Cardiac Surgery Flashcards
Unstable angina definition
rupture of atherosclerotic plaques of coronary arteries causing increased ischemia
STEMI & NSTEMI definition
disruption of atherosclerotic plaque of coronary arteries causing platelet aggregation and clot formation, causing high grade stenosis or occlusion of coronary
artery with or without associated emboli entering microcirculation downstream, resulting in ischemia and infarction of myocardium
Definitions of typical and atypical angina
typical angina that is severe and prolonged (>20 minutes)
typical angina satisfies all 3 criteria:
1) retro sternal pressing pain radiating to shoulder / jaw / arm
pain sometimes described as pressure, tightness, heaviness
pain usually diffuse and not localized
angina usually last minutes, rarely seconds or days
2) provoked with exertion or emotional stress
3) relieved with rest or nitroglycerin
atypical angina only satisfies 1-2 of the 3 criteria above
What does it mean if angina lasts < or > 20 minutes
angina lasting <20 minutes = myocardial ischemia angina
> 20 minutes = acute coronary syndrome (i.e. unstable angina or myocardial infarction)
CCS classification of angina
class 1 = no limitation of ordinary activity; angina with strenuous, rapid or prolonged exertion
class 2 = slight limitation of ordinary activity; angina with ordinary activity (walking stairs, walking uphill) after meals, in cold, in wind or under emotional stress
class 3 = marked limitation of ordinary activity; angina on walking or climbing short distances under normal condition and at normal pace
class 4 = inability to carry on ordinary activity; angina at rest
3 presentations of unstable angina
crescendo pattern with increase in frequency, duration or intensity
angina at rest without provocation
new onset of severe angina (CCS class 3) without previous angina
ACS investigations
ECG at presentation, often repeated if patient still has symptoms
blood laboratory tests: troponin and CK-MB (usually repeated at 6 and 9 hours after initial assessment if it is negative at 0 hour)
ECG ACS “rules”
on ECG, infarct follows 2 rules
1) territorial: where ST elevation in territorial leads (inferior = II, III, aVF; anterior = V1, V2, V3, V4; lateral = V5, V6, I, aVL)
inferior = II, III, aVF = right coronary artery (RCA)
lateral = I, aVL, V5, V6 = I, aVL by left circumflex (CCX) artery; V5, V6 by branch of left anterior descending (LAD) artery
anterior = V1, V2, V3, V4 = left anterior descending (LAD) artery
2) reciprocal changes: ST depression in leads opposite to territorial leads with ST elevation
reciprocal leads includes 1) lateral leads to inferior leads; 2) anterior leads to posterior leads; 3) sometimes anterior to inferior leads
by this rule, ST depression in anterior leads requires a 15 leads ECG (posterior leads V7, V8, V9) to rule out STEMI in posterior leads
Ischemia findings on ECG
on ECG, ischemia manifested commonly as ST depression or T wave inversion, but can also have biphasic T waves
ST depression or T wave inversion due to ischemia usually do not follow territorial leads
Cardiac enzyme markers and their meanings
cardiac enzyme markers include myoglobin, CK-MB, troponin I, troponin T
troponin I is most specific and sensitive, which will start to elevate 3-12 hours post infarct, peak at 10-24 hours post infarct and return to baseline in 3-10 days
delayed (i.e. after 6-9 hours) negative troponin rules out infarction
early (i.e. <6 hours) negative troponin does not rule out anything
Management for STEMI
Stabilize. Then patients with STEMI require all of the following
A) supplemental oxygen to achieve O2 saturation >92%
B) anti-platelets, most commonly Aspirin and (Clopidogrel or Ticagrelor)
cardiologist may also add glycoprotein IIb/IIIa inhibitor (GP IIb/IIIa)
C) anti-thrombin, most commonly Heparin (unfractionated or low molecular weight) or Fondaparinux
D) vessels opened, either percutaneous coronary intervention (PCI) or fibrinolytic agent (tPA)
PCI (balloon angioplasty to open occluded coronary vessel) if within 90 minutes of catheter lab
multiple blocks or occlusion not amenable to PCI may be candidate to coronary artery bypass graft (CABG) surgery
tPA if >90 minutes of catheter lab given no contraindication to anti-fibrinolytic
E) symptomatic treatment
morphine and nitroglycerin to relieve chest pain
Who should not receive nitro
Patients taking sildenafil
