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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