APEX- Josh > Unit 3 - CV Patho > Flashcards

Unit 3 - CV Patho Flashcards

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1
Q

Stratify cardiac risk assessment based on ?

A
  • Patient history
  • Type of surgery
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2
Q

Risk of perioperative MI for gen. population &
Risk for pt who has had previous MI?

ACC/ AHA guidelines recommended minimum time after MI for elective surgery?

A
  • General Population- 0.3%

Previous MI:
- >6 months- 6%
- 3-6 months- 15%
- < 3 months- 30 %
HIGHEST risk greatest within 30 days

ACC/ AHA guidelines: 4-6 weeks

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3
Q

when should a patient be referred to a cardiologist before surgery?

A

General anesthesia
- NYHA classification of 3 or 4 scheduled for a high/intermediate risk surgery
- Minor surgery under MAC ok to proceed if preop suggests stable cardiac disease

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4
Q

High cardiac risk based on surgical procedure (4)

A

> 5%
- Emergency surgery (especially in elderly)
- Open aortic surgery
- Peripheral vascular surgery
- Long surgical procedures w/ significant volume shifts and/ or blood loss

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5
Q

Intermediate cardiac risk based on surgical procedure

A

1-5%
- CEA
- Head & neck surgery
- Intrathoracic/ intraperitoneal surgery
- Orthopedic surgery
- Prostate surgery

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6
Q

Low cardiac risk based on surgical procedure

A

<1%
- Endo procedures
- Cataract surgery
- Superficial procedures
- Breast surgery
- Ambulatory procedures

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7
Q

6 General risk factors for perioperative cardiac morbidity & mortality for non-cardiac surgery

A
  1. High risk surgery
  2. Hx of IHD (greatest risk with unstable angina)
  3. Hx CHF
  4. Hx cerebrovascular disease
  5. DM
  6. Serum Cr > 2 mg/dL
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8
Q

Unstable Angina

A

Confers the greatest risk of peri-op MI
- angina @ rest
- New onset angina (<2 months)
- increasing symptoms (intensity, frequency, duration)
- Duration exceeding 30 minutes
- Symptoms becoming less responsive to medical Therapy

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9
Q

3 important biomarkers released by infarcted myocardium

Most sensitive?

A
  1. creatine kinase-MB
  2. troponin I
  3. troponin T

troponins are more sensitive

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10
Q

when do biomarkers released by infarcted myocardium initially elevate

A

3-12 hours

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11
Q

Peak elevation: CK-MB, Trop I, Trop T

A
  • CK-MB: 24 hours
  • Troponin I: 24 hours
  • Troponin T: 12-48 hours
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12
Q

Initial elevation: CK-MB, Trop I, Trop T

A

All three: 3-12 h

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13
Q

Return to baseline: CK-MB, Trop I, Trop T

A

CK-MB: 2-3 d
Trop I: 5-10 days
Trop T: 5-14 days

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14
Q

Lead II

A
  • Identifies inferior wall ischemia
  • Monitors dysrhythmias (particularly w/ narrow QRS where P-wave analysis critical) i.e JR, Afib, Aflutter
    ** V1 can monitor dysrhythmias as well **
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15
Q

Leads for detecting intraoperative LV ischemia

A

V3, V4, V5

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16
Q

which lead may be best for detecting ischemia & why

A

Classic teaching: V5

V4

closest to isoelectric level on baseline EKG

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17
Q

combination of what 3 leads has an ischemic detection rate of up to 96%

A

leads II, V4, V5

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18
Q

intraop EKG monitoring in CAD pt

A

5-lead is best approach: RA, RL, LA, LL, and a V lead to monitor for LV ischemia

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19
Q

goal of myocardial ischemia interventions

A

make the heart smaller, slower, and better perfused

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20
Q

Treatment for increased O2 demand

A
  • Increased HR: B-Blocker
  • Increased BB: Increase Anesthetic
  • Increased PAOP: Nitro
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21
Q

Treatment of decreased O2 supply intra-op MI

A
  • Decreased HR: Anticholinergic, Pacing
  • Decreased BP: Vasoconstrictor, reduce depth of anesthesia
  • Increased PAOP: Nitro, Inotrope
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22
Q

Most MI occur when

A

Postoperative period, within 48 h

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23
Q

what is diastolic compliance

A

describes filling pressure that results from a given EDV

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24
Q

what happens to the diastolic pressure-volume curve with decreased compliance

A

curve shifts up and left (stiffer)

