7566854
| Question | Answer |
| What is the pathophysiology of mitral stenosis? | Immune-mediated damage, annular calcification, or infection that damages the mitral valve -> inflammation, fusion of the chordae tendonae, leaflet thickening, & potential mitral regurgitation. Damage reduces mitral valve orifice side making it more difficult for blood to pass from the left atrium to the left ventricle -> increast LA pressure. |
| What cardiac state and ECG heart tracings can be caused by mitral stenosis? | * Pulmonary edema --> right heart failure * Left atrial enlargement --> Afib |
| What is the clinical presentation of mitral stenosis? | * Dyspnea: due to lower cardiac output & edema * Hemoptysis: Increased LA pressure ruptures small bronchial veins * Thromboembolism: In LA -> stroke, PE, MI * RHF due to pulmonary HTN |
| What are the physical exam findings in mitral stenosis? | * Loud S1 * Opening snap * Murmur: Rumbling, mid-diastolic murmur |
| What diagnostic studies can be used for diagnosing mitral stenosis? | * EKG: LAE, RVH * CXR: LA, RV, RA enlargement, palm edema * ECHO: Gold std. non-invasive |
| What are the orifice sizes in mitral stenosis from normal to severe disease? | * Normal: 4 - 6 * Mild: 1.5 - 2 * Moderate: 1 - 1.5 * Severe: < 1 **Usually asymptomatic > 1.5 |
| How is asymptomatic mitral stenosis treated? | * No therapy is required |
| How is mitral stenosis with mild symptoms treated? | Medical Management * Diuretics: for pulmonary edema * Rate control and anticoagulants: for Afib |
| How is mitral stenosis with severe symptoms treated? | Surgical Management * Balloon valvotomy: contraindicated in heavily calcification, severe subvalvular calcification, or mild mitral regurgitation. * Mitral valve replacement: When balloon is contraindicated |
| What is the pathophysiology of mitral regurgitation? | During systole some of the blood in the left ventricle moves back into the left atrium because the mitral valve is not fully closed --> reduced cardiac output. In the next cycle, regurgitated blood plus regular atrial blood will move into the LV --> LV volume overload, LV dilation, LV dysfunction, pulmonary congestion. |
| What are the clinical symptoms of mitral regurgitation? | * Dyspnea: due to decreased cardiac output and pulmonary congestion * Weakness * Left Heart Failure: Due to volume overload * More susceptible to infective endocarditis |
| What are the physical exam findings in mitral regurgitation? | * Murmur: Holosystolic, heard immediately after S1 and can continue beyond A2. Can be heard best at the apex and radiates to the axilla. Murmur is louder if the LV volume increases or when afterload increases. |
| What diagnostic studies can be used for diagnosing mitral regurgitation? | CXR: Dilated left ventricle, pulmonary edema ECHO: Gold Std. Should see mitral regurgitation, dilated left ventricle and maybe left atrium, decreased left ventricle function. |
| What is the treatment for patients with mild symptoms related to mitral regurgitation? | Medical Management * Diuretics: reduce pulmonary congestion * Vasodilators: If symptomatic to reduce afterload making it easier to pump into the aorta rather than the LA. * Periodic follow-up to assess LV enlargement and reduced ejection fraction. |
| What are the treatments for symptomatic patients with mitral regurgitation? | Surgical Management * Done when symptomatic or Ejection Fraction < 60% and End Systolic Diameter is > 40mm. * Mitral Repair: If structural problem * Mitral Replacement: Functional problem |
| What is the pathophysiology of mitral valve prolapse? | * Myxotamous degeneration of the mitral leaflets and chords. * The weakened valve together with the chordal lengthening lead to prolapse into the left atrium during systole. |
| What are the clinical symptoms of mitral valve prolapse? | * Most patients are asymptomatic for life. |
| What are the physical exam findings for mitral valve prolapse? | * Mid-systolic click * Late systolic murmur (Can have one or both) |
| What diagnostic studies can be used for mitral valve prolapse? | ECHO |
