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
Mitral stenosis clinical presentation
pulmonary congestion: dyspnea, orthopnea, paroxysmal nocturnal dyspnea
other: hemoptysis, hoarseness from impingement of recurrent laryngeal nerve
complication: atrial fibrillation, thromboembolism
physical exam: opening snap then decrescendo murmur during diastole at apex
Mitral stenosis investigation
echocardiogram: mitral valve area, pulmonary hypertension
severe mitral stenosis if mitral valve area <1.2cm2
Mitral stenosis medical management
avoid exertion
treat atrial fibrillation (anti-coagulation, rate or rhythm control) and CHF according to CHF guidelines (ACEI, beta-blocker, Furosemide)
beta-blocker, digitalis
Mitral stenosis intervention
procedure = percutaneous balloon valvuloplasty, surgical open mitral commissurotomy, mitral valve replacement (surgical or percutaneous)
indication for intervention 1. symptomatic NYHA class 3-4 CHF
- echocardiogram: severe mitral stenosis <1.5cm2 or pulmonary hypertension
- complication: atrial fibrillation or recurrent thromboembolism
Mitral regurgitation pathophysiology
cause: rheumatic heart disease, ruptured cordae, papillary dysfunction (post myocardial infarction), mitral prolapse, LV dilatation, infective endocarditis
mitral regurgitation -> increased left atrial enlargement -> pulmonary congestion -> pulmonary hypertension
mitral regurgitation -> decreased cardiac output -> forward heart failure
Mitral regurgitation clinical presentation
pulmonary congestion: dyspnea, orthopnea, paroxysmal nocturnal dyspnea
low cardiac output: fatigue
physical exam: holosystolic systolic murmur radiating to axilla
Mitral regurgitation investigation
echocardiogram: severity of mitral regurgitation, left ventricular function, visualization of mitral leaflet, papillary muscle, cord abnormalities
Mitral regurgitation medical management
diuretics, ACEI
Mitral regurgitation intervention
procedure
1st line = surgical repair of mitral valve (annuloplasty ring, leaflet repair, chordae transfer / replacement)
2nd line = valve replacement (surgical or percutaneous) if surgical repair not possible
indication for intervention
1. if mitral valve surgical repair possible and patient is a good surgical candidate, then as early as possible
- symptomatic especially if NYHA class 3-4 CHF
- echocardiogram: low LVEF <60%, left ventricular dilatation, pulmonary hypertension
- complication: atrial fibrillation
Types of cyanotic congenital heart disease
5 T’s
tetralogy of Fallot
Transposition of Great Vessel
Truncus artheriosus
Total anomalous pulmonary venous drainage
Tricuspid atresia
other: hypo plastic left heart syndrome, Ebstein’s anomaly
What is cyanotic congenital heart disease
right to left shunt resulting in de-oxygenated blood in systemic circulation
Causes of acyanotic congenital heart disease
left to right shunt: atrial septal defect, ventricular septal defect, patent ductus arteriosus
Obstructive: aortic coarctation, aortic stenosis, pulmonic stenosis
What is Eisenmenger’s syndrome
left to right shunt cause left ventricular dysfunction -> congestive heart failure, right ventricular hypertrophy, pulmonary hypertension -> reversal to right to left
shunt
Congenital heart disease diagnosis
almost all congenital heart disease diagnosed based on echocardiogram
Atrial septal defect epidemiology
~10% congenital heart disease
Atrial septal defect types and pathophysiology
3 types: osmium primum, osmium scandium (most common type 50-70% cases), sinus venosus
continuous left to right shunt through atrial septal defect
Atrial septal defect clinical presentation
usually asymptomatic in childhood
physical exam: widely split and fixed S2, systolic ejection murmur
Atrial septal defect complications
congestive heart failure, pulmonary hypertension
Atrial septal defect management
surgery: suture closure of atrial septal defect (may be done by percutaneous catheter)
VSD epidemiology
30-50% congenital heart disease
VSD clinical presentation
mild = asymptomatic
mild to severe = exercise intolerance, recurrent asthma / upper respiratory tract infection episodes
physical exam: holosystolic murmur at left lower sternal border with thrill, mid-diastolic rumble at apex
VSD complications
congestive heart failure, pulmonary hypertension
VSD management
