Unit 3 - CV Patho Flashcards
what is the risk of perioperative MI if the patient had an MI < 3 months ago?
30%
what is the risk of perioperative MI in the general population?
0.3%
when should a patient be referred to a cardiologist before surgery?
a pt with an NYHA classification of 3 or 4 who is scheduled for a high- or intermediate-risk surgery
risk of perioperative MI if MI > 6 months
6%
risk of perioperative MI if previous MI within 3-6 months
15%
highest risk of reinfarction
within 30 days of acute MI
ACC/AHA minimum recommended time before considering elective surgery in a patient with recent MI
4-6 weeks
6 risk factors for perioperative cardiac morbidity & mortality for non-cardiac surgery
- high risk surgery
- history of IHD (greatest risk with unstable angina)
- history CHF
- history cerebrovascular disease
- DM
- serum Cr > 2 mg/dL
what factor confers the greatest risk of perioperative MI
unstable angina
3 important biomarkers released by infarcted myocardium
what’s more sensitive of MI diagnosis?
- creatine kinase-MB
- troponin I
- troponin T
troponins are more sensitive
when do biomarkers released by infarcted myocardium initially elevate
3-12 hours
peak elevation with infarcted myocardium:
CK-MB
Troponin I
Troponin T
- CK-MB: 24 hours
- Troponin I: 24 hours
- Troponin T: 12-48 hours
when does CK-MB return to baseline after MI?
2-3 days
when do troponin I levels return to normal after infarction?
5-10 days
when do troponin T levels return to normal after infarction
5-14 days
EKG lead that aids in identification of inferior wall ischemia & monitors for dysrhythmias
lead II
best leads for detecting intraoperative LV ischemia
V3, V4, V5
which lead may be best for detecting ischemia & why
V4
closest to isoelectric level on baseline EKG
combination of what 3 leads has an ischemic detection rate of up to 96%
leads II, V4, V5
intraop EKG monitoring in CAD pt
RA, RL, LA, LL, and a V lead to monitor for LV ischemia
goal of myocardial ischemia interventions
make the heart smaller, slower, and better perfused
how to treat intraop increased myocardial O2 demand caused by increased PAOP
nitroglycerin
what is diastolic compliance
describes filling pressure that results from a given EDV
what happens to the diastolic pressure-volume curve with decreased compliance
curve shifts up and left
higher EDP for given EDV
what happens to diastolic pressure-volume curve with increased compliance
shifts down and right
lower EDP for given EDV
5 conditions that make the heart “stiffer” and decrease compliance
(things that affect the diastolic pressure-volume relationship)
- age > 60
- ischemia
- pressure overload hypertrophy (aortic stenosis or HTN)
- HOCM
- pericardial pressure (increased external pressure)
what happens to filling pressures in a poorly compliant ventricle
higher filling pressures required to prime poorly compliant ventricle
CVP and PAOP with reduced ventricular compliance
may overestimate LVEDV
why is there a risk of pulmonary edema in a poorly compliant ventricles
higher filling pressures required
2 conditions that dilate the heart and increase compliance
- chronic aortic regurg
- dilated cardiomyopathy
what type of heart failure is associated with a pumping problem
HF with reduced ejection fraction
aka systolic failure
what type of heart failure is assoc. with a filling problem
HF with preserved EF
aka diastolic failure
3 etiologies of systolic heart failure (HFrEF)
- myocardial ischemia
- valve insufficiency
- dilated cardiomyopathy
7 etiologies of diastolic failure (HFpEF)
- myocardial ischemia
- valve stenosis
- HTN
- hypertrophic cardiomyopathy
- cor pulmonale
- obesity
- aging
what is HF with reduced EF?
