgery be delayed in favor of optimization?

A

SBP > 180
DBP > 110

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43
Q

Measuring the BP on the arm (or worse the leg) in the patient in the sitting position will (over/under)estimate the BP in the brain

A

overestimate (the brain BP is lower)

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44
Q

HTN crisis occurs wehn the BP exceeds what?

When is it deemed a hypertensive EMERGENCY?

A

180/120

when there is evidence of end-organ damage (otherwise its called HTN urgency)
CNS: encephalopathy, stroke, papilledema
Cardiac: CHF
Renal: HTN-induced acute renal dysfunction

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45
Q

What is the MOST common cause of secondary HTN?
A. PIH
B. Coarctation of the aorta
C. Renal Artery Stenosis
D. Cigarette Smoking

A

C. Renal artery stenosis

A narrowed renal artery (atherosclerosis or fibromuscular dysplasia) reduces renal blood flow. In attempt to increase GFR, the kidenys activate the RAAS system

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46
Q

What is the definitive treatment of renal artery stenosis?

What shouldn’t these patients be give if B/L stenosis and why

A

renal artery endarterectomy or nephrectomy

No ACE inhibitors bc they can significantly reduce GFR and preciptate renal failure in pts with B/L renal artery stenosis

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47
Q

Match the HTN drug it its drug class
Drugs: perindopril, terazosin, eprosartan, nisoldipine

A

perindopril → ACE
terazosin → alpha blocker
eprosartan → ARB
Nisoldipine → CCB

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48
Q

Drug that reduces afterload, preload, vs preload and afterload

A

hydralazine → afterload reduction
nitroglycerine → preload reduction
Sodium nitroprusside → preload and afterload reduction

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49
Q

What 3 things can be targeted to reduce blood pressure?

A

ANS → alpha/beta blockers
Myocardium and VSM → CCBs, arteriodilators, venodilators
Kidney → ACEi’s, ARBs, loop diuretics, thiazide diuretics, K sparing diuretics, aldosterone antagonists

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50
Q

suffix “-zosin”
drug class, how they reduce BP

what other 2 drugs fall in this class that dont end in zosin?

A

Alpha-1 antagonists
→decrease intravascular calcium → vasodilation → decreased SVR (afterload)

Phenoxybenzamine (long acting, non-competitive, selective); phentolamine (short acting, competitive, non-selective)

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51
Q

Selective B1 antagonists and how do they reduce BP

A

MABE AB
Metoprolol, Atenolol, Bisprolol, Esmolol, Acebutolol, Bextolol
→reduction in: inotropy, chronotropy, dromotropy, & renin release from juxtaglomelular aparatus

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52
Q

non-selective beta blockers

A

TPPNS
Timolol, Pindolol, Propanolol, Nadolol, Sotalol

*in addition to beta 1 effects, beta 2 blockade results in vasoconstriction in the muscle (not as profound decrease in BP)

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53
Q

Alpha-2 agonists - 2 most common and how do they reduce blood pressure

A

precedex and clonidine
-reduce sympathetic outflow

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54
Q

-“ipine” - what drug class, what do they target, and how do they reduce BP

A

CCBs - dihydropyridinines
→ target vasculature → decreases intravascular calcium → vasodilation → decreased SVR (Afterload)

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55
Q

What CCBs are the non-dihydropyridines , what classes are they, and how do they work?

Which produces more myocardial depression?

specific uses for each

A

Diltazem (Benzothiazepine)
Verapamil (Phenylalkamine)

→targets mycoardium > vessels
→ reduces: inotropy, chornotropy, dromotropy, SVR (afterload)

verapamil (dont use if on beta blockers > can result in CHB)

verapamil - angina, MI, SVT (afib/flutter)
diltazem - chronic HTN, arrhythmia protection (afib/flutter)

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56
Q

How do loop diuretics work?

3 examples

A

inhibit NA-K-2Cl transporter in the thick ascending loop of henle

→diuresis → reduced venous return (preload)

fureosemide, bumetanide, ethracrynic acid

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57
Q

4 Thiazide diuretics (mneumonic), how do they combat HTN

A

MICH
Metolazone, Indapamide, Chlorthialidone, HCTZ

inhibits the NA-Cl transporter in the DCT
→diuresis → reduced venous return (decreased preload)

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58
Q

K+ sparing diuretics vs Aldosterone antagonists
-examples of each, where do they work

A

K sparing = Triameterene & amloride
Aldosterone antagonists = Spironolactone

they inhibit K+ excretion and NA reabsorption by the principle cells in the collecting ducts

→ K sparing diruetics work indepdently of aldosterone
→ aldosteron antagonists also block aldosterone at mineralcorticoid receptors

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59
Q

A patient with a hx of CAD with an EF of 35% develops AFIB with RVR. Which is the BEST treatment for this patient
A. Verapamil
B. Diltaizem
C. Nifedipine
D. Nicardipine

A

B. Diltaizem

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60
Q

Rank the order in which the following CCBs impair contractility from most to least
→ nifedipine, verapamil, nicardipine, diltazem

A

Verapamil → nifedipine → diltazem → nicardipine

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61
Q

What is the only CCB proven to reduce the M&M from cerebral vasospasm?

A

Nimodipine

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62
Q

What are the 3 types of voltage-gated calcium channels; which ones do all clinically used CCBs bind to and what happens?

A

L type = long-lasting or slow channel
N type = neural
T type = transient

*CCBs bind to the alpha-1 subnit of the L-type calcium channel
→ this prevents calcium from entering the cardiac and VSM cells

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63
Q

Which CCB is useful as a coronary antispasmodic?

A

Nicardipine

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64
Q

MOA of clevidipine

A

Arterial vasodilator → reduces SVR without affecting preload

lipid emulsion (EDTA preservative)

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65
Q

How is clevidipine metabolized?

