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APEX ANESTHESIA FLASHCARDS > UNIT 3 Cardiovascular > Flashcards

UNIT 3 Cardiovascular Flashcards

1
Q

define: chronotropy, inotropy, dromotropy, & lusitropy

A

chronotropy: HR
inotropy: contractility
dromotropy: conduction velocity
lusitropy: rate of myocardial relaxation

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2
Q

describe the function of the Na+ K+ pump

A

maintains the cell’s resting potential: keeping the inside of the cell negative & the outside relatively positive

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3
Q

list the 5 phases of the ventricular AP & describe the ionic movement during each phase

A 
0 = depolarization (Na+ influx) from fast voltage Na+ channels **THIS IS WHERE CARDIOPLEGIA WORKS**

1 = initial repolarization  (K+ efflux & Cl- influx). Inactivation of Na+ channels

2 = plateau (Ca++ influx) Activation of slow voltage calcium channels. Prolongs absolute refractory state. Maintains Na+ in their inactive state 

3 = repolarization (K+ influx) K leaves faster than calcium 

4 = restoration of resting membrane potential (Na+/K+ pump)
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4
Q

list the 3 phases of the SA node AP & describe the ionic movement during each phase

A 
4 = spontaneous depol (leaky to Na+) from I-F funny gates (activated by Hyperpolarization), then at -50 MV calcium from T-type channels help out to depolarize it

0 = depol (Ca++ influx) calcium from L-type channels 

3 = repol (K+ efflux)

TP -45
RMP is -60

SA NODE IS FASTER THAN AV NODE. HR is determined by intrinsic firing rate of SA node and autonomic tone.

Autonomic tone determined by SNS and PNS.

SNS: NE stimulates B2 receptor and increases Na+ and Ca2+ conductance = increase HR

PNS: Acetylcholine stimulates M2 receptor and increases K+ conductance = hyperpolarizes to decrease HR

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5
Q

what process determines the intrinsic HR, and what physiologic factors alter it?

A

HR is determined by the rate of spontaneous phase 4 depol in the SA node

increase HR by manipulating 3 variables:
- rate of spont phase 4 depolarization (Reaches TP faster)
- threshold becoming more negative
- resting membrane potential becoming less negative

When RMP and TP are close: easier for cell to depolarize
When RMP and TP are far: harder for cell to depolarize

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6
Q

what is the calculation for MAP?

A

SBP/3 + 2DBP/3

OR

[(COxSVR)/80] + CVP

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7
Q

what is the formula for SVR?

A

[(MAP-CVP)/CO]x80

normal 800-1500 dynes/sec/cm^5

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8
Q

what is the formula for PVR?

A

[(MPAP-PAOP)/CO]x80

normal 150-250dynes/sec/cm^5

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9
Q

describe the frank-starling releationship

A

relationship b/n preload (ventricular volume) & CO
- increased preload causes increased myocyte stretch = increased ventricular output

the increase in output d/t increased preload only occurs to a point
- overstretch to the ventricular sarcomeres = decreased CO

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10
Q

what factors affect myocardial contractility?

A

increased:
- SNS stimulation, catecholamines
- calcium
- digitalis
- PDE inhibitors

decreased:
- myocardial ischemia
- severe hypoxia
- acidosis
- hypercapnia
- hyperkalemia
- hypocalcemia
- IA, propofol
- BB, CCB

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11
Q

discuss excitation-contraction coupling in the cardiac myocyte

A

myocardial cell membrane depolarizes

  • during phase 2: Ca++ enters via L-type Ca++ channels in T tubules
  • Ca++ influx turns on ryanodine 2 receptor, which releases Ca++ from sarcoplasmic reticulum
  • Ca++ binds troponin C (myocardial contraction)
  • Ca++ unbinds troponin C (myocardial relaxation)
  • most of Ca++ is returned to sarcoplasmic reticulum via SERCA2 pump
  • Ca++ binds a storage protein (calsequesterin) inside the sarcoplasmic reticulum
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12
Q

what is afterload & how do you measure it in the clinical setting?

A

afterload = the force the ventricle must overcome to eject it’s SV

we can use SVR/PVR

SVR = [(MAP-CVP)/CO]x80
PVR = [(mPAP-PAOP)/CO]x80
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13
Q

what law can be used to describe ventricular afterload?

A

Laplace

Tension or wall stress = Pressure x Radius / thickness

  • intraventricular pressure is the force that pushes the heart apart
  • wall stress is the force that holds the heart together

wall stress is reduced by
- decreased intraventricular pressure
- decreased radius
- increased wall thickness

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14
Q

list 3 conditions that set afterload proximal to the systemic circulation

A
  • aortic stenosis
  • hypertrophic cardiomyopathy
  • coarctation of the aorta
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15
Q

use the wiggers diagram to explain the cardiac cycle

A

Know this shit

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16
Q

relate the 6 stages of the cardiac cycle to the LV pressure volume loop

A
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17
Q

how do you calculate ejection fraction?

A

measure of systolic function (contractility). % of blood that is ejected from the heart during systole

EF = SV/EDV x100

Normal 60-70%
Mild dysfunction 41-49%
Moderate dysfunction 26-40%
Severe dysfunction <25%

SV = EDV-ESV

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18
Q

can you calculate the SV and/or EF with a pressure volume loop?

