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APEXANESTHESIA > 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; separates charge across the cell membrane keeping the inside of teh cell relatively 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)
1 = initial repol (K+ efflux & Cl- influx)
2 = plateau (Ca++ influx)
3 = repol (K+ influx)
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+)
0 = depol (Ca++ influx)
3 = repol (K+ efflux)
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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
  • threshold becoming more negative
  • resting membrane potential becoming less negative
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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 (ventricular output)
- increased preload –> increased myocyte stretch –> increased ventricular output

the increase in output d/t increased preload only occurs to a point
- after this point, overstretch occurs to the ventricular sarcomeres –> decrease in # of cross bridges that can be formed –> 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
wall stress = PR/thickness

  • intraventricular pressure is the force that pushes teh 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

pay attention to the following:

  • where systole & diastole occur
  • 6 stages of the cardiac cycle
  • 4 pressure waveforms
  • how the pressure waveforms match up to the EKG
  • how the valve position changes match up to the EKG
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16
Q

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

A
  1. rapid filling (L lower baseline)
  2. reduced filling (later baseline)
  3. atrial kick (L lower corner)
  4. isovolumic contraction (R pressure increase)
  5. ejection (top slope)
  6. isovolumic relaxation (L pressure decrease)
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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

SV/EDV x100

normal 60-70%
LV dysfunction when EF <40%
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 = righ 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 CPP?

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 & demand?

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)

increased demand

  • tachycardia
  • HTN
  • SNS stimulation
  • increased wall tension
  • increased end diastolic volume
  • increased afterload
  • increased contractility
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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 
S1 = closure of MV &amp; TV (right lower corner)
S2 = closure of AV &amp; PV (left upper corner) 
S3 = may suggest systolic dysfunction (L bottom baseline)
S4 = may suggest diastolic dysfunction (R bottom baseline)
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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

volume overload:

  • eccentric hypertrophy
  • sarcomeres are added in series

pressure overload

  • concentric hypertrophy
  • sarcomeres are added in parallel
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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

mitral stenosis:
- short, L shifted
aortic stenosis:
- tall, R shifted
aortic regurg
- acute: R shifted, decreased pressure, and diagonal isovolumetric relaxation
- chronic: enlarged volume, no change in pressure, diagonal isovolumetric relaxation
mitral regurg:
- acute: R shifted, decreased pressure, diagonal isovolumetric contraction
- chronic: enlarged volume, decreased pressure, diagonal isovolumetric contraction

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28
Q

list the hemodynamic goals for the 4 common valvular defects.

A

aortic stenosis: slow HR, high preload, high/normal afterload, SR
aortic regurg: high HR, high/normal preload, low SVR
mitral regurg: high HR, high preload, low SVR, avoid increased PVR
mitral stenosis: slow/normal HR, avoid increased PVR

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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
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

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
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
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
  • values must be evaluated in the context of the patient’s EKG

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

35
Q

how do you treat intraoperative MI?

A

goals: 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

36
Q

what factors reduce ventricular compliance?

A 
age >60yrs
ischemia
pressure overload hypertrophy (i.e. aortic stenosis/HTN)
IHHS
pericardial pressure (external)

take away point: higher filling pressures are required to prime the ventricle

37
Q

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

A

systolic: the ventricle doesn’t empty well
- hallmark = decreased EF w/ an increased end diastolic volume. Volume overload commonly causes systolic dysfunction

diastolic: the ventricle doesn’t fill well
- when the heart is unable to relax and accept the incoming volume b/c compliance is reduced. defining characteristic = symptomatic heart failure w/ normal EF

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)
- decreased afterload to reduce workload (SNP), but maintain CPP
- 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
39
Q

list 6 complications of HTN

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

how does HTN contribute to CHF?

A

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

(all patho leads to one another)

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.

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%)

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
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
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

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

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

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.

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

50
Q

What is pulsus paradoxus?

A

an exaggerated decrease in SBP during inspiration (SBP falls by >10mmHg). 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

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

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)
53
Q

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

A

because hemodynamics are minimally affected, 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 (can precipitate CV collapse)

  • IA
  • propofol
  • TPL
  • high dose opioids
  • neuraxial

better to use: ketamine, N2O, benzos, opioids

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
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
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

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)
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)
59
Q

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

  • bare metal stent
  • drug eluting stent
  • s/p angioplasty
  • s/p 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)

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.

61
Q

Why is an LV vent used during CABG surgery?

A

Removes blood from LV. This blood usually comes from the Thebesian veins & bronchial circulation (anatomical shunt)

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

63
Q

List 4 contraindications to intra-aortic balloon pump.

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

Describe the Crawford classification system of aortic aneurysms.

A

of thoracoabdominal aneurysms

type 1: all or most of descending thoracic aorta & only upper abdominal aorta
type 2: all or most of descending thoracic aorta & most of abdominal aorta
type 3: only the lower descending thoracic aorta & most of abdominal aorta
type 4: none of the descending thoracic aorta but most of the abdominal aorta

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

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 * vessel radius
T=PR

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

67
Q

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

A

placed above the artery of Adamkiewicz may cause ischemia to the lower portion of the anterior SC. This can result in anterior spinal artery syndrome (aka Beck’s syndrome).

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

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

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 (doesn’t detect subcortical problems)

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

regional must cover C2-C4

72
Q

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

A

baroreceptor

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

The pt requires emergency decompression of the surgical site. If the surgeon isn’t readily available, this falls on you. Cricothyroidotomy may be required.

APEXANESTHESIA (12 decks)

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