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CARDIOVASCULAR ACUTE/SUBACUTE BACTERIAL ENDOCARDITIS ➔ A bacterial infection of the endocardium ➔ Duke criteria ◆ Positive blood culture for infective endocarditis (IE) ● Isolation of typical organisms from two positive cultures of blood samples drawn > 12 hours apart, or all of three or a majority of four separate cultures of blood ● Typical organisms include viridans strep, S. bovis, HACEK (H. aphrophilus, A. actinomycetemcomitans, C. hominis, E. corrodens, and K. kingae), or community-acquired S. aureus or enterococci ◆ Endocardial involvement as evidenced by positive echocardiogram for IE defined as… ● Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or ● Abscess, or ● New partial dehiscence of prosthetic valve ➔ Frequency of affected valves is aortic > mitral >> tricuspid ➔ Vascular phenomena ◆ Major arterial emboli ◆ Septic pulmonary infarcts ◆ Mycotic aneurysm ◆ Intracranial hemorrhage ◆ Conjunctival hemorrhages ◆ Splinter hemorrhages

◆ Janeway lesions ➔ Immunologic phenomena ◆ Glomerulonephritis ◆ Osler’s nodes ● Tender fingertip nodules ◆ Roth spots ● Retinal hemorrhages ➔ First line treatment is vancomycin ◆ Therapy can be narrowed with blood culture results

ANGINA ARRHYTHMIAS PROLONGED QT SYNDROME ➔ QTc > 430 msec in men and > 450 msec in women ➔ Causes of prolonged QT (QT WIDTH) ◆ QT ● Prolonged QT syndromes including Romano-Ward and Jervell and Lange-Nielsen ◆ Wolff-Parkinson-White (WPW) syndrome ◆ Infarction ◆ Drugs ◆ Torsades ◆ Hypocalcemia, hypokalemia, hypomagnesemia ➔ Symptoms include syncopal episodes, predisposition to paroxysmal episodes of ventricular tachycardia and torsades de pointes by “R-on-T phenomenon” ◆ QRS fires at the same time (so, prematurely) as ventricular repolarization (T wave) is happening, so not all tissue is ready for depolarization

➔ If inherited, give beta blockers to decrease sympathetic stimulus and implantable overdrive pacemaker/defribillator SINUS BRADYCARDIA ➔ A sinus rhythm (P before every QRS complex) with upright P waves in I and aVF and narrow QRS complexes with a rate < 60 ➔ If the RR distance is at least one inch, consider…(One INCH) ◆ Overmedication ◆ Inferior wall MI, increased intracranial pressure ◆ Normal variant ◆ Carotid sinus hypersensitivity ◆ Hypothyroidism SINUS TACHYCARDIA ➔ HR > 100 bpm and regular, usually < 150, with a P wave prior to every QRS complex and upright P waves in I and aVF ATRIAL ECTOPY WANDERING ATRIAL PACEMAKER (WAP) ➔ More than 3 different P wave morphologies ➔ QRS following each P wave ➔ Usually asymptomatic but the patient may complain of palpitations or anxiety MULTIFOCAL ATRIAL TACHYCARDIA (MAT) ➔ Wandering atrial pacemaker with a rate > 100 bpm ➔ Associated with COPD and theophylline overdose ➔ Rate is often difficult to control WOLFF-PARKINSON-WHITE (WPW) SYNDROME ➔ A syndrome in which there is an accessory electrical pathway that causes SVT in older children and adults ➔ The heart beats too fast for adequate filling and may led to shock

➔ Diagnosis ◆ EKG changes ● Narrow QRS complex ● HR > 200 ● P waves present ● Slurred upstroke of QRS (delta wave) that may not be evident during tachyarrhythmia ➔ Don’t give ABCD to someone with WPW because they preferentially block AV node conduction, which would leave the accessory tract completely unopposed ◆ Adenosine ◆ Beta blockers ◆ CCBs ◆ Digoxin SICK SINUS SYNDROME (SSS) ➔ Sinus arrest is a pause of the SA node signal that usually results in ectopic or escape beats and rhythms that take over as source for ventricular impulse

CARDIAC TAMPONADE ➔ A pericardial effusion that restricts ventricular filling and eventually stroke volume, leading to systemic hypotension, shock, PEA, and death ➔ Electrical alterans ➔ Beck’s triad is JVD, hypotension, and muffled heart tones ➔ One of the reversible causes of PEA is cardiac tamponade ◆ Either a bedside ultrasound or pericardiocentesis should be performed in a patient in PEA ➔ Treatment ◆ Immediate decompression via needle pericardiocentesis, pericardial window, or thoracotomy with manual decompression