heart can’t pump enough blood to satisfy body’s metabolic requirements
volume overload
what is HF with preserved EF
heart can’t relax and accept incoming volume d/t decreased ventricular compliance
contractility with HFpEF
generally preserved unti late in disease
compensation for HFrEF
- increased SNS
- increased RAAS
- increased preload
EDV, EDP, ESV, SV, LV mass, and LV geometry in chronic HFrEF (systolic failure)
- increased EDV
- increased EDP
- increased ESV
- decreased/normal SV
- increased LV mass
- eccentric hypertrophy
EDV, EDP, ESV, SV, LV mass, and LV geometry in chronic HFpEF (diastolic failure)
- normal EDV
- increased EDP
- normal ESV
- normal or decreased SV
- increased LV mass
- concentric hypertrophy
defining characteristic of HFpEF (diastolic failure)
symptomatic heart failure with normal EF
5 ways the body adapts to heart failure & consequences of each
- SNS activation - increased myocardial work
- excessive vasoconstriction - decreased CO
- chronic SNS activation - downregulation of beta receptors
- fluid retention - ventricular dilation, increased wall stress
- myocardial remodeling - decreased myocardial performance
how can myocardial remodeling with heart failure be reversed
ACE inhibitors & aldosterone antagonists
3 physiologic functions of BNP
- natriuresis
- diuresis
- vasodilation
why does the failing heart release natriuretic peptides into systemic circulation
improve Na+ and fluid balance
useful biomarker for assessing risk in pt with heart failure
BNP
MOA of neprilysin inhibitors
neprilysin degrades natriuretic peptides
inhibition can be used to treat heart failure by increasing concentration of natriuretic peptides in blood
goals of HFrEF (systolic failure)
(preload, afterload, contractility, HR)
- diuretics if preload too high
- decrease afterload to reduce myocardial work, maintain CPP (SNP)
- augment contractility with inotropes PRN (dobutamine)
- HR usually high; may need to stay high to preserve CO with low EF
HD goals of HFpEF (diastolic failure)
(afterload, contractility, HR)
- keep afterload elevated to perfuse thick myocardium (neo)
- contractility usually normal
- slow/normal HR to increase diastolic time and CPP
most common cause of right heart failure
left heart failure
6 conditions that increase PVR and right heart work
- hypoxia
- hypercarbia
- acidosis
- hypothermia
- high PEEP
- N2O
4 surgical procedures with high cardiac risk (risk > 5%)
- emergency surgery (especially in elderly)
- open aortic surgery
- peripheral vascular surgery
- long surgical procedures with significant volume shifts/blood loss
5 surgical procedures assoc. with intermediate cardiac risk (risk = 1-5%)
- CEA
- head/neck surgery
- intrathoracic or intraperitoneal surgery
- orthopedic surgery
- prostate surgery
5 surgical procedures assoc. with low cardiac risk (risk < %)
- endoscopic procedures
- cataract surgery
- superficial procedures
- breast surgery
- ambulatory procedures
what is the modified NY association functional classification of heart failure
class 1: asymptomatic class 2: symptomatic with moderate activity class 3: symptomatic with mild activity class 4: symptomatic at rest
how is coronary perfusion pressure calculated
aortic diastolic pressure - LVEDP
what’s the difference in primary and secondary HTN
primary: no identifiable cause (95%)
secondary: identifiable cause (5%)
treatment of RV failure
- inotropes (milrinone, dobutamine)
- pulmonary vasodilators (iNO, sildenafil)
- reverse causes of increased PVR
how does HTN cause organ damage
increased BP increases myocardial work
higher arterial driving pressure damages nearly every organ in the body
6 complications of HTN
- concentric LVH
- IHD
- CHF
- arterial aneurysm (aorta, cerebral)
- stroke
- ESRD
how does LVH contribute to infarction
- leads to CHF
- increased MvO2 results in coronary insufficiency
diagnosis of HTN
BP measured on 2 separate occasions at least 1-2 weeks apart to confirm
normal, elevated, and HTN stages 1-3
- normal: SBP < 120 & DBP < 80
- elevated: SBP 120-139 & DBP < 80
- stage 1 HTN: SBP 130-139 or DBP 80-89
- stage 2 HTN: SBP > 140 or DBP > 90
- stage 3 HTN (crisis): SBP > 180 and/or DBP > 120
cause of primary HTN
increased CO, SVR, or both (SVR almost always the cause)
what plays an integral role in increasing SVR
vascular smooth muscle tone (increased intracellular Ca2+ concentration)
what leads to increased SVR in primary HTN
SNS overactivity, chronic vasoconstriction
how does chronic vasoconstriction assoc. with primary HTN lead to water and Na+ retention
- results in increased renin release
- increases AT1, AT2 and aldosterone
- increases Na+/water retention
why do pts with primary HTN have a vasodilator deficiency
decreased NO and prostaglandins
how do patients with primary HTN develop increased vascular stiffness
collagen and metalloproteinase depositition in arterial intima
cerebral perfusion pressure remains constant with BP of:
50-150 mmHg
BP beyond the limits of autoregulation is dependent on:
pressure
cerebral autoregulation curve in pts with chronic HTN
shifted to right, narrower
difficult to predict on individual basis
how does HTN contribute to CHF?
