Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Typical angina Precordial chest pain Associated w/myocardial ischemia but w/o necrosis Precipitated by stress, exercise, or exertion Caused by significant coronary stenosis NO CELL DEATH Discomfort in chest; sub sternal or retrosternal Burning, heavy or squeezing sensation Resting ECG: May show transient ST depression during chest pain; changes resolve with relief of pain, 25% will have normal ECG Cath: definitive dx procedure Stress test: most useful non- invasive procedure Promptly relieved by rest or Nitroglycerine Attain acceptable exercise tolerance, prevent frequent ischemia and infarction Lifestyle changes: smoking, weight, HTN, cholesterol Aspirin, NTG, BB, CCB PCI, CABG Atypical Angina Unrelated to exercise Most common in DM, females and elderly Palpitations w/o chest pain May see pain in r/l chest, abdomen, back, arm or jaw in absence of sub sternal pain Antacids Acute Myocardial Infarction Result of prolonged myocardial ischemia Cell death caused by occlusion (from plaque) Sudden onset by lasts 30 minutes or longer. Pain is more severe than angina and typically in crescendo pattern
Substernal pain that may radiate. Heaviness, pressure, burning, tightness Arrhythmias, hypotension, CHF, diaphoresis, wakness, SOB, cough, N/V Some pt. may have painless MI Cardiac enzymes: CK, CK- MB, troponin I and II CKMB/CK total >5% = MI ECG: most important dx test ST elevation of 1mm or more in at least 2 leads Oxygen Morphine Anti-platelet: Plavix, UFH or LMWH STEMI: BB, statins, cath Pericarditis Lasts many hours to days Pain worse with deep inspiration, movement or supine. More localized than angina Over sternum or apex; may radiate to neck/left shoulder Sharp, stabbing, knifelike Pericardial friction rub Improved with sitting up/leaning forward Aortic Dissection Sudden onset, relenting Occurs in setting of HTN Pain in anterior chest that may radiate to the back Excruciating, tearing, knifelike Murmur of AI, pulse, or BP asymmetry, cold extremity
Pulmonary Embolism Substernal or over area of pulmonary infarction Sudden onset, lasts minutes to hours. Pleuritic or angina-like pain Dypnea, tachycardia, hypotension, hypoxia, hemoptysis, signs of Rt. HF
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management Hypertension Primary: 90-95% of cases: there is no identifiable or treatable cause Secondary: identifiable/treatable cause (renal, endocrine, drug, etc) Causes include: renal HTN, sleep apnea, Cushing syndrome, coarction of aorta Symptoms not often present In long standing HTN: ventricular hypertrophy, aortic insufficiency murmurs, S4 heart sounds, S# gallop. Compare upper and lower extremity BPs BP elevated on at least 3 separate days or if >160/100
Normal BP <120/<80 Prehypertension: 120- 139/80-89 Stage 1: 140-159/90-99 Stage 2: >160/>100
Serum chemistries, CBC, lipids Home BP monitoring Eliminate treatable causes of secondary HTN Lifestyle modification Goal BP: <140/90 in most adults, <130/80 in DM and renal disease Diuretics, BB, ACEI, ARBS, CCB, etc ACEI contraindicated in pregnancy Congestive Heart Failure Systolic: Decrease in myocardial contractility which leads to reduced SV and CO; inadequate ventricular filling and subsequent chamber dilation. Diastolic: abnormal filling, secondary to impaired relaxation of the ventricle (may be due to a stiff non-compliant chamber of excessive hypertrophy. Acute: sudden reduction in CO and hypoperfusion without peripheral edema Chronic: Develops and progresses slowly. Seen in pts with dilated cardiomyopathy or multivalvular disease. Left-sided: hemodynamic overload secondary to AR, increased peripheral resistance from HTN, weakened muscle from MI, or valvular disease Right-sided: caused by left ventricular dysfunction, PHT, PE, COPD, congenital or valvular disease Left-sided: dyspnea on exertion, orthopnea, weakness and fatigue, weight gain, paroxysmal nocturnal dyspnea, oliguria, rales, S3 gallop, S4 gallop. Right sided: dyspnea on exertion, peripheral edema, JVD, hepatomegaly, hepatojugular reflux, ascites, weight gain, weakness and fatigue, nocturia Staging: ACC/AHA A: at risk for developing heart failure w/o evidence of cardiac dysfunction B: evidence of cardiac dysfunction w/o sx C:evidence of cardiac dysfunction w/sx D:symptoms of heart failure despite maximal therapy NYHA I: no sx at any level of exertion II: sx with heavy exertion III: sx with light exertion IV: sx with no exertion