A

yes

SV = width of loop
EDV = right side of loop at X axis
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19
Q

what is the best TEE view for diagnosing myocardial ischemia?

A

midpapillary muscle level in short axis

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20
Q

what is the equation for Cerebral PP?

A

CPP = aortic DBP - LVEDP

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21
Q

what region of the heart is most susceptible to myocardial ischemia? Why?

A

LV subendocardium

  • best perfused during diastole
  • as aortic pressure increases, LV tissue compresses its own blood supply & reduces BF (this area has high compressive pressure)
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22
Q

what factors affect myocardial oxygen supply?

A

decreased supply:

  • decreased coronary flow: tachycardia, decreased aortic pressure, decreased vessel diameter
  • increased end diastolic pressure
  • decreased CaO2: hypoxemia, anemia
    -** decreased O2 extraction: L shift of HgB dissociation curve, decreased capillary density**
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23
Q

discuss the NO pathway of vasodilation

A

NO = smooth m relaxant –> vasodilation

NO synthase catalyzes conversion of L-arginine to NO

  • NO diffuses from endothelium to smooth m
  • NO activates guanylate cyclase
  • guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
  • increased cGMP decreases intracellular Ca++ –> smooth m relaxation
  • phosphodiesterase deactivates cGMP to guanosine monophosphate (deactivates NO mechanism)
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24
Q

where do the heart sounds match up on the LV pressure volume loop?

A

Know where S1, S2, S3, S4 are

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25
Q

what are the two primary ways a heart valve can fail

A

stenosis:
- fixed obstruction to forward flow during chamber systole
- the chamber must generate a higher than normal pressure to eject the blood

regurgitation:
- the valve is incompetent: leaky
- some blood flows forward & some blood flows backward during chamber systole

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26
Q

how can the heart compensate for pressure overload? volume overload?

A

REVSS Regurgitation, eccentric, volume, series, systolic HF

SCPPD Stenosis, concentric, pressure, parallel, diastolic HF

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27
Q

describe pressure volume loops for the following pathophysiologies:

  • mitral stenosis
  • aortic stenosis
  • mitral regurg (acute & chronic)
  • aortic regurg (acute & chronic)
A

A = M.S.

B = A.S.

C = A.R.

D = M.R.

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28
Q

list the hemodynamic goals for the 4 common valvular defects.

A

aortic stenosis: F,S,C: Full preload, Slow HR, Constricted high SVR/afterload)

Mitral stenosis: avoid increase in PVR so no nitrous

aortic regurg/mitral regurg: FFF: Full preload, Fast HR, Forward (vasodilate low SVR/afterload)

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29
Q

what is the most common dysrhythmia associated w/ mitral stenosis?

A

afib

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30
Q

list 6 risk factors for perioperative cardiac M&M for noncardiac surgery.

A 
high risk surgery
hx of ischemic heart disease (unstable angina = greatest risk of peri-op MI)
hx of CHF
hx of CVA
DM 
Cr>2
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31
Q

what is the risk of perioperative MI in the patient w/ previous MI

A

general pop = 0.3%
MI >6mo = 6%
MI 3-6mo = 15%
MI <3 mo = 30%

highest risk of reinfarcation is w/in 30 days of an acute MI

ACC/AHA recommends at least 4-6 weeks before elective surgery

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32
Q

categorize high, medium, and low risk surgical procedures according to cardiac risk

A

high (>5%):

  • emergency (esp in elderly)
  • open aortic surgery
  • peripheral vascular surgery
  • long surgical procedures w/ significant volume shifts/blood loss

intermediate (1-5%):

  • carotid endarterectomy
  • head & neck surgery
  • intrathoracic/intraperitoneal surgery
  • orthopedic surgery
  • prostate surgery

low (<1%):

  • endoscopic procedures
  • cataract surgery
  • superficial procedures
  • breast surgery
  • ambulatory procedures
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33
Q

what is the modified new york association functional classification of heart failure?

A 
class I: asymptomatic
class II: symptomatic w/ moderate activity
class III: symptomatic w/ mild activity
class IV: symptomatic at rest
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34
Q

how do you interpret cardiac enzymes in the patient w/ a suspected ischemic event?

A

a cell requires O2 to maintain integrity of it’s cell membrane, and when deprived of O2, it dies & releases it’s contents into the systemic circulation

  • myocardium releases creatine kinase-MB, troponin I, and troponin T
  • troponins are more sensitive than CK-MB for MI diagnosis

CK-MB: elevation 3-12hrs, peaks in 24hrs, returns to baseline in 2-3 days

troponin I: elevation 3-12hrs, peaks 24hrs, returns to baseline in 5-10 days

troponin T: elevation in 3-12hrs, peaks 12-48hrs, returns to baseline in 5-14days

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35
Q

how do you treat intraoperative MI?

A

Make the heart slower, smaller, and better perfused (improve supply, decreased demand):

  • slow/normal HR (use BB or pacing, anticholinergic)
  • optimize BP (increase IA, vasodilator/vasoconstrictor)
  • decrease PAOP w/ NTG or inotrope
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36
Q

what factors reduce ventricular compliance?

A

Anything that makes the heart stiffer so there’s more pressure

  • age >60yrs
  • ischemia
  • pressure overload hypertrophy (i.e. aortic stenosis/HTN)
  • Hypertropic obstructive cardopmyopathy
  • Pericardial tamponade
  • pericardial pressure (external)

**take away point: higher filling pressures are required to prime the ventricle in reduced ventricular compliance*

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37
Q

what is the difference b/n systolic & diastolic heart failure?

