Cardiovascular

Rapid Review

• Background
  • An abdominal aortic aneurysm (often referred to as a ‘triple A’), is an abnormal dilation of the abdominal segment of the aorta. Smoking is a significant risk factor for development of this condition. As the aneurysm grows, there is an increased risk of rupture, which can be life threatening.
• Signs/Symptoms
  • “AAA Triad” (Abdominal pain, hypotension, pulsatile abdominal mass), syncope
• Diagnosis
  • Ultrasound useful for initial detection (abdominal aorta > 3.0 considered aneurysmal). CT is better at identifying potential ruptures.
• Treatment
  • If ruptured: maintain targeted SBP of 70-90 mm Hg and prep for immediate surgery. If non-ruptured: consult vascular surgery
• Disposition
  • Any acutely symptomatic patient with AAA should be admitted. They will likely require emergent surgical intervention.
  • Asymptomatic patients with AAA can usually be discharged with close vascular surgery follow-up

Rapid Review

• Background
  • Acute coronary syndromes result from acute obstruction of a coronary artery. Consequences depend on degree and location of obstruction and range from unstable angina to non–ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and sudden cardiac death.
• Signs/Symptoms
  • Chest discomfort (+/- dyspnea), nausea, and diaphoresis.
• Diagnosis
  • ECG (ST-segment elevation/depression)
  • Troponin
• Treatment
  • Initial treatment includes antiplatelets (aspirin and clopidogrel), pain control (nitroglycerin/morphine), anticoagulation (Heparin), beta-blocker (if no signs of heart failure), statin (high-dose atorvastatin).
  •  For STEMI, fibrinolytics and PCI are needed.
• Disposition
  • Admission is required for unstable angina and myocardial infarction. May require transfer to PCI capable facility
  • Stable angina can be safely discharged with PCP and cardiology follow up.

Rapid Review

• Background
  • The aorta is the largest blood vessel of the body and carries blood away from the heart. An aortic dissection occurs when the lining of the aorta begins to separate. Type A dissections move towards the heart and are a surgical emergency. Type B dissections move away from the heart and may be managed with medication to control blood pressure and heart rate.
• Signs/Symptoms
  • “Ripping/tearing” sensation, asymmetric pulses/BP 
• Diagnosis
  • CXR (show widened mediastinum). CT or transesophageal echo confirms the diagnosis.
• Treatment
  • “Anti-impulse therapy”. Reduce BP and HR as low as tolerable using IV beta-blockers (ex. esmolol, labetalol) and nitroprusside (after HR controlled). 
  • Provide analgesia
• Disposition
  • All patients with aortic dissection should be admitted to ICU with cardiothoracic/vascular surgery consultation.

Rapid Review

• Background
  • Aortic regurgitation (AR) is incompetency of the aortic valve causing backflow from the aorta into the left ventricle during diastole. May cause pulmonary edema and cardiogenic shock
  • Commonly caused by Marfan syndrome, aortic dissection, rheumatic fever, infectious endocarditis
• Signs/Symptoms
  • Symptoms: Same as heart failure (orthopnea, fatigue, dyspnea, nocturnal dyspnea). 
  • Signs: Diastolic murmur in LUSB, “water hammer pulses”,  widened pulse pressure, (+) de Musset sign, (+) Quincke pulse
• Diagnosis
  • Transthoracic echocardiography confirms diagnosis
• Treatment
  • Manage underlying cause (antibiotics for endocarditis, PCI for STEMI, surgery for dissection)
  • Treat heart failure w/ diuretics, inotropic agents, etc.
  • Definitive treatment is surgical valve replacement/repair.
• Disposition
  • Admission to ICU is warranted for acute aortic regurgitation or hemodynamic instability.
  • Some patients who are hemodynamically stable may be candidates for outpatient management, but only after consultation with cardiology.

Rapid Review

• Background
  • Aortic stenosis (AS) is narrowing of the aortic valve, obstructing blood flow from the left ventricle to the ascending aorta during systole. 
  • Common causes include degenerative calcification, rheumatic heart disease, and congenital bicuspid aortic valves.
• Signs/Symptoms
  • Symptoms: Classic triad (syncope, exertional dyspnea, chest pain)
  • Signs: Crescendo-decresendo systolic murmur (RUSB). Radiates into carotids. Decreases w/ valsalva
• Diagnosis
  • Transthoracic echocardiography confirms diagnosis
• Treatment
  • Asymptomatic: no treatment required
  • Symptomatic: consult interventional cardiology for aortic valve replacement, or valvuloplasty if unstable.
• Disposition
  • Admission is required for cases of critical aortic stenosis. ICU is required if hemodynamically unstable or signs of cardiogenic shock.