| What is the treatment for mitral valve prolapse? | *Usually not necessary *Consider antibiotic prophylaxis for dental procedures |
| What is the pathophysiology of tricuspid stenosis? | Damage to the tricuspid valve causes a reduced lumen size reducing flow from the right atrium to the right ventricle. The right atrial pressure increases which is translated back to the venous system. |
| What are the clinical findings associated with tricuspid valve stenosis? | * Hepatomegaly * Ascites * Edema * Jaundice * Murmur: Diastolic rumbling, increased with inspiration (Right ventricle) |
| What is the diagnostic test for tricuspid valve stenosis? | ECHO |
| What is the treatment for tricuspid valve stenosis? | Surgical * Tricuspid valve repair * Tricuspid valve replacement |
| Tricuspid regurgitation pathophysiology? | Results from failure of the tricuspid valve to close fully before the right ventricle contraction (usually due to the stretching apart of leaflets from RV dilation). As result, some blood flows back into the right atrium --> increased right atrial pressure. |
| What are the physical exam findings associated with tricuspid regurgitation? | * Murmur: systolic murmur at LLSB that is louder with inspiration due to increased venous return to the heart * Elevated JVP * Large pulsatile liver * Lower extremity edema * Ascites |
| What diagnostic test can be used for tricuspid regurgitation? | ECHO |
| What is the treatment for tricuspid regurgitation? | Medical Treatment * Treat underlying cause (CHF, etc.) * Diuretics: To reduce lower extremity edema Surgical Treatment * Tricuspid valve repair *Tricuspid valve replacement |
| What are the primary infections that cause bacterial endocarditis? | Acute: S. aureus Subacute: S. viridins or S. enerococcus |
| What populations are at greater risk for getting bacterial endocarditis? | * IV drug users * Post-surgery for prosthetic valve * Congenital heart defect * Indwelling catheter |
| What is the pathophysiology of bacterial endocarditis? | Formation of a small non-infected thrombus on the endothelial surface in the heart. Secondary infection near the thrombus with bacteria circulating in the blood stream. The bacteria proliferate and form vegetation on the heart valves. |
| What are the clinical and physical exam findings associated with bacterial endocarditis? | * New heart murmur * Fever * Splinter hemorrhages * Osler's nodes: painful, red raised lesions on hands and feet * Janeway lesions: non-tender small erythematous or hemorrhagic macular or nodular lesions on palms or soles |
| What diagnostic studies are used for diagnosing bacterial endocarditis? | ECHO: Look for vegetations Blood culture: look for causative organism |
| What is the treatment for bacterial endocarditis? | * Antibiotics: Prophylaxis during non-sterile procedures like dental, sinus, cystoscopy, and colonoscopy for high risk patients. **Amoxicillin 1 hr before procedure **Clindamycin if patient has penicillin allergy |
| What is the etiology of aortic stenosis? | * Degenerative calcified valve * Congenital bicuspid valve * Congenital unicuspid valve * Rheumatic heart disease |
| What are the populations at risk for developing aortic stenosis? | Most common in the elderly due to aging. Seen in children if congenital. |
| What is the pathophysiology of aortic stenosis? | Results in difficulty pumping blood from the left ventricle into the aorta due to a narrowed lumen and increased pressure (afterload). This results in left ventricular hypertrophy and over time, can lead to dilated left ventricle which can cause mitral regurgitation. |
| What are the clinical and physical exam findings associated with aortic stenosis? | * Angina: reduced cardiac output * Syncope: reduced cardiac output * Heart failure: seen as dyspnea (symptoms appear after years of flow obstruction) * Murmur: systolic crescendo-decrescendo heard in 2nd intercostal space radiating to the carotids * S4: before S1 * Parvus et Tardes Pulse: weak, delayed pulse in carotids * Systolic thrill * Sustained PMI |