A

systolic: the ventricle doesn’t empty well (pump issue)
- HF with decreased EF with an increased end diastolic volume
- Volume overload commonly causes systolic dysfunction

diastolic: the ventricle doesn’t fill well (filling issue)
- Heart is unable to relax and accept the incoming volume b/c compliance is reduced.
- Heart failure with normal EF

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38
Q

compare and contrast the hemodynamic goals in the patient w/ systolic vs. diastolic HF

A

systolic:
- preload is already high (can use diuretics if too high)
- decrease afterload to reduce workload (SNP)
- augment contractility as needed
- HR is usually high d/t increased SNS (& CO is HR dependent)

diastolic:
- preload required to stretch noncompliant (LVEDP doesn’t correlate w/ LVEDV)
- keep high afterload to perfuse thick myocardium
- normal contractility
- slow/normal HR to increase diastolic time

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39
Q

list 6 complications of HTN

A 
LVH
ischemic heart disease
CHF
arterial aneurysm
stroke
ESRD
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40
Q

how does HTN contribute to CHF?

A

HTN –> increased myocardial wall tension –> LVH –> myocardium O2 extraction –> coronary insufficiency –> CHF, infarctions, dysrhythmias

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41
Q

how does HTN affect cerebral autoregulation?

A

chronic HTN shifts the curve to the R, allowing the patient’s brain to tolerate a higher range of blood pressures. The pt is then not able to tolerate a lower blood pressure.

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42
Q

What’s the difference b/n primary & secondary HTN?

A

primary (essential) - more common (95%) & no identifiable cause

secondary - caused by some other pathology (5%)

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43
Q

list 7 causes of secondary HTN.

A 
coarctation of the aorta
renovascular disease
hyperadrenocorticism (Cushing's)
hyperaldosteronism (Conn's)
pheochromocytoma
pregnancy-induced HTN
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44
Q

What are the 2 major classes of calcium channel blockers? List examples of each.

A

dihydropyridines (mostly vascular smooth muscle vasodilation & decrease in SVR)

  • nifedipine
  • nicardipine
  • nimodipine
  • amlodipine

non-dihydropyridines (mostly myocardium: decrease in HR, contractility, conduction velocity, coronary vascular resistance)

  • verapamil
  • diltiazem
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45
Q

describe the pathophysiology of constrictive pericarditis

A

caused by fibrosis or any condition where the pericardium becomes thicker.

During diastole, the ventricles cannot fully relax, and this reduces compliance and limits diastolic filling.

Ventricular pressures increase, which creates a backpressure to the peripheral circulation.

The ventricles adapt by increasing myocardial mass, but over time this impairs systolic function

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46
Q

Describe the anesthetic management of constrictive pericarditis

A

CO is HR dependent: avoid bradycardia!

preserve HR & contractility

  • ketamine
  • pancuronium
  • IA w/ caution
  • opioids, benzos, etomidate OK

maintain afterload

aggressive PPV can decrease venous return & CO

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47
Q

describe the pathophysiology of pericardial tamponade

A

cardiac tamponade occurs when fluid accumulates inside the pericardium.
What separates it from a pericardial effusion is that the excess fluid exerts an external pressure on the heart limiting it’s ability to fill & act like a pump.

CVP rises in tandem w/ pericardial pressure.
As ventricular compliance deteriorates, L & R diastolic pressure (CVP & PAOP) begin to equalize.

LV pressure increases & volume decreases –> decreased coronary perfusion, decreased SV, decreased CO –> increased contractility, HR, RAAS activation

TEE is the best method of diagnosis

TX : pericardiocentesis or pericardiostomy

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48
Q

What is Kussmaul’s sign?

A

JVD or an increased CVP (most pronounced during inspiration).

indicates impaired RV filling d/t a poorly compliant RV or pericardium.

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49
Q

List two conditions commonly associated w/ Kussmaul’s sign

A

can occur w/ any condition that limits RV filling.

make sure you associate Kussmaul’s sign w/ constrictive pericarditis & pericardial tamponade

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50
Q

What is pulsus paradoxus?

A

SBP falls by >10mmHg during inspiration

Suggests impaired diastolic filling

negative intrathoracic pressure on inspiration –> increased venous return to RV –> bowing of ventricular septum toward LV –> decreased SV –> decreased CO –> decreased SBP

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51
Q

List 2 conditions commonly associated w/ pulsus paradoxus

A

Like Kussmaul’s sign, you should also associate pulsus paradoxus w/ constrictive pericarditis & pericardial tamponade

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52
Q

What is Beck’s triad? What conditions are associated w/ it?

A

occurs in those w/ acute cardiac tamponade

  1. hypotension (decreased SV)
  2. JVD (impaired venous return to RV)
  3. muffled heart tones (fluid accumulation in pericardial space attenuating sound waves)
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53
Q

what are the best anesthetic techniques for the patient w/ acute pericardial tamponade undergoing pericardiocentesis?

A

Local anesthesia is preferred.

If GA is required, your primary goal is to preserve myocardial function.

SV is severely decreased & increased SNS tone provide compensation.