A

by tissue and plasma esterases

1/2 life = 1 minute (full recovery 5-15 mins after stopping gtt)

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66
Q

Identify the anesthetic considerations for constrictive pericarditis (select 2):
- kussmaul’s sign is usually present
- it is mot commonly caused by a virus
- afterload should be reduced
- bradycardia should be avoided

A

Kussmaul’s sign is usually present
Bradycardia should be avoided

→constrictive pericarditis limits the hearts ability to move within the pericardial sac → decreased myocardial compliance and limits diastolic filling

acute pericarditis (not constrictive) is usually caused by a virus

Kussmauls sign is a paradoxical rise in CVP and JVD during inspiration resulting from RV filling defect (impared RV compliance)
→ since stroke volume is reduced, the cardiac output is HR dependent ( avoid bradycardia)
→ BP = CO x SVR → if CO is limited, the BP must be maintained by SVR → DO NOT REDUCE AFTERLOAD

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67
Q

Identify the anesthetic considerations for constrictive pericarditis (select 2):
- kussmaul’s sign is usually present
- it is mot commonly caused by a virus
- afterload should be reduced
- bradycardia should be avoided

A

Kussmaul’s sign is usually present
Bradycardia should be avoided

→constrictive pericarditis limits the hearts ability to move within the pericardial sac → decreased myocardial compliance and limits diastolic filling

acute pericarditis (not constrictive) is usually caused by a virus

Kussmauls sign is a paradoxical rise in CVP and JVD during inspiration resulting from RV filling defect (impared RV compliance)
→ since stroke volume is reduced, the cardiac output is HR dependent ( avoid bradycardia)
→ BP = CO x SVR → if CO is limited, the BP must be maintained by SVR → DO NOT REDUCE AFTERLOAD

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68
Q

T/F- constrictive pericarditis is usually caused by a virus

A

False- Acute pericarditis is usually caused by a virus

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69
Q

3 conditions that affect the pericardium and limit the hearts ability to move within the pericardial sac

A
  1. acute pericarditis
  2. constrictive pericarditis
  3. cardaic tamponade
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70
Q

Acute vs constrictive pericarditis

A

Acute is usually caused by a viral infection/inflammation. It doesn’t reduce diastolic filling unless the inflammation leads to constrictive pericarditis or cardiac tamponade.

→constrictive pericarditis is caused by fibrosis or any condition where the pericardium becomes thicker. it leads to reduced diastrolic filling.

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71
Q

treatment for constrictive pericarditis

A

pericardiotomy

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72
Q

3 main anesthetic considerations for constrictive pericarditis

A
  1. avoid bradycardia → since SV is reduced, CO is dependent on HR (CO= HR x SV)
  2. preserve contractility
    → ketamine, etomidate, benzos, opioids, pancuronium
    → volatile agents with caution
  3. maintain afterload

*Aggressive PPV can decrease venous return and CO

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73
Q

The pericardium is composed of ____ layers that are seperated by _______mls of clear fluid

A

2 layers:
Visceral layer → attached to myocardium
Parietal layer → anchored in the mediastinum

Seperated by 10-50mls of clear fluid

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74
Q

What is Kussmauls sign

& what does it indicate

A

an increase in CVP and JVD during inspiration

due to RV filling defect (impared RV complianc)
→constrictive pericarditis

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75
Q

What is pulsus paradoxus

& what is it indicative of?

A

Decreased SBP > 10mmHg during inspiration

indicative of impaired diastolic filling

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76
Q

What presents as ST elevation with normal enzymes

what else would be present

A

acute pericarditis

Acute CP with pleural component → increased CP with inspiration and postural change; releaved by leaning forward or supine
*Pericardial friction rub
*Fever

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77
Q

Treatment of acute pericarditis

A

usually resolves spontaneously

Drugs to relieve pain → salicylates, oral analgesics, corticosteroids

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78
Q

Why is it important to maintain spontaneous ventilation as long as possible for someone with constrictive pericarditis/tamponade

A

bc spontaneous respirations = negative pressure inside chest wall to draw in air → also helps blood flow more easily into the RA and supply preload

once positive pressure ventilation takes place- you lose that preload and CO

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79
Q

Is dressler’s syndrome associated with constrictive or acute pericarditis

A

acute

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80
Q

What are the 3 components of Becks triad

what do they indicate

A

Muffled heart tones, JVD, hypotension

→pericardial temponade occurs when the pericardium fills with fluid → this restricts the hearts movement and impairs its ability to function as a pump

*fluid accumulation in the pericardial sac → muffled heart tones
*decreased venous return to the heart → JVD
* decreased SV → hypotension

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81
Q

What is a pericardial effusion

A

accumulation of fluid inside the pericardial sac

it’s not an emergency and seldum requires intervention

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82
Q

Clinical presentation of cardiac tamponade (4):

A
  1. Becks triad:
    → muffled heart tones from fluid accumulation in the pericardial sac
    → JVD from decreased venous return to the right heart
    → hypotension from decreased stroke volume
  2. Pulsus paradoxus
    → decrease in SBP > 10mmHg during inspiration d/t impaired diastolic filling
  3. Kussmaul’s sign
    → paradoxical increase in CVP and JVD during inspiration d/t impaired RV compliance (impaired filling)
  4. Reduced EKG voltage (from fluid in the pericardial sac impeding transmission of signals)
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83
Q

How do CVP, PAOP coincide with

A

CVP = right cardiac diastolic filling pressure?
PAOP = left cardiac disastolic filling pressure?

i think, idk maybe

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84
Q

Describe the pressure-volume loop of cardiac tamponade

A

Left shift → from decreased LV EDV
Narrower loop → from decreased stroke volume
Higher/steeper slope during ventricular filling → decreased ventricular compliance

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85
Q

What is this and why does it happen

A

Pulsus paradoxus → decrease in SBP by >10mmHg during inspiration

*negative intrathroacic presssure on inspriation → increased venous return to the RV → bowing of interventricular septum toward the LV → decreased SV → decreased CO → decreased SBP