- increased myocardial wall tension
- LVH
- increased MvO2
- coronary insufficiency
what is the cerebral autoregulation curve
describes the range of BPs where cerebral perfusion pressure remains constant
why does the cerebral autoregulation curve shift to the right in pts with chronic HTN
helps the patient’s brain tolerate a higher range of BPs
comes at the expense of not tolerating a lower BP
6 causes of secondary HTN
- coarctation of aorta
- renovascular disease
- hyperadrenocorticism (Cushing’s syndrome)
- hyperaldosteronism (Conn’s disease)
- pheochromocytoma
- pregnancy-induced HTN
anticipated HD response to anesthesia in pts with HTN
- exaggerated hypotensive response to induction
- exaggerated hypertensive response to intubation & extubation
risk of using myocardial depressants and vasodilators with anesthesia in pts with HTN
hypertensive pts are volume contracted
agents that cause myocardial depression & vasodilation unmask volume contracted state
how to promote HD stability in patients with HTN
adequate hydration before induction
perioperative beta blocker use in hypertensive pts
- continue throughout periop period if already on
- starting DOS increases risk of hypotension, bradycardia, stroke, death
should ACE inhibitors and ARBs be taken DOS?
decision made on case-by-case basis
effects of ACE inhibitors and ARBs with GA
can produce vasoplegia and cause a state of hypotension unresponsive to vasopressors and fluids
may need to treat with vasopressin, terlipressin, methylene blue
surgery should be delayed for optimization when BP is what?
SBP > 180
DBP > 110
most common cause of intraoperative HTN
surgical stimulation
what is a hypertensive crisis
BP > 180/120
when is a hypertensive emergency declared
evidence of end-organ injury
- CNS: encephalopathy, stroke, papilledema
- cardiac: CHF
- renal: HTN-induced acute renal dysfunction
treatment of hypertensive crisis
depends on cause
beta blockers, CCBs, vasodilators (Nipride)
clinical findings with coarctation of aorta
- upper limb BP > lower limb BP
- weak femoral pulse
- systolic bruit
clinical findings with renovascular disease
- bruit (epigastric or abdominal)
- severe HTN in young pt
clinical findings with Conn’s disease
- HTN
- hypokalemia
- alkalosis
- weakness/fatigue
- paresthesia
- nocturnal polyuria & polydipsia
clinical findings of pheo
- headache
- palpitations
- diaphoresis
clinical findings of pregnancy-induced HTN
- peripheral and pulmonary edema
- headache
- sz
- RUQ pain
2 major classes of CCBs
- dihydropyridines: nifedipine, nicardipine, amlodipine, clevidipine
- non-dihydropyridines
example of CCB in phenylalkylamine class
verapamil
example of CCB in benzothiazepine class
diltiazem
how do alpha 1 antagonists reduce BP
- decreased vascular calcium causes vasodilation
- decreased SVR
how do beta 1 antagonists decrease BP
decreased: inotropy, chronotropy, dromotropy, renin release
vasoconstriction in muscle
beta 1 selective beta blockers
- acebutolol
- atenolol
- bisoprolol
- esmolol
- metoprolol
alpha:beta anagonistic properties in labetolol
IV = 1:7 PO = 1:3
how do alpha 2 agonists decrease BP
decreased SNS outflow
how do CCBs decrease BP
- decreased vascular calcium (vasodilation)
- decreased SVR
- decreased inotropy, chronotropy, dromotropy
class of CCBs that target vasculature
dihydropyridines
class of CCBs that target myocardium > vessels
non-dihydropyridines
how do arteriodilators and venous dilators decrease BP
increased NO
venodilators decrease venous return
how do ACE inhibitors decrease BP
- inhibits vasoconstriction d/t AT2
- inhibits aldosterone release
how do AT2 receptor blockers decrease BP
- inhibits vasoconstriction r/t AT2
- inhibits aldosterone release
how do loop diuretics decrease BP
inhibits Na-K-Cl transporter in thick portion of ascending loop of Henle
diuresis = decreased VR
how do thiazide diuretics decrease BP
inhibits Na-Cl transported in distal convoluted tubule
decreased VR
how do K+ sparing diuretics decrease BP
inhibit K+ excretion and Na+ reabsorption by principal cells of collecting ducts
MOA of CCBs
bind to alpha-1 subunit of L-type calcium channel & prevent calcium from entering cardiac and vascular smooth muscle cells
which cardiac marker is the least sensitive for MI?