Avoid drugs that depress myocardium or decrease afterload = this can precipitate CV collapse
- IA
- propofol
- high dose opioids
- neuraxial

better to use: ketamine, N2O, benzos, opioids

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54
Q

list 7 patient factors that warrant antibiotic prophylaxis against infective endocarditis.

A
  • previous infective endocarditis
  • prosthetic heart valve
  • unrepaired cyanotic congenital heart disease
  • repaired congenital heart defect if the repair is <6mo old
  • repaired congenital heart defect w/ residual defects that have impaired endothelialization at the graft site
  • heart transplant w/ valvuloplasty
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55
Q

list 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis

A

high risk procedures that are thought to be “dirty” procedures where the risk of transient bacteremia outweighs the risk of antibiotic therapy:

  • dental procedures involving gingival manipulation and/or damage to the mucosa lining
  • respiratory procedures that perforate the mucosal lining w/ incision or biopsy
  • biopsy of infective lesions on the skin or muscle
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56
Q

What are the 3 key determinants of flow through the LV outflow tract?

A

systolic LV volume
force of LV contraction
transmural pressure gradient

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57
Q

What factors tend to reduce cardiac output in the patient w/ obstructive hypertrophic cardiomyopathy?

A

things that distend the LVOT are good for CO, while things that narrow the LVOT are bad.

  1. systolic LV volume (distended by increased preload, HR, narrowed by decreased preload, HR)
  2. force of LV contraction (distended by decreased contractility, narrowed by increased contractility)
  3. transmural pressure gradient - pressure distends the LVOT (distended by increased Ao pressure, narrowed by decreased Ao pressure)
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58
Q

What hemodynamic conditions reduce CO in the patient w/ hypertrophic cardiomyopathy?

A 
increased HR (tx w/ BB, CCB)
increased contractility (tx w/ BB or CCB)
decreased preload (tx volume)
decreased afterload (tx phenylephrine)

So you want to decrease HR and contractility
Increase preload and afterload

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59
Q

How long should elective surgery be delayed in the patient w/:

  • bare metal stent
  • drug eluting stent
  • angioplasty
  • CABG
A

bare metal: 30 days (3 mo preferred)
drug eluting: 6-12mo (6 mo for newer generation, 12 for older)
s/p angioplasty: 2-4 weeks
s/p CABG: 6 weeks (3mo preferred)

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60
Q

What is the difference b/n alpha-stat and pH-stat blood gas measurements during CPB?

A

because the solubility of a gas is a function of temperature, it should make sense that hypothermia complicates interpretation of blood gas results during CPB. As temp decreases, more CO2 is able to dissolve in the blood. By extension, this affects the pH

alpha-stat: does not correct for patient’s temperature. Aims to keep intracellular charge neutrality across all temperatures. It is associated w/ better outcomes in adults
pH-stat: corrects for the patient’s temperature. Aims to keep a constant pH across all temperatures. It is associated w/ better outcomes in peds.

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61
Q

Why is an LV vent used during CABG surgery?

A

Removes blood from LV

Since blood pools up from the Thebesian veins & bronchial circulation

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62
Q

How does the intraaortic balloon pump function throughout the cardiac cycle? How does it help the patient?

A

counter pulsation device that improves myocardial O2 supply while reducing myocardial O2 demand

diastole:
- pump inflation augments coronary perfusion
- inflation correlates w/ dicrotic notch on aortic pressure waveform

systole:
- pump deflation reduces afterload & improves CO
- deflation correlates w/ R wave on EKG

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63
Q

List 4 contraindications to intra-aortic balloon pump.

A
  • severe aortic insufficiency
  • descending aortic disease
  • severe PVD
  • sepsis
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64
Q

Describe the Crawford classification system of aortic aneurysms.

A
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65
Q

Describe the Debakey & Stanford classification systems of aortic dissection.

A

Stanford:

  • A = involves ascending aorta
  • B = doesn’t involve ascending aorta

DeBakey:
- Type 1 = tear in ascending + dissection along entire aorta
- Type 2 = tear in ascending + dissection only in ascending aorta
- Type 3 = tear in proximal descending aorta w/:
3a = dissection limited to thoracic aorta
3b = dissection along thoracic & abdominal aorta

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66
Q

Which law describes the relationship b/n aortic diameter & risk of aortic rupture in the patient w/ a AAA

A

LaPlace

wall tension = transmural pressure x vessel radius

T=P x R

increased diameter –> increased transmural pressure –> increased wall tension

mortality increases significantly once AAA reaches > 5.5cm

surgical correction is recommended at this time or if it’s growing >0.6-0.8cm/yr

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67
Q

How does the aortic cross clamp contribute to the risk of anterior spinal artery syndrome?

A

A clamp placed above the artery of Adamkiewicz may cause ischemia to the lower portion of the anterior spinal cord.

This can result in anterior spinal artery syndrome (aka Beck’s syndrome).

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68
Q

How does anterior spinal artery syndrome present?

A

flaccid paralysis of LE
bowel/bladder dysfunction
loss of temp/pain sensation

preserved touch & proprioception so they can still feel

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69
Q

What is amaurosis fugax?

A

blindness in one eye, a sign of impending stroke

emboli travel from the ICA to the opthalmic artery, which impairs perfusion of the optic nerve & causes retinal dysfunction

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70
Q

A patient is undergoing CEA w/ EEG monitoring. What does this monitor tell you, and what conditions can lead to false conclusions?