Non-pharmacological: aimed at correcting reversible casues such as valvular lesions, myocardial ischemia, uncontrolled HTN, arrhythmias, or diet (low in salt etc) Valvular Heart Diseases Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management Acute Rheumatic Fever (ARF) Group A-hemolytic strep (follow epidemics of streptococcal pharyngitis) Has become rare with abx (especially PCN)
Acute onset, febrile illness, along with variable combinations of: Arthritis: polyarthritis, migration of pain, large joints Arthralgia Carditis:pancarditis, chest pain, friction rub, murmurs Chorea: neurological disorder, muscle weakness (milking sn) skin manifestations: erythema marginatum, rheumatic nodules. Jones criteria Want to suppress inflammatory response, provide symptomatic relief and minimize cardiac insult. Benzathine PCN Pen V-K Erythromycin (PCN allergy) NSAIDs Aortic Stenosis (AS) Outflow tract obstruction of blood from the LV that can occur at the valve (valvular), above the valve (supravalvular) or below the valve (subvalvular) AS happens as a result of adhesions and fusion of the commissures and cusps. Leaflets and ring become vascularized, resulting in retraction and stiffening of the cusps. Calcification occurs and the AV orifice is reduced to a smaller opening. Major compensatory mechanism of LV outflow tract obstruction is LVH
Most pts are asymptomatic, but some may get: angina, syncope, dizziness, dyspnea, dysonea on exertion (orthopnea, PND, pulmonary edema) Physical findings: palpable systolic thrill in the carotids or at the base, harsh, midsystolic ejection murmur, S4 gallop, single S2 sound, faint diastolic murmur, systolic ejection click in younger pts ECG: severe AS shows LVH, with or without ST-T changes. Possible LBBB or RBBB Echocardiogram: LV wall motion, outflow, mass and cavity size. AV thickening and area narrowing/gradient.
Prophylaxis abx for invasive procedures which prevents against endocarditis Mild AS pts can live a normal life Moderate AS pts should avoid severe physical activity. A-fib should be converted to a NSR Severe AS: if symptomatic despite meds, surgery for valvular replacement, biprostetic or mechanical valve Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management Aortic Regurgitation (AR) Abnormal regurgitant flow from the aorta back into the left ventricle, through a non-compliant aortic valve. Also referred to as aortic insufficiency.
In acute AR, the LV is of normal size and non-compliant.
In chronic AR there is LV compensation, increasing LV dilation to accommodate the increased LV volume. AR subjects the LV to volume overload primarily but also to excessive pressure load. Compensation results in LV dilatation (eccentric hypertrophy) with some increased LV muscle wall thickness. Symptoms: DOE, fatigue, reduction in exercise tolerance, uncomfortable palpitations, dizziness/light headedness. Physical Findings: bounding pulses, blowing, early- diastolic murmur heard best along the LSB, with the patient leaning forward after exhaling, low-frequency, mid-diastolic rumbling at the apex in severe AR (diastolic murmurs are soft), Quinkes sign (pulsatile blanching and reddening of the nail bed with pressure). Asymptomatic patients are monitored with echo to asses LVF
Afterload reduction vasodilators (CCB or ACEI) for asymptomatic pt with associated HTN
Symptomatic pts and even asymptomatic pt with severe AR and impaired LVF (EF<0.50) should be considered for surgical correction.