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86
Q

A patient with blunt chest trauma presents for pericardiocentesis. He exhibits JVD and kussmaul’s sign. What is the BEST induction agent for this patient?
A. Propofol
B. Etomidate
C. Ketamine
D. Midazolam

A

C. Ketamine

*the patient with pericardial tampone relies on an elevated SNS tone to maintain BP. Most GAs cause myocardial depression and reduced afterload (both of which ontribute to CV collapse)

→local anesthesia is the preferrred technique for pericardiocentesis

if GA is required, ketamine is the best option as it activates the SNS which increases HR, contractility, and afterload

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87
Q

Surgical management of cardiac tamponade (2)

A

Pericardiocenteisis (needle aspiration) and pericardiostomy

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88
Q

Optimal anesthetic mangement for cardiac tamponade

A

Local anesthethesia to preserve hemodynamic stability

if GA required, use drugs that preserve myocardia function such as : ketamine, n20, benzos, and opioids
→maintain NSR, preload, afterload, , and contractiltiy
→ spontaneous ventilation is preverred over PPV

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89
Q

Pericardiocentesis vs Pericardiostomy

complications

A

Pericardiocentesis → needle is used to aspirate pericardial fluid
Pericardiostomy → surgical opening and drainage of the pericardium (subxiphoid, thoracoscopic, or thoracotomy)

PTX, re-accumulation of pericardial fluid, puncture of the coronary vessels or myocardium

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90
Q

A patient presents to the preop clinic with hx of infective endocarditis; which procedure puts this pt at the HIGHEST risk of an adverse outcome:
A. cystoscopy
B. Colonoscopy
C. Dental implant
D. Coronary stent placement

A

Dental implant

→pts at high risk for developing bacteremia after certain “dirty procedures” should receive antibiotic prophylaxis

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91
Q

What is infective endocarditis

A

a bacterial infection of the heart valves and endocardium

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92
Q

What patients should receive prophylaxis for infective endocarditis? (3)

A

Hx IE
Prosthetic heart valve
Congential heart defect

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93
Q

What non-cardiac procedurs are indications for prophylaxis for infective endocarditis (3)

A
  1. Dental procedures with gingival manipulation
  2. certain resp procedures
  3. biopsies of infected lesions
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94
Q

What cardiac procedures are NOT indications of prophylaxis for infective endocarditis? (3)

A
  1. MVR
  2. CABG
  3. Coronary stent placement
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95
Q

IV antibiotics for IE prophylaxis (4)

A

ACCC
Ampicillin
Cefazolin
Ceftriaxone
Clindamycin

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96
Q

What is infective endocardities usually caused by?

A

Bacteremia

bacteria in the bloodstream

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97
Q

What is infective endocardities usually caused by?

A

Bacteremia

bacteria in the bloodstream

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98
Q

T/F- unrepaired cardiac valve disease requires prophlyatic antibotics for IE

A

False

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99
Q

T/F- bronchospy with biopsy requires prophlyactic antibiotic of IE

A

True

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100
Q

Which intervention is MOST likely to precipitate hemodynamic instablity in the patient with hypertrophic cardiomyopathy
A. Esmolol
B. Nitroglycerine
C. Phenylepherine
D. 500ml Bolus

A

B. Nitroglycerine

reduces preload → reduction in systolic LV volume → narrowed LVOT → worsens obstruction
- fluid bolus has opposite effect
- slower HR extends LV filling time so esmolol increases LV volume and reduces contractility with helps improve LVOT obstruction
- neo increases aortic pressure which increases transmural pressure , opening the LVOT

101
Q

Which intervention is MOST likely to precipitate hemodynamic instablity in the patient with hypertrophic cardiomyopathy
A. Esmolol
B. Nitroglycerine
C. Phenylepherine
D. 500ml Bolus

A

B. Nitroglycerine

reduces preload → reduction in systolic LV volume → narrowed LVOT → worsens obstruction
- fluid bolus has opposite effect
- slower HR extends LV filling time so esmolol increases LV volume and reduces contractility with helps improve LVOT obstruction
- neo increases aortic pressure which increases transmural pressure , opening the LVOT

102
Q

What 3 things determine blood flow through a LVOT

A
  1. Systolic LV volume (preload)
  2. Force of LV contraction
  3. Transmural pressure (increased aortic pressure increases transmural pressure, opening the LVOT)
103
Q

What is the most common cause of sudden cardiac death in young atheletes?

A

Hypertrophic cardiomyopathy

104
Q

Hypertrophic cardiomyopathy leads to what kind of obstruction during systole

2 causes

A

LV outflow tract (LVOT) obstruction

  1. congenital hypertrophy of the in interventricular septum
  2. SAM - systolic anterior motion of the anterior leaflet of the mitral valve
105
Q

3 conditions that worsen LVOT

4 treatments

A
  1. Decreased preload
  2. Increased contractility
  3. decreased afterload

Betablockers, CCB, Fluids, Phenylepherine

106
Q

4 other names for hypertrophic cardiomyopathy

A
  1. Obstructive hypertrophic cardiomyopathy (OHCM)
  2. Hypertrophic obstructive cardiomyopathy (HOCM)
  3. Asymetric septal hypertrophy (ASH)
  4. Idiopathic hypertrophic subaortic stenosis (IHSS)
107
Q

T/F- SAM can occur after mitral valve replacement

A

False -mitral valve REPAIR

NOT replacement!

108
Q

In a patient with a bare-metal cardiac stent presenting for bunionectomy, what is the MINIMAL amount of time that the patient should wait before undergoing surgery (answer in days)

A

30 days

109
Q

What should patients be on after getting a coronary stent and why?