CK-MB
what are the 3 best EKG leads to monitor intraoperative ST changes?
V3
V4
V5
how does a decrease in ventricular compliance affect PAOP
PAOP may overestimate LVEDV
how do patients with CHF maintain BP?
rely on elevated levels of circulating catecholamines (increased SNS tone)
why can a standard 2 mg/kg propofol induction cause CV collapse in pts with CHF
CHF patients rely on increased SNS tone to maintain BP
2 mg/kg propofol reduces SNS tone while simultaneously reducing contractility (instead, slow titration of lower dose)
primary mechanism of CHF that activates RAAS
CHF reduces renal blood flow
why do CHF patients release natriuretic peptides
atrial dilation increases release of ANP & BNP
how does CHF affect beta receptors
causes down-regulation
most common cause of secondary HTN
renal artery stenosis
how does renal artery stenosis cause secondary HTN
- narrowed renal artery reduces renal blood flow
- kidneys activate RAAS in attempt to increase GFR
why are ACE inhibitors contraindicated in a pt with bilateral renal artery stenosis
can significantly reduce GFR and precipitate renal failure
examples of arteriodilators
- hydralazine
- Nipride
examples of venodilators
- NTG
- Nipride
examples of loop diuretics
- furosemide
- bumetanide
- ethacrynic acid
examples of thiazide diuretics
- HCTZ
- metolazone
- indapamide
- chlorthalidone
potassium sparing diuretics
triamterene
amiloride
CCB that is a useful coronary antispasmodic
nicardipine
only CCB proven to decrease M&M from cerebral vasospasm
nimodipine
CCBs that reduce HR in pts with tachycardia, A-fib, or A-flutter
verapamil
diltiazem
CCB contractility impairment from greatest to least
verapamil > nifedipine > diltiazem > nicardipine
best CCBs for HTN r/t increased SVR
nifedipine, amlodipine, nicardipine (vasodilators)
MOA of clevidipine
arterial vasodilation decreases SVR without affecting preload
contraindications of clevidipine
- egg allergy
- soybean allergy
- impaired lipid metabolism (pathologic HLD, lipid nephrosis, acute pancreatitis with HLD)
- severe aortic stenosis
CCB prepared as a lipid emulsion
clevidipine
clevidipine dosing
1-2 mg/hr, max 16 mg/hr
PK of clevidipine
- onset 2-4 min
- half life 1 min (full recovery 5-15 min after gtt off)
- tissue and plasma esterase metabolism
function of pericardium
surrounds heart and provides minimal friction environment
where do the visceral and parietal layers of the pericardium attach
visceral - attached to myocardium
parietal - anchored to mediastinum
3 conditions that affect the pericardium
- acute pericarditis
- constrictive pericarditis
- cardiac tamponade
what causes constrictive pericarditis
fibrosis or any condition that causes pericardium to be thicker
effects of constrictive pericarditis
- ventricles can’t fully relax during diastole (decreased compliance and diastolic filling)
- increased ventricular pressure creates back pressure on peripheral circulation
- ventricles increase myocardial mass (impairs systolic function over time)
cause of acute pericarditis
usually inflammation
(most commonly viral)
does acute pericarditis affect diastolic filling
not usually unless inflammation leads to constrictive pericarditis or tamponade