CHEST PAIN ➔ ED evaluation of chest pain consists of a rapid determination as to whether the CP represents a potentially life-threatening cause ➔ Features of history that increase the likelihood that CP is due to ACS (in order of decreasing probability) ◆ Substernal location of CP ◆ Pain lasts from 30 minutes to 30 hours, of gradual onset ◆ Pain is described as crushing, squeezing, tightness, or pressure ● “Like an elephant is sitting on my chest” ◆ Pain is accompanied by diaphoresis or “impending sense of doom” ◆ Pain is similar to previous anginal pain ◆ Family history of first-degree male relative with ACS at age 50 or younger ◆ Pain radiating to left, right, or both arms ➔ Features of physical exam that increase the likelihood that CP is due to ACS (in order of decreasing probability) ◆ Diaphoresis ◆ Nausea/vomiting ◆ New S3 sound ◆ Hypotension ◆ Lung crackles ➔ LEVINE SIGN is when a patient puts a clenched fist to his chest to describe the pain of an MI

CONDUCTION DISORDERS ATRIAL FIBRILLATION ➔ Very rapid atrial depolarization (350-600 bpm) from many ectopic atrial foci, usually with ineffective conduction to the ventricles ◆ Rapid ventricular response gives ineffective systole from poor filling

● This is especially bad for people in heart failure because the loss of atrial kick leads to a decreased contribution to cardiac output ➔ Predisposes to atrial blood stasis and subsequent clotting, which can embolize and cause stroke ◆ Risk of acute ischemic stroke is increased fivefold ● So, patients with atrial fibrillation have to be anticoagulated ➔ Most common sustained cardiac dysrhythmia ➔ Causes of atrial fibrillation (PIRATES) ◆ Pulmonary disease ◆ Ischemia ◆ Rheumatic heart disease ◆ Anemia, atrial myxoma ◆ Thyrotoxicosis ◆ Ethanol ◆ Sepsis ➔ Diagnosis ◆ Narrow QRS complexes ➔ Do a transesophageal echo on people with atrial fibrillation to rule out atrial thrombi ➔ Treatment ◆ Control ventricular response rate to between 60 and 100 with AV nodal blocking drug ● CCB or BB acutely, digoxin long term ◆ Consider elective cardioversion if < 48 hours duration ● If > 48 hours duration, must anticoagulate for 4 weeks before cardioversion

◆ Anticoagulation in new-onset atrial fibrillation is mandatory because of the significant risk for embolization, which can result in stroke

ATRIAL FLUTTER ➔ Rapid atrial depolarization (240-350 bpm) from an abnormal focus within the atria and variable ventricular conduction described as a block ➔ Causes of atrial flutter (PIRATES) ◆ Pulmonary disease ◆ Ischemia ◆ Rheumatic heart disease ◆ Anemia, atrial myxoma ◆ Thyrotoxicosis ◆ Ethanol ◆ Sepsis

SUPRAVENTRICULAR TACHYCARDIA ➔ Most common pediatric dysrhythmia ➔ Narrow QRS complex tachycardia with regular RR intervals at a rate of 150-250, caused by either increased atrial automaticity or reentry phenomenon ➔ Symptoms include… ◆ Dyspnea ◆ Palpitations ◆ Angina ◆ Diaphoresis ➔ Diagnosis ◆ Chest x-ray is most often normal ◆ EKG changes ● Narrow QRS complex ● Tachycardia at a rate > 150

● Typically regular, P waves may or may not be visible ➔ Treatment ◆ Immediate synchronized cardioversion (50J) if hemodynamically unstable, in CHF or ACS ◆ Vagal maneuvers ● Carotid massage ● Diving reflex ● Valsalva maneuver ◆ Adenosine (contraindicated in patients with asthma) ● 6 mg rapid IV push followed by 20 mL flush ○ Repeat as needed x 2 with 12 mg each time ● Blocks AV nodal conduction ◆ Diltiazem (0.25 mg/kg IV over 2 minutes) or verapamil (0.15 mg/kg IV over 1 minute) or beta block to control rate

