Chest Pain Clinical Reasoning Flashcards
What is the classic presentation of stable angina?
Substernal exertional chest discomfort
Sxs resolve promptly with rest or nitroglycerin and do not change over the course of weeks
Usually pt has CHD risk factors
What is the cause of stable angina?
Mismatch between myocardial oxygen supply and demand.
Common first presentation of coronary heart disease (CHD) usually due to coronary artery stenosis
What are the important tests for workup of stable angina?
cardiac stress test, CT coronary angiogram, or angiogram
Laboratory testing: blood glucose and lipid panel to look for diseases which increase likelihood of ischemic process
What are the risk factors for CHD? (important to ask for chest pain workup)
male sex
age >55 yo in men, >65 yo in women
tobacco use
diabetes mellitus
hypertension
abnormal lipid profile
other: other vascular diseases, CKD, elevated inflammatory markers, lifestyle factors (sedentary, obesity, etc), cocaine use
How might women describe angina differently than men?
More likely to use terms like “burning” or “tender”
What 3 questions should you ask to categorize a patient’s chest pain as either typical angina, atypical angina, nonanginal?
- Where is your pain? (substernal = pos)
- Does your pain come on or get worse when you walk, walk fast, or climb stairs? (exertional = pos)
- Does your pain get better with rest? (yes = pos)
If all 3 positive screen –> typical angina
If only 2 positive –> atypical angina
If only 1 positive –> nonanginal chest pain
What do stress tests do?
attempt to induce and detect myocardial ischemia (can use exercise or drug induced if needed, ex. dobutamine)
Other than exertion, what are two triggers for stable angina?
Emotional stress, cold weather
How would you decide between a stress test or angiography for further workup for suspected stable angina?
Pt with high likelihood of disease may not benefit from stress test bc the test is not needed for diagnostic purposes or they may not be able to undergo revascularization
Angiography is the gold standard for diagnosing CHD. Indications are abnormal stress test indicating substantial ischemia, ischemia at a low workload on exercise test, diagnostic uncertainty.
Can move straight to angiography without stress test if sxs are disabling despite therapy or if they have heart failure
How can you treat stable angina?
Tx goal = relieve sxs, inhibit disease progression
- Lifestyle modification (smoking cessation, exercise, weight loss, low fat and low cholesterol diet)
- Medication to treat sxs:
- Beta blocker (first line, decrease oxygen demand)
- Nitrates (increase coronary blood flow, short acting used to relieve episodes)
- Medication to slow sx progression:
- aspirin
- high intensity statin
- BP control if pt has HTN
- ACE-I/ARB in patients at highest risk (ex. diabetes, heart failure)
- gylcemic control
What is the classic presentation for GERD?
heartburn (burning, substernal, chest discomfort), regurgitation, dysphagia, symptoms worse at night and after large meals, worse lying down
(note dysphagia raises possibility of obstructing lesion and mandates prompt eval, usually with upper endoscopy)
What factors typically make GERD symptoms worse? (aggravating factors)
- ingesting large (esp fatty) meals
- lying down after meal
- using tobacco
- eating foods that relax lower esophageal sphincter (chocolate, alcohol, coffee, peppermint)
How can you diagnose GERD?
suggestive symptoms and response to therapy generally considered diagnostic
EGD can be done in pts with alarm symptoms (dysphagia, odynophagia, weight loss, GI bleeding, iron deficiency anemia) or signs suggestive of complicated disease (early satiety, vomiting, extra-esophageal symptoms, unclear etiology of chest pain, longstanding sxs - to check for Barrett esophagus, require long term therapy, respond poorly to appropriate therapy)
what is the treatment for GERD?
8 week course of once per day proton pump inhibitor (PPI) = first line
H2 receptor blockers can be used for maintenance therapy (not initial tx)
motility agents may also be useful (not initial tx)
what is the classic presentation for acute MI?
Middle aged man with risk factors for CHD with crushing substernal chest pressure, pain radiating to left arm, diaphoresis, nausea/vomiting, shortness of breath, feeling of impending doom
*Note: we do a bad job at recognizing (and historically studying) MI in women, younger and older patients. There are also frequent atypical presentations
When does an MI happen?
prolonged failure to perfuse an area of myocardium leading to cell necrosis
what is the most common etiology of an acute MI?
coronary plaque ruptures causing thrombosis and subsequent blockage of a coronary artery
what are the broad differences between STEMI and nSTEMI?
STEMI
- transmural ischemia or infarction
- typically caused by complete occlusion of coronary artery
- initial diagnosis requires strict ECG criteria
nSTEMI
- less severe, usually injuring only subendocardial tissue
- typically caused by incomplete occlusion of a coronary artery
- higher subsequent risk for STEMI than for pts with STEMI
What is the first initial step for workup if suspected MI?
Next step?
EKG within 10 minutes of arrival to ED!
Obtain peripheral blood sample to check CK-MB and troponin
What cardiac biomarkers are measured in suspected MI?
serum creatine kinase MB subunit (CK-MB)
troponin
how can kidney disease affect troponin levels?
may be elevated (increased risk false positives)
How can MI present in women specifically?
- more likely to present without chest pain
- often report prodromal sxs (fatigue, dyspnea, insomnia)
- dyspnea, weakness, fatigue common sxs
what would the expected findings be for STEMI on EKG?
ST-segment elevation/depression, T-wave inversions, Q waves
What is the classic presentation for unstable angina (UA) or nSTEMI?
new or worsening sxs of CHD, only differentiated by absence (UA) or presence (nSTEMI) of myocardial enzyme elevation in peripheral blood samples
what distinguishes unstable angina from stable angina?
UA is angina that is new, worsening in severity or frequency, or occurs at rest
what is the pathophysiology of UA or nSTEMI?
primarily caused by acute plaque rupture followed by platelet aggregation