* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download ITE Review: Cardiovascular
Survey
Document related concepts
Cardiac contractility modulation wikipedia , lookup
Cardiovascular disease wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Heart failure wikipedia , lookup
Electrocardiography wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Aortic stenosis wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Coronary artery disease wikipedia , lookup
Atrial fibrillation wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Transcript
ITE Review: Cardiovascular Know ACLS -meds that can be given through ET tube…..LEAN -Lidocaine -Epinephrine -Atropine -Nalaxone -give 2-2.5 times normal dose dilute in normal saline Dysrhythmias: Know normal EKG morphology/intervals/etc Hypothermia -‘J wave’ or Osborn wave -sinus brady and afib w/out RVR most commonly seen -rewarm the patient Hypokalemia -U waves (best seen in V3) - PROLONGED QT……LEADING TO RISK OF VFIB/TORSADES Hyperkalemia -peaked T’s (5.5-6.5) -prolonged PR, flattened or absent P, wide QRS (6.5-8) -sine wave, vfib, asystole (>8) Hypocalcemia -prolonged QT Hypercalcemia -shortened ST and QT intervals Hypomagnesemia -prolonged PR and QT -usually associated with hypokalemia (if you don’t replace mag, K will stay low) Digitalis Effects -sagging ST, concave up (hockey stick) -most prominent in lateral leads…..does not indicate toxicity -toxicity -poisoning of the Na-K-ATPase pump: tachydysrhythmias -increasing vagal tone: bradydysrhythmias and AV blocks -risk factors: hypoxia, lyte imbalance, drugs -EKG: PVCs- most common -paroxysmal atrial tach with AV block – pathognomonic -Acute (think young OD) vs Chronic (think elderly, poor renal function) -treatment: acute: multiple doses of charcoal, give FAB 1 -FAB: ventricular dysrhythmias, K >5, lethal intoxication SVT -regular -vagal maneuvers -adenosine (xanthines increase dose, benzos/carbamazepine decrease dose) -Ca vs beta blockers to slow rate Atrial Fibrillation -irregularly irregular -generally 160-180, >200 think WPW -regular and slow, think digitalis -normal cardiac function (CA/beta blockers) -compromised cardiac function (dig/amiodarone) ->48 hr onset attempt to avoid cardioversion -think about anticoagulation WPW -short PR (<0.12) -delta wave -Kent bundle is the accessory -narrow regular complex treat like SVT -wide complex procainamide vs. amiodarone -afib or flutter, NO AV blockers, procainamide Atrial Flutter -sawtooth -vagal maneuvers or adenosine -rate control (beta/Ca block) Multifocal Atrial Tachycardia -irregularly irregular rhythm -p waves varying shapes, at least three different types in one lead -treat the underlying condition (COPD, CHF, theophylline toxicity) -then Ca blockers (avoid beta block), try mag Sick Sinus Syndrome -combinations of brady and tachydysrhythmias, most commonly in elderly -treatment based on brady or tachy -need referral to cardiologist for pacer Ventricular Tachycardia -3 or more consecutive PVCs with rate >120 -PVC= earlier, wider, absent preceding P wave, ST/T wave opposite of QRS -monomorphic: amiodarone, lidocaine, procainamide or sotalol Torsades de pointes -QRS axis swings from + to – in single lead -precipitated by prolonged QT -hypo K, hypomag -1A and 1C antidysrhythmics, cyclic antidepressents, droperidol 2 -magnesium sulfate, then overdrive pacing (isoproterenol) Ventricular Fibrillation -fine or course, zigzag pattern, no Ps, QRS or t waves -ACLS ***Remember cardiovert in cases of hemodynamic instability*** Know PEA and Bundle Branch Blocks AV Blocks -1st: pronlonged PR >0.20 sec -no treatment -Mobitz 1 (wenckebach): PR progressively lengthens and then drops beat -asymptomatic no treatment (symptoms get atropine or pacing) -Mobitz II: PR same duration, dropped beats -require pacing, avoid atropine -3rd : no atrial pulses conducted, no relationship between P and QRS -require pacing, try atropine (except wide complex with inferior MI) Pacemakers/AICD -transcutaneous vs temporary transvenous -used for unstable brady, overdrive pacing, early bradyasystolic arrest -Tips for transvenous pacing -apex of right ventricular ideal location -right IJ preferred access (2nd in left subclavian) -Pacemaker Failure -screening EKG, CXR, use of pacemaker magnet -magnet placement turns off sensing, turns pacer to fixed-rate -battery depletion, wire fracture, oversensing, lead malposition -runaway pacer: HR>200, usually from battery depletion, place magnet -AICD -indicated for pts who are high risk for fatal dysrhythmias -think Brugada, Hx of sudden cardiac arrest, poor EF -place magnet over to inactivate -CPR and defibrillate then same (don’t place pads overtop generator) Acute Coronary Syndrome -continuum from stable angina to unstable angina to acute myocardial infarction -stable angina: transient, episodic CP, predictable and reproducible, improved with rest or nitro -unstable angina: new in onset, occurs at rest or differs from stable angina, severely limiting or last longer -AMI: STEMI or CP with elevated cardiac markers -Atypical presentations: DM, elderly and women 3 -epigastric discomfort -fatigue/SOB -approx 12.5% of all MIs -Risk Factors: smoking, HTN, DM, hyperlipidemia, FHx 1st CAD <55, Hx of CAD, PVD EKG: Get one and know what a STEMI looks like -Anterior (LAD)- V1-V4, reciprocals in inferior leads -Lateral (LAD/circumflex)- I, avL, V5-6 -Inferior (right CA)- II, III, avF, depression in V1-4 -Right Ventricular Wall (right CA) – V3r and V4r, usually happens with inferior -think hypotensive and cardiogenic shock -Posterior (circumflex off right) – depression in anterior leads, abnormally tall R in V2 Treatment -ASA: 160-325 mg, chewing gives max benefit -Plavix: in STEMI or high risk NSTEMI -Heparin/lovenox: for AMI and unstable angina -Nitro: for pain, watch BP -beta-blockers: usually given on floor, at some point within 24 hours -Morphine: for pain after nitro -Thrombolytics (STEMI) -TPA/Alteplase, given within 30 minutes of ED arrival, if no CATH -PCI > 60-90 minutes away -no contraindications -PCI- for STEMI Complications -Dysrhythmias -vfib highest in first hour of infarct -LV failure (CHF, pulmonary edema, cardiogenic shock) ->25% function loss = pulm edema ->40% loss of function = shock -Conduction disturbances -1st degree and Mobitz 1 with inferior -Mobitz II with anterior – gets pacer -BBB with AMI more likely to develop CHF, AV block and vfib -new RBBB in AMI high risk of 3rd AV block and cardiogenic shock Congestive Heart Failure/Acute Cardiogenic Pulmonary Edema Etiology: left sided-ischemic heart disease. HTN, aortic/mitral valvular disease Right sided- left sided failure, pulm HTN, tricuspid/pulmonic disease Precipitating Factors -ischemia -afib -sodium overload and non compliance -increased hemodynamic demand 4 -HTN -COPD (leading cause of cor pulmonale) Signs and symptoms -SOB, ‘cardiac asthma’, pleural effusion, S3, JVD, dependent edema CXR/Symptom Progression -Stage 1: cephalization, dyspnea, PAWP 8-12 -Stage 2: interstitial edema (kerley B lines), dry cough, PAWP 18-25 -Stage 3: alveolar edema (butterfly pattern), wet cough, pink frothy sputum PAWP >25 Lab -BNP-marker for CHF -<100 reliably excludes diagnosis Treatment -place upright, get monitor strip -Oxygen: most important, don’t forget about BiPAP, if intubated think PEEP -meds: nitro, lasix, morphine -think pressors if in shock (dobutamine, norepinephrine) Cardiomyopathies -dilated (most common), restrictive or hypertrophic Idiopathic Dilated Cardiomyopathy -dilatation of all four chambers, systolic pump failure -get sings of left and right sided failure -afib most common dysrhythmia -treat with diuretic, vasodilators, (digitalis) Restrictive Cardiomyopathy -diastolic restriction of ventricular filling, mimics constrictive pericarditis -right sided failure symptoms predominate -exercise intolerance common -dilated atria, mitral/tricuspid regurg -treat with diuretics (avoid vasodilators) Hypertrophic Cardiomyopathy -left ventricular hypertrophy without dilation, usually septum greater -50% inherited -dyspnea on exertion, syncope and pre-syncope with exertion -sudden death with exercise induced dysrhythmias (usually older pt) -‘a wave’, systolic ejection murmur increased with valsalva, standing, exercise -EKG with LVH and left atrial enlargement, giant negative T waves -treat with propranolol, amio for ventricular dysrhythmias -avoid increasing myocardial contractility and/or reducing ventricular volume -septal myomectomy for severe cases (mortality of 3-8%) -antibiotic prophylaxis for dental procedures 5 Deep Venous Thrombosis -venostasis, hypercoagulability and vessel wall injury/abnormality (Virchow’s triad) Presentation -unilateral pain, swelling and edema (most reliable sign, >3cm) Phlegmasia cerulea dolens -ischemic form of venous occlusion -tensely swollen, painful and cyanotic (bullae may be present) -may result in venous gangrene (irreversible) Phlegmasia alba dolens (milk leg) -massive iliofemoral thrombosis associated with arterial spasm -swollen not tense, doughy, white skin, petechiae often present -temporary, as arterial spasm resolve leg become cyanotic appearing Risk Factors -PRIOR DVT, carcinoma, pregnancy/post partum, estrogen therapy -immobility, trauma/surgery, AIDS/SLE, inherited coagulopathies -KNOW WELLS! And when to use d-dimer for exclusion Diagnosis -duplex Ultrasonography (with repeat testing usually in 7 days) Treatment -aimed at preventing PE -anti-coagulate with heparin/lovenox and start Coumadin -thrombolytic therapy for <60 yo pts with massive limb threatening clot ie cerulea dolens -greenfield filter if can not anti-coagulate or have failed -admit those who: need close monitoring for bleeding -poor compliance/inadequate assistance -circulatory compromise -require IV heparin Pulmonary Embolism -third most common cause of death in US -primarily a complication of a DVT Risk Factors -DVT, obesity, prior DVT/PE, surgery (orthopedic), carcinoma, prolonged bed rest Presentation -DYSPNEA, pleuritic CP, apprehension, syncope (massive) -TACHYPNEA, tachycardia, hypotension (massive) -classic triad: dyspnea, pleuritic CP or tachypnea (present in at least 95%) -once again know WELL’s CXR -atelectasis, elevated hemidiaphragm, small pleural effusion: most common -hampton’s hump and westermark’s sign -dyspnea and hypoxia with normal CXR very suggestive 6 EKG -nonspecific ST/T wave and sinus tach are most common finding -look for right heart strain -peaked P in lead II -new RBBB, S1Q3T3 D-dimer -remember Well’s, negative test can not exclude moderate or high pretest! V/Q scan -need interpretation in the context of clinical suspicion -low-moderate pretest prob with normal study, excludes significant PE 98% -indeterminate or non-diagnostic will need further testing -high prob with high pretest is considered confirmatory -remember limited in lung disease sCTA -95% sensitivity for segmental or large PE, 75% for subsegmental -per Rivers: negative test with high pretest requires angiography Pulmonary Angiography -gold standard -can still miss small peripheral clots, also 2.5 mm w/out augmentation Duplex US -nondiagnostic VQ, use this as next step, if + treat Treatment -heparin/lovenox with Coumadin -Fibrinolytic -hemodynamic instability -RV dysfunction on bedside echo -TPA preferred, 100mg over 2 hours Pericardial Disorders Pericarditis -most common cause: idiopathic and viral -diagnosis -Hx: sharp precordial pain, relieved by sitting