| What diagnostic testing is used to diagnose aortic stenosis? | CXR: LVH, calcified valve EKG: LVH, LAE ECHO: most common. Immobile aortic valve and dilated aortic root Cardiac catheterization: Definitive test before surgery, can measure valve flow and area *Normal 3cm *Severe: <.6 |
| What is the treatment for aortic stenosis? | Surgical *Aortic valve replacement (anyone with symptoms) If asymptomatic treat the underlying HF and avoid strenuous activity (body cannot compensate due to low cardiac output) |
| What is the etiology of aortic regurgitation? | Acute *Infective endocarditis *Trauma *Aortic dissection/MI Chronic *Valvular: Rheumatic HD, bicuspid valve, SLE, other congenital causes *Aortic root disease: syphilis, HTN, osteo imperfecta |
| What populations are at risk for developing aortic regurgitation? | More common in men (75%) |
| What is the pathophysiology of aortic regurgitation? | Due to acute causes, valvular disease, or dilation of the aortic root which stretches the AV apart, blood flow regurgitates back into the LV, increasing LVEDV --> LV dilation and hypertrophy to increase blood outflow. Over time these compensations fail --> increased LVP, LAP, and pulmonary pressures. |
| What are the clinical and physical exam findings associated with aortic regurgitation? | *Dyspnea on exertion * Angina: reduced CO * Palpitations, syncope * Signs of LV failure * Murmur: diastolic decrescendo at LLSB * Widened pulse pressure: increased systolic, decreased diastolic * Corrigan's pulse: water-hammer pulse, pistol pulse. Rapidly increasing pulse that collapses as arterial pressure decreases due to regurgitation. * A2 soft/absent, S3 common |
| What diagnostic studies are useful for diagnosis of aortic regurgitation? | CXR: LVH, dilated aorta ECG: LVH ECHO: LVH, reverse of blood flow in the aorta, aortic root size |
| What is the treatment for aortic regurgitation? | Medical Treatment for asymptomatic, stable * Salt restriction * Diuretics * Vasodilators: reduce SVR * Digoxin: Increase contractility of the heart * ACEi: reduce afterload * Exercise restriction Surgical Treatment for acute or symptomatic * Aortic valve replacement |
| Acute Coronary Syndrome | The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion that can result in unstable angina, NSTEMI, STEMI, *Coronary heart disease is the leading cause of death in the US |
| What is the etiology/epidemiology of angina and NSTEMI ('non-ST-segment elevation myocardial infarction)? | Commonly due to coronary artery disease. Risk factors include: Age, DM, HTN, Dyslipidemia, *Tobacco use, Genetics, PAD, Obesity, Physical activity Usually > 50 yo with risk factors |
| What is the pathophysiology of angina and NSTEMI? | Supply of O2 to the heart is reduced due to low coronary flow. Can be due to thrombosis, hemorrhage, plaque rupture. |
| Stable angina | Refers to chest pain when O2 demand is increased such as during exercise. |
| What is the clinical presentation associated with unstable angina and NSTEMI? | *Chronic angina that has increasing frequency, duration, or intensity. *New-onset angina that is severe or worsening *Angina not relieved by rest |
| What diagnostic studies are useful in diagnosing an NSTEMI? | ECG: ST segment depression or T wave abnormalities to rule out/in MI Stress Test: After stabilization. Look for ST changes on ECG or wall motion abnormalities on ECHO. Cardiac Catheterization: visualize steno tic lesions Cardiac Enzymes: absent in unstable angina, present in NSTEMI |
| What is the treatment for acute angina and an acute NSTEMI? | Unstable angina: admit to cardiac unit with monitoring Acute medical treatment (UA/NSTEMI) * Aspirin * β blocker - first line * Heparin: LMWH to prevent clotting * Nitrates: first line. rapid vessel dilation |
| What is the treatment for severe NSTEMI or when medical treatment fails? | Surgical Management * Stent placement: * CABG |
| What is the long-term treatment for NSTEMI? | Aspirin, β blockers, nitrates, reduce risk factors |
| What is the etiology of Variant (Prinzmetal's) angina? | Coronary artery disease (75%) Normal vessels, as well. |