A

Dual antiplatelet therapy to prevent stent thrombosis

ASA & thienopyridine (clopidogrel or ticlopidine)

110
Q

The duration to postpone elective surgery after stent placement for the following:
Angioplasty without stent
Baremetal stent
DES

A

Angiplasty without stent → 2-4 weeks
BMS → 1-3 months
DES → 6-12 months

  • First generation DES = 12 months
  • *Current generation DES = 6 months
111
Q

T/F - for most surgeries aspirin can be continued throughout the perioperative period

When should clopidogrel and ticlopidine be stopped?

A

True

Clopidogrel → stop 7 days prior
Ticlopidine → stop 14 days prior

112
Q

Aspirin vs Thienopyridine (clopidogrel/ticlopidine) MOAs

A

Asprin → irreversible cyclooxygenase inhibitor
Thienopyridine → ADP antagonist

113
Q

How long to delay elective surgery in someone who had ACS

what about CABG?

A

ACS → 12 months minimum

CABG → 6 weeks ( 3 months preferred)

114
Q

How long should ASA be stopped prior to surgery is it is absolutely contraindicated

A

At least 3 days

115
Q

Best tx for stent thrombosis

A

PCI

want blood flow restored in < 90 minutes

116
Q

Best tx for stent thrombosis

A

PCI

want blood flow restored in < 90 minutes

117
Q

Priming the cardiopulmonary bypass machine with a balanced salt solution reduces all of the following except :

A. microvascular flow
B. plasma drug concentration
C. oxygen-carrying capacity
D. blood viscosity

A

A. Microvascular flow

  • because the CPB bypass circuit becomes an extension of hte patient’s circulation, it must be primed with enough volume to de-air the pump. The priming fluid can be a balanced salt solution or blood

-priming with anything other than blood produces hemodultion wich has the following effects:
→ decreased hematocrit, plasma concentration of drugs and plasma proteins, decreased o2 carrying capacity, decreased blood viscosity, increased microvascular flow

118
Q

3 benefits of the centrifugal pump over the roller pump

A
  1. less traumatic to blood cells
    → uses gravity and spins the blood thru a cone
  2. decreased risk of air emboli
    → bc it uses gravity, it cant produce excess negative pressure → decreased risk for air entrainment
  3. Decreased risk of line rupture if arterial inflow line is clamped
    → unable to produce excessively high postive pressure, so if confronted by an excessive afterload, the line wont rupture
119
Q

What is the preferred type of oxygenator for CBP?

A

Membrane oxygenator

A bubble oxygenator uses a blood-gas interface with no membrane and increases risk of cerebral air embolism

120
Q

What is the balanced salt solution comprised of that primes the CBP circuit? (4)

A

Mannitol
Albumin
Heparin
HCO3-

121
Q

5 effects of hemodilution during priming of the CBP circuit

A
  1. decreased hematocrit
  2. decreased o2 carrying capacity
  3. decreased blood viscosity
  4. decreased plama concentration of drugs and plasma proteins
  5. increased microvascular flow (due to decreased blood viscosity)
122
Q

What can happen if air enters the veinous line of hte CPB circuit?

A

airlock

123
Q

When is awareness MOST likely to occur during CABG with CPB?
A. Induction of anesthesia
B. Aortic cannulation
C. Rewarming
D. Sternotomy

A

Sternotomy

due to intense surgical stimulation

124
Q

An ACT greater than what is adequate heparinization for CBP

A

> 400

125
Q

Systolic BP should be what before aortic cannulation?

A

< 100 mmHg

126
Q

4 things to think of in the pre-bypass period

A
  1. awareness most common during sternotomy
  2. ACT > 400
  3. SBP < 100 before aortic cannulation
  4. Use cell saver or antifibrinolytics to conserve blood loss
127
Q

What is cardioplegia and what does it do and why?

A

Potassium-containing solution
→arrests the heart in diastole
→best way to reduce myocardial o2 consumption during CBP

128
Q

How much protamine to reverse heparin?

A

1mg protamine for every 100units of heparin given

or just fucking make it simple and say 10mg for every 1,000 units of heparin bc no one is giving < 100units of heparin

129
Q

3 things to consider post bypass

A
  1. Protamine dosing (10mg/1000units)
  2. Radial artery pressure may be artifically low
  3. Mycardial depression and heart block by necessitate vasoative meds and cardiac pacing
130
Q

For CBP, what if hte patient has a allergy or hx of HIT?

A

alternatives: Bilvalirudin, hirudin, or another factor 10 inhibitors

131
Q

Why is it important to avoid hypertension during cannulation of the aorta?

goal BP?

A

bci t can lead to aortic dissection

SBP < 100 (ideal 90-100) or MAP < 70

132
Q

Re: Cardioplegia:
Potassium (increases/decreases) RMP, which locks what kind of channels in what state?

A

increases RMP
locks NA+ channels in closed-inactive state

133
Q

How is the heart “restarted” after cardioplegia?

A

by infusing cornoary circulation with warm, normokalemic blood

134
Q

Antegrade vs retrograde cardioplegia

special considerations with antegrade

A

Antegrade → into aortic root → cornoary arteries

Retrograde → coronary sinus

antegrade- aortic valve must be competent and aorta clamped

135
Q

Since blood flow is non-pulsatile on pump how do we assess organ perfusion?

A

MAP

136
Q

How does protamine work?

A

it’s a postive base which forms a complex with heparin (negative acid) and neutralizes it

137
Q

Two side effects of protamine

A

systemic vasodilation and pulmonary vasoconstriction = side effects

anaphylaxis = allergy

administration over 10-15 mins reduces known side effects

138
Q

2 antifibrinolytics commonly used during cardiac surgery

A

aminocaproic acid (amicar)
tranexamic acid (TXA)

139
Q

Pick the statements that MOST accurately describe intra-aortic balloon pump (select 2)

  • increases afterload
  • tip of balloon should be positioned 2cm proximal to the brachiocephalic artery
  • it inflates during diastole
  • it is contraindicated in severe aortic insufficency
A
  • inflates during diastole
  • -contraindicated in severe AI
140
Q

How does an intraaortic balloon pump work?