Mitral Regurgitation (MR) regurgitant blood flow from the LV back into the LA usually a result of an incompetent MV. Occurs during systole. The severity of MR and the ratio of forward CO to backflow are dictated by 5 factors: 1.) Size of the mitral orifice during regurge 2.)Systolic pressure gradient between LV and LA 3.)Systolic vascular resistance 4.) Compliance of the LA 5.)Duration of regurge with each contraction
Acute MR may present with flash pulmonary edema, it is a result of sudden rupture of the chordae tendineae (THIS IS A MEDICAL EMERGENCY!) Symptoms of chronic MR are usually from low cardiac output, especially during exertion: fatigue, weakness, dyspnea, orthopnea, PND, Peripheral edema Chronic MR as a result of rheumatic fever: holosystolic murmur heard best at the apex, radiating into the left axila. Acute MR: murmur may have a decrescendo quality, an S3 may also be heard indicating an increase in volume return to LV
CXR: may show pulmonary edema in acute and enlarged LA and LV in chronic ECG: in chronic MR may show LAE and LVH Echo: evaluates the mitral valve for gradient flow; LA and LV size and function Cath: identifies coronary ischemic etiology (papillary muscle dysfunction)
Acute: IV diuretics, vasodilators
Chronic: repair or replace and continual monitoring by echo
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management Mitral Stenosis (MS) Stiffening of the mitral apparatus resulting in decreased forward flow from the LA into the LV Most common cause of MS is rheumatic fever A stenotic MV obstructs the outflow of blood into the LV resulting in an increase in pressure in the LA. This increase in pressure is then sent back into the pulmonary system (increases venous and capillary pressure) Dyspnea on exertion, dyspnea at rest, reduced exercise tolerance, orthopnea, PND Symptoms with advanced MS: pulmonary hypertension (PHT), JVD, hepatomegaly, ascites, edema. Physical findings: Ventricular tap in patients, loud S1, high pitched opening snap, diastolic rumble diuretics to reduce vascular congestion in AF beta blockers CCB valvuloplasty is the treatment of choice. Mitral Valve Prolapse Asymptomatic billowing of the mitral valve leaflets retrograde into the LA during systole; it can be accompanied with MR. Enlargement of the valve leaflets (posterior leaflet); normal collagen and elastin matric on the valve fibrosa is fragmented and replaced with myxomatous connective tissue. usually asymptomatic but may have chest pain or palpitations from associated arrhythmias. Midsystolic click: tensing of leaflet or chordae Late systolic murmur best heard at the apex: from regurgitant flow back into LA Made by Echo which reveals posterior displacement of one or both of the leaflets. ECG is usually normal unless there is an underlying LAE or LVH.
Tricuspid Stenosis (ST) rare and usually the result of long term RF OS, JVD diastolic murmur heard best at the sternum and increased with inspiration Surgery
Tricuspid Regurge (TR) Most commonly from RV enlargement and usually functional and not structural pulsatile liver systolic murmur louder on inspiration in the left sternal border Treat underlying conditions responsible for RV size and/or pressure. Also treat with diuretics or surgical repair. Pulmonic Stenosis (PS) Rare and almost always caused by a congenital deformity of the valve. carcinoid syndrome (encasement and immobilization of the leaflets) a systolic murmur balloon valvuloplasty Pulmonic Regurge (PR) Primarily in the setting of severe pulmonary hypertension, dilation of the annulus and enlarged pulmonary artery Causes a high-pitched, decrescendo murmur along the LSB. Treat underlying conditions to help alleviate regurgitation. Myocardial and Pericardial Diseases Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management Myocarditis Inflammatory disease of the myocardium Causes: Viral: direct invasion of the monocytes by virus: Coxsackie B, echovirus, HIV Bacterial
Pleuritic chest pain: worsens with inspiration especially if pericardial involvement Nonspecific: fever, malaise, myalgia tachycardia, pericardial friction rub, mitral and tricuspid murmurs ECG: ST segment and T wave abnormalities Endomyocardial biopsy: evidence of myocardial inflammation and necrosis needed (but not finding it does not exclude diagnosis)