A

monitors cortical electrical function NOT subcortical

  • risk of cerebral hypoperfusion w/ loss of amplitude, decreased beta wave activity, and slow wave activity
  • high incidence of false negatives (hypercarbia, hypoxia, seizures, hypothermia, ketamine, N2O, light or too heavy anesthesia, opioids)
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71
Q

What regional technique can be used for the patient undergoing a CEA? What levels must be blocked?

A

cervical plexus block (superficial or deep)

C2-C4

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72
Q

What reflex can be activated during CEA or following carotid balloon inflation?

A

baroreceptor

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73
Q

A pt in the PACU develops a hematoma following R CEA. Her airway is completely obstructed. What is the best treatment at this time?

A

emergency decompression of the surgical site

If the surgeon isn’t readily available, this falls on you. Cricothyroidotomy may be required.

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74
Q

Name two presenting signs of cyanide toxicity associated with sodium nitroprusside

A
  • Tachyphylaxis (where you need to increase dosage)
  • Metabolic acidosis
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75
Q
A
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76
Q
A
77
Q
A
78
Q

Name some things that increase contractility

A
79
Q
A

Afterload

SV is decreased by:
- decreased preload
- decreased contractility
- increased afterload

decrease afterload = SV will increase

80
Q
A
81
Q

Mediators of coronary vasodilation include:

A
  • Adenosine
  • Beta 2 agonist: increases CAMP: decreases MLCK sensitivity to calcium
  • Histamine 2: increases CAMP: decreases MLCK sensitivity to calcium
  • Muscarinic: increases nitric oxide
82
Q

Things that cause coronary vasoconstriction:

A
  • Histamine 1
  • Alpha agonist
  • Hypocarbia
83
Q

When does primentzal angina occur?

A

It occurs at rest due to overreactive alpha receptors

84
Q

List 3 things responsible for coronary autoregulation

A

1) local metabolism- ex: adenosine potent vasodilator

2) myogenic response: ability to maintain vessel diameter. When diameter increases: contracts, when it decreases: dilates

3) ANS: example is prinzmetal angina

85
Q
A
86
Q

What causes vasodilation and vasoconstriction?

G-protein cAMP Pathway

Nitric oxide cMP Pathway

Phospholipase C Pathway

A

G-protein cAMP Pathway → Vasodilation

Nitric oxide cMP Pathway → Vasodilation

Phospholipase C Pathway → Vasoconstriction

87
Q
A

Loop width is reduced, ESV shifts to the right

88
Q

Bradycardia is caused by:

A) making the threshold potential more negative.
B) increasing potassium conductance.
C) increasing the slope of phase 4 depolarization.
D) making the resting membrane potential more positive.

A

B) increasing potassium conductance.

Threshold potential becomes more negative, shorter ddistance between RMP and TP, so it takes longer for the cell to reach TP. This slows HR

89
Q

How much of the cardiac output does the myocardium receive at rest?

A

5%

90
Q

The sarcoplasmic reticulum releases calcium when:

A) repolarization occurs.
B) the SERCA2 pump is turned on.
C) calcium stimulates the ryanodine receptor.
D) troponin binds to the actin/myosin complex.

A

C) calcium stimulates the ryanodine receptor.

Ca+2 activates the ryanodine receptor (RyR2), which releases a large quantity of Ca+2 from the sarcoplasmic reticulum.

This is called calcium-induced calcium-release.

91
Q

Choose the statements that most accurately describe the coronary circulation. (Select 3.)

A) The right coronary artery perfuses the apex of the heart.
B) The left circumflex artery supplies the left bundle branch.
C) Leads Il, Ill, and AVF monitor the right coronary artery.
D) The left anterior descending artery perfuses the anterior 2/3 of the septum.
E) Left coronary artery dominance occurs in 80% of the population.
F) The SA nodal artery most commonly arises from the right coronary artery.

A

A) The right coronary artery perfuses the apex of the heart.
B) The left circumflex artery supplies the left bundle branch.
C) Leads Il, Ill, and AVF monitor the right coronary artery.
D) The left anterior descending artery perfuses the anterior 2/3 of the septum.
E) Left coronary artery dominance occurs in 80% of the population.
F) The SA nodal artery most commonly arises from the right coronary artery.

92
Q

Contractility is dependent on:

A) preload
B) afterload
C) neither

A

Neither

93
Q

Which phases of the cardiac cycle are associated with an open mitral valve and a closed aortic valve? (Select
3.)

A) Diastasis
B) Isovolumic ventricular contraction
C) Isovolumic ventricular relaxation
D) Ventricular ejection
E) Atrial systole
F) Rapid ventricular filling

A

A) Diastasis
B) Isovolumic ventricular contraction
C) Isovolumic ventricular relaxation
D) Ventricular ejection
E) Atrial systole
F) Rapid ventricular filling

94
Q

Most common cause of Aortic stenosis?

A

Bicuspid aortic valve and calcification (occurs at birth, instead of 3 leaflets there’s 2)

95
Q

Which drug is MOST likely to increase the degree of prolapse in the patient mitral valve prolapse?

Sevoflurane
Ketamine
Phenylephrine
Etomidate

A

Ketamine

A large ventricle tends to reduce MV prolapse, while a small ventricle tends to increase MV prolapse. For this reason, the primary management goal for MVP is to prevent excessive cardiac emptying.