BUNDLE BRANCH BLOCK LEFT BUNDLE BRANCH BLOCK ➔ Conduction is blocked before the anterior and posterior fascicles split ➔ EKG changes ◆ No Q waves in I, aVF, V5, or V6 ◆ Large, wide R waves in I, aVL, V5, and V6 ➔ Use the Sgarbossa criteria to look for ischemia with known LBBB, where a score greater than or equal to 3 predicts an MI ◆ ST segment elevation > 1 mm concordant (in the same direction) with its QRS axis is 5 points ◆ ST segment elevation > 1 mm in V1-V3 is 3 points ◆ ST segment elevation > 5 mm, discordant with QRS is 2 points

RIGHT BUNDLE BRANCH BLOCK

➔ Ischemia is not masked with RBBB, except in leads V1-V3 ➔ EKG changes ◆ Regular sinus rhythm (RSR) described as “rabbit ears” in morphology in V1, V2 ◆ Wide S waves in I, aVL, V5, and V6

VENTRICULAR TACHYCARDIA ➔ > 3 ectopic ventricular beats in a row ◆ Wide QRS complexes with no preceding P wave ➔ Will readily convert to ventricular fibrillation (which is bad) ➔ Treatment ◆ If stable… ● Procainamide 20-50 mg/min IV until arrhythmia is suppressed, hypotension ensues, QRS duration increases > 50%, or maximum dose (17 mg/kg) is reached ○ Avoid in patients with CHF ● Amiodarone 150 mg IV bolus over 10 minutes ○ Can be repeated once and should be followed with maintenance infusion of 1 mg/min for 6 hours ● Sotalol 100 mg IV (1.5 mg/kg) over 5 minutes ○ Avoid if prolonged QT ◆ If pulseless, treat like ventricular fibrillation

VENTRICULAR FIBRILLATION ➔ Early defibrillation is the most important therapy for this rhythm ◆ It takes precedence over establishing IV access, intubation, or the administration of any drug ◆ 360J if monophasic monitor, 150J-200J if biphasic monitor ➔ Medications of use include…

◆ Epinephrine 1 mg IV q 3-5 minutes or vasopressin 40 U IV x 1 ◆ Amiodarone 300 mg IV for VF, then infusion ● Lidocaine can be used if amiodarone is not available ○ 1-1.5 mg/kg IV, able to repeat once ◆ Magnesium sulfate 1-2 g IV, then infusion if torsades de pointes is present ● “Twisting of the points”

PREMATURE BEATS PREMATURE ATRIAL COMPLEXES (PACs) ➔ Abnormal electrical focus triggers an atrial contraction before the sinus node fires, thus triggering a QRS and ventricular contraction ➔ There is a compensatory pause before the next sinus beat ◆ Longer RR interval ➔ Benign and asymptomatic

CORONARY HEART DISEASE ➔ ACS can be classified as STEMI, n-STEMI, or unstable angina ◆ n-STEMI and unstable angina are thought to represent the ends of the same disease process spectrum ● Unstable angina with elevated serum cardiac biomarkers is an n-STEMI ➔ Obtain cardiac biomarkers, CBC, electrolytes, coagulation studies, and drug levels (i.e. digoxin) if relevant ➔ Sublingual NTG provides analgesia and coronary dilation, where up to 1.2 mg can be given ◆ If the patient responds transiently to NTG but their pain returns, IV NTG can be started ➔ Morphine reduces excess catecholamine release, 4 mg given initially for analgesia

NON-ST ACUTE MYOCARDIAL INFARCTION

ST SEGMENT ELEVATION ACUTE MYOCARDIAL INFARCTION ➔ Diagnosis of STEMI ◆ Elevation of > 1 mm in ST segments of two or more contiguous segments ◆ New LBBB ➔ Sgarbossa criteria for impending MI in LBBB ◆ ST elevation > 1 mm in leads with dominant R waves (concordant with QRS complex) ◆ ST elevation > 5 mm in leads with dominant S waves (discordant with QRS complex) ◆ ST depression > 1 mm in V1, V2, or V3 ➔ Reperfusion therapy ◆ Given for STEMI within 12 hours of onset, where the two options are thrombolytics (alteplase, reteplase, tenecteplase, streptokinase, urokinase) or PCI (percutaneous coronary intervention) ● Absolute contraindications to thrombolytic therapy include... ○ History of intracranial hemorrhage ○ History of ischemic stroke longer than 3 hours ago but less than 3 months ago ○ Cerebral vascular malformation ○ Intracranial malignancy ○ Symptoms or signs suggestive of an aortic dissection ○ Bleeding diathesis ○ Active bleeding ○ Significant closed-head or facial trauma within the last 3 months ● Relative contraindications to thrombolytic therapy include… ○ History of chronic, severe, or poorly controlled hypertension