up and leaning forward -PE: friction rub is pathognomonic (triphasic, lower left sternal border) -EKG: diffuse concave up ST elevation with PR depression -echo: to look for effusion -BUN/Crt: important to r/o uremia -treatment -outpatient for idiopathic/viral if reliable with NSAIDs -inpatient for others and treat underlying cause (dialysis for uremia, cessation of drug, antimicrobials for infection) Pericardial Tamponade -Beck’s triad: hypotension, JVD, muffled heart tones (happens just prior to arrest) -tachycardia is earliest finding 7 -diagnosis -EKG: low voltage, electrical alternans (pathognomonic) -echo: gold standard -large effusion, diastolic collapse of RV and RA -swinging motion -treatment -monitor, IV, O2 -aggressive volume resuscitation and pressors if needed -cardiac/CT consult and pericardiocentesis (under US) Myocarditis -inflammation of the heart muscle Presentation -range from nonspecific fatigue to florid CHF -usually preceded with viral illness -watch for tachycardia disproportionate to fever Diagnosis -EKG: non specific, most common sinus tach -CXR: usually normal (could see signs of CHF) -Echo: dilated chambers with diffuse or focal hypokinesis -Labs: mild to moderate leukocytosis, elevated ESR -trop rise and fall slowly -endomyocardial biopsy for definitive Etiology -virus is most common cause -also remember drugs, parasites and systemic disease (SLE, Kawasaki) Treatment -supportive, admit to ICU, bed rest -treat CHF like CHF (ACE inhibitors particularly helpful) -immunosuppressives and NSAIDs contraindicated -IVIG for Kawasaki Endocarditis -localized infection of the endocardium with hallmark of vegetation -congenital/acquired valvular disease and prosthetic are most commonly affected Causative Organisms: most commonly bacteria -native valves: non-viridan strep -prosthetic valves: coag-neg staph (<60 day post-op), staph aureus/strep epi (>60) -IVDA/immunocompromised: staph aureus Left vs Right: IVDA on right (pulmonary) Clinical Presentation -fever: most common -signs of metastatic infection -Roth spots (retinal hemorrhage), Osler nodes (tender nodules on volar finger) -Janeway lesions (non tender macular on fingers, palms, soles), splinter hemorrhages 8 Diagnosis -blood cultures most useful, + in >90% -Duke Criteria -Major: positive blood culture, evidence of endocardial involvement -Minor: predisposition, fever, vascular and/or immunologic phenomenon, Microbiologic evidence, echo evidence -need two major, or one major and 3 minor, or 5 minor Treatment -native valve: ampicillin/nafcillin + gent or vanc + gent -prosthetic: vanc + gent + rifampin Conditions needing Prophylaxis -prosthetic valve -hx of endocarditis -cyanotic congenital heart lesions (unrepaired, most CHD need it) -acquired valvular disease (ie rheumatic fever) -hypertrophic cardiomyopathy -indicated for procedures with significant manipulation of infected tissue -not needed for foley, routine dental cleaning, intubation (ie clean procedures) Aortic Dissection and AAA Dissection (most common lethal aortic disease, 2-3 times more common than AAA) -male predominant, age 50-70 -Risk factors: HTN (don’t forget connective tissue disorders, syphilis) -Classification: Stanford (and Debakey) -type A (I&II) more deadly -Presentation -pain most common symptom (abrupt, sharp, tearing/ripping) -unequal pulses -Diagnosis -CXR: upright, widened mediastinum, calcium sign -right side: deviation of trachea -left side: pleurapical cap, depressed left mainstem bronchus, effusion -EKG: usually abnormal -STEMI most common misdiagnosis (usually inferior) -Definitive Testing -TEE: most expedient, S&S about 100%, ‘unstable’ pts Contraindicated with esophageal disease -Aortography: traditional gold standard, S&S =90%, not done in ED -CTA: almost 100% S&S, may miss rapidly moving flap -Treatment -10-15 units of blood on standby, surgical consultation -control HR and BP, esmolol first then nitroprusside -treat pain with IV narcotics 9 Expanding and Ruptured AAA -true aneurysm involves all three layers of the arterial wall, 95% infrarenal -most often occur with atherosclerotic disease -males >60 (Caucasian….heavy smoker) -Presentation: -think middle age to elderly white male with syncope or near syncope and -severe abdominal and back pain (might have scrotal hematoma, look) -PE with classic pulsatile abdominal mass +/- tenderness -Diagnosis and management -high likelihood in Hx and PE is enough for OR -IVs, monitor, 10 units of blood on standby, surgical consultation -bedside echo or if ‘stable’ CTA with close supervision HTN Emergency and Urgency Emergency -(severely elevated DBP >140), END ORGAN DAMAGE -Presentation: encephalopathy, acute intracranial events, dissection, pulmonary edema, ischemia, eclampsia, AKI -Treatment: arrest and reverse the end organ damage by lowering BP rapidly -do so in controlled manner -use IV meds, goal reduce BP by 30% in first hour -Encephalopathy: nipride -ischemic stroke: only treat >220/120 (180 for TPA), labetalol Nicardipine -ICH: labetalol, nicardipine -SAH: nimodipine or nicardipine -dissection: nipride (in combo with esmolol) -MI: nitro -Pulmonary Edema: nitro -Eclampsia: magnesium and hydralazine Urgency -DBP >115 with no end organ damage -asymptomatic patient discharge to follow up with PCP -use oral agents to gradually lower BP over 24-48 hrs Valvular Heart Disease Prosthetic Valves -Mechanical -lifespan >20 yrs -loud metallic click -LIFE LONG ANTICOAGULATION (> hemolysis, more thombogenic) -Bioprosthetic -lifespan 8-10 years 10 -sounds similar but louder than native valve -anticoagulation optional (ASA sufficient) -Complications -thromboembolic events -paravalvular leak: immediate-suture rupture, delayed-endocarditis -more common in mechanical -endocarditis: <2 mo post-op staph/strep epi, after strep viridans Mitral Valve Prolapse (click murmur syndrome) -most common, 5-10% of population, young women -presentation: young women-palpitations, athlete and elderly-syncope -high-pitched, late systolic murmur with mid-systolic click -treat only symptomatic pts with…. Beta blockers for CP or dysrhythmias ASA or anticoagulation with hx of TIA/stroke Mitral Stenosis -rheumatic heart disease etiology for >90% -presentation: exertional dyspnea (most common), hemoptysis -diastolic murmur heard best at apex -afib most common complication -treatment: rate control afib, ABx prophylaxis Mitral Regurgitation Acute -usually rupture of chordae tendineae or papillary muscle after… -MI, trauma, infection -presents in fulminant CHF/pulmonary edema -apical systolic murmur (radiating to axilla) -treat with hemodynamic support and consult CT surgery Chronic -evolves slowly and usually coexists with mitral stenosis -high pitched holosystolic murmur, wide-split S2 -afib in 75% of pts -ABx prophylaxis Aortic Stenosis -<65 bicuspid valve, >65 calcification -symptoms late after opening <1cm (exertional dyspnea/syncope) -harsh systolic crescendo-decrescendo murmur radiating to carotids -Treatment -mild symptoms: d/c, avoid strenuous activity -CHF: admit and decrease preload/afterload -refer all symptomatic pts for surgical therapy 11 Aortic Regurgitation Acute -think dissection -present with severe dyspnea -short diastolic murmur at left sternal border Chronic -exertional fatigue and dyspnea -decrescendo diastolic blowing murmur Tricuspid Stenosis -think endocarditis from IVDA -presents with fatigue and systemic edema -diastolic murmur accentuated with inspiration -rarely exists in isolation and usually other valve disease is dominant Tricuspid Regurgitation -usually hx of pulmonary HTN -holosystolic murmur at xiphoid -afib in 80% of pts 12