To Keep the Heart Full, You’ll Want to Avoid:
• SNS stimulation → myocardial contractility
• Decreased SVR
• Hypovolemia
• Upright posture (reverse Trendelenburg or sitting position)

96
Q

Which of the following is the LEAST likely to precipitate pulmonary edema with mitral stenosis?

Uterine contraction
Judicious fluid administration
Atrial fibrillation
Trendelenburg position

A

Judicious fluid administration

In the patient with severe mitral stenosis, any condition that increases left atrial volume can precipitate pulmonary edema. Of all the answer choices, judicious fluid administration is least likely to raise left atrial pressure significantly.

Both uterine contraction and Trendelenburg position increase preload. Atrial fibrillation reduces cardiac output and increases back pressure in the pulmonary circulation.

97
Q
A
98
Q

What factors increase myocardial demand?

A
  • tachycardia
  • HTN
  • SNS stimulation
  • increased wall tension
  • increased end diastolic volume
  • increased afterload
  • increased contractility
99
Q
A

Myocardial ischemia and aging

100
Q

Name things that cause cardiac compliance

A

Know all these in detail

101
Q

How does a decreased compliance affect PAOP and CVP?

A

It may overestimate LVEDP

102
Q

List things that INCREASE compliance

A
  • dilated cardiomyopathy
  • chronic aortic insufficiency
103
Q
A

Increased sympathetic tone

To maintain blood pressure, patients with CHF rely on elevated levels of circulating catecholamines (increased SNS tone).

Anesthetic techniques that reduce SNS tone can precipitate cardiovascular collapse.
For instance, a standard propofol induction (2 mg/kg) is not a good idea because it reduces SNS tone while simultaneously reducing myocardial contractility. Propofol is a suitable option, however the patient may require slow titration of a much lower dose.

CHF reduces renal blood flow, and this is the primary mechanism that activates the renin-angiotensin-aldosterone system.
Atrial dilation (from CHF) increases the release of atrial and brain natriuretic peptides. ANP and BNP cause natriuresis (Na and water excretion).

104
Q

Adaptation to heart failure

A
  • remodeling: can be reversed with ace inhibitors and spirnolactone
105
Q

Name things that increase PVR

A
  • hypoxia
  • hypercarbia
  • acidosis
  • hypothermia
  • high PEEP
  • PPV
  • atelectasis
  • nitrous oxide
  • polycythemia
106
Q

How does CHF affect beta receptors?

A

Causes down regulation

107
Q

Name some causes of secondary HTN

A

The most common cause of secondary HTN is renal artery stenosis

108
Q

Know the differences between constrictive and acute pericarditis

A
109
Q

Cardiac tamponade

A
110
Q

Systolic HF with reduced EF anesthetic management

A
  • preload is fine this is a pumping problem
    -we want to reduce afterload, so we can give sodium Nitroprusside
  • give contractility as needed
  • keep HR high if the EF is low
111
Q

Diastolic HF with preserve EF management

A
  • This is a filling problem
  • keep afterload elevated with neo
  • want heart low to give it more time to fill
112
Q

Metolazone, indapamide

A

Thiazide diuretics. Inhibits NaCl in distal convoluted tubule

113
Q
A

Diltiazem - benzothiazepine best for a patient with reduced contractility

114
Q
A
  • Kassuamal’s usually present
  • avoid Bradycardia
115
Q

Constrictive pericarditis

A

is caused by fibrosis or any condition where the pericardium becomes thicker.

The ventricles cannot fully relax during diastole, and this reduces compliance and limits diastolic filling.

Ventricular pressures increase, and this creates back pressure on the peripheral circulation.

The ventricles adapt by increasing myocardial mass, but over time this impairs systolic function.

116
Q

Constrictive pericarditis is caused by?

S/S:

Tx:

A

Caused by:
- Cancer (radiation)
- Cardiac surgery
- Rheumatoid arthritis
- Tuberculosis
- Uremia

S/S:

  • Due to increase venous pressure and decrease in CO
  • Kussmaul’s sign: JVD during inspiration
  • Pulsus paradoxus (less common)
  • Distended neck veins
  • Hepatomegaly
  • Peripheral edema
  • Atrial dysrhythmias d/t atrial distension
  • pericardial knock

Tx: Pericardiotomy

CO is dependent on HR: Avoid bradycardia. Preserve HR and contractility

117
Q

Acute pericarditis causes:

A
  • Infection (viral most common)
  • Dresser’s syndrome - inflammation from necrotic myocardium s/p MI (Dressler’s syndrome is a form of pericarditis seen following myocardial infarction.)
  • Systemic lupus erythematosus
  • Scleroderma
  • Trauma
  • Cancer (same has constrictive pericarditis)
118
Q

Acute pericarditis S/S:

A
  • Acute chest pain with pleural component
  • Pain with inspiration & postural changes, relieved by leaning forward or supine
  • Pericardial friction rub
  • ST elevation w/ normal enzymes
  • Fever

Tx:
- Usually resolves spontaneously
- Drugs to relieve pain: salicvlates, oral analgesics

119
Q

Constrictive pericarditis tx:

A

Avoid bradycardia! Since cardiac output is dependent on heart rate

Preserve heart rate and contractility
- Pancuronium
- opioids, etomidate, benzos are ok!
- Maintain afterload
- Aggressive PPV can decrease venous return & CO

120
Q

Cardiac tamponade: what increases and decreases?

