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Apex NCE Board Prep 2020 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q 
Define the terms: 
chronotropy 
inotropy 
dromotropy 
lusitropy
A
  • chronotropy: heart rate
  • inotropy: contractility
  • dromotropy: conduction velocity (how fast action potential travels per time)
  • lusitropy: rate of myocardial relaxation (during diastole)
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2
Q

Describe the function of the Sodium-Potassium pump

A
  • it maintains the cells resting membrane potential
  • keeps the inside of the cell negative relative to the outside (outside is positive)
  • it removes the Na that entered the cell during depolarization and replaces the K that left the cell during repolarization
  • takes out 3 Na ions and puts back 2 K ions
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3
Q

List the 5 phases of the ventricular action potential

A
  • Phase 0: Depolarization - Na influx
  • Phase 1: Initial repolarization: K efflux and Cl influx
  • Phase 2: Plateau phase: Ca influx (slow)
  • Phase 3: Repolarization: K efflux
  • Phase 4: Na/K Pump restores RMP
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4
Q

List the 3 phases of the SA node action potential

A
  • Phase 4: Spontaneous depolarization- leaky to Na (Ca influx at the very end of phase 4)
  • Phase 0: Depolarization - Ca influx
  • Phase 3: Repolarization- K efflux
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5
Q

What process determines the intrinsic heart rate?

What physiologic factors alter it?

A
  • rate of spontaneous phase 4 depolarization of the SA node
  • can increase heart rate by manipulating 3 variables:
    1. rate of phase 4 increases (reaches TP sooner)
    2. TP becomes more negative (shorter distance to RMP)
    3. RMP becomes more positive (shorter distance to TP)
  • when RMP and TP are close it is easier for the cell to depolarize
  • when RMP and TP are further apart it is harder for the cell to depolarize
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6
Q

Equation for MAP

A

SBP + 2(DBP) / 3

[(CO x SVR) / 80] + CVP

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7
Q

Equation for SVR

A

[(MAP - CVP) / CO] x 80

norm: 800-1500 dynes/sec/cm

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8
Q

Equation for PVR

A

[(PMAP - PAOP) / CO] x 80

norm: 150-250 dynes/sec/cm

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9
Q

Describe Frank-Starling

A
  • relationship between ventricular volume (preload) and ventricular output (cardiac output)
  • increased preload = increased myocyte stretch = increased cardiac output
  • decreased preload = decreased myocyte stretch= decreased cardiac output
  • increased preload causes an increased CO to a certain point. After that additional volume overstretches the sarcomeres, decreases number of crossbridges and reduces cardiac output. Leads to pulmonary congestion and increases PAOP
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10
Q

What factors cause increased myocardial contractility?

A
  • SNS stimulation
  • catecholamines
  • calcium
  • digitalis
  • phosphodiesterase inhibitor
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11
Q

What factors cause decreased myocardial contractility? (labs, drugs, ect.)

A
  • myocardial ischemia
  • severe hypoxia
  • hypercarbia
  • hyperkalemia
  • hypocalcemia
  • volatile anesthetics
  • propofol
  • beta blockers
  • calcium channel blockers
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12
Q

Excitation-contraction coupling in the cardiac myocyte

A
  • action potential causes cell to depolarize
  • During plateau phase (2), Ca+ enters the myocyte through the L-type Ca+ channels in the t-tubules
  • Ca+ influx turns on ryanodine receptor which then causes calcium release from the SR (Ca-induced Ca-released)
  • Ca+ binds to troponin C (contraction)
  • Ca+ unbinds from troponin C (relaxation)
  • Ca+ goes back to SR via SERCA2 pump
  • Ca+ that is in the SR binds to storage protein calsequestrin
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13
Q

What is afterload and how do you measure it in the clinical setting?

A
  • the force the ventricle must overcome to eject its stoke volume
  • measured by SVR
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14
Q

What law can be used to describe ventricular afterload?

A

wall stress = (intraventricular pr. x radius)/ ventricular thickness

  • intraventricular pressure is the force that pushes the heart apart
  • wall stress is the force that holds the heart together
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15
Q

How is wall stress reduced?