higher EDP for given EDV

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25
what happens to diastolic pressure-volume curve with increased compliance
shifts down and right lower EDP for given EDV
26
5 conditions that make the heart "stiffer" and decrease compliance (things that affect the diastolic pressure-volume relationship)
1. age \> 60 2. ischemia 3. pressure overload hypertrophy (aortic stenosis or HTN) 4. Hypertrophic Obstructive Cardiomyopathy 5. pericardial pressure (increased external pressure)
27
what happens to filling pressures in a poorly compliant ventricle? Clinical takeaways?
higher filling pressures required to prime poorly compliant ventricle - Preservation of NSR & atrial kick critically important to maintain priming function - Elevated filling pressures put patients at higher risk for pulm. edema - Any condition that reduces vent. compliances, **CVP & PAOP may overestimate LVEDV**
28
2 conditions that dilate the heart and increase compliance
1. chronic aortic insufficiency 2. dilated cardiomyopathy
29
what are 2 classifications of heart failure?
- Pumping problem: reduced ejection fraction (systolic failure) - Filling problem: preserved EF (diastolic failure)
30
3 etiologies of systolic heart failure (HFrEF)
1. myocardial ischemia 2. valve insufficiency 3. dilated cardiomyopathy
31
7 etiologies of diastolic failure (HFpEF)
1. myocardial ischemia 2. valve stenosis 3. HTN 4. hypertrophic cardiomyopathy 5. cor pulmonale 6. obesity 7. aging
32
what is HF with reduced EF? Compensatory mechanisms?
heart can't pump enough blood to satisfy body's metabolic requirements --> volume overload - less O2-rich blood delivered to periphery - A-V O2 content difference increased - Compensatory mechanisms: Increase SNS, RAAS, & preload
33
what is HF with preserved EF
heart can't relax and accept incoming volume d/t decreased ventricular compliance - Normal EF & contractility generally preserved until late in disease
34
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
35
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
36
5 ways the body adapts to heart failure & consequences of each
1. SNS activation - increased myocardial work 2. excessive vasoconstriction - decreased CO 3. chronic SNS activation - downregulation of beta receptors 4. fluid retention - ventricular dilation, increased wall stress 5. myocardial remodeling - decreased myocardial performance
37
how can myocardial remodeling with heart failure be reversed
ACE inhibitors & aldosterone antagonists
38
3 physiologic functions of BNP What degrades natriuretic peptides?
1. natriuresis 2. diuresis 3. vasodilation neprilysin - inhibition can be used to treat heart failure by increasing concentration of natriuretic peptides
39
why does the failing heart release natriuretic peptides into systemic circulation
improve Na+ and fluid balance through natriuresis, diuresis, and vasodilation
40
Anesthetic goals HFrEF (preload, afterload, contractility, HR)
- Preload: already high, diuretics if too high - Afterload: decrease to reduce myocardial work (SNP), maintain CPP - Contractility: augment with inotropes PRN (dobutamine) - HR: usually high d/t increased SNS; higher is needed to preserve CO
41
Anesthetic goals HFpEF (preload, afterload, contractility, HR) (preload, afterload, contractility, HR)
- Preload: Volume required to stretch noncompliant ventricle; LVEDP doesn't correlate w/ LVEDV **(TEE best)** - Afterload: keep elevated to perfuse thick myocardium (neo) - Contractility: usually normal - HR: slow/normal to increase diastolic time and CPP
42
most common cause of right heart failure
left heart failure
43
6 conditions that increase PVR and right heart work
- hypoxia - hypercarbia - acidosis - hypothermia - high PEEP - N2O
44
how is coronary perfusion pressure calculated
aortic diastolic pressure - LVEDP
45
treatment of RV failure
- inotropes (milrinone, dobutamine) - pulmonary vasodilators (iNO, sildenafil) - reverse causes of increased PVR
46
how does HTN cause organ damage
Elevated afterload increases myocardial work & higher driving pressure damage nearly every organ in the body
47
6 complications of HTN
- concentric LVH - IHD - CHF - arterial aneurysm (aorta, cerebral) - stroke - ESRD
48
Complications for HTN-- Chart
HTN ---> increased myocardial wall tension --> LVH & increased MVO2 ---> LVH ---> CHF ---> increased MvO2 ---> coronary insufficiency ---> infarct dysrhythmias ---> CHF
49
Diagnostic Criteria for HTN Normal Elevated Stage 1 Stage 2 Stage 3
Normal SBP<120 & DBP <80 Elevated SBP 120-129 & DBP <80 Stage 1 SBP 130-139 or DBP 80-89 Stage 2 SBP> 140 or DBP>90 Stage 3 (HTN Crisis) SBP > 180 &/or DBP >120
50
Cause of primary HTN Cause of secondary HTN
(95%) idiopathic- increased CO, SVR, or both (SVR almost always the cause) (5%)
51
What regulates BP
feedback network of the SNS (baroreceptors), RAAS, & ADH
52
what plays an integral role in increasing SVR
vascular smooth muscle tone (increased intracellular Ca2+ concentration)
53
Common explanations for HTN
- SNS overactivity --> chronic vasoconstriction --> Inc. SVR - chronic vasoconstriction---> inc. renin release --> inc. angiotensin I, II, & aldosterone --> inc. Na+ & H20 retention - Vasodilator deficiency (dec. NO, prostaglandins0 --> Inc. SVR - Collagen & metalloproteinase deposition in arterial intima --> inc. vasc. stiffness --> inc. SVR - Diet (inc. Na+ and/or dec. K+ or Ca2+ intake)
54
cerebral perfusion pressure remains constant with BP of:
50-150 mmHg
55
BP beyond the limits of autoregulation is dependent on:
pressure
56
cerebral autoregulation curve in pts with chronic HTN
shifted to right, narrower difficult to predict on individual basis
57
what is the cerebral autoregulation curve
describes the range of BPs where cerebral perfusion pressure remains constant
58