nitroglycerin should not be given to patients with suspected right ventricular infarct, because it decreased preload and causes cardiovascular collapse (hypotensive shock)
all patients with inferior infarct should have right leads (V4R) to rule out right ventricular infarct, which would have ST elevation in V4R, before giving nitroglycerin
Management of unstable angina or NSTEMI
some elements may change according to risk
A) supplemental oxygen to achieve O2 saturation >92%
B) anti-platelets, most commonly Aspirin and (Clopidogrel or Ticagrelor)
cardiologist may also add glycoprotein IIb/IIIa inhibitor (GP IIb/IIIa)
C) anti-thrombin, most commonly Heparin (unfractionated or low molecular weight) or Fondaparinux
D) vessels opened, either percutaneous coronary intervention (PCI) or fibrinolytic agent (tPA)
decision depend on risk stratification
E) symptomatic treatment
morphine and nitroglycerin to relieve chest pain
Management of unstable angina or NSTEMI risk stratification
management based on risk stratification by TIMI score
TIMI score based on 7 criteria, each worth 1 point each
1) age >65
2) >3 cardiac risk factors (diabetes, smoking, dyslipidemia, hypertension, family history of premature cardiovascular disease)
3) known coronary artery disease with stenosis >50%
4) aspirin use within last 7 days
5) severe angina with >2 episodes within 24 hours
6) ECG ST changes (elevation or depression >0.5mm)
7) elevated cardiac markers
TIMI score predicts risk of death, MI or ischemia within next 14 days
Non-ST elevated ACS low risk group classification and management
ECG: normal
TIMI score 0-2
Management:
(ASA, statin, nitro for all)
B-blocker
Early discharge with follow up
Non-ST elevated ACS intermediate risk group classification and management
ECG: normal or T wave inversion
TIMI score 3-4
Other: Previous CABG or PCI
Management: (ASA, statin, nitro for all) Heparin Clopidigrel Observation
Non-ST elevated ACS high risk group classification and management
ECG: ST shift or deep T wave inversion
TIMI score 5-7
Other:
Positive or negative cardiac markers
Refractory ischemia, heart failure or hypotension
Management:
(ASA, statin, nitro for all)
Heparin
GP IIb/IIIa inhibitor or bivalirudin with Clopidigrel
B-blocker
Early catheterization (for assessment and revascularization)
Aortic dissection pathophysiology
tear or disruption of intimal layer of aorta where blood flow tears and continues to dissect intimal layer
Aortic dissection complications
rupture of aorta, causing exsanguination
clot in false lumen, compromising downstream blood vessels branching from the aorta, resulting in ischemia of tissue such as brain, heart, kidney, GI tract, limbs
bleeding into pericardium resulting in cardiac tamponade
Aortic dissection history/risk factors
1 risk factor = hypertension
structural risk factors: connective tissue disease (Marfan’s, Ehler-Danlos syndrome), bicuspid aortic valve, aortic co-arctation, valve replacement, coronary artery bypass graft surgery
other risk factors including smoking
Aortic dissection clinical presentation
in general, patient with aortic chest pains look unwell and are hemodynamically unstable (tachycardia, hypertension or hypotension, syncope)
abrupt onset
typically, sharp tearing chest pain 10/10 radiating to back between scapula, maximum at onset
pain can be described as searing, throbbing and may radiate to jaw or abdomen
associated symptoms mainly due to ischemia of brain, heart, GI system and limbs
brain ischemia results in stroke (loss of consciousness, aphasia, limb weakness, paralysis)
heart ischemia results in angina, syncope, myocardial infarction, cardiac tamponade
GI ischemia results in abdominal pain
limb ischemia results in limb pain, cold & pulseless leg
rupture into body cavity ->
hemothorax causing hemoptysis, dyspnea hemoperitoneum causing hypotensive shock, peritonitis
pericardium causing cardiac tamponade
Aortic dissection mortality
40% immediate mortality
1% mortality risk per hour for next 48 hours
5-20% mortality even with surgery
Aortic dissection physical exam
vitals: hypertensive (or hypotensive if cardiac tamponade), tachypnea, tachycardia
cardiovascular exam: discrepancy in blood pressure (>20-30mmHg) between 2 arms, weak one sided pulse, aortic regurgitation murmur (decrescendo diastolic murmur)
neurological: focal neurological deficit
abdominal exam: pain, pulsatile abdominal mass