Most cases resolve w/o treatment so supportive treatment of symptoms Avoid exercise
Cocaine Use Rapid onset of action; increased myocardial oxygen demand increases the HR, systemic arterial pressure, and LV contractility, marked vasoconstriction and enhance platelet aggregation and thrombus. Most damage with repeated use. It can cause angina, MI, LVH, dysrhythmias, cardiomyopathy, SCD
urine drug screen Oxygen, Benzodiazepines, thrombolytics, PCI NTG and Verapamil: NO BBs (cocaine affects both alpha and beta receptors and a BB may cause the alpha to work unopposed on the heart) Pericarditis Inflammation of the visceral and parietal membrane that covers the entire heart Causes: Idiopathic, Viral: coxsackie B, echovirus, adenovirus, mono, Hep B, Bacterial: purulent, TB, Fungal: histoplasmosis; Dresslers syndrome, connective tissue disorders, neoplastic disease, drugs, trauma, parasites, uremia. Chest pain: abrupt onset, sharp, stabbing pain, pleuritic, worse when supine, relieved/reduced by sitting Dyspnea, anxiety, myalgia pericardial friction rub (CLASSIC), tachypnea, fever, dysrhythmias (SVT), restricted breathing (aka splitting) ECG: diffuse ST elevation with concavity and no reciprocal depression, also PR elevation CXR, echo, lab studies (CBC, TB, ESR, ANA, renal and thyroid, RF)
Usually self-limiting; rest; treatment of underlying causes Pain meds, non- steroidal/steroidal, NO anticoagulants due to risk of developing hemopericardium Pericardial resection (rare)
Cardiac Tamponade Emergent condition in which fluid accumulates in the pericardium. The blood significantly elevates the pressure on the heart, preventing the hearts ventricles from filling properly. End result is ineffective pumping of blood, shock, and often death Becks triad: hypotension, jugular venous distension and muffled heart sounds Constant chest pain, fatigue, dyspnea, tachycardia, hypotension, signs of compression of adjacent structures.
Decreased/muffled heart sounds CXR, ECG, Echo, Pulsus Paradoxus (fall of 10mmHg with inspiration)
IV fluids and O2 (for shock) drainage (pericardiocentesis) surgery(pericardiotomy)
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management Constrictive Pericarditis Secondary to progressive scarring of the pericardium Filling of the heart chambers is restricted; elevation and equalization of diastolic pressures in all four cardiac chambers. right-sided heart failure, exertional dyspnea, cough, orthopnea, fatigue, muscle weakness, chest pain is rare. salt restriction, avoid drugs that reduce HR, surgical removal or the pericardium
Hypertrophic Cardiomyopathy Most common genetic CV disease Most common cause of sudden death in young people, including athletes Sudden cardiac death is most visible and devastating consequence Symptoms can occur late Suspected by heart murmur, positive family history, abnormal EKG, or onset of symptoms SCD: Most common before age 25-30. Most pts who die suddenly have mild or no symptoms. Risk of SCD declines with age but does not disappear. 2-D echo is principal diagnostic tool: LVH varies from massive and diffuse to mild segmental wall thickening. Intervention to reduce SCD: Pharmacology AICD: primary prevention Implant at age 20: 4:1 excess of ICD implants to lives saved.
Atrial Fibrillation Most common sustained arrhythmia in adults Fibrillation in which the normal rhythmic contractions of the cardiac atria are replaced by rapid, irregular twitching of the muscular wall. Biggest concern for those with AF is a CVA (stroke) Often associated with other CV disorders such as: HTN, CHF, DM, ischemia, valvular, congenital Chaotic rhythm with an atria rate in excess of 350 to 600 bpm; quivering atria; no concerted contractile effort. This results in an irregular rhythm P-waves on the ECG are not present. 4 kinds: paroxysmal, recurrent, persistent, or permanent Rarely life-threatening May be asymptomatic if the rate is controlled. Fatigue, dizziness, dyspnea, palpitations Syncope, TIA, CVA
Thyroid function study Echocardiogram Other cardiac studies to assess for occult disease CHADS score: 0-1: aspirin 2 or more: oral coagulation therapy In rapid a-fib, rate control is key, but be cautious of BP diltiazem IV Cardioversion (within first 48 hours) Anticoagulation: Warfarin is the DOC Target INR for AF is 2.0 to 3.0 An exception to anticoagulation treatment is lone atrial fibrillation