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