A

it inflates during diastole to increase CPP (increases o2 supply)

deflates during systole → redcues after load (decreased o2 demand)

141
Q

Who is IABP contraindicated in? (Main one + 3 more)

Why?

A

pt’s with aortic insufficency
→ descending aortic aneuyrsm
→peripheral vascular disease
→sepsis

Ballon inflation would force blood retrograde into the left ventricle (no bueno)

142
Q

Where should the tip of a balloon of the AIBP be placed

what happens if it is in a more proximal position?

A

2cm distal to the left subclavian artery

a more proximal position can lead to occlusion of the left common carotid and/or brachiocephalic arteries

143
Q

indications for IABP (4)

A
  1. Cardiogenic shock
  2. MI
  3. intractable angina
  4. Difficult seperation from CPB
144
Q

Most common complications of IABP (3)

A

vascular injury
infection @ insertion site
thrombocytopenia

145
Q

How is a IABP placed?

A

through the femorlal artery and advanced along the descending aorta

146
Q

balloon inflation with IAP correlates with what on the arterial waveform?

A

the diacrotic notch (AV closure, start of diastole)

147
Q

When does the aortic valve close

A

at the beginning of diastole

*this is when IABP balloon inflates

148
Q

When does the IABP balloon deflate and what does it occur with on the EKG?

A

-just before onset of systole
-R Wave

149
Q

T/F- timing of IABP is generally unaffected by pacemaker spikes or electrocautery

A

True

150
Q

T/F- pts on long term IABP require anticoagulation

A

true

151
Q

What do these point correlate with

how is IABP function during these points

A

R Wave→ Start of Systole → balloon deflates

T Wave → start of diastole → balloon inflates

152
Q

In the patient with an LVAD, organ perfsion is LEAST dependent on:
-preload
-pump speed
-afterload
-inotropy

A

Inotropy

LVAD unloads the failing heart by pumping blood from the LV to the aorta, so CO ( thus organ perfusion) are depdendent on → LV preload, pump speed, & pressure gradient across the pump (afterload)

153
Q

What is an LVAD

A

A mechanical device that unloads the failing heart by pumping blood from the LV to the aorta.

154
Q

What 3 things is cardiac output (and thus organ perfusion) depdendent on in someone with an LVAD

A
  1. LV preload
  2. Pump Speed
  3. Afterload (pressure gradient across the pump)
155
Q

T/F- with an LVAD, flow can be pulsatile or non-pulsatile

A

True
If non-pulsatile, then SpO2 and NIBP will be ineffective

→ consider arterial line, serial ABGs, and cerebral ox

156
Q

Why is regional anesthesia avoided in the patient with an LVAD

A

bc they are anticoagulated

157
Q

What is the most common cause of death in the LVAD patient

A

Sepsis

158
Q

With an LVAD, the inflow cannula is inserted where?

Where does blood go from there?

A

inserted into the apex of the LV

from there, blood flows through the LVAD pump and is returned to the aorta through the outflow cannula

159
Q

When would an LVAD be used (3)

A
  1. bridge to recovery
  2. bridge to transplant
  3. destination therapy
160
Q

what 3 conditions would require surgical correction before an LVAD can be placed?

A
  1. intracardiac shunt (PFO)
  2. AI
  3. TR
161
Q

What can produce a suction event with an LVAD, what happens

whats the consequences

how to manage it

A

the combination of a low preload with a relatively high pump speed → LV suck down (part of the LV is sucked into the LV cavity) → occludes teh inflow cannula

tx: fluid administration (to increase preload) & reducing pump speed

consequences → hypotension and ventricular dysrhythmias.

→leftward shift of the interventricular septum alters RV geometry, reducing RV contractility n& compliance

162
Q
A

B.

crawford type II d/t mandatory period of stopping blood flow to the renal arteries and some of the radicular arteries that perfuse the anterior spinal cord and possibly the artery of Adamkiewicz.

163
Q

Acute dissection of hte ascending aorta (what Debakey or standford classifcation) is considered a surgical emergency

what’s something you need to consider in your anesthetic plan

A

DeBakey 1 or 2
or Stanford A

Aortic valve is often affected, so consider AI in your anesthetic plan

164
Q

What are aortic aneurysms classified by?

A

The region of the aorta affected

165
Q

Aortic Dissection - Standford Type A classification vs Type B

A

A = involves the Asecnding Aorta
B= does not involve ascending aorta

166
Q

DeBakey classification system

A

Type 1 → tear in ascending + dissection along entire aorta

Type 2 → tear in ascending + dissection ONLY in the ascending aorta

Type 3 → Tear in the proximal descending aorta with:
3A: dissection limited to thoracic aorta
3B: dissection along thoracic and abdominal aorta

167
Q

Acute dissection of the ascending aorta (Debakey ___ or Standford ___) is considered a surgical emergency

what should you consider in the anesthetic plan

A

Stanford A (involves Ascending aorta)
or
Debakey 1 or 2
(1 = tear in ascending, dissection along entire aorta; 2 = tear in ascending, dissection in the ascending aorta only)

the aortic valve is often affected so treat as if pt has AI

168
Q

How is dissection of the descending aorta generally handled

A

medical management (meds for HR, BP, pain)

surgical repair does not always produce a significant benefit

however, these patients often do ultamiely require surgery

169
Q

Surgical intervention is recommended when the diameter of a AAA is > ____cm or grows more than ____ cm per year

A

5.5 cm

or grows > 0.6-0.8cm per year

170
Q

T/F- risk of aneurysmal rupture is best described by Poiseuille’s law

A

False - law of la place (La Pop!)

171
Q

what 3 s/s suggest rupture of AAA?

This triad is present in what % of patients

A

acute onset of back pain, hypotension, and pulsatile abdominal mass

only present in ~ 50% of patients

172
Q

What is the most common cause of postop death in AAA repair patients?