Rapid Review

• Background
  • Cardiac dysfunction in the presence of adequate intravascular volume, causing hypotension and inadequate tissue perfusion
  • Typically caused by acute MI (most common), massive PE, cardiac tamponade, or tension pneumothorax
• Signs/Symptoms
  • Symptoms: Lethargy, somnolence, confusion
  • Signs: Hypotension (< 90), tachycardia, JVD, decreased urine output
• Diagnosis
  • Mostly clinical diagnosis (based on vitals, EKG, troponin, etc.)
  • Can confirm with echocardiography (depressed ventricular function)
• Treatment
  • Treat underlying cause
  • Stabilize with fluids (cautiously) and vasopressors (Norepinephrine preferred)
• Disposition
  • Admission to critical care unit
  • Early consultation with cardiology and cardiothoracic surgery is key for survival.

Rapid Review

• Background
  • Cardiac tamponade is accumulation of blood in the pericardial sac of sufficient volume and pressure to impair cardiac fillings
• Signs/Symptoms: 
  • “Beck’s Triad” (hypotension, muffled heart tones, and distended neck veins).  May present with chest pain and dyspnea
• Diagnosis
  • Clinical diagnosis; ECG may show low QRS voltage, CXR will show an enlarged cardiac silhouette. Ultrasound will show RV diastolic collapse.
• Treatment
  • Pericardiocentesis
• Disposition
  • Acute or new cardiac tamponade will need ICU admission. Depending on etiology, will need further intervention by intervential cardiology, cardiotheroacic surgery, or trauma surgery. 
  • Small, stable pericardial effusions in asymptomatic patients can be discharged with close follow up. 

Rapid Review

• Background
  • Infection and inflammation of the endocardial surface of the heart. Typically caused by S. aureus or S. viridians.
  • May be acute (infection of normal valves) or subacute (indolent infection of abnormal valves
  • Major risk factors include IVDU, cardiac prosthesis, immunocompromised.
• Clinical Presentation
  • Symptoms: Fever (90%), malaise, weight loss
  • Signs: “FROM JANE” (Fever, rosh spots, osler nodes, murmur, janeway lesions, anemia, nail bed hemorrhages, emboli)
• Diagnosis
  • Duke’s Criteria (Includes)
  • Echocardiography + Blood cultures
• Treatment
  • IV antibiotics (ex. Vancomycin + Gentamicin)
  • Consult CT surgery if decompensated heart failure, pulmonary edema, cardiogenic shock
• Disposition
  • Admission is required for all cases of suspected infectious endocarditis. ICU if hemodynamically unstable. 

Rapid Review

• Background
  • Broad disease characterized by inadequate blood flow to meet metabolic demands. Heart failure can be right-sided or left-sided. Left-side heart failure is further categorized into heart failure with reduced ejection fraction (HFrEF or “systolic failure) or heart failure with preserved ejection fraction (HFpEF or “diastolic failure”)
• Signs/Symptoms
  • Largely depends on type of HF. Left-sided HF typically causes SOB, fatigue, orthopnea, rales/crackles on lung sounds. Right-side HF typically causes pitting edema, abdominal fluid accumulation, and JVD
• Diagnosis
  • Mostly clinical; BNP will be elevated, CXR may show cardiomegaly and effusions. Cardiac ultrasound is the most useful diagnostic tool.  
• Treatment
  • Fluid overload and pulmonary edema can be managed with CPAP/BPAP, nitroglycerin, and furosemide. Hypotension can be managed with norepinephrine. 
• Disposition
  • Unstable patients with cardiogenic shock, pulmonary edema, or concomitant ischemia will need ICU admission. Stable patients may be admitted to the medical wards.
  • Mild exacerbations of chronic CHF that respond well to treatment in the ED can be discharged if follow up is available within 1 week.