ANGINA PECTORIS

○ Severe uncontrolled hypertension on presentation > 180/110

UNSTABLE ANGINA

mmHg ○ Recent (within 2-4 weeks) internal bleeding ○ Traumatic or prolonged (> 10 minutes) CPR ○ Major surgery within the preceding 3 weeks ○ Current use of anticoagulant with INR 1.7 ○ Pregnancy

➔ Angina is considered unstable if… ◆ It lasts for more than 20 minutes or its frequency is increased from baseline ◆ Its onset is new and markedly limits physical activity

◆ Onset occurs at rest PRINZMETAL’S ANGINA

DYSPNEA ON EXERTION ACUTE CARDIOGENIC PULMONARY EDEMA ➔ Most common cause is noncompliance with medications ➔ Diagnosis ◆ Hazy appearance on chest x-ray ◆ Obtain CBC, electrolytes, cardiac biomarkers, and BNP ➔ Treatment ◆ First line treatments (NOt BAD) ● Nitroglycerin reduces preload and thus pulmonary capillary wedge pressure ● Oxygen therapy

● BiPAP (or CPAP) is useful in severe edema as a temporizing measure until pharmacologic therapy can take effect ● Aspirin is given as part of protocol to rule out acute coronary syndrome ● Diuretics, where loops are used to produce venodilation (which reduces pulmonary capillary pressure by causing diuresis) ○ With furosemide, peak onset of diuresis occurs in about 30 minutes and lasts about 6 hours ◆ Second line modalities can be used to boost inotropic support ● Dobutamine causes increased stroke volume and cardiac output by mainly working on beta-1 receptors with minimal effect on alpha-1 receptors ○ Initial dose is 2.5 microgram/minute ● Dopamine is reserved for hypotensive patients in whom arterial pressure increase is required, due to stimulation of alpha-1 adrenergic receptors in addition to beta-1 (cardiac) receptors ○ Cardiac dosing is 3-10 micrograms/min ◆ Nesiritide is recombinant BNP, so is vasodilatory ● Use is limited to inpatient who has failed first line therapy

HEART FAILURE ➔ Condition characterized by inadequate systemic perfusion to meet the body’s metabolic demands due to “failure” of the heart’s pump function ➔ Pathophysiology ◆ Systolic dysfunction ● Low cardiac output leads to backflow of blood into the lungs, which increases the pulmonary pressure

● Normally, neurohormonal pathways and the sympathetic nervous system compensate ● Release of catecholamines aggravates the ischemia ● Symptoms appear when the body is no longer able to sufficiently compensate ◆ Diastolic dysfunction ● Problem is impaired left ventricular relaxation ● Leads to elevated diastolic pressures and poor ventricular filling, which causes pulmonary edema ● Diastolic heart failure becomes symptomatic when heart rate increases (exertional), because it decreases the amount of time the left ventricle has to fill (relaxation time) ◆ Echocardiogram helps distinguish between systolic and diastolic dysfunction ➔ Diagnosis ◆ EKG changes ● Findings commonly seen in congestive heart failure include… ○ LVH ○ LBBB ○ Intraventricular conduction delay ○ Non-specific ST segment and T-wave changes ➔ Treatment ◆ Definitive treatment of heart failure is a heart transplant ● Circulatory assist devices can provide a bridge to heart transplant ○ Circulatory assist devices are mechanical devices that allow an increase in myocardial oxygen supply and the decreased workload of the left ventricle

◆ Three types of circulatory assist devices ● Counterpulsation devices ○ Intra-aortic balloon pump ● Cardiopulmonary assist devices ● LV assist devices ➔ Patients with combined systolic and diastolic left ventricular dysfunction also have a worse prognosis than patients with either in isolation

HYPERTENSIVE EMERGENCIES ➔ Defined as hypertension that causes end-organ damage ➔ Signs of end-organ damage ◆ Brain ● Hypertensive encephalopathy ○ Loss of integrity of the blood-brain barrier and resulting cerebral edema ● Intracerebral hemorrhage ○ A result of long-standing HTN, vascular disease, or aneurysm rupture ◆ Eye ● Hypertensive retinopathy ○ Cotton-wool spots (focal ischemia) ○ Hemorrhage ○ Papilledema (optic disc edema from hypoxia) ◆ Heart ● LV failure and pulmonary edema due to increased afterload ◆ Kidney ● Acute renal failure ○ Causes and is caused by HTN

