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MBBS IV - Junior Clerkship WCS > JC 12 (Medicine) - Acute Myocardial Infarction and Aortic Dissection > Flashcards

JC 12 (Medicine) - Acute Myocardial Infarction and Aortic Dissection Flashcards

1
Q

Difference in troponin levels between ACS with/ without ST elevation

A

ACS + ST elevation = Troponin elevated

ACS without ST elevation/ with ST depression/ T wave inversion = Troponin normal/ marginally elevated

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2
Q

Pathophysiology of acute myocardial infarction

Difference between myocardial ischemia and infarction

A

Fibrous cap of plaque ruptures
» blood clot forms around the rupture
» blocked coronary artery
» death of heart tissue due to prolonged ischemia

o Ischemia = lack of blood supply, no myocardial cell death, reversible
o Myocardial infarction = cell death, cannot regenerate, irreversible

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3
Q

Phases of myocardial infarction

Which phase is salvageable?

A
  1. Evolving phase (first 6 hours to 12 hours from the time of pain)
     Infarcted muscles are acidotic, with loss of Ca and influx of K+ → arrhythmia
     Potential for recovery of heart muscle if:
    a) Improve blood supply by revascularization
    b) Decrease oxygen demand (lower BP, HR)
  2. Convalescence phase
     Infarcted muscles will not recover, irreversible
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4
Q

Treating myocardial infarct during convalescence phase is not useful. T or F?

A

False

treatment during convalescence phase can improve mortality and morbidity by:

a) Avoiding remodeling of infarct (thinning of the infarct wall and dilation of
infarct zone) → avoid aneurysm, ventricular septal rupture, heart failure

b) Improving collateral circulation

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5
Q

ST elevation myocardial infarction

  • Predisposing factors/ triggers
A

 Unusual heavy exercise
 Emotional stress (including surgery, infection, exercise)
 Progression from unstable angina
 Surgical procedures
 Infection e.g. pneumonia
 Circadian periodicity (peak incidence between 0600-1200)

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6
Q

ST elevation myocardial infarction:

Presentation

A

 Severe (maybe intolerable)
 Prolonged (usually > 30 minutes, not relieved by rest)
 Nature: constricting, crushing, compressing, heavy weight
 Radiation: left arm (ulnar aspect), lower jaw
 Other symptoms: SOB, weakness, dizziness, palpitation, nausea, vomiting (Bezold-Jarisch reflex)

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7
Q

ST elevation myocardial infarction

Differential diagnosis

A
  1. Acute pericarditis
     Sharp (knifelike)
     Aggravated by respiratory movement
     Radiates to the trapezius ridge (= characteristic site of pericardial pain)
  2. Pulmonary embolism: hemoptysis
  3. Aortic dissection:
     Ripping / tearing sensation
     Radiation to back
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8
Q

Diagnostic criteria for acute myocardial infarction (type 1 and 2) **

A
  1. Detection of rise and/or fall of cardiac biomarkers above 99th percentile of ULN
  2. Evidence of ischemia:
    - Clinical symptoms of ischemia
    - ECG changes: New St-T wave changes/ New LBBB/ New Pathological Q waves
    - Cardiac imaging evidence: New loss of viable myocardium/ new loss of wall motion
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9
Q

Types of cardiac imaging for diagnosis of myocardial infarction

A

Echocardiogram

Angiogram + PTCA (percutaneous transluminal coronary angioplasty)

Nuclear imaging (Tc-99m)

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10
Q

List ECG changes associated with myocardial infarction

A

New ischemia:
- ST elevation in any leads (e.g. II, III, aVF for inferior infarct, V2-V6 for anterior infarct)
- New Pathological Q waves: Any Q wave or QS complex in V2-V3
- Hyperacute T waves
- Pseudonormalization of T waves
- Wellen syndrome: Deep inverted/ Biphasic T wave in V2-3
- ST elevation in aVR: left main stem occlusion

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11
Q

Causes of false positive ST- elevation

A 
Electrical dysfunctions
 Metabolic disturbances (e.g. hyperkalemia)

Cardiac disease:
 Peri-/myocarditis
 Benign early repolarization
 LBBB
 Pre-excitation
 Brugada syndrome
 LVH with strain pattern
 Post- cardioversion
 Ventricular apical aneurysm

Acute Infarct/ Hemorrhage:
 Pulmonary embolism (e.g. long haul flight)
 Subarachnoid hemorrhage

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12
Q

Causes of false-negative ST elevation (check)