LV pressure:
Ventricular filling:
Ventricular volume:
Stroke volume:
Cardiac output:
SNS:
Coronary perfusion pressure:

A

LV pressure: increased
Ventricular filling: decreased
Ventricular volume: decreased
Stroke volume: decreased
Cardiac output: decreased
SNS: increased and contractility
Coronary perfusion pressure: decreased

121
Q

Drugs that ok with use with cardiac tamponade

A
  • ketamine
  • opioids
  • nitrous oxide
  • benzos
122
Q

Do you need prophylaxis antibiotics for unrepaired cardiac valve?

A

No

Read all this well!!!

You will need abx for bronchscopy with biopsy and previous valve replacement, and unrepaired congenital disease

123
Q

Asymmetrical septal hypertrophy

A
124
Q

Hypertrophic obstructive cardiomyopathy

A

Pro tip: Treat it similar to aortic stenosis

Full, slow, constricted. Increase afterload! And decrease contractility with BB and CCB

125
Q

List 2 things that cause LVOT

A
126
Q

List 3 surgical options to correct LVOT

A
127
Q

Priming bypass circuit with anything other than blood products can cause a decrease in what? And increase in??

A
128
Q

How much protamine to reverse heparin?

A

1mg of protamine for 100 units of heparin

129
Q

IABP

A

Position it 2cm distal to the LEFT of subclavian artery

130
Q

IABP

Review placement

A

Notice where the balloon inflates

131
Q

LVAD

A

Inotrophy

132
Q

LVAD

A

LVAD is a mechanical device that unloads the failing heart by pumping blood from the left ventricle to the aorta.
The inflow cannula is inserted into the apex of the left ventricle.

From here, blood flows through the LVAD pump and is returned to the aorta through the outflow cannula.

Avoid regional bc they’re on anticoagulants

133
Q
A
134
Q

AAA

A
135
Q

AAA

A

Caused by destruction of elastin and collagen in vessels

Law of Laplace = wall stress / radius

SX when > 5.5 cm or if it grows more than 0.6-0.8cm per year

Ruptures in left retroperitoneum = allowing it to tamponade and clot formation

MI is most common post operative death

S/S hypotension, back pain, pulsatile abdominal mass

136
Q
A
137
Q

Aortic cross clamping

A
138
Q

Aortic cross clamping: what increases and decreases?

  • MAP
  • CO
  • SVR
  • Venous return
  • AoDP
  • Total body VO2
A
  • MAP: increased
  • CO: decreased
  • SVR: increased
  • Venous return: increased
  • AoDP: increased
  • Total body VO2: increased
139
Q

How is wall stress, cardiac output, renal blood flow affected by aortic clamping?

A

Wall stress is increased

CO is decreased

Renal blood flow is decreased

140
Q

Aortic cross clamp removal: what is increased or decreased?

  • Preload, afterload, contractility, AoDP
  • PAOP, PVR, total VO2
A
  • Preload, afterload, contractile, AoBP are decreased
  • PAOP increased, PVR increased, total VO2 increased
141
Q

Artery of Adamkiewicz

A
142
Q

Anesthesia considerations for anterior spinal cord syndrome

A
143
Q

Sensation, motor, temperature/pain?

Corticospinal tract-

Spinothalamic tract-

Dorsal column tract-

A

Corticospinal tract- motor

Spinothalamic tract- sensory: temperature sensation, pain sensation

Dorsal column tract- sensory

144
Q

Subclavian steal syndrome

A
145
Q

Carotid artery angioplasty stenting

A

Biggest risk of activating baroreceptor reflex, anticholinergics are helpful

Common complication- thromboembolic stroke due to arthrosclerotic debris

146
Q
A

Systolic anterior motion (SAM) is a complication of mitral valve repair

Nitroprusside and Dobutamine make it worse

Tx is similar to HOCM and nitro and Dobutamine make it worse

Neo and fluid bolus improves it

147
Q

MAP =

A

CO x SVR

148
Q

Impact on O2 supply and demand:

  • Tachycardia
  • Increased Aortic diastolic pressure:
  • Increased preload:
A
  • Tachycardia: decrease supply, increase demand
  • Increased Aortic diastolic pressure: increased supply, increased demand
  • Increased preload: decreased supply, increased demand
149
Q
A

KEY: Diastolic murmur at midclaviclar line MSD: mitral stenosis DIASTOLIC MURMUR

think of all things associated with MSD:
Endocarditis, SLE, RA, rheumatic fever, carcinoid syndrome

150
Q
A

Dilation and pulmonary edema

151
Q

CO x 1000/ HR

A

SV

152
Q

List some things that reduce preload

A
153
Q

Review what’s on the X and Y axis

A
154
Q

Review this

A

Systole: IC and ejection

155
Q

What is happening at isovolumic relaxation?

A

MV and AV are CLOSED

156
Q

Label the arteries

A
157
Q
A

Raise concentration gradient with the inhalation agent and give them a BB

158
Q

S/S of angina

A
159
Q

Severe aortic stenosis

A

Peak velocity > 4

Mean gradient > 40 mmHg

Aortic valve < 1 cm2

160
Q
A
161
Q

Hypoplastic left heart syndrome

A
  • Underdeveloped Left Ventricle: The left ventricle, normally responsible for pumping oxygenated blood to the body, is too small to perform its function.
  • Mitral and Aortic Valve Defects: These valves are often either narrowed or closed, restricting blood flow from the left atrium to the left ventricle and from the ventricle to the aorta.
  • Narrowed or Small Ascending Aorta: The main artery that carries blood from the heart to the rest of the body is too small to provide adequate blood flow.