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
59
6 causes of secondary HTN
1. coarctation of aorta 2. renovascular disease 3. hyperadrenocorticism (Cushing's syndrome) 4. hyperaldosteronism (Conn's disease) 5. pheochromocytoma 6. pregnancy-induced HTN
60
anticipated HD response to anesthesia in pts with HTN
- exaggerated hypotensive response to induction - exaggerated hypertensive response to intubation & extubation
61
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
62
how to promote HD stability in patients with HTN
adequate hydration before induction
63
perioperative beta blocker use in hypertensive pts
- continue throughout periop period if already on - starting DOS increases risk of hypotension, bradycardia, stroke, death
64
should ACE inhibitors and ARBs be taken DOS?
decision made on case-by-case basis
65
effects of ACE inhibitors and ARBs with GA should ACE inhibitors and ARBs be taken DOS?
-can produce vasoplegia and cause a state of hypotension unresponsive to vasopressors and fluids - may need to treat with vasopressin, terlipressin, methylene blue decision made on case-by-case basis
66
surgery should be delayed for optimization when BP is what?
SBP \> 180 DBP \> 110
67
most common cause of intraoperative HTN
surgical stimulation
68
what is a hypertensive crisis
BP \> 180/120
69
when is a hypertensive emergency declared
evidence of end-organ injury - CNS: encephalopathy, stroke, papilledema - cardiac: CHF - renal: HTN-induced acute renal dysfunction
70
treatment of hypertensive crisis
depends on cause beta blockers, CCBs, vasodilators (Nipride)
71
Findings with coarctation of aorta
- upper limb BP \> lower limb BP - weak femoral pulse - systolic bruit Diagnostic - Aortography - Echo - CT/ MRI
72
Findings with renovascular disease
- bruit (epigastric or abdominal) - severe HTN in young pt Diagnostic - CT/ Angiography - MRA - Aortagraphy - Duplex US
73
Findings with Conn's disease
- HTN - hypokalemia - alkalosis - weakness/fatigue - paresthesia - nocturnal polyuria & polydipsia Diagnostic - Cp aldosterone, renin - Cp/ Urine K
74
Finding for Cushing's Syndrome (hyperadrenocorticism)
- Wt gain (truncal obesity) - Hyperglycemia - Muscle & bone weakness - Weakened immunity - Hirsutism - Moon face Diagnostic - Dexamethasone suppression test - Glucose Tolerance Test - Urinary Cortisol - Adrenal CT/ MRI
75
Findings of pheo
- headache - palpitations - diaphoresis Diagnostic - Plasma metanephrines - Urinary catecholamines -Urinary VMA
76
Findings of pregnancy-induced HTN
- peripheral and pulmonary edema - headache - sz - RUQ pain Diagnostic - Urine protein - Plt count - Uric acid - CO
77
2 major classes of CCBs
- Dihydropyridines: nifedipine, nicardipine, amlodipine, clevidipine Non-dihydropyridines - Phenylalkylamine: Verapamil - Benzothiazepine: Diltiazem
78
how do alpha 1 antagonists reduce BP
- decreased vascular calcium causes vasodilation - decreased SVR
79
how do beta 1 antagonists decrease BP
decreased: inotropy, chronotropy, dromotropy, renin release vasoconstriction in muscle
80
beta 1 selective beta blockers
- acebutolol - metoprolol - esmolol - bisoprolol - atenolol | AMEBA
81
alpha:beta anagonistic properties in labetolol
``` IV = 1:7 PO = 1:3 ```
82
how do alpha 2 agonists decrease BP
decreased SNS outflow
83
how do CCBs decrease BP
- decreased vascular calcium (vasodilation) - decreased SVR - decreased inotropy, chronotropy, dromotropy
84
Class of CCBs that target vascular tone
Dihydropyridines - Nifedipine - Amlodipine - Nicardipine
85
Class of CCBs that target HR
Non-dihydropyridines - Verapamil - Diltiazem (>verapamil for preservation of contractility when reduced HR required)
86
CCB impairment of contractility in order (highest to lowest)
verapamil > nifedipine > diltiazem > nicardipine
87
how do arteriodilators and venous dilators decrease BP
increased NO venodilators decrease venous return
88
how do ACE inhibitors decrease BP
- inhibits vasoconstriction d/t AT2 - inhibits aldosterone release
89
how do AT2 receptor blockers decrease BP
- inhibits vasoconstriction r/t AT2 - inhibits aldosterone release
90
how do loop diuretics decrease BP
inhibits Na-K-Cl transporter in thick portion of ascending loop of Henle diuresis = decreased VR
91
how do thiazide diuretics decrease BP
inhibits Na-Cl transported in distal convoluted tubule decreased VR
92
how do K+ sparing diuretics decrease BP
inhibit K+ excretion and Na+ reabsorption by principal cells of collecting ducts
93
MOA of CCBs
bind to alpha-1 subunit of L-type calcium channel & prevent calcium from entering cardiac and vascular smooth muscle cells
94
how do patients with CHF maintain BP?
Increased SNS tone- rely on elevated levels of circulating catecholamines
95
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)
96
primary mechanism of CHF that activates RAAS
CHF reduces renal blood flow
97
why do CHF patients release natriuretic peptides
atrial dilation increases release of ANP & BNP
98
how does CHF affect beta receptors
causes down-regulation
99
most common cause of secondary HTN
renal artery stenosis
100
how does renal artery stenosis cause secondary HTN
- narrowed renal artery reduces renal blood flow - kidneys activate RAAS in attempt to increase GFR
101
why are ACE inhibitors contraindicated in a pt with bilateral renal artery stenosis
can significantly reduce GFR and precipitate renal failure
102
examples of arteriodilators
- hydralazine - Nipride
103
examples of venodilators
- NTG - Nipride
104
examples of loop diuretics
- furosemide - bumetanide - ethacrynic acid
105
examples of thiazide diuretics
- HCTZ - metolazone - indapamide - chlorthalidone
106
potassium sparing diuretics
triamterene amiloride
107
CCB that is a useful coronary antispasmodic? Decrease M&M for cerbral vasospasm?
Nicardipine Nimodipine
108