surgery: closure of ventricular septal defect with surgical patch (may be done by percutaneous catheter)
PDA epidemiology
5-10% congenital heart disease
PDA clinical presentation
may be asymptomatic, but have apneic / bradycardia spell
physical exam: tachycardia, bounding pulses, hyperactive precordium, continuous machinery murmur best heard at left intra-clavicular area radiating to back
PDA management
Indomethacin (PGE2 antagonist) for closure in premature infant
surgery: closure of PDA by surgical ligation (or spring to clot and close PDA by percutaneous catheterization)
Coarctation of the aorta pathophysiology
narrowing of aorta, most commonly at level of ductus arteriosus
Coarctation of the aorta clinical presentation
often asymptomatic
physical exam: low ankle brachial index (ABI), high blood pressure at upper extremity & low blood pressure at lower extremity, weak / absent pulses in lower extremity, radial-femoral
delay, systolic murmur with late peak at apex / left axilla / left back
Coarctation of the aorta complication
hypertension
Coarctation of the aorta management
if pre-ductus arteriosus, then prostaglandin to keep ductus arterioles patent
surgery: catheterization balloon dilatation +/- stent of aorta at site of coarctation
Pulmonary stenosis pathophysiology
stenosis causing obstruction of blood flow to pulmonary artery and lung
90% stenosis at valve, but obstruction can be at sub-valvular or supra-valvular
Pulmonary stenosis clinical presentation
spectrum from asymptomatic to congestive heart failure
physical exam: wide split S2, systolic ejection murmur at left upper sternal border, pulmonary ejection click
Pulmonary stenosis management
surgery: surgical repair at site of obstruction
Tetrology of Fallot pathophysiology
1) ventricular septal defect
2) right ventricle outflow tract obstruction (pulmonary stenosis)
3) over-riding aorta
4) right ventricular hypertrophy
Tetrology of Fallot clinical presentation
cyanosis, hypoxic tet spells in extertional states, paroxysmal rapid & deep breathing
physical exam: loud single S2 due to pulmonary stenosis, systolic ejection murmur at left upper sternal border
Tetrology of Fallot management
medical management: supplemental oxygen, knee-chest position, fluid bolus, morphine sulfate, beta-blocker
surgery: repair of ventricular septal defect, widening of pulmonary valve
Tranposition of Great Arteries epidemiology
5% of congenital heart disease
Tranposition of Great Arteries pathophysiology
systemic: body -> right atrial -> right ventricle -> aorta -> body; pulmonary: lungs -> left atrium -> left ventricle -> pulmonary artery -> lungs
Tranposition of Great Arteries clinical presentation
progressive cyanosis unresponsive to supplemental oxygen as ductus arteriosus closes
Tranposition of Great Arteries treatment
prostaglandin to keep ductus arterioles open
surgery: surgical repair with connection of aorta to left ventricle and pulmonary artery to right ventricle
Total Anomalous Pulmonary Venous Connection epidemiology
2% of congenital heart disease
Total Anomalous Pulmonary Venous Connection pathophysiology
pulmonary veins draining into right atrium instead of left atrium, usually requiring atrial septal defect shunt to stay alive
Total Anomalous Pulmonary Venous Connection management
surgery: re-routing pulmonary vein into left atrium
Truncus arteriosus pathophysiology
single great vessel arising from heart connecting left and right ventricle to aorta, pulmonary and coronary arteries
the trunks overlie a ventricular septal defect
Truncus arteriosus management
surgery: closure of ventricular septal defect to include trunks on left ventricle + reconnecting pulmonary artery from trunks to right ventricle
Ebstein anomaly pathophysiology
malformed tricuspid valve displaced into right ventricle, causing right ventricular dysfunction, tricuspid stenosis or tricuspid regurgitation
associated with patent foramen oval to allow right to left shunting
Ebstein anomaly management
surgery: tricuspid valve repair or valve replacement + atrial septal defect closure
Hypoplastic left heart syndrome epidemiology
1% of congenital heart disease
Hypoplastic left heart syndrome pathophysiology
hypoplasia of left ventricle, mitral and / or aortic valve, small ascending aorta
circulation dependent on ductus potency for systemic circulation
