Cardiology

• Chest pain: pressure, squeezing, or heaviness — radiating to left arm, jaw, or neck
• Diaphoresis (sudden, profuse sweating)
• Nausea, vomiting; pallor
• Dyspnea (especially with inferior or RV involvement)
• Sense of impending doom
• Atypical presentation in women/elderly/diabetics: back pain, fatigue, nausea without chest pain

vs. Unstable angina: STEMI produces ST elevation on 12-lead ECG and eventual troponin rise indicating cell death. Unstable angina is ACS without ST elevation or troponin. Both require aspirin and urgent transport — the distinction is made with ECG and labs.

New hypotension with inferior MI (leads II, III, aVF) = suspect right ventricular MI. Nitrates and diuretics are contraindicated — these patients depend on preload. Give fluids cautiously; call early alert.

• Chest pain occurring at rest (not triggered by exertion)
• Chest pain not relieved after three doses of nitroglycerin
• New-onset angina within the past 2 months
• Crescendo pattern: episodes becoming more frequent, longer, or more severe
• Presentation mimics stable angina — distinction is clinical context
• No reliable way to distinguish from NSTEMI without troponin

vs. Stable angina: Stable angina is predictably provoked by exertion and relieved by rest or NTG. Unstable angina occurs at rest or with minimal activity and is not consistently relieved. Field treatment is identical to STEMI: aspirin, nitroglycerin, transport — give oxygen only if SpO2 <94% (routine oxygen in ACS is no longer recommended).

Unstable angina not relieved by NTG x3 should be treated as NSTEMI in the field. These patients can progress to complete occlusion rapidly — early catheterization saves lives.

• Severe dyspnea; orthopnea (can't lie flat); paroxysmal nocturnal dyspnea
• Bilateral basilar crackles (wet lungs)
• Pink frothy sputum (severe alveolar flooding)
• JVD and peripheral pitting edema
• Tachycardia; diaphoresis; hypertension or hypotension (shock)
• Cardiac history (prior HF, MI, valve disease)

vs. COPD exacerbation: CHF has bilateral crackles, JVD, and responds to CPAP and nitroglycerin. COPD has wheezing, a smoking history, and barrel chest — no JVD, no frothy sputum. When uncertain, CPAP is appropriate for both.

Flash pulmonary edema deteriorates within minutes. Apply CPAP immediately. Nitroglycerin (if SBP >100 and no RV infarct) reduces preload and afterload rapidly. Do not delay for IV access before CPAP.

• Hypotension (SBP <90 mmHg) unresponsive to fluid
• Tachycardia; narrow pulse pressure
• Cool, pale, clammy, mottled skin (vasoconstriction)
• JVD (backed-up venous pressure)
• Bilateral crackles (pulmonary edema from pump failure)
• Altered mental status; decreased urine output

vs. Distributive (septic) shock: Cardiogenic shock has cool/pale skin, JVD, and pulmonary edema. Septic shock early has warm/flushed skin, wide pulse pressure, and fever without JVD or pulmonary edema. Fluids are cautious in cardiogenic; aggressive in septic.

Cardiogenic shock complicating inferior MI — suspect right ventricular infarction. NTG and diuretics drop preload further and can cause cardiac arrest. Identify early; alert receiving hospital.

• Beck's Triad: hypotension + JVD + muffled (distant) heart sounds
• Pulsus paradoxus: SBP drops >10 mmHg with inspiration
• Tachycardia (compensatory)
• Narrow pulse pressure
• Dyspnea; anxiety; pallor
• Electrical alternans on ECG (alternating QRS height — swinging heart)

vs. Tension pneumothorax: Both cause JVD and hypotension (obstructive shock). Tamponade has muffled heart sounds with equal bilateral breath sounds. Tension PTX has unilateral absent breath sounds and tracheal deviation (late). Mechanism guides the differential: penetrating chest trauma vs. spontaneous.

Electrical alternans + refractory hypotension = immediate pericardiocentesis required. During cardiac arrest from tamponade, pericardiocentesis is the resuscitative intervention — CPR alone is ineffective.

• Sudden, severe tearing or ripping chest pain radiating to the back (between shoulder blades)
• Unequal blood pressures arm-to-arm (>20 mmHg difference)
• Pulse deficits in extremities
• Syncope; neurological deficits (if carotids involved)
• Hypertensive history; Marfan syndrome risk factor
• Pain maximal at onset (vs. MI which builds)

vs. STEMI: Dissection pain is tearing/ripping, maximal at onset, and radiates to the back. MI pain is pressure/squeezing and builds over minutes. Critical distinction: thrombolytics are absolutely contraindicated in aortic dissection and can be fatal.

Proximal (Type A) dissection involving the coronary arteries can produce an inferior STEMI picture. Giving thrombolytics to a dissection patient can cause exsanguination. Unequal arm BPs + tearing back pain = dissection first.

• VF: coarse irregular waves, no organized P/QRS/T — shockable
• Pulseless VT (pVT): wide QRS tachycardia without palpable pulse — shockable
• Asystole: flat line or minimal electrical activity — non-shockable
• PEA: organized rhythm on monitor with no palpable pulse — non-shockable
• All: unresponsive, apneic or agonal breathing, no pulse
• PEA: search for reversible H's and T's (Hypovolemia, Hypoxia, Tension PTX, Tamponade, Toxins, Thrombosis)

Shockable (VF/pVT) vs. non-shockable (asystole/PEA) determines whether defibrillation is indicated. Defibrillating asystole does NOT help and wastes time. Confirm asystole in two leads before withholding a shock.

Fine VF can look like asystole on low gain. Always check at least 2 leads at adequate gain before calling asystole and withholding defibrillation. A single shock to fine VF can convert it to a perfusing rhythm.