Download ITE Review: Cardiovascular

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
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-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
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-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
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-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
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-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
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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
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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
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-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
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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
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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
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-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
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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
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