A

 Prior Q waves and/or persistent ST- elevation
 Paced rhythm
 LBBB

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13
Q

Classification of acute myocardial infarction (5 classes)

A
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14
Q

Types and subtypes of cardiac biomarkers for myocardial infarction **

A
  1. CPK (creatinine phosphokinase):
    - CK-MB isoenzyme – short half-life and good for detecting reinfarction
    - CK-MM – also in skeletal muscle
  2. SGOT (serum glutamic oxaloacetic transaminase)
  3. LDH-1 (Lactic dehydrogenase) *
  4. Troponin T or I **
  5. Myoglobin **
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15
Q

Compare the timing of cardiac biomarkers after myocardial infarction

A

Myoglobin = FIRST biomarker, but non-specific and fast elimination

CK-MB = Second, short half-life, good for reinfarction

Troponin T or I = Third, long half-life, more sensitive and specific than CK-MB, good for MI with delayed presentation

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16
Q

List acute treatment options for acute myocardial infarction

A

General:
 Bed rest, O2, morphine
 Coronary care unit +/- resuscitation

Fibrinolytic therapy***

  • Non-specific: Streptokinase, Urokinase
  • Tissue-type plasminogen activator (t-PA)
  • TPA derivatives: TNK-tPA, lanoteplase, reteplase

PTCA (percutaneous transluminal coronary angioplasty)***

  • Angiogram and PCI
  • Emergency coronary artery bypass graft (CABG)
17
Q

Indication for fibrinolytic therapy for acute myocardial infarction

A

o AMI – pain + ST elevation in 2 contiguous chest leads

o Time of onset of pain < 12 hours **

o Absence of contraindications (absolute and relative c/i)

18
Q

Absolute contraindications to fibrinolytic therapy for myocardial infarction

A

Cerebral:

  • Prior intracranial hemorrhage
  • Structural cerebral vascular lesions
  • Malignant cerebral neoplasms
  • Recent ischemic stroke (3 months)

Vascular:

  • Aortic dissection
  • Bleeding/ bleeding tendency

Trauma:
Recent closed head/ facial trauma (3 moinths)

19
Q

Relative contraindications to fibrinolytic therapy for myocardial infarction

A

CVD History:

  • Chronic severe hypertension/ uncontrolled hypertension on presentation
  • History of ischemic stroke, intracranial pathologies
  • Anticoagulant use

Surgical risk:

  • Major surgery, long CPR
  • Recent internal bleeding
  • Allergy to streptokinase

Miscellaneous:

  • Pregnancy
  • Peptic ulcers
20
Q

Criteria for successful fibrinolysis after myocardial infarction

A

Clinical: decrease pain

ECG criteria:
 Early resolution of ST elevation at 90min
 Preservation of R wave

Biochemical evidence – early peaking of CPK (11-12h)
 Vs. normal peak: 22-24h

Imaging: radionuclide imaging, angiography

21
Q

MoA of fibrinolysis therapy for myocardial infraction

A

Streptokinase
 Activates plasminogen to plasmin&raquo_space;> plasmin lyses fibrin in clots

Tissue-type plasminogen activator (t-PA)
 In the presence of fibrin, t-PA is activated and activates
plasminogen at the site of the clot
 More rapid lysis, fewer bleeding complications
 Administered with heparin

(TPA derivatives: TNK-tPA, lanoteplase, reteplase)

22
Q

Limitations of fibrinolytic therapy for myocardial infarction

A
  1. Only 50% of patients receiving fibrinolysis achieved optimal myocardial perfusion
  2. 1/3 re-occlusion by 3 months
  3. Delayed presentation and undiagnostic ECGs
23
Q

MoA of percutaneous transluminal coronary angioplasty

A

PCI:
- Balloon angioplasty and stent insertion into coronary artery to restore blood flow

CABG:
- Coronary artery bypass graft: graft from saphenous artery, radial artery, internal thoracic arteries

24
Q

Indications for PCI over fibrinolytic therapy

A
  • presented 3-12 hrs after onset
  • contraindicated against fibrinolysis: cardiogenic shock, stroke …etc
  • Unclear diagnosis
  • Previously failed fibrinolysis/ Rescue PCI
  • Post-thrombolysis PCI to increase efficacy of treatment
  • Ischemia-driven PCI after thrombolysis
25
Q

Long-term prophylaxis treatment after myocardial infarction

A

Antiplatelet therapy: lower acute mortality and re-infarction
- Aspirin + Clopidogrel / prasugrel / ticagrelor or GP IIb/IIIa inhibitors