only CCB proven to decrease M&M from cerebral vasospasm
nimodipine
109
MOA, dosing, pharmacokinetics of clevidipine
MOA: arterial vasodilation reduces SVR without affecting preload Dosing: start @ 1-2 mg/ hr (max= 16 mg/ hr) Onset: 2-4 min t1/2: 1 min (full recovery 5-15 min after stopping) Metabolized by plasma & tissue esterases (no need to adjust dose for renal/ liver failure)
110
contraindications & s/e of clevidipine
- egg or soybean allergy - impaired lipid metabolism (pathologic HLD, lipid nephrosis, acute pancreatitis with HLD) - severe aortic stenosis S/E - hypotension & reflex tachycardia - impair cardiac contractility (per manufacturer)
111
CCB prepared as a lipid emulsion
clevidipine
112
Pharmacokinetics of clevidipine
- onset 2-4 min - half life 1 min (full recovery 5-15 min after gtt off) - tissue and plasma esterase metabolism
113
function of pericardium
surrounds heart and provides minimal friction environment composed of 2 layers separated by 10-50 mL of clear fluid
114
where do the visceral and parietal layers of the pericardium attach
visceral - attached to myocardium parietal - anchored to mediastinum
115
3 conditions that affect the pericardium
1. acute pericarditis 2. constrictive pericarditis 3. cardiac tamponade all limit hearts ability to move within the pericardial sac
116
Causes and effects of constrictive pericarditis
Fibrosis or any condition that causes pericardium to be thicker 1. ventricles can't fully relax during diastole (decreased compliance and diastolic filling) 2. increased ventricular pressure creates back pressure on peripheral circulation 3. ventricles increase myocardial mass (impairs systolic function over time)
117
Causes and effects of acute pericarditis
usually inflammation (most commonly viral) Doesn't usually affect diastolic filling unless inflammation--> constrictive pericarditis or tamponade
118
Constrictive pericarditis (chart info) - Causes - S/s - Tx - Anes. Mgngmnt
Causes- cancer (radiation), cardiac surgery, RA, TB, uremia S/s: - Kussmaul's sign- JVD during inspiration - Pulsus paradoxus (less common)- decrease SBP >10 with inspiration/ indicates impaired diastolic filling - Inc. venous pressure- distended neck veins, hepatomegaly, ascites, peripheral edema - atrial dysrhythmias d/t atrial distention - Pericardial knock Tx: Pericardiotomy (hemorrhage & dysrhythmias common, Mortality= 6-19%) Anes. Mngmnt: (similar to AS) - avoid bradycardia (CO dependent on HR) - preserve contractility (ketamine, pancuronium, VA w/ caution, opioids, benzos, etomidate ok) - maintain afterload - Agressive PPV --> dec. ven. return & CO
119
Acute pericarditis (chart info)
Causes: viral infection, Dressler's syndrome (inflammation from necrotic myocardium s/p MI), SLE, scleroderma, trauma, cancer (radiation) S/s: acute chest pain with pleural component (inc. pain with inspiration, postural changes- relieved when leaning forward or supine, pericardial friction rub, ST elevation with normal enzymes, fever Tx: usually resolves spontaneously (Meds to relieve pain: salicylates, oral analgesics, corticosteroids)
120
what separates pericardial tamponade from effusion
Tamponade- excess fluid exerts pressure on myocardium, limiting ability to fill and act as a pump Effusion- seldomly requires treatment
121
CVP/ PAOP in pericardial tamponade
CVP rises in tandem with pericardial pressure; as ventricular compliance deteriorates, left and right diastolic pressure (CVP and PAOP) begin to equalize
122
Pericardial tamponade diagnosis
- TEE (best method) - Becks Triad: hypotension, JVD, muffled heart tones - Pulsus Paradoxus - Kussmaul's sign - Reduced EKG voltage - Mass effect: compression of heart, lungs, trachea & esophagus
123
Causes of symptoms in Kussmaul's sign
Neg. intrathoracic pressure on insp.--> Inc. venous return to RV --> Bowing of ventricular septum toward LV --> Dec. SV, CO, SBP
124
best treatment of pericardial tamponade Complications
Pericardiocentesis & pericardiostomy - pneumo, re-accumulation of fluid, & puncture of coronary vessels or myocardium
125
Effects of increased pericardial volume (chart)
Inc. pericardial pressure --> inc. LV pressure & dec. ventricular volume - inc. LV pressure --> dec coronary perfusion & ventricular filling - dec. ventricular volume --> dec. SV--> dec. CO - Dec. CO --> inc. contractility, HR, renal fluid retention
126
Pressure volume loop in pericardial tamponade
- loop shifts to left (decreased LVEDV) - narrower (decreased SV) - higher slope during ventricular filling (decreased ventricular compliance)
127
What is Beck’s triad and what causes of the symptoms?
Seen in pleural effusions - **Hypotension**: decreased SV - **JVD**: impaired VR to right heart - **Muffled heart tones**: fluid accumulation in pericardial space attenuates sound waves (same for EKG voltage)
128
Preferred anesthetic technique for acute pericardial tamponade undergoing pericardiocentesis
local anesthesia - If GA required- preserve myocardial function
129
Drugs to avoid & safer options with pericardiocentesis
Avoid: volatiles, propofol, thiopental, high dose opioids, neuraxial anesthesia Safer: Ketamine (best choice d/t SNS activation), N2O, benzos, opioids
130
why should spontaneous ventilation be maintained until pericardial tamponade relieved
PPV can impair venous return and CO (CV collapse)
131
what happens to SNS tone, HR, inotropy, LVEDP, LVEDV, coronary perfusion pressure, CO, and SV with pericardial tamponade
- SNS increased - HR increased - inotropy increased - LVEDP increased - LVEDV decreased - CPP decreased - CO decreased - SV decreased
132
why do pts with pericardial tamponade have increased contractility and afterload
increased SNS tone
133
Hemodynamic goals for cardiac tamponade