peripheral vascular exam: acute limb ischemia (cold, dusky, pulseless leg)
Aortic dissection investigations
chest X-ray: wide mediastinum loss of normal aortic contour, hemothorax
12% patients with aortic dissection have normal chest X-ray, so normal chest X-ray does not rule out aortic dissection
bed side trans-thoracic (TT) or trans-esophageal (TE) ultrasound: pericardial effusion and tamponade on TT or TE, dissection flap on TE
ECG: left ventricular hypertrophy, ischemic changes, pericarditis, heart block
chest CT angiography: gold standard to diagnose aortic dissection, where it shows aortic branch involvement and pericardial effusion
chest CT angiography requires patient to be stable
Aortic dissection diagnosis
diagnosis based on chest CT angiography
Aortic dissection management
1) stabilize patient: ABCs
IV medication to lower blood pressure
2) specific treatment
Stanford type A dissection = involvement of ascending aorta with higher mortality risk (compromises vessels to head and coronaries, with pericardial sac), treated with surgery with cardiopulmonary bypass
surgery = open aorta at proximal extent of dissection and then sew graft to intimal flap and adventitia circumferentially
surgical complication: renal failure, mesenteric ischemia, stroke, paraplegia, persistent leg ischemia, death
60% mortality rate peri-operative and post-operative
Stanford type B dissection = no involvement of ascending aorta, treated with IV beta-blocker (Labetalol) to lower blood pressure and may involve surgical consultation
intervention only if complications (rupture or significant occlusion of true lumen causing ischemia) , where treatment can be surgical repair or endovascular catheterization
Pulmonary embolism pathophysiology
PE often originate from deep leg veins from proximal to deep: external iliac -> common femoral -> deep femoral, superficial femoral -> popliteal -> anterior & posterior tibial, peroneal
from leg deep vein thrombosis, a clot broke off as embolus, which then entered circulation and became lodged in pulmonary circulation (artery branches), which can have 2 potentially deadly consequences
1) dead space (ventilation but no perfusion) and hypoxemia
2) increased pulmonary vasculature resistance, causing right ventricular strain and possible failure, leading to cardiovascular collapse
Virchow’s triad risk factors
Stasis: immobilization such as from bed-ridden, post-surgery, long leg cast, long flights / train rides
hypercoagulable state: inherited thrombotic disorder (protein C/S deficiency, Factor V Leiden), malignancy, inflammatory disorders (systemic lupus erythematosus, inflammatory bowel disease), pregnancy & post-partum, hormone replacement / oral contraceptive pill
endothelial injury: central venous catheter, surgery
PE clinical presentation
abrupt or gradual onset
pain on one side of chest, typically do not radiate, worse with inspiration
associated symptoms include dyspnea, syncope, cough, hemoptysis and palpitation
severe PE cause cardiovascular collapse including syncope and cardiac arrest
associated with deep vein thrombosis (leg swelling, pain)
PE physical exam
vital signs: fever, hypotension, tachycardia, tachypnea, low oxygen saturation (hypoxemia)
general appearance: respiratory distress
cardiovascular exam: increased JVP, peripheral edema, S3 or S4
respiratory exam: decreased breath sounds, rales
leg: signs of DVT such as swelling, erythema, warmth, palpable cord and tenderness
PE investigations
chest X-ray: band atelectasis, decreased lung volume on affected side, pulmonary infarct / hemorrhage, edema, Hampton’s hump (wedge shape against pleura)
most PE patients will have normal chest X-ray, so chest X-ray mainly to rule out other causes including congestive heart failure, pneumonia, pneumothorax, pleural effusion
ECG: tachycardia in 40% PE cases, right ventricular strain (inverted T wave and ST depression in V1-V4) in 30% cases, right bundle branch block (RBBB) in 20% cases, S1Q3T3 (S wave in lead I, Q wave in lead III, inverted T wave in lead III) in 20% cases, atrial fibrillation
normal ECG does not rule out PE, but can rule out STEMI and pericarditis
arterial blood gas: hypoxemia, hypocapnia, high Aa gradient, respiratory alkalosis
laboratory test: D-dimer positive
compression ultrasound (CUS) of leg: deep vein thrombosis
bed side ultrasound of heart: right ventricle dilatation