Hypoplastic left heart syndrome management
medical: intubation, correction of metabolic acidosis, prostaglandin to keep ductus arterioles open
surgery: Norwood procedure (connect aorta to right ventricle with connection of pulmonary artery to aorta, such that right ventricle pump blood into both systemic and pulmonary circulation), then heart transplant in adulthood
Aortic dissection epidemiology
incidence of 5 in 1 million
3 males to 1 female ratio
peak incidence age 50-65 years old
Aorta segments
aorta have 5 segments from proximal to distal
1) aortic root from aortic valve to sinotubular junction, giving branch to coronary arteries
2) ascending aorta from sinotubular junction to brachiocephalic artery, no branches
3) aortic arch from brachiocephalic artery to left subclavian artery, giving branch to brachiocephalic artery, left common carotid artery and left subclavian artery
4) descending thoracic aorta from left subclavian artery to diaphragm, giving branch to intercostal arteries
5) abdominal aorta from diaphragm to bifurcation to common iliac artery, giving branch to celiac trunk, superior mesenteric artery, renal arteries, inferior mesenteric arteries and lumbar arteries
Stanford and Debakey classifications for aortic dissection
Stanford Classification include type A and B
type A: involvement of ascending aorta
type B: no involvement of ascending aorta
DeBakey classification include 1, 2, 3A, 3B
1 = involvement of ascending and descending aorta
2 = involvement of ascending aorta only
3 = involvement of descending aorta only, where 3A = involvement of thoracic aorta; 3B = involvement of thoracic and abdominal aorta
Stanford A = DeBakey 1 and 2
Stanford B = DeBakey 3
Major risk factors for coronary artery disease
history of cardiovascular disease
5 big risk factors:
1. dyslipidemia (high LDL, low HDL)
- smoking
- diabetes
- hypertension
- family history of premature cardiovascular disease
Other risk factors:
metabolic syndrome, defined as central obesity based on waist circumference (>94cm for men; >80cm for women) plus >2 of following:
hypertriglyceridemia (>1.7)
low HDL cholesterol (<1 for men, <1.3 for women)
hypertension (>130/85 or treatment for hypertension)
high fasting glucose (>5.6 mmol/L) or diabetes
weight and BMI (normal = 18-25; overweight = 26-29; obese = >30)
inflammatory diseases: lupus, rheumatoid arthritis, psoriasis, elevated hs-CRP
ethnicity especially south Asian
Framingham risk score
Framingham risk score used to calculate future risk of cardiovascular disease for patients with NO history of cardiovascular disease
Framingham risk score based on 7 variables: age, gender, total cholesterol, HDL cholesterol, blood pressure, diabetes, smoking history
Benefits of revascularization therapy
revascularization improves symptoms & quality of life and reduce risk of MI & premature death
Types of revascularization therapy
2 types of revascularization therapy
1) percutaneous coronary intervention (PCI)
catheter dilating stenosed coronary artery with balloon and then placing stent
PCI require 1 year of Aspirin plus Clopidogrel post PCI
2) coronary artery bypass graft (CABG)
surgical grafting patient’s own blood vessel (saphenous vein or internal mammary artery) to connect aorta to coronary artery downstream from site of stenosis as bypass
Consideration and indication for revascularization therapy
Revascularization may be considered in patients with ischemic heart disease and any of the following:
- angina symptoms refractory to medication therapy
- inadequate cardiovascular quality of life despite medication therapy
revascularization indicated in patients with any high-risk features on non-invasive test associated with >3% annual risk of MI or death
final decision on revascularization therapy usually by cardiologist and cardiac surgeon taking into account of patient factors, revascularization options and local practices
Medication post revascularization
revascularization should address underlying cause of narrowing of blood vessel, so patient do not need to be on beta blocker or ACEI post PCI or CABG
Indications for CABG
isolated proximal disease in large coronary arteries (>1.0-1.5mm) is ideal for CABG; small diffusely diseases coronary arteries are not suitable for CABG
strong recommendation for CABG > Percutaneous Coronary Intervention (PCI)