HR- maintain HR (CO is HR dependent since SV is reduced) Rhythm- NSR (properly timed atrial kick required to prime less compliant ventricles) Preload- maintain or inc. (avoid PPV, hypovolemia, venous pooling; all dec. preload) Contractility- maintain or inc. (inotropes prn) Afterload- maintain (essential to compensate for dec. SV & CO)
134
Infective endocarditis def. & ACC/AHA guidelines for antibiotic prophylaxis
- Bacterial infection of heart valves & endocardium - Only if high risk of developing IE & more likely to suffer adverse outcomes (who is at risk, does surgical procedure increase the risk, & what is the appropriate treatment tx?)
135
6 patients at highest risk of infective endocarditis (need preop antibiotic prophylaxis); 3 patients that don't need abx
1. previous infective endocarditis 2. prosthetic heart valve 3. unrepaired cyanotic CHD 4. repaired CHD ( rx \< 6 months) 5. repaired CHD with residual defects that have impaired endothelialization at graft site 6. heart transplant with valvuloplasty No abx needed: unrepaired valve disease (incl. mitral prolapse, CABG, stents)
136
3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis. 4 surgical procedures that don't need abx?
1. dental procedures involving gingival manipulation and/or damage to mucosal lining 2. respiratory procedures that perforate mucosal lining (incision/biopsy) 3. biopsy of infective lesions on skin or muscle No abx needed: upper/ lower GI endo, cysto, TEE, dermatologic procedures
137
IE abx PO prophylaxis options
Amoxicillin 2 g (50 mg/ kg peds) PCN allergy - Clinda 600 mg (20 mg/ kg peds) - Azithro 500 mg (15 mg/kg peds) - Clarithro 500 mg (15 mg/kg peds)
138
IE abx IV prophylaxis options
Ampicillin 2g (50 per peds) Ancef 1g (50 per peds) Ceftriaxone 1g (50 per peds) PCN allergy - Clinda 600 mg (20 per peds)
139
Most common autosomal dominant CV disease? Most common cause of sudden cardiac death in young athletes? Other names for the disease process?
Hypertrophic obstructive cardiomyopathy (HCOM) - Obstructive hypertrophic cardiomyopathy (OHCM) - Hypertrophic obstructive cardiomyopathy (HOCM) - Asymptomatic septal hypertrophy (ASH) - Idiopathic hypertrophic subaortic stenosis (IHSS)
140
what causes LVOT obstruction in HCOM
1. congenital hypertrophy of interventricular septum 2. systolic anterior motion of anterior leaflet of mitral valve
141
3 key determinants of flow through LVOT
1. systolic LV volume 2. force of LV contraction 3. transmural pressure gradient
142
Conditions that narrow LVOT (inc. obs & dec. output) HCOM?
- decreased systolic volume (preload or inc. HR) - increased contractility - decreased aortic pressure
143
Conditions that distend LVOT (dec. obstruction & inc. CO)
- increased systolic volume (inc. preload or dec. HR) - decreased contractility - increased aortic pressure
144
venturi effect in SAM
blood rapidly flows across LVOT velocity increases through stricture
145
how is hypertrophic obstructive cardiomyopathy diagnosed
TEE
146
SAM can be a postop complication after which surgery
mitral valve **repair** (not replacement)
147
what happens if some of LV stroke volume can't pass into aorta
- takes retrograde path across mitral valve - leads to mitral regurg
148
sign of turbulent flow through LVOT obstruction or mitral regurg
systolic murmur
149
what leads to diastolic dysfunction in HCOM
LVH
150
why is it v important to promptly treat A-fib or junctional rhythms in pt with hypertrophic obstructive cardiomyopathy
preserving LA contraction is very important
151
why is nitroglycerin not a good choice for a pt with hypertrophic obstructive cardiomyopathy
reduces preload - reduces systolic LV volume - narrows LVOT - worsens obstruction
152
is esmolol good or bad for HCOM pt?
good - slower HR extends LV filling time, so esmolol increases systolic LV volume also decreases contractility, which improves LVOT obstruction
153
is phenylephrine a good or bad choice for HCOM pt
good - increases aortic pressure, which increases transmural pressure and opens LVOT
154
3 surgical options to correct LVOTO
1. septal myomectomy 2. alcohol injection into septal perforator arteries 3. mitral valve replacement
155
how long should elective surgery be delayed after PCI angioplasty without stent
2-4 weeks
156
how long should elective surgery be delayed in pt after PCI with bare metal stent?
30 days (3 months preferred)
157
how long should elective surgery be delayed in pt after PCI with drug eluding metal stent in stable ischemic heart disease?
first generation DES = 12 months minimum current generation DES = 6 months minimum
158
how long should elective surgery be delayed in pt after PCI with drug-eluding metal stent in pt with acute coronary syndrome?
12 months minimum
159
how long should elective surgery be delayed in pt after a CABG?
6 weeks (3 months preferred)
160
what meds are involved in dual antiplatelet therapy (DAPT)
- aspirin - thienopyridine (ADP receptor antagonist, usually clopidogrel or ticlopidine)
161
when should a pt on DAPT stop taking aspirin before surgery
continue unless absolutely contraindicated if contraindicated stop 3 days preop
162
when should a pt on DAPT stop taking clopidogrel before surgery
7 days preop
163
when should a pt on ticlodopine for DAPT stop taking preop?
14 days before surgery
164
what can be given to reverse platelet inhibition in emergency surgery on a pt taking DAPT
platelets
165
should UFH/Lovenox be used to "bridge" patients off antiplatelet therapy?
no - paradoxically increases platelet aggregation in the stent
166
whats the best treatment for stent thrombosis
PCI best outcome if blood flow restored \< 90 min
167
purpose of roller pump in CPB
compresses blood tubing, creates occlusion point as it mechanically propels blood forward
168
CPB pump flow with afterload changes
remains constant d/t roller pump
169
how can roller clamp cause tubing rupture