| What is the pathophysiology of Variant (Prinzmetal's) angina? | Transient coronary vasospasm usually accompanied by a fixed atherosclerotic lesion. |
| What is the clinical presentation associated with Variant (Prinzmetal's) angina? | * Angina at rest * Ventricular arrhythmia * ST elevation during chest pain: transient and without cardiac enzyme elevation |
| What diagnostic studies are sued for diagnosis of Variant (Prinzmetal's) angina? | Coronary angiography: Give patient IV ergonovine to provoke chest pain and image the vessels to see vasospasm |
| What is the treatment for Variant (Prinzmetal's) angina? | * Calcium channel blockers: vasodilate * Nitrates: vasodilate |
| What is the etiology and epidemiology for myocardial infarction? | * Most common etiology is coronary artery disease * usually in patients with a history of angina, CAD risk factors, prior MI, arrhythmias. Men > women 30% death rate if do not make it to hospital |
| What is the pathophysiology of myocardial infarction? | Necrosis of the myocardium as a result of interrupted blood supply. Usually due to thrombosis in a coronary artery due to atherosclerotic plaque rupture which occludes the vessel. |
| What is the clinical presentation of a myocardial infarction? | * Angina: severe squeezing, burning, crushing chest pressure that radiates to the neck, ulnar side of the left arm, jaw, epigastrum, or back. Often vague in nature. * Asymotomatic (25%): More common in DM * Dyspnea * Fatigue * N/V * Diaphoresis * Syncope * Sense of impending doom * V fib: #1 cause of sudden cardiac death; requires immediate defib/CPR. |
| What are the physical exam findings associated with a myocardial infarction? | * Patient unable to rest comfortably * Vital signs and PE may be normal * Signs of heart dysfunction: JVD, rales, systolic murmur, S3, S4 |
| What diagnostic testing is used for diagnosing a myocardial infarction? | ECG: ST elevation, T wave inversion,Q waves (transmural STEMI) ST depression, T wave inversion (subendotelial NSTEMI) Cardiac Enzymes: Troponins (I & T) are most important to order, have greatest sensitivity and specificity. Increase at 3-5 hrs, peak 24-48 hrs, reduce in 5-14 days. Obtain every 8 hours Creatinine Phosphokinase: (CPK, CPK-MB): are released from skeletal muscle more than heart and other tissues and are less sensitive and specific. Increase in 4-8 hours, peak at 24 hrs, normal in 48-72 hrs. Obtain every 8 hrs. CPK-MB more specific than CPK. Myoglobin: peaks within 2 hrs so will show up before others, but is not specific. |
| What is the treatment for a myocardial infarction? | Primary goal: Restore coronary blood flow Strongest benefit in first 2 hours: *Thrombolytics (streptokinase): not used as sole therapy much due to contraindications (60% of patients ineligible) and higher rates of occlusion. Not used in NSTEMI because of increased risk of bleed. *PTCA: Percutaneous transluminal coronary angioplasty. STD of CARE for STEMI. S/t in combo with lytics. Involves insertion of a balloon tipped catheter into the femoral artery and guiding it to the coronaries. The balloon is inflated to open the vessel and break off the clot. S/t a permanent stent is also inserted. |
| What is the pharmacological and lifestyle treatment for a myocardial infarction? | * Aspirin/clopidogrel: antiplatelet. Reduces mortality. Long-term therapy. * β blockers: reduce HR, contractility, afterload, reduce mortality. Long-term therapy * ACEi: vasodilate, reduce mortality (largest benefit in CHF or interior wall MI), long0term therapy. * Statins: stabilize plaques, lower cholesterol, give regardless of lipid levels, reduce risk of CAD, CVD, mortality, long-term therapy. * O2 * Nitrates: pain * Morphine: pain * Smoking cessation: 50% reduction for anther CV event. Within 3 years CV risk normalizes. Poss nicotine replacement. * Exercise: Cardiac rehab --> reduces mortality by 25% * Mediterranean diet: low meat, lots of fish, bread, veggies, fruits |
