Valvular Emergencies October 11, 2005 Dr. Kanagala.

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Presentation transcript:

Valvular Emergencies October 11, 2005 Dr. Kanagala

Introduction There may be abnormalities of cusps, chordae, or papillary muscles causing valvular dysfunction. Significant valvular abnormality increases stroke rate 3.2 times and death rate 2.5 times

Chronic Valve Disease There may be decades between onset of dysfunction and symptoms Dilation or hypertrophy may preserve cardiac function Account for around ninety percent of valvular disease

Acute Valve Disease Acute valve disease can result in dramatic symptoms.

Diagnosing a New Murmur Consider murmur in context of patient’s medical condition Patient may have normal cardiac anatomy, but murmurs can be associated with other disease states. Examples include anemia, thyrotoxicosis, sepsis, fever, renal failure, and pregnancy

Diagnosing a New Murmur A diastolic murmur or new murmur warrants cardiology referral for evaluation/echo. Urgency for accurate diagnosis and referral or admission depends on severity of symptoms not presence of murmur unless aortic stenosis and syncope is suspected. Patient may be at risk for recurrent cardiovascular event.

Innocent or Physiologic Murmur No abnormal symptoms or signs Soft, systolic ejection murmur begins after S1 and ends before S2, and heart sounds are normal Review of symptoms reveals no symptoms compatible with cardiovascular disease, and complete physical exam is normal.

Mitral Stenosis Most common cause is rheumatic heart disease Progressive stenosis may lead to pulmonary hypertension causing pulmonary and tricuspid incompetence Most patients develop atrial fibrillation

Clinical Features of Mitral Stenosis Symptoms include: tachycardia, anemia, pregnancy, infection, emotional upset, A- fib, exertional dyspnea, paroxysmal nocturnal dyspnea, acute pulmonary edema, hemoptysis, orthopnea, PAC, systemic emboli and infarction, right sided heart failure

Clinical Features continued… mid-diastolic rumbling murmur with crescendo toward S2 With onset of Afib the presystolic accentuation of the murmur disappears. S1 is loud and followed by a loud opening snap (high pitched, heard at apex)

Clinical Features continued… Apical impulse is small and tapping Systolic blood pressure is normal or low Signs of pulmonary hypertension include thin body habitus, peripheral cyanosis, and cool extremities

Diagnosis ECG: notched or biphasic P waves and right axis deviation Chest X-ray: straightening of left heart border, findings of pulmonary congestion like kerley B lines and increase in vascular markings Confirmed with echocardiography (TEE)

Treatment Diuretics for pulmonary congestion Afib treatment Anticoagulation if at risk for embolic events With severe mitral stenosis patients should be warned to avoid strenuous physical activity If hemoptysis occurs due to mitral stenosis and pulmonary hypertension, thoracic surgery may be warranted

Mitral Incompetence Causes include MI, MVP syndrome, rheumatic heart disease, coronary artery disease, collagen vascular disease Inferior MI due to right coronary occlusion is most common ischemic cause

Acute Mitral Incompetence Causes MI Mitral valve prolapse syndrome Rheumatic heart disease Coronary artery disease Collagen vascular disease Inferior MI due to right coronary occlusion is the most common cause of ischemic mitral valve incompetence

Acute Mitral Incompetence Presents with dyspnea, tachycardia, and pulmonary edema S3 and S4 is usually heard Acutely, a harsh apical systolic murmur starts with S1 and may end before S2 Patients may deteriorate quickly due to cardiogenic shock or cardiac arrest

Acute Mitral Incompetence Intermittent mitral incompetence usually presents with acute episodes of respiratory distress due to pulmonary edema and can be asymptomatic in between attacks Pronounced dyspnea may mask angina that accompanies the ischemia

Chronic Mitral Incompetence Late systolic left parasternal lift High pitched holosystolic murmur starting with S1 and may end before S2, heard best in fifth intercostal space, mid-left thorax, and radiates to the axilla First heart sound is soft and often obscured by the murmur S3 heard and followed by a diastolic rumble

Diagnosis ECG: acute inferior MI, left atrial enlargement, LVH, new onset pulmonary edema CXR: minimally enlarged left atrium, pulmonary edema, left ventricular enlargement Echocardiography is essential. TEE done once patient is stable

Acute Mitral Incompetence Treatment Pulmonary edema: oxygen, diuretics, nitrates, intubation Nitroprusside: increases forward output by increasing aortic flow and partially restoring mitral valve competence as left ventricular size diminishes Dobutamine may be required for hypotensive patients

Mitral Incompetence Treatment Aortic balloon counter pulsation Surgery may be warranted if mitral valve rupture Evaluate for and treat endocarditis Treat atrial fibrillation with heparin, control ventricular rate with beta blockers and calcium channel blockers Keep INR 2-3

Mitral Valve Prolapse Click murmur syndrome May be congenital Male, age above 45, and the presence of regurgitation place patient at higher risk for complications

Mitral Valve Prolapse Clinical Features Most are asymptomatic Atypical chest pain Palpitations Fatigue Dyspnea unrelated to exertion Midsystolic click Second heart sound may be diminshed by late systolic murmur with crescendos into S2

Mitral Valve Prolapse Diagnosis ECG: usually normal Chest X-ray: may be normal, or show pectus excavatum, straight thoracic spine, or scoliosis

Treatment of Mitral Valve Prolapse Usually not needed in ED Beta blockers may be used for patients with palpitations, chest pain, or anxiety Suggest avoidence of alcohol, tobacco, and caffeine to relieve symptoms Patients with Afib/ risk for embolization: warfarin with INR of 2-3 Patients with MVP and Afib without mitral regurg., HTN, heart failure, and above 65 can be managed with aspirin 160mg qd.