if arterial inflow line is clamped, pump continues pushing forward and can rupture inflow tubing
170
complication with roller pump on CPB if venous reservoir runs dry
air embolism
171
what type of CPB is less traumatic to blood cells
centrifugal pump
172
which CPB tends to not entrain air
centrifugal pump - can't produce excessive negative pressure, tends to not entrain air
173
disadvantage of centrifugal CPB pump
lack of an occlusion point if afterload is excessively high, blood backs up towards venous circulation and decreases circulating blood volume
174
component of CPB where gas exchange occurs
oxygenator
175
which CPB oxygenator is safer
membrane oxygenator (uses blood-membrane-gas interface)
176
which CPB oxygenator carries risk of cerebral air embolism
bubble oxygenator (uses a blood-gas interface)
177
what is the CPB circuit primed with
- mannitol - albumin - heparin - bicarb
178
when is awareness most common with CPB
during sternotomy
179
ACT goal for CPB
\> 400 seconds
180
what should be used for anticoagulation for CPB if pt has heparin allergy
- bivalirudin - hirudin - another factor 10 inhibitor
181
SBP goal before aortic cannulation
\< 100 mmHg (HTN can cause dissection)
182
best way to reduce myocardial O2 consumption during CBP
cardioplegia (K+ containing solution that arrests heart in diastole)
183
where is antegrade cardioplegia introduced
into aortic root solution enters coronaries
184
required for antegrade cardioplegia to work
competent aortic valve & clamped aorta
185
where is retrograde cardioplegia introduced
through a cannula into coronary sinus
186
alpha-stat ABG
- doesn't correct for pt's temp - aims to keep constant pH across all temps
187
which blood gas measurement in CPB is assoc. with better outcomes in adults
alpha-stat
188
which blood gas measurement in CPB is assoc. with better outcomes in peds
pH-stat
189
pH-stat ABG
- corrects for pt's temp - aims to keep constant pH across all temperatures
190
dose of protamine after off bypass
~1 mg for each 100 units heparin given
191
radial artery pressure immediately after CPB
may be artificially low
192
common post-bypass AEs
- myocardial depression - heart block (may need vasoactives and pacing)
193
why is MAP not a good surrogate for organ perfusion during CPB
blood flow is non-pulsatile
194
what is the difference in full bypass and partial bypass
- full: all venous return drained in venous reservoir - partial: heart receives and pumps a fraction of venous return
195
why is an LV vent used during CABG surgery?
- removes blood from LV - this blood usually comes from Thesbian veins and bronchial circulation (anatomic shunt)
196
how does protamine reverse heparin
neutralization reaction (forms acid/base complex)
197
how should post-bypass protamine dose be calculated
account for amount of heparin predicted to remain in circulation after bypass if based on initial heparin dose, may contribute to protamine overdose
198
administration of protamine
over 10-15 min to reduce systemic vasodulation and pulmonary vasoconstriction
199
indications for IABP
- cardiogenic shock - MI - intractible angina - difficult CPB separation
200
contraindications for IABP
- aortic insufficiency - descending aortic disease (aneurysm) - severe PVD - sepsis
201
where is IABP inserted
through femoral artery and advanced along descending aorta
202
what is an IABP?
a counterpulsation device that improves myocardial o2 supply while reducing O2 demand
203
how does IABP function in diastole?
pump inflation augments coronary perfusion
204
how does IABP function in systole?
pump deflation reduces afterload and improves CO
205
what do IABP inflation and deflation correlate with on monitoring waveforms?
- inflation correlates with dicrotic notch and T wave - deflation correlates with R wave
206
where should the IABP distal tip be and why
- 2cm distal to left subclavian - more proximal can occlude left common carotid and brachiocephalic arteries
207
how is proper IABP position confirmed
- CXR - TEE - fluoro
208
effects of priming the CPB circuit with anything other than blood
hemodilution: - decreased Hct - decreased plasma concentration of drugs and plasma proteins - decreased O2 carrying capacity - decreased blood viscosity - increased microvascular flow
209
what can happen if air enters the venous line of CPB circuit
air lock
210
MOA of potassium based cardioplegia
- arrests heart in diastole - K+ increases RMP, which locks voltage-gated Na+ channels in closed-inactive state
211
contraindication to antegrade cardioplegia
incompetent aortic valve
212
when does the IABP inflate and deflate
- inflates during diastole (increases coronary perfusion pressure/O2 supply) - deflates during systole (reduces afterload, decreases O2 demand)
213
when is aortic pressure higher with IABP
higher in diastole than during unassisted systole
214
most common IABP complications
- vascular injury - infection at insertion site - thrombocytopenia
215
purpose of an LVAD
mechanical device that unloads failing heart by pumping blood from LV to aorta
216
where is the inflow cannula of LVAD inserted
in apex of LV
217
conditions that require surgical correction before LVAD can be used
- PFO - AI - tricuspid regurg
218
purpose of LVAD
- bridge to recovery - bridge to transplant - destination therapy
219
why might SpO2 and NIBP be ineffective with LVAD
flow may be non-pulsatile depending on native function consider AL and cerebral ox
220
most common cause of death with LVAD
sepsis
221
common long-term complication with LVAD
GI bleeding (requires anticoagulation)
222
what 3 things are CO dependent on in a pt with LVAD
1. LV preload 2. pump speed 3. pressure gradient across pump (afterload)
223
what is LV suck down with LVAD & how is it treated
