UNIT 3 Cardiovascular Flashcards by Jesica Nguyen

define: chronotropy, inotropy, dromotropy, & lusitropy

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

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describe the function of the Na+ K+ pump

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

0 = depolarization (Na+ influx)

1 = initial repolarization  (K+ efflux &amp; Cl- influx)

2 = plateau (Ca++ influx)

3 = repolarization (K+ influx)

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

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

4 = spontaneous depol (leaky to Na+)
0 = depol (Ca++ influx)
3 = repol (K+ efflux)

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

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. (Shorter distance between RMP and TP)
- resting membrane potential becoming less negative (Shorter distance between RMP and TP)

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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what is the calculation for MAP?

SBP/3 + 2DBP/3

[(COxSVR)/80] + CVP

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what is the formula for SVR?

[(MAP-CVP)/CO]x80

normal 800-1500 dynes/sec/cm^5

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what is the formula for PVR?

[(MPAP-PAOP)/CO]x80

normal 150-250dynes/sec/cm^5

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describe the frank-starling releationship

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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what factors affect myocardial contractility?

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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discuss excitation-contraction coupling in the cardiac myocyte

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

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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what law can be used to describe ventricular afterload?

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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list 3 conditions that set afterload proximal to the systemic circulation

aortic stenosis
hypertrophic cardiomyopathy
coarctation of the aorta

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use the wiggers diagram to explain the cardiac cycle

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

rapid filling (L lower baseline)
reduced filling (later baseline)
atrial kick (L lower corner)
isovolumic contraction (R pressure increase)
ejection (top slope)
isovolumic relaxation (L pressure decrease)

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how do you calculate ejection fraction?

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

yes

SV = width of loop
EDV = righ side of loop at X axis

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what is the best TEE view for diagnosing myocardial ischemia?

midpapillary muscle level in short axis

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what is the equation for CPP?

CPP = aortic DBP - LVEDP

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

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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what factors affect myocardial oxygen supply & demand?

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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discuss the NO pathway of vasodilation

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

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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what are the two primary ways a heart valve can fail

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

volume overload: (Regurgitation) “Really Series”
- eccentric hypertrophy
- sarcomeres are added in series

pressure overload (stenosis)
- concentric hypertrophy
- sarcomeres are added in parallel

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describe pressure volume loops for the following pathophysiologies:

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

A = M.S.

B = A.S.

C = A.R.

D = M.R.

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list the hemodynamic goals for the 4 common valvular defects.

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

afib

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

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

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

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

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

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

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

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

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

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

how do you treat intraoperative MI?

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

what factors reduce ventricular compliance?

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

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

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

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

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

list 6 complications of HTN

LVH
ischemic heart disease
CHF
arterial aneurysm
stroke
ESRD

how does HTN contribute to CHF?

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

(all patho leads to one another)

how does HTN affect cerebral autoregulation?

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.

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

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

secondary - caused by some other pathology (5%)

list 7 causes of secondary HTN.

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

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

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

describe the pathophysiology of constrictive pericarditis

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

Describe the anesthetic management of constrictive pericarditis

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

describe the pathophysiology of pericardial tamponade

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

What is Kussmaul’s sign?

JVD or an increased CVP (most pronounced during inspiration). indicates impaired RV filling d/t a poorly compliant RV or pericardium.

List two conditions commonly associated w/ Kussmaul’s sign

can occur w/ any condition that limits RV filling.

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

What is pulsus paradoxus?

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

List 2 conditions commonly associated w/ pulsus paradoxus

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

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

occurs in those w/ acute cardiac tamponade.

hypotension (decreased SV)
JVD (impaired venous return to RV)
muffled heart tones (fluid accumulation in pericardial space attenuating sound waves)

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

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

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

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

list 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis

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

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

systolic LV volume
force of LV contraction
transmural pressure gradient

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

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

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

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

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

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

bare metal stent
drug eluting stent
s/p angioplasty
s/p CABG

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)

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

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.

Why is an LV vent used during CABG surgery?

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

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

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

List 4 contraindications to intra-aortic balloon pump.

severe aortic insufficiency
descending aortic dz
severe PVD
sepsis

Describe the Crawford classification system of aortic aneurysms.

Describe the Debakey & Stanford classification systems of aortic dissection.

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

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

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

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

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).

How does anterior spinal artery syndrome present?

flaccid paralysis of LE
bowel/bladder dysfunction
loss of temp/pain sensation
preserved touch & proprioception

What is amaurosis fugax?

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

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

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)

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

cervical plexus block (superficial or deep)
local infiltration

regional must cover C2-C4

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

baroreceptor

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

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

Name two presenting signs of cyanide toxicity associated with sodium nitroprusside

Tachyphylaxis (where you need to increase dosage)

Metabolic acidosis

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UNIT 3 Cardiovascular Flashcards

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