Aortic Stenosis Most common cause: degenerative heart disease/ calcific aortic stenosis Most common cause in young adults: congenital heart disease Third most common cause in US, but most common cause world wide: rheumatic heart disease

Aortic Stenosis: Clinical Features Classic triad of dyspnea, chest pain, and syncope Exercise may induce symptoms Dyspnea is typically first symptom, followed by PND, exertional syncope, and angina Atrial Fibrillation is less common than in mitral disease but 10% of patients have it at time of surgery

Clinical Features Continued… A small amplitude pulse Slow rate of of increase of carotid pulse LVH Paradoxical splitting of S2 S3, S4 present Classic harsh systolic ejection murmur heard best at second intercostal space radiating to right carotid artery Sudden death

Clinical Features Continued… Brachioradial delay ECG: LVH, in 10% of patients LBBB/RBBB ChestX-ray: starts out normal, but eventually LVH and CHF

Treatment of Aortic Stenosis Pulmonary Edema: oxygen and diuretics New onset Afib: heparin and cardioversion Limit vigorous activity Patients with symptoms secondary to aortic stenosis such as syncope should be admitted

Aortic Incompetence Majority of acute cases due to infective endocarditis Aortic dissection of the root is the second most common cause May be due to trauma

Causes: Increased ventricular pressure: elevates pressure in left ventricle, pulmonary congestion results Appetite suppressant drugs have been linked to aortic incompetence

Causes: Calcific degeneration, Ankylosing spondylitis Congenital disease, Ehlers-Danlos syndrome Systemic hypertension, Reiters Myxomatous proliferation Rheumatic heart disease Marfan syndrome Syphils

Aortic incompetence Clinical Features… Dyspnea Acute pulmonary edema with pink, frothy sputum Fever, chills: Endocarditis Systemic emboli Sinus tach Dissection of ascending aorta

Clinical Features Continued… Sudden death Tachycardia, tachypnea and rales High pitched blowing diastolic murmur heard after S2 Some may have palpitations May have stabbing chest pain, fatigue or dyspnea LV failure

Clinical Features Continued… 2/3 have no symptoms for up to 20 years despite a significant lesion Wide pulse pressure with prominent ventricular impulse Water hammer pulse Accentuated precordial apical thrust Pulsus biferens Duroziez sign Quincke pulse

Aortic Incompetence: Diagnosis Acute: The chest x-ray shows acute pulmonary edema Chronic: The ECG shows LVH and chest x- ray shows cardiomegally, aortic dilation, and possibly CHF ECHO is crucial TEE if aortic dissection suspected

Acute Aortic Incompetence: Treatment Pulmonary Edema: oxygen, intubation Diuretics and nitrites can be used, but may not be effective Nitroprusside plus ionotropic agents can be used to augment forward flow and reduce LVEDP to prepare for surgery Caution when using beta blockers-risk of blocking compensatory tachycardia Emergency surgery

Chronic Aortic Incompetence Treatment: Vasodilators like Ace inhibitors or Nifedipine

Right Sided Valvular Heart Disease Causes Endocarditis in drug users due to organisms such as S.Aureus-isolated symptomatic tricuspid pathology COPD/pulmonary HTN RV failure with dilation Rheumatic heart disease Blunt trauma Congenital: tetrology of Fallot Pulmonary valve incompetence

Clinical Features Dyspnea, orthopnea: most common JVD Peripheral edema Hepatomegaly Splenomegaly ascites

Clinical Features Tricuspid Valve Incompetence: soft blowing holosystolic murmur heard along left lower sternal border Tricuspid Valve Stenosis: rumbling crescendo decrescendo diastolic murmur that occurs just before S1. It is heard at lower left sternal border

Diagnosis Must obtain Echocardiogram

Treatment Address the underlying problem diuretics

Prosthetic Valve Disease Two groups exist: mechanical non-tissue vs. bioprostheses using porcine, bovine or human valves Survival is better with mechanical, and bleeding more common in bioprosthetic valves Valves may become stenotic and small amounts of regurgitations common due to incomplete closure

Complications Thrombi on valve Degeneration of valve Sutures around valve disrupted Valve failure Bleeding/embolism Endocarditis/ ring abscess May have increased susceptibility to hemodynamic compromise from new onset A fib.

Complications Lifelong anticoagulation is needed to decrease risk of thromboembloism and valve thrombosis

Clinical Features Dyspnea CHF Minor/major embolic events Neurologic symptoms: thromboemboli due to valve thrombi or endocarditis Bleeding due to anticoagulation

Clinical Features Abnormal heart sounds Mechanical model: systolic murmur Aortic Bioprosthesis: short midsystolic murmur Mitral Bioprosthesis: loud diastolic murmur

Diagnosis Chest x-ray: can help identify change in position relative to previous films CBC, RBC, PT/INR If you suspect valve dysfunction-echo May need cardiac cath

Treatment May need cardiac surgery referral if there is acute dysfunction Treatment of prosthetic acute valvular dysfuntion due to thrombotic obstruction is thrombolytic therapy Lesser degrees of mechanical valve obstruction: anticoagulate to INR of 2-3.5

Treatment Disposition can be difficult decision if patient has worsening symptoms- consult cardiology

Question 1: Which of the following are clinical features of Aortic Incompetence? A) Water Hammer Pulse B) Pulsus Biferens C) Duroziez Sign D) All of the Above

Question 2: T/F The most common cause of Aortic Stenosis in young adults is congenital heart disease.

Question 3: Causes of Acute Mitral Incompetence include: A) MI B) Mitral Valve Prolapse C) Rheumatic Heart Disease D) All of the above

Answers 1)D 2)T 3)D