- low preload + relatively high pump speed produces suction - part of LV sucked into LV cavity, occludes inflow cannula - treated with IVF to increase preload, decrease pump speed
224
consequences of suction with LVAD
- hypotension - ventricular dysrhythmias - L shift of interventricular septum - decreased RV contractility - decreased compliance
225
consequences of mechanical shear stress with LVAD
- coagulopathy - platelet dysfunction
226
Crawford aneurysm classification: type 1
involves all or most of descending thoracic aorta and upper abdominal aorta
227
Crawford aneurysm classification: type 2
involves all or most of descending thoracic aorta, most of abdominal aorta
228
Crawford aneurysm classification: type 3
involves lower descending thoracic aorta and most of abdominal aorta
229
Crawford aneurysm classification: type 4
involves most of abdominal aorta only
230
DeBakey aneurysm classification: type 1
tear in ascending aorta + dissection along entire aorta
231
DeBakey aneurysm classification: type 2
tear + dissection only in ascending aorta
232
DeBakey aneurysm classification: type 3a
tear in proximal descending aorta with dissection limited to thoracic aorta
233
DeBakey aneurysm classification: type 3b
tear in proximal descending aorta with dissection along thoracic & abdominal aorta
234
Crawford vs. Debakey aneurysm classification
- Crawford: classifies aortic aneurysms into 4 types based on involvement in thoracic/abdominal aorta - DeBakey: classified according to location of dissection
235
Stanford Aneurysm classification
- type A: involves ascending aorta - type B: doesn't involve ascending aorta
236
in which types of dissection should you be worried about aortic insufficiency
DeBakey 1/2 or Stanford A (involve ascending aorta)
237
which type of aortic aneurysms are most difficult to repair
crawford types 2 & 3
238
which type of aortic aneurysm has the most significant perioperative risks & why
crawford type 2 - paraplegia - renal failure mandatory period for stopping blood flow to renal arteries and some radicular arteries that perfuse anterior spinal cord
239
aortic aneurysms that are surgical emergencies
acute dissection of ascending aorta | (Debakey 1/2, Stanford A)
240
type of aortic aneurysm that is often managed medically
dissection of descending aorta (meds for HR, BP, pain)
241
incidence of AAA in pts \> 50
3-10%
242
independent risk factors for AAA
- cigarette smoking - male - advanced age
243
how is AAA most commonly detected
- pulsatile abdominal mass - generally asymptomatic
244
primary mechanism of AAA
destruction of elastin and collagen that form matrix of vessel wall
245
pathologic changes that cause abdominal aorta to weaken/dilate
- atherosclerosis - inflammation - endothelial dysfunction - platelet activation
246
what AAA measurements correlates with risk of rupture
diameter (increased radius = increased transmural pressure = increased wall stress)
247
when is surgical correction of AAA recommended
when \> 5.5cm or if it grows \> 0.6-0.8 cm/year
248
risk of AAA rupture when \> 8 cm diameter
30-50%
249
classic triad of symptoms in AAA rupture
- hypotension - back pain - pulsatile abdominal mass \*\*only in ~50% of patients\*\*
250
where do most AAA rupture
left retroperitoneum
251
most common cause of AAA postop death
MI
252
how does aortic cross clamp contribute to risk of anterior spinal artery syndrome?
- clamp above artery of Adamkiewicz may cause ischemia to lower anterior spinal cord - can result in anterior spinal artery syndrome (Beck's syndrome)
253
how does anterior spinal artery syndrome present
- flaccid paralysis of lower extremities - bowel and bladder dysfunction - loss of temp and pain sensation - preserved touch and proprioception
254
why dont most AAA rupture pts immediately exsanguinate
most aneurysms rupture in left retroperitoneum, allowing for tamponade and clot formation
255
effects of aortic cross clamp: - venous return - CO - MAP - SVR - PAOP
- VR increased (blood shift proximal to clamp) - CO decreases or doesn't change (depends on reserve) - MAP increased (inc. preload & SVR) - SVR increases (mechanical effect, catecholamine release, RAAS activation) - PAOP increased/unchanged (inc venous return)
256
physiologic effects of removing aortic cross clamp - LV wall stress - MVO2 - coronary blood Q - renal blood Q - total body VO2 - SvO2
- LV wall stress increased (inc preload/afterload) - MVO2 increased - coronary blood Q increased - renal blood Q decreased - total body VO2 decreased (aerobic metabolism distal to clamp) - SvO2 increased (decreased total body VO2)
257
infrarenal clamp time associated with increased risk ARF
\> 30 min
258
effects of aortic cross clamp removal: - venous return - CO - MAP - SVR - PAOP
- VR decreased (central hypovolemia, capillary leak) - CO decreased (dec. preload & contractility) - MAP decreased (dec. preload & SVR) - SVR decreased (anaerobic metabolites, vasodilation) - PAOP increased (increased PVR)
259
effects of aortic cross clamp release: - LV wall stress - MVo2 - coronary blood Q - renal blood Q - total body VO2 - SvO2
- LV wall stress decreased - MVo2 decreased (increased if PAOP increased) - coronary blood Q decreased - renal blood Q decreased/unchanged (depends on MAP) - total body VO2 increased (cells distal to clamp receive O2) - SvO2 decreased (increased total body VO2)
260
advantages of EVAR over open repair
- decreased operative time - decreased transfusion rate - shorter LOS - decreased morbidity - no need for aortic cross clamp - avoid resp risks assoc. with midline abdominal incision
261
complications of EVAR
- baroreceptor reflex activation - massive hemorrhage - aortic rupture - cerebral embolism - endoleak
262
what is an endoleak
EVAR complication - original graft fails to prevent blood from entering aortic sac
263
endoleak treatment
sometimes resolve spontaneously (especially early), may require placement of 2nd graft or open repair