CT pulmonary angiography (CTPA) or ventilation perfusion scan (VQ scan) as confirmatory tests: can visualize embolism or decreased perfusion
PE diagnosis
patients first stratified into a) very low risk; b) low risk; c) high risk, which dictates confirmatory tests to rule in or out PE
1) PERC rule to stratify patient into very low risk patients ruled out by PERC if patient meets NONE of the following criteria age >50 tachycardia HR>100 oxygen saturation <94% prior DVT or PE recent trauma or surgery hemoptysis exogenous estrogen use symptoms and signs of DVT
patient PERC negative with low clinical suspicion of PE requires no further work-up for PE (i.e. only chest X-ray, ECG and blood work, no D-dimer, no CTPA, no VQ scan)
patient PERC positive need to be stratified into low or high risk based on Well’s score
2) Well’s score to stratify patient into low or high risk
pretest probability of PE based on Well’s score divide into low risk (<4 points) or high risk (>4 points)
investigations based on Well’s score
in low risk patients, PE can be ruled out with a negative D-dimer
in low risk patients with positive D-dimer, CTPA is needed to rule out PE
in high risk patients, PE is ruled in or out with CTPA
What is the Modified Well’s Score for PE
Active cancer +1
Hemoptysis +1
Recent immobilization or surgery +1.5
Tachycardia (>100 beats/min) +1.5
Past history of DVT or PE +1.5
Signs or symptoms of DVT based on clinical judgment +3
No alternative diagnosis as or more likely than PE +3
PE management
1) stabilize and address ABC (supplemental oxygen if hypoxemia, IV fluids if hypotension)
2) break clots in PE
for massive PE causing cardiovascular compromise (hypotension, tachyarrhythmia, syncope, cardiac arrest), fibrinolytics
for hemodynamically stable PE, anticoagulants commonly low molecular weight heparin (LMWH) for short term while starting warfarin for long term
PE disposition
patients risk stratified by simplified PE Severity Index (PESI) for determining disposition
simplified PESI includes following variables, each worth 1 point:
age >80 years
history of cancer
history of heart failure or chronic lung disease
tachycardia >110 beats / min
hypotension where systolic blood pressure <100mmHg
hypoxia where oxygen saturation <90%
low risk = 0 point; high risk > 1 point
patients with low risk have low risk (1%) for 30 day mortality, thus can be discharged home to be followed up as outpatient
patients with high risk have higher risk (10%) for 30 day mortality, thus need to be admitted as inpatient
Definition of systolic dysfunction
heart unable to contract or pump blood efficiently into circulation caused by impaired contractility or increased after load
reduced ejection fraction
Definition of diastolic dysfunction
heart unable to fill properly between each beat caused by decreased compliance
preserved ejection fraction
Clinical presentation of heart failure
F = Fatigue A = Activities limited, exercise intolerance C = Chest congestion E = Edema including ascites, peripheral edema S = Shortness of breath including dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND)
NYHA classification of heart failure
heart failure symptoms graded on New York Heart Association (NYHA) classification, which dictate prognosis and management
Class I: no symptoms; able to perform ordinary activities without limitations
Class II: mild dyspnea and fatigue with moderate exertion; occasional swelling of ankles and feet; somewhat limited in exercise and strenuous activities; no symptoms at rest
Class III: symptoms (dyspnea) with minimal exertion; noticeable limitation inability to exercise and participate in mildly strenuous activities; comfortable only at rest
Class IV: symptoms (dyspnea) at rest; unable to do any physical activity without discomfort
ACC / AHA staging of heart failure
ACC / AHA staging of heart failure based on structural changes and symptoms
Stage A: patient at high risk of heart failure, but has no structural heart disease currently
Stage B: structural heart disease (myocardial infarction, left ventricular hypertrophy, low ejection fraction, valvular disease) but no symptoms
Stage C: current or prior symptoms of heart failure; structural heart disease with symptoms
Stage D: refractory heart failure; marked symptoms despite maximal medication and hospitalization
Types of valve prosthesis and their advantages, disadvantages and contraindication
valve prosthesis can be mechanical or bioprosthetic
