Working Problem 4- Myocardial Infarction Flashcards
What biomarkers do you look out for in myocardial infarction?
Troponin T and I Preferred marker Protein located in cardiac muscle Poor sensitivity first 6 hours after onset of symptoms Repeat in 8-12 hours after onset of symptoms Can be elevated with Pulmonary embolism Aortic dissection Renal failure Sepsis Cardiac trauma or surgery CHF
How does a patient with pericarditis present?
Inflammation of the pericardial sac Pain is due to irritation of the parietal pleura Sharp pleuritic substernal pain Radiates to the back, neck, or shoulder Worse with cough, inspiration, supine Improves with leaning forward Pericardial friction rub, tachycardia, dyspnea EKG-diffuse ST elevation Troponin is elevated in up to 22%
How does a patient with spontaneous pneumothorax present?
Sudden rupture of a lung bleb
Tall thin males age 20-40
Underlying lung disease
Smokers
Sudden onset of sharp pain, worse with inspiration, and SOB
Physical exam-decreased breath sounds on the affected side
Tension pneumothorax-Immediate life threat
Decreased venous return to the heart
Severe respiratory distress, tachycardia, hypotension
How does a patient with Aortic dissection present?
Sudden onset of sharp, tearing, maximal pain
Pain radiates to the neck or back
Physical exam
Majority will be hypertensive
Difference in blood pressure between arms
Murmur of aortic regurgitation
Neurologic deficits (Chest pain with neurologic deficit, THINK DISSECTION)
How does chest wall pain show up in a patient?
30% of ED visits
Well localised,sharp,positional pain
Reproducible by palpating a specific area of chest wall
Costochondritis-pain and tenderness at costochondral or costosternal joints
What is the function of troponin T,I and C
Troponin C = calmodulin, which binds the Ca++
Troponin I inhibits the myosin ATPase until Ca++ binds to
the Troponin C component, which changes protein interactions
and permits contraction to occur
Troponin T anchors the complex to Tropomyosin
Tropomyosin is a long thin structural protein linked to the actin filaments
Why is troponin I prefered over T?
Troponin T requires a special machines and it is more troublesome
Quality control is better for Troponin T because Troponin I exists in
several different molecular forms in plasma and breakdown products
occur, so that different brands of reagents give different results
Therefore you must consult the laboratory reference range
However, Troponin I results are probably at least 99% as reliable as
Troponin T in the clinical arena
What is unstable angina?
Unstable angina (UA) is an acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage. It is characterised by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of MI.
How do you assess unstable angina?
Typical features include age >45 years; smoker; with long-standing hypertension, diabetes, or hypercholesterolaemia. A history of peripheral vascular disease or pre-existing heart disease should be determined.
Most patients present with chest pain, although women, people with diabetes, and older people may present with atypical symptoms.
Typical cardiac chest pain is described as a retrosternal pressure or heaviness that radiates to the jaw, arm, or neck, and may be intermittent or persistent. Angina is considered to be unstable if it is prolonged (lasting more than 20 minutes), if it occurs at rest, or if it is new-onset severe angina, crescendo angina, or post-myocardial infarction. Pain may be accompanied by other symptoms such as diaphoresis, nausea, dyspnoea, and syncope.
Atypical presentations include epigastric pain, recent-onset indigestion, stabbing chest pain, pleuritic chest pain, or isolated dyspnoea.
What are the investigations done for unstable angina?
- ECG - may be normal or have transient ST segment depression (>0.05 mV) or T-wave inversion (>0.2 mV)
- Cardiac biomarkers - not elevated
- FBC - normal
- Electrolytes and renal function - normal
- Blood sugar – normal, elevated in diabetes
- Lipid profile - normal or increased total cholesterol and LDL
- Coagulation profile - normal
- CXR - in patients with heart failure, will show pulmonary oedema; excludes alternative diagnoses or triggers of chest pain
- Echocardiogram - transient regional wall motion abnormalities
- Coronary angiography - stenosis of coronary artery
What is the management for unstable Angina?
• Emergency Treatment
o Oxygen, nitrates, morphine
o Antiplatelet therapy – aspirin/clopidogrel
• Confirmed UA (non-elevated biomarkers)
o Antiplatelet therapy – aspirin or clopidogrel
o Beta-blocker or calcium channel blocker
o Intravenous nitrates
o ACE inhibitor
o Early coronary catheterisation and intervention
o Glycoprotein IIb/IIIa inhibitor
o Anticoagulation - heparin
o Statin
o Cardiac rehabilitation – lifestyle modifications
What is STEMI?
MI is myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand. This is usually caused by occlusion in the coronary arteries. ST-elevation MI (STEMI) is suspected when a patient presents with persistent ST-segment elevation in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history.
How does STEMI lead to cardiogenic shock?
If a sufficient quantity of myocardium undergoes ischaemic injury, left ventricular (LV) pump function becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end diastolic pressure give rise to diastolic dysfunction.
How do you assess STEMI?
description of the chest pain (i.e., onset, nature, location, radiation, intensity, duration, associated features) and an enquiry about any associated symptoms or major risk factors for CAD (e.g., hypertension, diabetes, dyslipidaemia, obesity, chronic renal insufficiency, smoking) are essential. Other risk factors for MI include male gender, advanced age, and cocaine use in younger people.
• Classically the pain is described as diffuse, severe, ‘heavy’ or ‘crushing’, located centrally in the chest, with radiation to the left arm or jaw and occurring at rest. However, it may be atypical by location (i.e., epigastric, jaw, arm, neck pain) or by nature (i.e., burning, throbbing, uneasiness).
• Associated features include nausea, vomiting, dyspnoea, palpitations, weakness, dizziness, and light-headedness.
• The clinical picture of acute MI is variable, and no signs are specific to this condition. On general inspection, patients are typically distressed, diaphoretic, tachycardic, and appear pale or grey. Rales on lung examination suggest heart failure. An audible S3 or S4 on cardiac examination indicates poor cardiac muscle compliance of the infarcted muscle.
• Alternatively, the patient may be in cardiogenic shock with a decreasing level of consciousness, profound hypotension, acute SOB, and imminent cardiac arrest.
What are the investigations done for STEMI?
- ECG - new left bundle branch block (LBBB) or ST-segment elevation of at least 1 mm in 2 or more contiguous leads
- Cardiac biomarkers - elevated CK, CK-MB, and troponin
- CXR – normal
- Coronary angiogram - presence of thrombus with occlusion of the artery
- Echocardiogram - hypokinesis, dyskinesis, or akinesis