264
amaurosis fugax
blindness in one eye sign of impending stroke. emobli travel from internal carotid to opthalmic artery & impairs perfusion of optic nerve causes retinal dysfunction
265
what perfuses the posterior 1/3 spinal cord
posterior spinal arteries
266
perfuses anterior 2/3 spinal cord
anterior spinal artery (1)
267
where does artery of Adamkiewicz originate
on left side between T11-T12 - 75% of population: originates between T8-T12 - another 10%: originates L1-L2
268
what are watershed areas
some regions of spinal cord only have a single blood supply
269
why does a patient with Beck syndrome present with flaccid paralysis of lower extremities
the corticospinal tract is perfused by anterior blood supply
270
why does pt with Beck's syndrome have bowel & bladder dysfunction
ANS fibers perfused by anterior blood supply
271
why does pt with beck syndrome lose pain and temp sensation
spinothalamic tract perfused by anterior blood supply
272
why does a pt with beck syndrome have preserved touch & proprioception
dorsal column perfused by posterior blood supply
273
thoracic cross clamp time that significantly increases risk of cord ischemia
\> 30 min
274
method to reduce spinal cord O2 consumption
moderate hypothermia (30-32 deg C)
275
what does spinal cord perfusion pressure depend on
pressure gradient between anterior spinal artery and CSF CSF will drain with decreased pressure and increased gradient
276
BP goals during cross clamp to prevent beck's syndrome
maintain proximal HTN (MAP ~ 100)
277
monitoring that monitors posterior cord
SSEP
278
spinal cord protecting drugs
- corticoteroids - CCBs - mannitol
279
incidence of amaurosis fugax
in 25% of pts with high grade stenosis
280
regional techniques for CEA
- local infiltration - superficial plexus block (C2-C4) - deep cervical plexus block (C2-C4)
281
risk of regional anesthesia in CEA pt
risk of ipsilateral phrenic nerve block - caution with severe COPD
282
cerebral perfusion pressure =
MAP - ICP
283
what does cerebral perfusion depend on during carotid artery clamp (CEA)
collateral flow from circle of willis (contralateral carotid and vertebral vessels)
284
EEG findings that indicate risk of cerebral hypoperfusion
- loss of amplitude - decreased beta wave activity - slow wave activity
285
things that increase frequency in EEG
- mild hypercarbia - early hypoxemia - seizure - ketamine - N2O - light anesthesia
286
things that decrease EEG frequency
- extreme hypercarbia - hypoxia - cerebral ischemia - hypothermia - anesthetic OD - opioids
287
what is cerebral oximetry what indicates cerebral perfusion is at risk
uses NIRS to monitor cerebral O2 sat (rSO2) in frontal lobe perfusion at risk when reduced 25%+ from baseline
288
use of transcranial doppler in CEA
assess continuous blood flow velocity in middle cerebral artery (where most emboli lodge) may indicate when shunt should be placed
289
anesthesia considerations for SSEP
- requires light plane of anesthesia - monitors sensory pathways only - volatiles decrease amplitude and increase latency (mirror ischemia)
290
where is carotid stump pressure measured
distal to clamp
291
carotid stump pressure that indicates risk of ipsilateral cerebral hypoperfusion
stump pressure \< 50m mmHg
292
risk assoc. with carotid shunt placement
increased risk embolic stroke
293
BP goal during carotid clamping (CEA)
keep BP normal/slightly elevated - brain perfusion is pressure dependent d/t loss of autoregulation
294
what reflex can be activated during CEA or following carotid balloon inflation
baroreceptor reflex
295
ETCO2 goal in CEA
maintain normocapia or mild hypocapnia cerbral vessels distal to stenosis may be maximally dilated - hypercarbia dilates cerebral vessels and shunts blood from hypoperfused tissue
296
lab value that increases risk stroke or death in CEA
blood sugar \> 200 mg/dL DOS
297
5 complications assoc. with CEA
- hematoma - RLN injury - hemodynamic instability (altered baroreceptor sensitivity) - stroke (usually embolic) - carotid denervation
298
when is carotid denervation a problem
hx bilateral CEA reduced ventilatory response to hypoxia
299
what is carotid artery angioplasty stenting (CAS)
uses percutaneous transvacuolar access to pass stent to carotid
300
ACT goal for CAS
\> 250 sec
301
most common complication of CAS & how is it treated
thromboembolic stroke treat w recombinant tPA
302
what is subclavian steal syndrome
occlusion of subclavian or innominate artery proximal to origin of ipsilateral vertebral artery (usually on left side) causes vertebral blood flow to reverse flow toward ipsilateral subclavian artery
303
BP in subclavian steal
much lower in ipsilateral arm
304
treatment of choice for subclavian steal syndrome
subclavian endarterectomy
305
s/s subclavian steal
- syncope - vertigo - ataxia - hemiplegia - arm ischemia - weak pulse in ipsilateral arm
306
why does the RV subendocardium remain well perfused throughout cardiac cycle
vs. LV subendocardium - thinner wall doesn't generate enough pressure to occlude its own circulation
307
when is LV subendocardium primarily perfused
during diastole
308
which region of myocardium receives the least amount of perfusion during systole & why
LV subendocardium tissue compresses its own blood supply as aortic pressure increases
309
why is LV subendocardium predisposed to ischemia
high compressive pressures in LV + decreased coronary flow during systole increases coronary vascular resistance
310
2 factors assoc. with highest O2 consumption
pressure work HR
311
MOA of aldosterone antagonists & example
- inhibit K excretion & Na reabsorption by principal cells of collecting ducts - block aldosterone at mineralocorticoid receptors spironalactone
APEX- Josh
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