A

MI

173
Q

3 independent risk factors for AAA

What is the incidence of AAA in the US for patients over 50yo?

A
  1. Ciggs
  2. Male gender
  3. Advanced age

3-10%

174
Q

T/F- most aneurysms rupture in the right retroperitoneum

A

false - left retroperitoneum

175
Q

Why don’t all patients with an aortic aneurysm rupture exsanguinate immediately?

A

Bc most aneurysms rupture in the left retroperitoneum, allowing for tamponade and clot formation

176
Q

What is the most common placement for the aortic cross clamp?

A

Infrarenal

177
Q

Applying aortic cross-clamp creates ________ by :

→Reducing:
→Shifting:
→Increasing:

A

A central hypervolemia by:
Reducing → venous capacity
Shifting → more blood proximal to the clamp
Increasing→ venous return

178
Q

Removing the aortic cross clamp creates _______ by:

  • restoring:
  • shifting:
  • ## decreasing:

creating a….

A

Central hypovoemia by:
Restoring → venous capacity
Shifting → blood to the lower body
Decreasing → venous return (increased size of tank)

a capillary leak that contributes to loss of intravascular volume

179
Q

Removing the aortic cross clamp creates _______ by:

  • restoring:
  • shifting:
  • ## decreasing:

creating a….

A

Central hypovoemia by:
Restoring → venous capacity
Shifting → blood to the lower body
Decreasing → venous return (increased size of tank)

a capillary leak that contributes to loss of intravascular volume

180
Q

Application of the cross-clamp starves the distal tissues of oxygen → these cells convert to anerobic metabolism, which leads to what 5 changes?

A
  1. increased lactic acid production → metabolic acidosis
  2. prostagladins
  3. activated complement
  4. myocardial depressant factors
  5. hypothermia
181
Q

T/F- even an infra-renal clamp reduces renal blood flow

A

true

pt still at risk of AKI

182
Q

2 things associated with IV contrast dye

A
  1. allergic reaction
  2. renal injujry
183
Q

When does an endoleak occur with AAA repair?

What do they do if there is one?

A

when the original graft fails to prevent blood from entering the aortic sac.

Some of them resolve spontaneously (esp early postop leaks), while others may require placement of a second graft or an open repair

184
Q

Occlusion of hte artery of Adamkiewicz during thoracic aneurysm repair may result in all of hte following EXCEPT:

A. Flaccid paralysis of the lower extremities
B. Bowel and bladder dysfunction
C. Loss of proprioception
D. Loss of temperature and pain sensation

A

D. Loss of proprioception

185
Q

An aortic cross-clamp placed above the artery of adamkiewicz can cause ischemia to where?

What syndrome can this result in?

A

ischemia to the** lower portion of the anterior spinal cord **

Anterior spinal artery syndrome (Beck’s syndrome)

*generally speaking, the anterior cord conttains motor neurons, and the posterior cord sensory neurons

186
Q

What does anterior spinal artery syndrome result in? (what tracts/fibers/columns contribute to each)

AKA

what’s preserved?

A
  1. Flaccid paralysis of the lower extremities → corticospinal tract affected
  2. Bowel and bladder dysfunction → autonimic nerve fibers affected
  3. loss of temp and pain sensation → spinalthalmic tract affected

Beck’s syndrome

Touch & proprioception are preserved (dorsal column is spared)

187
Q

How many posterior vs anterior spinal arteries are there?

A

Posterior = 2
Anterior = 1

188
Q

The posterior spinal arteries perfuse what portion of the spinal cord?

A

the posterior 1/3

189
Q

The anterior spinal artery perfuses what portion of the spinal cord?

A

The anterior 2/3

190
Q

label

A
191
Q

Backtrack blood flow from the posterior and anterior spinal arteries coming off the aorta (2 pathways)

A

Aorta →
Segmental artery → anterior/posterior radicular artery → anterior/posterior spinal artery
&
**subclavian artery → vertebral artery → anterior/posterior spinal arteries **

192
Q

What does the artery of adamkiewicz perfuse?

A

the anterior spinal cord in the **thoracolumbar **region

193
Q

aThe artery of adamkiewicz most comonly originates on the (right/left) side between what what levels in 75% of the population

Where does it arise in the freaky 10% of hte population ?

A

T8-T12 in 75%
T11-T12

L1-L2 in the freaky 10% of people

194
Q

What is the radicularis magna ?

A

The artery of adamkiewicz

*anterior spinal cord in the thoracolumbar region
*T 11-12
*left side

195
Q

Thoracic aortic cross clamp times > _ minutes pose a significant risk for cord ischemia

A

> 30 mins

196
Q

5 spinal cord protective strategies for thoracic aortic surgery

A
  1. keep cross-clamp times < 30 mins
  2. moderate hypothermia (30-32 C) → reduces cord o2 consumption
  3. CSF drainage
  4. proximal HTN during cross-clamping → map ~ 100mmHg
  5. Avoid hyperglycemia

also can do CSF drainage to increase the perfusion pressure gradient

197
Q

Injury to what spinal tract results in flaccid paralysis of the lower extremities

A

corticospinal tract

motor (anterior spinal artery)

198
Q

Injury to what spinal tract results in flaccid paralysis of the lower extremities

A

corticospinal tract

motor (anterior spinal artery)

199
Q

Injury to what spinal tract would account for loss of pain and temp sensation?

A

Spinothalmic trract

(anterior spinal artery)

200
Q

What is the BEST monitor of neurologic integrity during CEA?

A

an awake patient

gross

201
Q

What is the BEST monitor of neurologic integrity during CEA?

A

an awake patient

gross

202
Q

What is Amaurosis fugax?

What is it a sign of?

