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
-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 (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
-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
-epigastric discomfort
-fatigue/SOB
-approx 12.5% of all MIs
-Risk Factors: smoking, HTN, DM, hyperlipidemia, FHx 1st CAD 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
-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
-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 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
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
-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: 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 calcification
-symptoms late after opening ................
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