Ch. 5 Chest Pain, Diaphoresis, Nausea Flashcards
Aortic Dissection
Description:
Association:
Can present with:
CXR:
Description: Acute, tearing chest pain radiating to the back
Ass: HTN, Marfan’s syndrome
Can present with:
- stroke,
- MI,
- tamponade,
- acute aortic insufficiency (**may expect diastolic murmur from AR)
CXR: widened mediastinum
Acute Coronary Syndrome
Includes STEMI, NSTEMI, unstable angina
- Chest pain described as “elephant on chest”
- SOB
- Diaphoresis
- +n/v
- Tachycardia
- Hypotension
Coronary vasospasm
Common in younger patients, cocacine users, women
Coronary narrowing caused by autonomic dysfunction/mimics typical angina associated with true MI
Pericarditis
Pleuritic chest pain tha timproves with leaning forward
- Dyspnea
- Cough
- Fever
- Friction rub
- Pulsus paradoxus (drop in blood pressure on inspiration) if tamponade present
Pulmonary embolism
Pleuritic chest pain (i.e. worse with inspiration)
- Dyspnea
- Hypoxia
- Hypotension if embolus is massive
- Right heart strain & abnormal ECG findings may be present
Diffuse esophageal spasm
Esophageal motility disorder
- Chest pain
- Dysphagia
- Food regurgitation
- May be triggered by reflux, caffeine, spicy foods
Esophageal perforation
Most commonly after invasive procedures such as endoscopy
Also in alcoholics with forceful vomiting (i.e., Boerhaave syndrome)
Pneumothorax
Collapsed lung may present as acute pain
What are the classic hx and PE findings seen in MI?
- Chest pain
- Diaphoresis
- Anxiety
- Tachycardia
- Tachypnea
- +n/v
If there is a large area of ischemic damage to the heart, pt may have HF presenting with bilateral rales (pulmonary edema), JVD, new S3 or S4, new murmurs, hemodynamic instability (i.e., cardiogenic shock)
What group of women is at highest risk for MI? Why?
Postmenopausal women
Decline in estrogen levels believed to contribute to higher CVD risk profile as estrogen promotes growth and maintenance of intimal layer of arterial wall (maintaining its ability to expand and accommodate blood flow)
WHat is the difference between UA, NSTEMI, and STEMI?
What are the series of events that take place during an acute MI?
Thrombus formation following plaque rupture = primary mechanism involved in coronary vessel obstruction leading to ischemia and, eventually, myocyte necrosis and tissue death
Work up:
- What are the initial dx steps for suspected MI?
- What is the role of measurement of cardiac enzyme levels in the blood
- What is the best cardiac enzyme to dx a second MI on top of recent MI?
- What to watch out for in pts with kidney disease
- ECG + blood test for cardiac enzymes / chest radiograph to r/o pneumothorax and aortic dissection
- Troponin-I and CKMB measured every 8 hrs in first 24 hrs of suspected MI
- CKMB = first to rise but has low specificity
- Troponin-I has highest sensitivity for MI and increases in 3 hrs, peaks in 6 hrs, gradually decreases over 7 days
-
CKMB = best marker for repeat MI
- Peaks within 12-40 hrs following MI and decreases 2-3 days after
- CKMB and troponin are cleared through kidneys –> have longer 1/2 life in presence of kidney disease
What is the role of ECG?
Coronary anatomy and ECG changes?
Helps determine whether there is actually ischemia or infarction and, if so, the location of the ischemia or infarction
What is the initial management of STEMI?
MONABASH
What are the complications of MI?