A

Temporary blindness in one eye

impending stroke

*occurs in 25% of patient s with high grade stenosis

*emboli travel from ICA > opthalmic artery → impaired perfusion of the optic nerve → rentinal dysfunction

203
Q

Why is it important to know someones blood glucose level prior to taking them to surgery for CEA?

A

bc hyperglycemia > 200 has been associated with increased risk of stroke and death

*treat with insulin, avoid glucose containing solutions

204
Q

During cross clamping of the carotid, BP should be elevated; what should BP be after release of cross clamp and why?

A

<145 to reduce bleeding at the graft site

205
Q

The 4 significant postop risks associated with CEA?

A
  1. hematoma
  2. labile BP
  3. RLN injury
  4. Stroke (embolic most common)
206
Q

The 4 significant postop risks associated with CEA?

A
  1. hematoma
  2. labile BP
  3. RLN injury
  4. Stroke (embolic most common)
207
Q

What kind of blocks are done for CEA?

what levels

A

superficial and deep cervical plexus

C2-C4

208
Q

Why would you avoid regional anesthesia in a COPD patient presenting for CEA ?

A

risk of ipsilateral phrenic nerve block → dyspea d/t hemidiaphragm paralysis

209
Q

Cerebral perfusion pressure =

A

MAP - ICP (or CVP)

whichever is higher *

210
Q

label

A
211
Q

Cerebral oximetry uses what kind of technology to monitor cerebral oxygen in which lobe?

*The patient is at risk when cerebral o2 is reduced how much from baseline?

A

near-infrared spectroscopy (NIRS)

*Frontal lobe

> /= 25% from baseline

212
Q

Transcranial Doppler assesses continous blood flow velocity where?

what’s special about this area?

A

Middle cerebral artery

it’s where most emboli lodge

*it may indicate if a shunt is needed

213
Q

Where do most emboli lodge in the brain?

A

in the middle cerebral artery

214
Q

Carotid stump pressure measures pressure (distal/proximal) to the clamp

What is there a risk of and at what pressure?

What is a low stump pressure an indication for?

A

Distal

ipsilateral hypoperfusion if < 50mmHg

the need for a shunt to be placed
*most sugeons will avoid shunts a t all costs becuase they increase risk of embolic stroke, but a low stump pressure would be a good indication for a need for one

215
Q

If doing a CEA and you hear them say they need to place a shunt, what should come to mind?

A

increased risk for embolic stroke

216
Q

Why do we want to maintain BP @ patients normal or slightly elevated during carotid cross clamp?

A

Bc blood vessels in the ischemic area maximally dilate and become pressure depedent (loss of autoregulation)

217
Q

Besides concerns of bleeding of the new graft, what is another reason to reduce BP < 145 after clamp comes off carotid?

A

bc HTN → reperfusion injury → cerebral edema

218
Q

label

A
219
Q

What should you do if you end up in PACU and there is a hematoma developing on your CEA patient

A

remove the sutures to decompress the wound

220
Q

Which is more common postop CEA - hypertension or hypotension?

why

when does it subside?

A

HTN

exposing baroreceptors alters their sensitivity

within 24 hours

221
Q

Main reason agaisnt B/L CEA

A

carotid body denervation results in decreased ventilatory response to hypoxia

*peripheral chemoreceptors

222
Q

Goal ACT during carotid artery angioplasty stenting

how much heparin should they get? ex 80kg pt

A

> 250 sec

50-100units/kg

80kg should get 4,000 - 8,000 units of heparin

223
Q

What part of carotid artery angioplasty stenting can activate the baroreceptor reflex?

A

balloon inflation

*pretreat with atropine/glyco

224
Q

In the patient with RIGHT subclavian steal syndrome, arterial flow is diverted from the:

A. right vertebral artery → right subclavian artery
B. Right subclavian artery → left subclavian artery
C. Left vertebral artery → right subclavian artery
D. Left subvlavian artery → right subvlavian artery

A

A. Right vertebral artery → right subclavian artery

*Subclavian steal syndrome can reduce cerebral perfusion. If there’s an occlusion of the subclavian or innominate artery proximal to the origin of the ipsilateral artery, then there can be retrograde flow that travels down the vertebral artery (instead of towards the brain).

225
Q

Subclavian steal occurs when there is an occlusion of what, where?

What does it result in?, tx?

s/s? (5)

A

occlusion of the subclavian or innominate artery PROXIMAL to the origin of the ipsilateral vertebral artery

BP may be diminished in that arm; tx = subclavian endarderectomy

  1. syncope
  2. vertigo
  3. ataxia
  4. hemiplegia
  5. ishemia
226
Q

label

A
227
Q

Subvlavian steal syndrome “steals” blood from which vessel?

A

The vertebral artery (posterior cerebral circulation)

228
Q

A Patient with a hx of heart failure with preserved EF is scheduled for a lap chole; the primary anesthetic consideratio includes:

A. Fluid restriction
B. Preventing tachycardia
C. Targeting a MAP of 60mmHg
D. administering a postive chronotrope

A

B. Preventing tachycardia

HFpEF → heart is less able to accept the incoming volume bc ventricular compliance is reduced

*maximizing coronary blood flow is the highest priorrity for this patient → a slower HR improves O2 supply (increased diastolic time) while simultaneously reducing O2 demand

LV coronary perfusion presssure is AoDBP - LVEDP where optimal = higher AoDBP and lower LVEDP; however, LVEDP does not correlate to LVEDV
*these patients require adequate preload to stretch a non-compliant ventricle

229
Q

estimate the CPP (coronary)

A

42mmHg

CPP = Aortic DBP - LVEDP

use PA diastolic pressure as a surrogate for PAOP

230
Q

Anesthetic considerations for the patient with SYSTOLIC heart failure includes a/an:

A. avoidance of inotropes to reduce myocardial o2 demand
B. increased afterload to perfuse hypertrophied myocardium
C. increased heart rate to maximize cardiac output
D. increased preload to stretch a noncompliant ventricle

A

C. increased heart rate to maximize CO

*The hallmark of systolic heart failure is a decreased EF with an increased end-diastolic volume (bc the ventricle does not empty well).