| Anatomy What are the layers of the heart? | *Endocardium: includes the valves, inners surface of atria and ventricles, is contiguous with the vascular endothelium *Myocardium: heart muscle *Pericardium: Outer lining of the heart which includes a serous layer and a fibrous layer. The serous layer is divided into two visceral pericardium (adheres to the myocardium) and parietal pericardium (adheres to the fibrous layer). These are separated by a small space filled with a little pericardial fluid in normal patients. |
| What is the etiology of pericarditis? | *Infections: (HIV, Tb, fungal) *Post-infarction: (Dressler's syndrome inflammation after an MI that spreads to the pericardium) *Trauma *Collagen vascular disease (Lupus) *Radiation *Metabolic (uremia, myxedema) *Neoplastic (breast, lung, melanoma, lymphoma) *Idiopathic/viral (most common) |
| What is the epidemiology of pericarditis? | 5% of patients admitted to ER for non-ischemic chest pain. |
| What is the pathophysiology of pericarditis? | Inflammation of the pericardium --> friction and rubbing between the layers of serous pericardium causing significant pain and potentially effusion. If effusion occurs, the pressure around the heart increases, leading to impaired filling and pumping (low CO) causing shock. This is referred to as cardiac tamponade. |
| What is the clinical presentation associated with pericarditis? | History *Recent virus *Pleuritic chest pain: subacute, worse when inhaling, relieved when leaning forward. Physical exam: *Friction rub: heart in systole and diastole |
| What diagnostic testing is used when diagnosing pericarditis? | CXR: Water bottle heart ECG: Diffuse ST elevation +/- PR depression, PR elevation in aVR, low voltage; electrical alternans (alternating amplitude of QRS) ECHO: evaluate for effusion, rule out wall motion issues Labs: for any of the suspected causes |
| What is the treatment for pericarditis? | *Treat underlying cause *NSAIDs: first line if viral or idiopathic to reduce inflammation *Colchine: anti-inflammatory *Steroids: if refractory pain *Pericardiocentesis: if effusion |
| What is the etiology of cardiac tamponade? | Anything that causes pericarditis, but most commonly: *Neoplasm (50%) *Idiopathic/viral *Uremia |
| What is the pathophysiology of cardiac tamponade? | Additional fluid enters the pericardial space increasing the pericardial pressure. This increased pressure impairs ventricular filling and results in low CO which can lead to cardiogenic shock. |
| What are the clinical findings associated with cardiac tamponade? | History: Fatigue, dyspnea, +/- CP Physical Exam *Beck's Triad: hypotension, muffled heart sounds, elevated JVP *Kussmaul sign: Increased JVP on inspiration (normally, it would decline since more blood would be going into the heart)+/- *Pulsus Paradoxus: difference in SBP of ten or more on inspiration vs expiration. Due to inspiration producing RV filling and the IV septum shifting to the left because there is no room for the heart to expand. The SV from the LV is reduced. |
| What diagnostic studies are used in diagnosing cardiac tamponade? | CXR: Water bottle heart ECG: Diffuse ST elevation +/- PR depression, PR elevation in aVR, low voltage; electrical alternans (alternating amplitude of QRS) ECHO: evaluate for effusion, rule out wall motion issues Labs: for any of the suspected causes |
| What is the treatment for cardiac tamponade? | *Pericardiocentesis *Normal saline volume expansion *Vasopressors *Pericardotomy: recurrent effusions |
| What is the etiology of constrictive pericarditis? | All the causes of pericarditis *Tb: most common worldwide cause *Idiopathic/viral: most common in developed nations |
| What is the pathophysiology of constrictive pericarditis? | After an acute pericarditis, fibrosis of the pericardium develops and impairs pericardial elasticity. In diastole, the ventricle initially fills rapidly until the cardiac volume reaches the limits of the fibrosed pericardium. Then, the filling is severely reduced. Both RV/LV pressures increase. Systolic function remains intact. |
| What is the clinical presentation associated with constrictive pericarditis? | *Mostly signs of RHF *Peripheral edma *Ascites *Hepatomegaly *Elevated JVP *Kussmaul sign *Pericardial knock: high pitched heart sound during diastole that results from cessation of ventricular filling |