Rapid Review

• Background
  • Hypertensive emergency is defined as acute elevation of BP (typically >180/120) with evidence of end-organ damage
  • May or may not be the result of an underlying disease or injury
• Signs/Symptoms
  • Symptoms: Dyspnea, headache, chest pain, AMS
  • Signs: (+) JVD, (+) lung crackles, (+) S3, (+) asymmetric pulses
• Diagnosis
  • Clinical diagnosis. Requires elevated BP + is by acute end organ damage. 
  • Evaluate for end organ damage with EKG, troponin, BMP, UA, BUN, CXR, and bedside ultrasound.
• Treatment
  • Reduce BP by 10-20% in first hour, then 5-15% over next 23 hours
  • Common agents include nicardipine, clevidipine, fenoldopam, nitroglycerin, labetalol, and sodium nitroprusside. Preferred agent based on patient’s comorbidities. 
• Disposition
  • Admission is usually required if titratable antihypertensives are used.
  • Discharge is appropriate if patient does not have any evidence of end-organ damage.

Rapid Review

• Background
  • Mitral regurgitation (MR) is incompetency of the mitral valve causing flow from the left ventricle (LV) into the left atrium during ventricular systole. May progress to heart failure, endocarditis, or arrythmias
  •  Commonly caused by mitral valve prolapse, rheumatic heart disease, myocardial infarction.
• Signs/Symptoms
  • Symptoms: Similar to heart failure (dyspnea, fatigue, weakness, edema)
  • Signs: Holosystolic murmur in mitral area, radiates to axilla. May show signs of cardiogenic shock.
• Diagnosis
  • Echocardiography confirms diagnosis (transesophageal preferred)
• Treatment
  • Stabilize w/ vasodilators (nitroglycerine, nitroprusside) and inotropes (dobutamine). 
  • Definitive treatment is surgical valve replacement/repair.  
• Disposition
  • Admission to cardiothoracic ICU if hemodynamically unstable requiring immediate valve replacement/repair. 
  • If no signs of cardiogenic shock, they may be observed in a non-ICU setting.

Rapid Review

• Background
  • Pericarditis is an inflammation of the pericardial sac around the heart, without myocardial involvement. May or may not develop pericardial effusion.
  • Most commonly idiopathic (25-80%) or caused by infection (ex. Coxsackie virus). 
• Signs/Symptoms
  • Symptoms: sharp, pleuritic chest pain (85-90%). Improves while sitting up, worsens when lying back
  • Signs: Tachycardia, friction rub murmur
• Diagnosis
  • Clinical diagnosis. Need at least 2 out of 4 criteria (chest pain, friction rub, new/worsening pericardial effusion, ECG changes)
  • Classic ECG changes include PR depression, PR elevation, and diffuse ST segment elevation.
• Treatment
  • NSAIDs (Ibuprofen or Ketorolac) + Colchicine. Steroids may be used for refractory cases.
  • If pericardial effusion is present on echocardiogram, pericardiocentesis may be needed. Consult cardiology.
• Disposition
  • Discharge is appropriate for most patients, though admission may be needed if they are hemodynamically unstable or have large pericardial effusions.

Rapid Review

• Background
  • Peripheral arterial occlusion is a sudden decrease in perfusion that can occur from thrombotic plaque deposition of peripheral arteries (80%) or an embolism (20%). Most commonly occurs in femoral artery bifurcation.
  • Often occurs in patients w/ a history of atrial fibrillation or recent MI. 
  • 20-30% of patients will require limb amputation, despite treatment.
• Signs/Symptoms
  • Sudden onset of the “6 P’s” (parasthesia, pallor, pulselessness, poikilothermia, paralysis, pain out of proportion on exam)
• Diagnosis
  • Formal angiogram is gold standard
  • CTA can be used as an alternative (SN 96%, SP 95%)
• Treatment
  • Anticoagulation (unfractionated heparin, aspirin)
  • Consult vascular surgery for definitive treatment 
• Disposition
  • Admission is required with vascular surgery consultation for all patients with acute arterial occlusion or ABI < 5. 

Rapid Review

• Background
  • Superficial thrombophlebitis is an inflammation of a superficial vein caused by a thrombus. Typically a benign, self-limited disease
  • Most commonly occurs in patients w/ a history of catheter placement, varicose veins, or pregnancy.
• Signs/Symptoms
  • Symptoms: dull pain
  • Signs: “palpable cord”, erythema, induration
• Diagnosis
  • Clinical diagnosis
  • Ultrasound may be useful if considering DVT
• Treatment
  • Supportive care (NSAIDs, warm/cool compresses, compression therapy)
  • Consider antibiotics if cellulitis suspected
• Disposition
  • Majority of patients can be safely discharged if no evidence of DVT/PE.