A
  • decreased intraventricular pressure
  • decreased radius
  • increased wall thickness
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16
Q

Three conditions that set afterload proximal to the systemic circulation

A
  • aortic stenosis
  • hypertrophic cardiomyopathy
  • coarctation of the aorta
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17
Q

Use the Wiggers diagram to explain the cardiac cycle

A
  • starts with both atrial and ventricular pressures close to zero
  • atrium is getting filled from pulmonary circulation
  • atrial pressure is slightly higher so blood enters ventricle through MV and increases ventricular volume
  • aortic pressure is high at the top but falling
  • atria depolarizes and contracts
  • blood enters ventricle through MV and increases ventricular volume and pressure
  • ventricle depolarizes and contracts = shuts MV valve
  • MV and AV are closed = isovolumetric contraction
  • ventricular pressure rises but volume stays the same
  • increased ventricular pressure causes a tug on MV valve when it closes = quick jump in atrial pressure
  • ventricular pressure rises fast and opens AV
  • increase in aortic pressure (blood flows in) and ventricular pressure still increased (being actively stretched)
  • tug on MV valve is released = drop in atrial pressure
  • atrial pressure starts to rise as it gets blood back from the lungs
  • aortic and ventricular pressure fall = ventricular relaxation
  • ventricular pressure falls faster and AV slams shut
  • causes back flow of blood = dicrotic notch
  • both valves closed = isovolumetric relaxation
  • ventricular and aortic pressure continue to fall and blood flows to systemic circulation
  • atrial pressure exceeds ventricular as it is filled with blood from the lungs and the MV valve will open again
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18
Q

Relate the 6 stages of the cardiac cycle to the LV pressure-volume loop

A
  1. rapid filling = diastole
  2. reduced filling = diastole
  3. atrial kick = diastole
  4. isovolumetric contraction = systole
  5. ejection = systole
  6. isovolumetric relaxation = diastole
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19
Q

Ejection Fraction Calculation

A

EF = EDV - ESV / EDV x 100

  • EF is mesure of systolic function (contractility)
  • is the percentage of the blood that is ejected during systole
  • normal EF = 60-70%
  • LV dysfunction when EF < 40%
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20
Q

Best TEE view for diagnosing MI

A

mid papillary muscle level in short axis

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21
Q

Equation for coronary perfusion pressure

A

CPP = AoDBP - LVEDP

LVEDP = PAOP = Diastolic PA pressure

  • CPP can be improved by increasing AoDBP or decreasing LVEDP
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22
Q

What region of the heart is most susceptible to ischemia?

A
  • LV subendocardium
  • as aortic pressure increases, the LV tissue compresses the subendocardium and reduces blood flow
  • the high compressive pressure and decreased coronary blood supply during systole increases coronary vascular resistance and can lead to ischemia
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23
Q

What factors cause decreased myocardial oxygen delivery?

A 
DECREASED CORONARY FLOW 
- tachycardia
- decreased aortic pressure 
- decreased vessel diameter 
- increased end diastolic pressure 
DECREASED CaO2 
- hypoxemia
- anemia 
DECREASED OXYGEN EXTRACTION 
- left shift of Hgb dissociation curve (decrease P50) 
- decreased capillary density
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24
Q

What factors cause increased myocardial oxygen demand?

A
  • tachycardia
  • HTN
  • SNS stimulation
  • increased wall tension
  • increased EDV
  • increased afterload
  • increased contractility
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25
Q

Nitric oxide pathway of vasodilation

A
  • nitric oxide synthase converts L-arginine to nitric oxide
  • NO diffuses from endothelium into smooth muscle
  • NO activates guanylate cyclase
  • guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate (cGMP)
  • cGMP reduces intracellular Ca, causing smooth muscle relaxation
  • phosphodiesterase deactivates cGMP
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26
Q

Where are the heart sounds on the LE pressure-volume loop?

A

S1: at closure of MV (and tricuspid) = onset of systole
S2: at closure of AV (and pulmonic) = onset of diastole
S3: could be heard during early ventricular filling = may be systolic dysfunction
S4: could be heard at late filling just before MV closes = may be diastolic dysfunction

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27
Q

What are the two primary ways a heart valve can fail?

A
  1. stenosis
    • fixed obstruction to froward flow; must generate higher pressures
  2. regurgitation
    • valve is leaky and some blood flows forward and backward
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28
Q

Heart’s pressure compensation

A
  • concentric hypertrophy results from pressure overload

- sarcomeres are added in parallel

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29
Q

Heart’s volume overload compensation

A
  • eccentric hypertrophy results from volume overload

- sarcomeres are added in series

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30
Q

Hemodynamic goals for aortic stenosis

A

slow, skinny, normal

  • increase preload
  • maintain or increase SVR (CO depends on BP since SV is fixed at the stenotic valve)
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31
Q

Hemodynamic goals for aortic regurgitation

A

fast, full, forward

  • increase preload
  • decrease SVR
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32
Q

Hemodynamic goals for mitral stenosis

A

slow, full, constricted

  • maintain normal preload, SVR and contractility
  • avoid increases in PVR
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33
Q

Hemodynamic goals for mitral regurgitation

A

fast, full, forward

  • increase preload
  • decrease afterload
  • avoid increase in PVR
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34
Q

Most common dysrhythmia associates with mitral stenosis?