→ since the heart cant squeeze well, a greater volume of blood remains in the ventricle after each contraction (decreased SV) - only way to maintain cardiac output is to increase HR.

231
Q

What is the hallmark of systolic heart failure

Anesthetic considerations for preload/afterload/hr/contractility

A

a decreased EF with an increased EDV (ventricle doesn’t empty well)

Preload → already high, don’t let it get higher
Afterload → decrease to reduce the LV workload
HR → mintain high/normal range
Contractility → inotropic support as needed

232
Q

Which of the following are MOST closely associated with diastolic heart failure (select 3):

-dialated CM
-essentail HTN
-TR
-3rd heart sound
-ischemic heart disease
-AS

A

Aortic Stenosis
Ischemic heart disease
Essential hypertension

diastolic failure is associated with decreased ventricular compliance; the heart is unable to relax to accept the incoming volume → AKA: the ventricle doesn’t fill properly (explains why LVEDP overestimates the EDV

233
Q

What is the defining characteristic of diastolic dsyfunction?

A

symptomatic heart failure with a normal EF.

234
Q

3 most common causes of diastolic heart failure

other conditions it’s associated with (6)

A

AS, ischemic heart disease, long-standing essential HTN

concentric hypertrophy, old age, valve stenosis, HOCM, cor pulmonale, obesity

235
Q

Which drugs ahve been proven to reverse LV remodeling in the patient with heart failure (select 2)
-clonidine
-esmolol
-enalapril
-spironolactone

A

Enalapril & Spironolactone

*ACE inhibitors and aldosterone inhibitors are first line agents in the patient with heart failure

236
Q

what compliance curve correlates with the condition that produces the ABP waveform

A

The blue one

that waveform illustrates biferiens pulse and can occur in the patient with AI

237
Q

Which region of the myocardium receives the LEAST amount of perfusion during systole?

A. RV epicardium
B. RV subendocardium
C. LV epicardium
D. LV subendocardium

A

D. LV Subendocardium

it’s primarly perfused during diastole (very little to no perusion durin

238
Q

An elevated CK-MB is MOST consistent with:
A. AS
B. MI
C. Rheumatic fever
D. CHF

A

B. MI

239
Q

What are the 3 substances released by the cardiac myocytes wehn they are deprived of o2 and the cell membrane explodes lol

A

CKMB, Troponin I, Troponin T

240
Q

Which factors primarily affect myocardial O2 supply (select 2)

-P50
-Inotropy
-Diastolic time
-Wall tension

rank in order from hightest to lowest o2 cx

A

P50 & Diastolic time

Heart rate & Pressure work > contractility > wall stress > volume work

241
Q

An increase in which of the following is associated with teh HIGHEST increase in myocardial o2 consumption (select 2)

-wall stress
-HR
-volume work
-pressure work

A

HR & Pressure work

242
Q

Which agents reduce myocardial o2 demand? (select 2):

-dobutamine
-metoprolol
-mso4-
-atropine

A

metoprolol & morphine

243
Q

Calcium channel blockers produce their CV effects by binding to the:

A. Alpha-1 subunit of the L-type calcium channel
B. alpha-1 subunit of the T-type calcium channel
C. Beta subunit of the L-type calcium channel
D. Beta subunit of the T-type calcium channel

A

A. Alpha-1 subunit of the L-type calcium channel (long-lasting/slow channel)

N = neural, T = transient

this binding prevents calcium from entering cardiac and vascular smooth muscle cells

244
Q

A patient presents with diaphroesis, chest pain, and SOB. His BP is 220/110. Select the BEST IV drug for this patient:

A. Nimodipine
B. Nifedipine
C. Nicardipine
D. Verapamil

A

C. Nicardipine

Nicardipine and nifedipine are potent vasodilators, however only nicardipine is available for IV administration → they are best used to decrease SVR and/or releave angina

*verapamil reduces HR and contractility & also causes mild coronary vasodilating properties. It is primarily used for controlling SVT and/or angina. & causes LITTLE systemic vasodilation

245
Q

What is the MOST common cause of acute pericarditis?

A. RA
B. Viral infection
C. SLE
D. Radiation

A

B. Viral infection

*most common cause for constrictive is radiation or previous cardiac surgery

246
Q

Which abnormality is MOSt likely to occur in the patient with pericardial tamponade?

A. Pulsus alternans
B. Pulsus tardus
C. Pulsus paradoxus
D. Pulsus Parvus

A

C. Pulsus paradoxus

Normally the systolic BP decreases a little during inspiration (a few mmHg), but in the patient with pulsus paradoxus, the SBP decreases by 10mmHg or more

247
Q

Antibiotic prophylaxis agaisnt endocarditis may be indicated if a patient has a history of (select 2):

A. MVP
B. unrepaired cyanotic heart disease
C. prostethetic heart valve
D. cardiac stent placement

A

B & C
unrepaired cyanotic heart disease & prosthetic heart valve

248
Q

Which of the following are MOST likely to reduce stroke volume in the patient with hypertrophic cardiomyopathy:(3)
-Esmolol
-Neo
-Ephedrine
-Nitroprusside
-Hypervolemia
-Valsalva maneuver

what is your main concern with these patients?

A

Valsalva, ephedrine, nitroprusside

LVOT obstruction = main concern

-valsalve decreases preload

249
Q

All of the following diseases cause secondary hypertension EXCEPT:

A. Coarctation of the aorta
B. Conn’s disease
C. Hashiomoto’s disease
D. Cushing’s syndrome

A

C. Hashimoto’s disease (atoimmune dz resulting in hypothyroid)

Conn’s disease (hyperaldosteronism) → too much aldosterone
Cushing’s syndrome (hyperadrenocorticism) → too much glucocorticoid

Cardiac (7 decks)

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