So they need a PDA to bypass the small left ventricle. PDA is temporary and critical!

They will need a Noorwood surgery where the right ventricle connects to the lungs and the aorta

162
Q

Tricuspid Atresia

A

Absence or blockage of the tricuspid valve in the heart, preventing blood flow from the right atrium to the right ventricle.

Absent or Closed Tricuspid Valve/

Will need PDA or ASD to keep it open

  • Small right ventricle, enlarged left ventricle
  • decreased pulmonary blood flow (that occurs via a ventricular septal defect, patent ductus arteriosus, or bronchial vessels), - - arterial hypoxemia.
  • (right-to-left shunt) via an atrial septal defect prior to ejection into the systemic circulation causing a cyanotic defect.
163
Q
A
164
Q
A
165
Q
A
166
Q
A
167
Q
A
168
Q

Truncus Arteriosus

A

is a rare congenital heart defect in which a single large blood vessel (called the truncus arteriosus) arises from the heart, instead of the normal two separate vessels—the pulmonary artery and the aorta.

  1. Single Outflow Vessel: Instead of the normal two outflow tracts (the aorta and pulmonary artery), a single vessel exits the heart.
  2. Ventricular Septal Defect (VSD): There is usually a large hole between the two ventricles of the heart (a ventricular septal defect), allowing oxygen-poor blood from the right ventricle and oxygen-rich blood from the left ventricle to mix before being pumped through the truncus arteriosus.
  3. Mixed Blood Circulation: Because of the mixing of oxygenated and deoxygenated blood

TX: closure of VSD and to separate aorta and pulmonary artery

169
Q
A
170
Q
A
171
Q
A
172
Q

Name some features of Carvedilol

A
173
Q

Hyperkalemia and hypokalemia affects RMP by

A

Hyperkalemia increases RMP

Hypokalemia decreases RMP

174
Q

how to calculate CVO2

If you have hgb, spo2, and svo2

A

CVO2 = SpO2 - SvO2

Use 1.34 x hgb

(1.34 x hgb x SpO2) - (1.34 x hgb x SvO2)

175
Q

Things that affect myocardial SUPPLY

A

Diastolic time, AoDP, P50

176
Q

Highest increase in myocardial O2 CONSUMPTION

A

Heart rate > pressure work > contractility > wall stress > ventricle work

Highest rate and pressure work are the highest increase!!!!!!!!!

177
Q

Things that reduce preload

A

Avoid in HOCM

178
Q

Which of the following ECG changes is an indication of subendocardial ischemia?

A

Depression of the ST segment is typically associated with subendocardial ischemia

179
Q

Eisenmenger’s syndrome

A

Eisenmenger’s syndrome is a reversal of a left-to-right intracardiac shunt due to an increase in the pulmonary vascular resistance. Once the pulmonary vascular resistance reaches a level that is equal to or exceeds systemic vascular resistance, the shunt reverses to a right-to-left shunt.

180
Q

Which substance is released from the ventricles in response to increased wall stress?

A

Increased wall stress will cause the ventricles to release B-type natriuretic peptide.

The atria to release atrial natriuretic peptide

Both are released to produce diuresis, increased sodium excretion, and vasodilation.

181
Q

Which substance is released from the ventricles in response to increased wall stress?

A

Increased wall stress will cause the ventricles to release B-type natriuretic peptide.

The atria to release atrial natriuretic peptide

Both are released to produce diuresis, increased sodium excretion, and vasodilation.

182
Q

What is the most common cardiac defect through which a paradoxical embolus will occur?

A

A paradoxic embolus occurs when air or a thrombus transfers from the venous system to the arterial system by passing through a defect in the heart.

The most common defect through which this can occur is a patent foramen ovale.

183
Q

What are the primary determinants of stroke volume?

A

Preload, afterload, and cardiac contractility

184
Q

What are the primary determinants of stroke volume?

A

Preload, afterload, and cardiac contractility

185
Q

Supraventricular tachycardia most commonly occurs due to a reentry circuit consisting of

A

anterograde conduction over the slower AV nodal pathway

186
Q

Which agent is a competitive alpha-1 and alpha-2 receptor antagonist used primarily in the preoperative treatment of pheochromocytoma?

A

Phentolamine is a competitive alpha-1 and alpha-2 receptor antagonist used primarily in the preoperative treatment of pheochromocytoma.

Its preffered bc its short acting and reversible

187
Q

Where is the MAP on a flow loop?

A
188
Q

Class of anti-arrhythmic drugs

A

Class 1A: Double Quarter Pounder: Disopyridine, quinidine, procainamide (all end in -ine or -ide) moderate sodium channel blocking, prolongs AP

Class 1B: Lettuce Pickles: Lidocaine, Phenytoin Weaker sodium channel blockers

Class 1C: Fries Please: Flecainide and Propafenone

2: Beta blockers: slows depolarization of phase 4

3: Potassium channel blockers, prolongs phase 3 repolarization: Amiodarone, Bretylium

4: CCB: decreases conduction through AV node: verapamil, diltiazem

APEX ANESTHESIA FLASHCARDS (14 decks)

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