A

Atrial fibrillation

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35
Q

Six risk factors for preoperative cardiac morbidity and mortality for non-cardiac surgery

A
  • high risk surgery
  • Hx of ischemic heart disease
  • Hx of CHF
  • Hx of cerebrovascular disease
  • DM
  • creatinine > 2 mg/dL
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36
Q

Risk of preoperative MI in the pt with a previous MI

A
  • general population = 0.3%
  • if MI > 6 mo = 6%
  • if MI 3-6 mo = 15%
  • IF MI < 3 mo = 30%
37
Q

When is the highest risk of reinfarction after an acute MI?

A

within 30 days

*recommended to wait minimum of 4-6 weeks before elective surgery in patient with a recent MI

38
Q

High cardiac risk surgical procedures

A
  • emergency surgery (esp. elderly)
  • open aortic surgery
  • peripheral vascular surgery
  • long surgeries with lots of blood loss
39
Q

Intermediate risk cardiac surgical procedures

A
  • carotid
  • head and neck surgery
  • intrathoracic or intraperitoneal surgery
  • orthopedic surgery
  • prostate surgery
40
Q

Low cardiac risk procedures

A
  • endoscopic
  • cataracts
  • superficial procedures
  • breast surgery
  • ambulatory procedures
41
Q

Modified New York Association Functional Classification of Heart Failure

A
  • class I: asymptomatic
  • class II: symptomatic with moderate activity
  • class III: symptomatic with mild activity
  • class IV: symptomatic at rest
42
Q

Biomarkers released by infarcted myocardium

A
  • creatine kinase- MB
  • troponin I
  • troponin II
  • troponins are more sensitive
43
Q

Creatine Kinase- MB: initial elevation, peak, return to baseline

A
  • initial: 3-12 hrs
  • peak: 24 hrs
  • baseline: 2-3 days
44
Q

Troponin I: initial elevation, peak, return to baseline

A
  • initial: 3-12 hrs
  • peak: 24 hrs
  • baseline: 5-10 days
45
Q

Troponin II: initial elevation, peak, return to baseline

A
  • initial: 3-12 hrs
  • peak: 12-48 hrs
  • baseline: 5-14 days
46
Q

Treatment of intra-op MI

A
  • caused by increased O2 demand or decreased O2 supply
  • increased demand (high HR, BP, PAOP): give beta blocker, increase gas, vasodilator, Nitroglycerine
  • decreased supply (low HR and BP, hight PAOP): give anticholinergic, pace, decrease gas, vasoconstrictor, nitro, inotrope
  • nitroglycerine decreases PAOP
47
Q

What factors reduce ventricular compliance?

A
  • age > 60
  • ischemia
  • pressure overload hypertrophy (AS or HTN)
  • hypertrophic obstructive cardiomyopathy
  • pericardial pressure
48
Q

Systolic Heart Failure and hallmark symptoms

A
  • ventricle can’t empty/squeeze well
  • hallmark: decreased EF with increased EDV
  • caused by volume overload
49
Q

Diastolic Heart Failure

A
  • ventricle can’t fill properly because it is unable to relax (decreased vent compliance)
  • hallmark: symptomatic heart failure with normal EF
50
Q

Hemodynamic goals for systolic heart failure

A
  • preload: already high (give diuretics if too high)
  • afterload: decrease to reduce workload
  • contractility: use inotropes as needed (dobutamine)
  • heart rate: usually high d/t increased SNS tone; if EF is low then a higher HR is needed to preserve CO
51
Q

Hemodynamic goals for diastolic heart failure

A
  • preload: maintain/increase (volume needed to stretch noncompliant ventricle
  • afterload: elevated to perfuse thick myocardium
  • contractility: usually normal
  • heart rate: slow/normal to increase filling time
52
Q

Six complications of HTN

A
  • left ventricular hypertrophy
  • ischemic heart disease
  • CHF
  • arterial aneurysm (aorta, cerebral circus)
  • stroke
  • end-stage renal disease
53
Q

How does HTN cause CHF

A
  • HTN increases myocardial wall tension
  • increased wall tension causes increased MVO2 and left ventricular hypertrophy
  • LVH leads to diastolic CHF
  • increased MVO2 causes coronary insufficiency leading directly to CHF and/or infarction dysrhythmias which go on to cause CHF
54
Q

How does HTN affect cerebral autoregulation?