◆ Pregnancy ● Eclampsia ◆ Vascular ● Aortic dissection ➔ Diagnosis ◆ Labs will show elevated BUN and Cr ● Also get a UA, cardiac enzymes, CBC, and electrolytes ◆ Chest x-ray may show pulmonary edema or cardiomegaly ◆ EKG changes ● LVH ● Ischemic change ◆ CT head ➔ Treatment ◆ Parenteral therapy is preferred because of rapidity of action and ease of titration. Also, the treatment can be stopped if the patient becomes hypotensive. ● Common IV agents include… ○ Vasodilators ◆ Nitroprusside ● A powerful direct vasodilator ● Prolonged use may cause cyanide toxicity ◆ Nicardipine ● Antihypertensive response is comparable to nitroprusside with much fewer side effects ◆ Hydralazine ◆ Enalapril ◆ Fenoldopam

HYPOTENSION

CARDIOGENIC SHOCK

○ Adrenergic inhibitors ◆ Labetalol ● A combined alpha and beta blocker ● Main drawback is prolonged duration of action ◆ Esmolol ◆ Phentolamine

ORTHOSTATIC HYPOTENSION

ORTHOPNEA PALPITATIONS PERICARDIAL EFFUSION ➔ Excessive fluid in the pericardial space ➔ Causes include… ◆ Trauma ◆ Uremia ◆ Infection ◆ Post-irradiation ◆ Post MI ◆ Aortic dissection ◆ Tumors ➔ Symptoms include fever, pleuritic and positional chest pain (pain relieved by leaning forward), myalgias, pericardial friction rub, and pulsus paradoxus ◆ Pulsus paradoxus is an exaggeration of more than 10 mmHg of the normal variation during the inspiratory phase of respiration, in which the blood pressure declines as one inhales and increases as one exhales

◆ Additionally, patient may present in the shock state with more pronounced vital sign alterations ➔ Diagnosis ◆ Chest x-ray shows cardiomegaly ◆ EKG changes ● Differing QRS amplitudes (“alterans”) ● Axes shifting because of each ventricle swaying within a fluid-filled pericardial sac with each beat ◆ Echo ● Effusion ● Decreased systolic and diastolic dysfunction ● Collapse of RV/right atrial free walls in diastole ➔ Treatment ◆ Pericardiocentesis if unstable ◆ Pericardial window made in the OR if stable

VENOUS INSUFFICIENCY ➔ Incompetent valves in the peripheral venous system cause venous stasis of peripheral blood, microextravasation of RBCs, and fluid causing pigment (hemosiderin) deposition in local tissues (stasis dermatitis) and pitting edema ➔ Treatment ◆ A mild diuretic in a low dose ◆ Compression stockings ◆ Elevate legs when sitting down

SYNCOPE VALVULAR DISEASE AORTIC STENOSIS

➔ Valve hardening obstructs blood flow from the left ventricle, resulting in progressive LVH, decreased cardiac output, hypertrophic and later dilated cardiomyopathy ➔ Predisposes to endocarditis ➔ Symptoms include dyspnea on exertion, angina, syncope on exertion, sudden death, and weak (parvus) and slow-rising (tardus) carotid pulse ◆ CRESCENDO-DECRESCENDO MURMUR heard best at the base of the heart with radiation to the carotids ➔ Diagnosis ◆ Chest x-ray show cardiomegaly with or without pulmonary edema ◆ EKG shows LVH with or without ischemic change ◆ Echo estimates the severity of the obstruction ➔ Treatment ◆ Definitive treatment is valve replacement ◆ Gentle hydration can be used if the patient is hypotensive

AORTIC REGURGITATION ➔ Regurgitation of blood flow back into the ventricle which leads to dilated cardiomyopathy and heart failure ➔ Symptoms include dyspnea, angina, and presence of an S3 heart sound ◆ HIGH-PITCHED BLOWING DIASTOLIC MURMUR heard best at the base of the heart, with or without a systolic flow murmur ◆ Will have a “water-hammer pulse,” which means that they have a peripheral pulse with a quick upstroke and then collapse ◆ Presence of wide pulse pressure ◆ Signs of aortic regurgitation include... ● Duroziez sign is the presence of a diastolic femoral bruit when the femoral artery is compressed enough to hear a systolic bruit

● Hill’s sign refers to a systolic pressure in the legs 20 mmHg higher than in the arms ● Quincke’s sign is a visible capillary pulse in the nails ● De Musset’s sign is a bobbi...