general rule: mechanical prosthesis for age <70 for durability; bio-prosthetic valve for age >70 for no anti-coagulation
1) Mechanical Valve
advantage: good durability
disadvantage: increased risk of thromboembolism requiring long-term anti-coagulation, not indicated in small aortic root sizes
anti-coagulation with Warfarin target INR 2-3 for aortic valve; 2.5-3.5 for mitral valve, 1-2% hemorrhage risk per year
contraindication: pregnancy or possibility of pregnancy (due to risk of anti-coagulation), bleeding risk
2) Bio-prosthetic Valve
advantage: decreased risk of thromboembolism where long term anti-coagulation is not indicated, good flow in small aortic root sizes
disadvantage: limited long term durability
contraindication: dialysis
Valve prosthesis interventions and their contraindications, advantages and disadvantages
intervention to replace valve can be surgery or percutaneous (i.e. via catheterization)
1) Surgery
contraindication: unsuitable surgical candidate due to comorbidity
advantage: standard of care, able to operate on patients where catheterization is contraindicated (see below)
disadvantage: invasive, requires cardiopulmonary bypass
2) Percutaneous
balloon valvuloplasty for stenosis, valve replacement for regurgitation
advantage:
contraindication: severe coronary artery disease / recent myocardial infarction, cannot take anti-coagulants
Aortic stenosis pathophysiology
cause: calcification of aortic valve, rheumatic heart disease, congenital aortic stenosis
outflow obstruction -> increased after load -> left ventricular hypertrophy -> eventual systolic dysfunction -> congestive heart failure
Aortic stenosis clinical presentation
symptomatic at late stage: SAD = syncope, angina, dyspnea (exertional) in order of angina (5 years life expectancy) -> syncope (3 years life expectancy) -> dyspnea (2 years life
expectancy)
physical exam: delayed and decreased volume carotid pulse, systolic ejection murmur at right upper sternal border
Aortic stenosis investigation
echocardiogram: valve area, pressure gradient, left ventricular hypertrophy (LVH), left ventricular ejection fraction (LVEF)
normal aortic valve area = 3-4cm2 mild stenosis = 1.5-3cm2 moderate stenosis = 1-1.5cm2 severe stenosis <1cm2 critical stenosis <0.5cm2
Aortic stenosis relative contraindications
avoid ACEI and nitrate
Aortic stenosis intervention
procedure = aortic valve replacement, surgical or percutaneous catheterization
indication for intervention:
1. symptomatic
- aortic valve area <1cm2 (exception = normal exercise test with no decrease in blood pressure and normal echocardiogram without left ventricular hypertrophy)
- echocardiogram: LVH, low LVEF, aortic valve gradient >50mmHg
Aortic regurgitation pathophysiology
cause: aortic root dilatation, bicuspid aortic valve, infective endocarditis
aortic regurgitation -> volume overload in left ventricle -> transfer of volume into left atrium and lung -> congestive heart failure
aortic regurgitation -> regurgitation in cause low diastolic pressure (due to regurgitation) and also increased systolic pressure (due to increased stroke volume)
Aortic regurgitation clinical presentation
acute: pulmonary edema from lung congestion
chronic: exertional dyspnea, angina, fatigue
physical exam: wide pulse pressure, bounding water hammer pulse, early diastolic decrecendo murmur (best at end expiration with leaning forward) at lower left sternal border
Aortic regurgitation investigation
echocardiogram: quanitfy aortic regurgitation, visualization of leaflet or aortic root anomalies
Aortic regurgitation medical management
avoid exertion
treatment of CHF according to CHF guidelines (ACEI, beta-blocker, Furosemide)
Aortic regurgitation intervention
procedure = aortic valve replacement, surgical or percutaneous catheterization
if aortic root dilatation, then aortic root replacement with valved conduit (Bentall procedure)
indication for intervention 1. symptomatic especially if NYHA class 3-4 CHF
- echocardiogram: low left ventricular ejection fraction (LVEF) <50% or dilated left ventricle
Mitral stenosis pathophysiology
cause: rheumatic heart disease
mitral stenosis -> increased left atrial pressure -> pulmonary congestion -> pulmonary hypertension -> right heart failure
mitral stenosis -> increased left atrial pressure -> atrial enlargement -> atrial fibrillation -> increased risk of thromboembolis