A
  • shifts the curve to the right allowing the brain to tolerate higher pressures
  • also makes the brain not able to tolerate lower pressures
  • BP past the zone of autoregulation is pressure dependent
55
Q

Primary vs. secondary HTN

A
  • primary (essential) HTN has no identifiable cause (95% of cases)
  • secondary HTN is caused by some other pathology (5% of cases)
56
Q

Seven causes of secondary hypertension

A
  • renal artery stenosis
  • coarctation of the aorta
  • hyperadrenocorticism (Cushing’s)
  • hyperaldosteronism (Conn’s)
  • pheochromocytoma
  • pregnancy-induced HTN
57
Q

Classes of calcium channel blockers

A

DIHYDROPYRIDINES: target vascular smooth muscle

  • nicardipine
  • nifedipine
  • nimodipine
  • amlodipine

NON-DIHYDROPYRIDINES: target myocardium

  • verapamil
  • diltiazem
58
Q

Pathophysiology of constrictive pericarditis

A
  • fibrosis or any condition that causes the pericardium to become thicker
  • ventricles can’t fully relax during diastole which reduces compliance and limits filling
  • causes back pressure to peripheral circulation
  • ventricles compensate by increasing in mass
  • over time systolic function becomes impaired
59
Q

Anesthetic management of constrictive pericarditis

A
  • avoid bradycardia: CO is dependent on HR
  • preserve HR and contractility (ketamine, pancuronium, caution with gas)
  • maintain afterload
  • aggressive PPV can decrease venous return and CO
60
Q

Pathophysiology of pericardial tamponade

A
  • fluid accumulation in the pericardium that exerts external pressure on the heart decreasing its ability to fill and pump
  • increased CVP with increasing pericardial pressures
  • CVP and PAOP equalize as ventricular compliance deteriorates
61
Q

Kussmal’s sign

A
  • backing up of blood d/t impaired RV filling causing JVD and increased CVP
  • is more pronounced during inspiration
62
Q

Two common conditions associated with Kussmal’s sign

A
  • constrictive pericarditis

- pericardial tamponade

63
Q

Pulsus Paradoxus

A
  • exaggerated decrease is SBP (more than 10 mmHg) during inspiration
  • suggests impaired diastolic filling
  • negative intrathoracic pressure on inspiration = increased VR to RV = bowing for ventricular septum towards LV = decreased SV, CO and SBP
64
Q

2 conditions associated with pulses paradoxus

A
  • constrictive pericarditis

- pericardial tamponade

65
Q

Beck’s traid and what is it associated with

A
  • JVD
  • muffled heart tones
  • hypotension
  • associated with acute cardiac tamponade
66
Q

Anesthesia for acute pericardial tamponade undergoing pericardiocentesis?

Drugs to use and drugs to avoid.

A
  • local is preferred
  • if general, need to preserve myocardial function
  • SV is severely decreased, but increased SNS tone provides compensation
  • avoid: gas, propofol, thiopental, high dose opioids, neuraxial
  • safe to use: ketamine (best), N2O, Benzes, opioids
  • any drug that depresses the myocardium decreases afterload and can cause CV collapse
67
Q

Six patient factors that warrant abx prophylaxis agains infective endocarditis

A
  • previous endocarditis infection
  • unrepaired cyanotic heart disease
  • prosthetic heart valve
  • congenital heart repair less than six months ago
  • repaired congenital heart with residual defects
  • heart transplant with valvuloplasty
68
Q

Three surgical procedures that warrant abx prophylaxis against infective endocarditis

A
  • dental procedures with gingival manipulation
  • respiratory procedures that perforate the mucosal lining
  • biopsy of the invective lesions on the skin or muscle
69
Q

Three determinants of LV outflow tract

A
  • systolic LV volume
  • force of LV contraction
  • transmural pressure gradient
70
Q

What factors reduce cardiac output in the patient with obstructive hypertrophic cardiomyopathy?