| What diagnostic studies are used to diagnose constrictive pericarditis? | CT: assess the pericardial thickness ECHO: reveals an abnormal filling pattern Cardiac Cath: Elevated diastolic pressures |
| What is the treatment for constrictive pericarditis? | *Pericardectomy: do this before the patient develops HF. AKA pericardial stripping. *Diuretics/Salt restriction: To manage fluid overload if no signs of HF. |
| What is the etiology of myocarditis? | *Idiopathic (>50%) *Viral (coxsackie, echovirus, adenovirus, parvovirus, EBV) *Infectious: (bacterial or fungal) *Autoimmune *Drug related: (Cocaine, EtOH, anthracyclines, hypersensitivity) *Metabolic: (hyperthyroidism, thiamine deficiency, pregnancy) *Neoplastic: (amyloidosis, multiple myeloma) |
| What is the pathophysiology of myocarditis? | Inflammation of the myocardium leads to heart muscle damage which may potentially weaken its ability to pump blood. |
| What are the clinical findings associated with myocarditis? | History: Recent viral syndrome, CHF symptoms (dyspnea, orthopnea, edema) Physical Exam *Congestive signs: Elevated JVP, peripheral edema, crackles, displaced PMI/S3 *Low flow: Tachycardia hypotension, cool clammy extremities, weak pulses, decreased urination, AMS |
| What diagnostic studies are used for diagnosing myocarditis? | CXR: cardiomegaly and pulmonary congestion, Karley B lines ECG: non-specific ST-T changes. ST elevation. Nothing classical ECHO: enlarged heart Cardiac MRI: gadolinium enhancement Endomyocardial biopsy: Gold std, but super invasive so rarely done. |
| What is the treatment for myocarditis? | *Treat underlying cause *Supportive treatment: afterload reduction, inotropes, diuretics *Potentially a role for ACEi/ARB and steroids (for rare etiologies) |
| What is the epidemiology of ventricular septal defect? | This is the most common congenital heart disease and is often associated with other defects or syndromes. (50% of children with down syndrome) Associated with fetal alcohol syndrome. |
| What is the pathophysiology of a ventricular septal defect? | In a VSD there is usually a left to right shunt from the high to low pressure ventricle. If large, there is increased flow to the PA, capillaries, PV, LA, and LV. This can also expose pulmonary vasculature to high pressure which over time could lead to pulmonary vascular disease, CHF, and edema. |
| What is the clinical presentation associated with ventricular septal defect? | The presentation depends on size and location. *Large defects: Tachypnea, Slow growth and poor feeding at 3-6 weeks, Murmur: loud pansytolic murmur and diastolic rumble. Accentuated S2, Active precordium (the cardiac beat is easily felt over the left side of the chest) *Small defects: Normal growth, quiet precordium, harsh holosystolic murmur with thrill. |
| What diagnostic testing is used to diagnose ventricular septal defect? | ECHO: look for the shunt, size, pressures, Gold Std. CXR: cardiomegaly, pulmonary edema EKG: LAE, LVH, superior QRS axis with inlet defects. Cath: pressures, PVR |
| What is the treatment for ventricular septal defect? | *Small defect: follow up for spontaneous closure *Large defect: anticongestive therapy (Lasix, ACEi) *Surgery: Large defects and supracristal defects |
| What is a perimembranous ventricular septal defect? | Most common. Located under the aorta in the LV and tricuspid in the RV. May or may not close spontaneously. |
| What is a muscular ventricular septal defect? | Occurs through trabecular septum and can be singular or multiple. Close spontaneously. |
| What is an inlet ventricular septal defect? | Located in the posterior septum, are usually large and require fixing. It is really an atrioventricular defect. |
| What is a supracristal ventricular septal defect? | Located in the RV outflow region just under the pulmonary valve and aorta. Can lead to aortic valve disease so all require surgery. |
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