- 2+ vessel disease in diabetic patients
- 3 vessels disease especially if left ventricular ejection fraction (LVEF) <50%
- 2 vessel disease with significant proximal left anterior descending (LAD) disease and (LVEF <50% or ischemia on non-invasive testing)
- 1 or 2 vessel disease without significant LAD disease who survived sudden cardiac death or sustained ventricular tachycardia (VT)
- significant left main coronary artery disease
other recommendation for CABG > PCI
- unstable or disabling angina unresponsive to medical therapy and PCI
- coronary artery rupture, dissection or thrombosis after PCI
- post-infarct angina
strong recommendation for CABG or PCI
- 1 or 2 vessel disease without significant LAD disease but with large area of viable myocardium and high risk criteria on non-invasive testing
- recurrent stenosis associated with large area of viable myocardium or high risk criteria on non-invasive testing
recommendation for CABG or PCI
- 1 vessel disease with significant proximal LAD involvement
- repeat CABG for multiple saphenous vein graft stenosis with high risk criteria on non-invasive testing
- 1 or 2 vessel disease without significant LAD disease but with moderate area of viable myocardium and high risk criteria on non-invasive testing
CABG procedure and different approaches
CABG = using graft (can range from 3-6 grafts) to connect from aorta to coronary arteries distal to sites of occlusion
grafts used include saphenous vein grafts (SVG), left internal thoracic / mammary artery (LIMA), right internal thoracic / mammary artery (RIMA), radial artery free graft, right gastroepiploic artery
SVG, LIMA and RIMA most commonly used, where IMAs have better long term patency (95% patency for IMA vs. 50% patency for SVG in 10 years)
CABG can be done with or without cardiopulmonary bypass (CPB)
CPB = pump and oxygenation apparatus that remove blood from inferior & superior vena cava -> performs gas exchange -> return blood into aorta, which allows cardiac arrest for open heart procedure
off-pump coronary artery bypass graft surgery (OP-CAB) = surgery performed on beating heart, where stabilization devices hold heart in place and positioning device allow lifting of heart
OP-CAB is more technically demanding, but is as safe and well tolerated by most patients
compared to CABG on CPB, OP-CAB decreases in-hospital morbidity, blood product transfusion, ICU stay, hospital stay, CK-MB / troponin I levels
OP-CAB and CABG on CPB have similar long term outcome
OP-CAB used in patients who are poor candidates for CPB such as older / sicker patient, calcified aorta, poor LVEF, severe peripheral vascular disease, severe COPD, chronic renal failure, coagulopathy, transfusion issues, anterior / lateral wall revascularization
Absolute and relative contraindications for off-pump CABG
absolute contraindication for OP-CAB: hemodynamic instability, poor quality target vessel, diffusely diseased vessel, calcified coronary vessels
relative contraindication for OP-CAB: cardiomegaly, congestive heart failure, critical left main disease, small distal target, recent or current acute myocardial infarction, cardiogenic shock, LVEF <35%
Advantage of CABG
CABG can dramatically improve LVEF, which is an important prognostic factor in ischemic heart disease, thereby increasing survival
CABG improves survival in >2 vessel disease in diabetic patients, compared to PCI
CABG complication
important CABG complications
- hemorrhage, graft thrombosis
- myocardial infarction, stroke
- dysrhythmias
- sternal dehiscence
- post-pericardiotomy syndrome (pericarditis), cardiac tamponade
redo CABG have higher operative mortality (2-3 times higher than prior operation), usually indicated in symptomatic patients who failed medical therapy and angiography showing progression of disease
complication of CPB
- micro-embolization of gaseous and particulate matter -> stroke and neurocognitive defect
- immune suppression
- trauma to formed blood element: thrombocytopenia, platelet dysfunction
- heparin rebound (increase anti-coagulation from increased heparin level in blood post CPB)
- systemic inflammatory response syndrome (SIRS) leading to neurological injury, pulmonary dysfunction, heart dysfunction / myocardial infarction, renal dysfunction, coagulopathy
- failure to wean from CPB