A
  • hypovolemia (decreased systolic volume)
  • hypotension (decreased Ao pressure)
  • increased contractility
  • goal is to distend the LVOT to decrease the obstruction and increase CO (increase systolic volume, decrease contractility, and increase Ao pressure)
71
Q

What hemodynamic conditions reduce CO in patient with hypertrophic cardiomyopathy?

A
  • increased HR (treat with B-blockers or CCBs)
  • increased contractility (treat with B-blockers or CCBs)
  • decreased preload (treat with volume)
  • decreased afterload (treat with Neo)
72
Q

How long should elective surgery be delayed in pt with bare metal stent?
Drug eluting stent?
Post CABG?

A
  • bare metal stent: 30 days
  • drug eluting stent
    • stable ischemic heart disease = 12 mo for first gen and 6 mo for current gen
    • acute coronary syndrome = 12 mo minimum
  • s/p CABG: 6 weeks (3 mo preferred)
73
Q

Alpha-stat vs pH-stat blood gas measurement during CPB

A
  • alpha-stat: doesn’t account for pt temp when measuring blood gas/pH (better outcomes in adults)
  • pH stat: corrects for the pt temp (better outcome in peds)
  • decreased temp allows for more CO2 to dissolve in the blood
74
Q

Why is a left ventricular vent used during CABG surgery?

A

removes blood from the LV (blood that comes from the thebesian veins and bronchial circulation)

75
Q

How does intra-aortic balloon pump function throughout the cardiac cycle

A

DIASTOLE

  • inflates during diastole to augment coronary perfusion
  • inflation correlates with dicrotic notch

SYSTOLE

  • deflates during systole to reduce afterload and improve CO
  • deflation correlates with R wave on EKG
  • IAoBP improves O2 supply and decreases O2 demand
76
Q

Four contraindications to the intra-aortic balloon pump

A
  • severe aortic insufficiency
  • descending aortic disease
  • severe PVD
  • sepsis
77
Q

Crawford classification of aortic aneurysms

A

Describes thoracoabdominal aneurysms

  • type 1: all or most of descending thoracic and only upper of abdominal aorta
  • type 2: all or most of descending thoracic and most of abdominal aorta
  • type 3: lower only descending thoracic and most of abdominal aorta
  • type 4: none of descending thoracic and most of abdominal aorta
78
Q

Stanford classification of aortic dissection

A
  • Type A: involves ascending aorta

- Type B: does not involve ascending aorta

79
Q

DeBakey classification of aortic dissection

A
  • Type 1: tear in ascending aorta and dissection along entire aorta
  • Type 2: tear in ascending aorta and dissection only in ascending aorta
  • Type 3: tear in proximal descending aorta
    • 3a- dissection only in thoracic aorta
    • 3b- dissection along thoracic and abdominal aorta
80
Q

When is surgical correction for a AAA recommended?

A
  • when the aneurysm exceeds 5.5 cm or if it grows more than 0.6-0.8 cm/year
81
Q

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

A
  • AoX clamp placed above artery of Adamkiewicz may cause ischemia to lower portion of spinal cord
  • can result in anterior spinal syndrome (aka Beck’s syndrome)
82
Q

How does anterior spinal syndrome present?

A
  • flaccid lower extremities
  • bowel and bladder dysfunction
  • loss of temp and pain
  • preserved touch and proprioception
83
Q

What is amaurosis fugax?

A
  • blindness in one eye that is a sign of impending stroke

- clot travels from internal carotid to ophthalmic artery

84
Q

What information does EEG monitoring provide during a carotid endarterectomy?

A
  • cortical electrical function (no subcortical)

- risk of cerebral hypo perfusion with loss of amplitude, decreased beta wave, and/or slow wave activity

85
Q

Causes of false-negatives with EEG monitoring

A

Increased frequency

  • mild hypercarbia
  • early hypoxia
  • seizure activity
  • ketamine
  • N2O
  • Light anesthesia

Decreased frequency

  • extreme hypercarbia
  • hypoxia
  • cerebral ischemia
  • hypothermia
  • anesthetic overdose
  • opioids
86
Q

Regional technique that is used for a carotid and what levels must be blocked

A
  • cervical plexus block (superficial or deep)
  • local infiltration
  • C2-C4 must be blocked
87
Q

What reflex can be activated during a carotid endarterectomy?

A

baroreceptor reflex

88
Q

what needs to be done if post-op carotid develops hematoma that causes airway compromise?

A
  • emergency decompression of surgical site

- cricothyroidotomy if surgeon isn’t immediately available

Apex NCE Board Prep 2020 (5 decks)

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