Anti-thrombin therapy (anticoagulants): prophylaxis vs DVT

  • Heparin, LMWH
  • Fondaparinux
  • Bivalirudin
  • Warfarin: Only if LV thrombus/ venous thrombosis or embolization
26
Q

Long-term cardio-protective treatment after myocardial infarction

A

Lower oxygen demand:

  • Betablockers e.g. metoprolol, timolol, oral or IV
  • CCB e.g. diltiazem
  • Nitrates

Lower remodeling/ dilatation

  • Beta-blockers
  • ACEi/ ARB
  • Aldosterone receptor antagonist
27
Q

Complications of acute myocardial infarction (limited to the heart alone)

A 
 Heart failure
 Arrhythmias
 VSD (anterior MI)
 Mitral regurgitation complicating papillary muscle dysfunction
 Pericarditis
28
Q

Follow-up tests and secondary prevention of acute myocardial infarct

A

Tests:
 Residual ischaemia – exercise test, angiogram
 Electrical instability – 24h ECG for ventricular tachycardia or arrhythmia

Secondary prevention:
 Risk factors modulation: exercise, stop alcohol and smoking, lipid (aggressive lipid lowering with statin)

 Beta blocker (oral), aspirin, ACEI/ARB

 Cardiac rehabilitation and prevention

29
Q

Aortic dissection

Pathophysiology

A

Blood violates aortic intimal and adventitial layers (intimal tears)
» blood goes into media&raquo_space; separates wall of aorta&raquo_space; False lumen is created

Dissection may extend proximally, distally, or in both directions

30
Q

Difference between aortic dissection and anuerysms

A

o Vs. true aneurysm: permanent dilatation of aorta (all layers)
o Vs. false aneurysm: adventitia is covered but wall of intima and media are damaged

31
Q

Classification of aortic dissection

A

Stanford Classification:
o Type A: ascending aorta involved
o Type B: all dissections not involving the ascending aorta

32
Q

Complications of Type A and Type B aortic dissection

A

Type A (emergency surgery needed, rapidly fatal)
 Coronary artery&raquo_space; MI
 Pericardial sac&raquo_space; cardiac tamponade
 Damage aortic valve&raquo_space; acute severe aortic regurgitation and congestive heart failure
 CVA, syncope

Type B (medical treatment unless severe)
 Acute ischemic lower limb, paraplegia (femoral artery, iliac artery)
 Renal infarct (renal artery)
 Mesenteric infarct (celiac artery)

33
Q

Causes of aortic dissection

A

o Coexisting hypertension (80%)

o Genetic disease: Marfan’s syndrome, familial aortic aneurysm/dissection, Ehlers-Danlos, Loeys- Dietz aneurysm syndrome

o Bicuspid aortic valve

o Trauma

34
Q

Aortic dissection

Presentation

A

Symptoms:
o Chronic: asymptomatic
o Acute: severe tearing pain, radiates to anterior chest or interscapular/ abdominal area

Signs:
o BP: high or low (tamponade)
o Pulse deficits (radiofemoral delay)
o Complications: aortic regurgitation (collapsing pulse, early diastolic decrescendo murmur)

35
Q

First-line investigations for aortic dissection

A

CXR: abnormal widening of mediastinum

CT thorax (& CT aortogram): thrombosed false lumen

MRI: for chronic dissection follow-up

Transesophageal echocardiogram: rapid imaging

36
Q

Prognosis of aortic dissection

A

o Mortality rates approach 1% per hour within first 48 hours (within 2 days: 50% patients die)

o Survival >90% with prompt diagnosis and management

o Death in aortic dissection results from progression of dissection

37
Q

Transoesophageal echocardiogram (TEE) for aortic dissection

  • Advantages and disadvantages
A

Advantages:
 Combining transthoracic and TEE demonstrate sensitivities and specificities >95%
 Very rapid (~10 minutes)
 Done at bedside with minimal risk

Problems:
 Limited visualization of the distal aorta
 False-positive results are possible

38
Q

Management of aortic dissection

A
  1. Haemodynamic stabilization: Control BP: SBP 100-120mmHg
    E.g. IV nitroprusside, pre-treated with IV Labetalol
    Surgical drainage of cardiac tamponade
  2. Definitive treatment:
    - Resection and graft surgeries

DO NOT give anticoagulants (giving heparin generates more dissection)

MBBS IV - Junior Clerkship WCS (131 decks)

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