Post-Pericardiotomy Syndrome (Pericarditis) pathophysiology
unknown pathophysiology
Post-Pericardiotomy Syndrome (Pericarditis) clinical presentation
usually onset weeks to 3 months post-operatively
systemic symptoms: fever, malaise
cardiac symptoms: pleuritic chest pain
physical exam: pericardial friction rub
complication: atrial fibrillation, pericardial effusion -> cardiac tamponade, pleural effusion
Post-Pericardiotomy Syndrome (Pericarditis) investigation
ECG: PR depression, diffuse ST elevation
Post-Pericardiotomy Syndrome (Pericarditis) treatment
medical treatment:
1st line = high dose PO aspirin or NSAID
2nd line = corticosteroids
CABG general indication
Strict criteria to be a surgical candidate
Requires suitable anatomy (proximal severe occlusion in large vessel)
CABG invasiveness
Invasive
CABG recovery
Higher short term morbidity
Higher rate of complication
Longer hospital stay
CABG cost
Expensive
CABG long term outcomes
Improvement in LVEF
Better survival (in >2 vessel disease)
Effective long term
PCI general indication
More lenient criteria for PCI candidate
More lenient criteria for anatomy
PCI invasiveness
Less invasive
PCI recovery
Less short term morbidity
Lower rate of complication
Shorter hospital stay
PCI cost
Less expensive
PCI long term outcomes
Usually does not improve LVEF
Worse survival (in >2 vessel disease)
Higher rate of re-intervention
Myocardial infarction complications
CRASHH PAD = Cardiac Rupture, Arrhythmia, Shock (cardiogenic), Hypertension / Heart Failure, Pericarditis, Aneurysm, DVT/PE
myocardial infarction in chronological order
post-infarct any time
recurrent myocardial infarction any time
arrhythmia within first 2 days:
tachycardia: sinus tachycardia, atrial fibrillation, ventricular tachycardia, ventricular fibrillation
bradycardia: sinus bradycardia, AV block (1st, 2nd, 3rd degree)
cardiogenic shock / congestive heart failure within first 2 days
myocardial rupture within 1-7 days
pericarditis & Dressler’s syndrome (pericarditis weeks post MI) within 1-7 days and 2-8 days
thromboembolism 7-10 days, DVT up to 6 months
Myocardial infarction surgical complications presentations and the pathophysiology, clinical presentation, diagnosis and management of those presentations
surgical complications usually present with onset 1-7 days post MI and usually present with:
- Cardiogenic Shock
pathophysiology: infarct decreases cardiac output, resulting in cardiogenic shock, which may lead to acute congestive heart failure
clinical presentation: cardiogenic shock (hypotension, elevated JVP, multi-organ dysfunction), symptoms and signs of acute congestive heart failure
treatment: emergency CABG may improve cardiac function and reduce mortality - Free Wall Rupture
pathophysiology: rupture (laceration or tearing) of ventricular or atrial walls, which was weakened from infarct
clinical presentation: acute cardiac tamponade (Beck’s triad = hypotension, distended JVP, distant & muffled heart sounds) -> immediate death
diagnosis: cardiac tamponade on echocardiogram
treatment: surgical repair to close rupture with suture or patch after resecting infarcted area - Papillary Muscle Rupture
pathophysiology: posterior / inferior MI may also involve papillary muscle, where failure to papillary muscle interferes with closure of mitral valve, resulting in acute mitral regurgitation
clinical presentation: pan-systolic murmur, acute congestive failure with pulmonary edema
diagnosis: papillary muscle dysfunction and mitral regurgitation on echocardiogram
treatment: mitral valve replacement via surgery - Ventricle Septal Rupture
pathophysiology: anterior and inferior infarct of ventricle septum, resulting in perforation
clinical presentation: pan-systolic murmur
diagnosis: ventricular septal defect on echocardiogram
treatment: surgical repair of ventricular septal defect with suture or patch - Ventricular Aneurysm
pathophysiology: infarct of myocardium result in dyskinetic portion of myocardium, which results in aneurysms causing blood stasis forming clot
clinical presentation: acute congestive heart failure, cardiogenic shock
diagnosis: visualization of ventricle aneurysm on echocardiogram
treatment: ventricular aneurysm with refractory heart failure or ventricular arrhythmia are treated with surgical resection of aneurysm (reconstructive surgery)
