Cardiology

Bradycardia
Initial Assessment
Is patient symptomatic or hypotensive (SBP<80)? If so, place in Trendelenburg, begin ACLS (Atropine 0.5mg IV, transcutaneous pacing), place pacemaker pads, give fluid bolus, call for back-up.
Start Dopamine 5 mcg/kg/min while waiting for cardiology fellow to come in and place a temporary wire.
Place on cardiac monitor; check rhythm strip and 12 lead EKG
Differential Diagnosis

Medications
Beta-blockers, calcium channel blockers, digoxin, amiodarone, other antiarrhythmics, morphine

Cardiac
Sick sinus syndrome, inferior MI, Mobitz type 2 heart block, 3rd degree heart block, Afib with slow ventricular response, increased vagal tone

Other
Respiratory insufficiency/apnea
Hypothyroidism
Increased intracranial pressure
Normal in athletes
Evaluation
ABCs, "eyeball" test-does patient appear comfortable, uncomfortable, or critical
H&P focusing on distinguishing between above causes
Chart review/review of medications
12 lead EKG
Cardiac enzymes, if indicated by H&P
Management
ACLS, if appropriate-Atropine 0.5mg IV, transcutaneous pacing, consider starting dopamine 5 mcg/kg/min until backup/fellow arrives if hypotensive.
Treat underlying cause
If patient is hypotensive, symptomatic, has HR<40, or EKG shows 2^nd degree AV block Mobitz type II or 3^rd degree heart block call for ICU/CCU back-up and call Cardiology consult fellow as patient may need urgent temporary transvenous pacer. Discontinue medications-but beware of rebound tachycardia.
Common Class I indications for pacemaker placement
Third degree AV block (typical symptoms include syncope, seizures, dizziness, confusion, limited exercise tolerance, and congestive heart failure)
Second degree AV block Mobitz type II with symptomatic bradycardia
Symptomatic sinus bradycardia with HR <40 or pauses >3sec
Sinus node dysfunction with tachycardia-bradycardia syndrome, episodic sinus arrest, or sinoatrial block
Neurocardiogenic syncope with >3sec pause after carotid sinus massage
Postoperative cardiac surgery with AV block not expected to resolve
Bifascicular block with intermittent complete heart block that is symptomatic
Bifascicular block with 2^nd degree AV block Mobitz type II

Tachycardia
Initial Assessment
Is patient symptomatic or hypotensive (SBP<80)? If so, place pt in Trendelenburg, begin ACLS (synchronized DC cardioversion or defibrillate), give fluid bolus, and call for back-up.
Place pt on cardiac monitor; check rhythm strip and 12 lead EKG
Evaluation
ABCs, "eyeball" test-does pt appear comfortable, uncomfortable, or critical
Focused H&P looking for evidence of ischemia or congestive heart failure, syncope, altered level of consciousness
Chart review/review of medications
12 lead EKG
Cardiac enzymes, if indicated by H&P
Differential Diagnosis/Management
Initiate ACLS, if appropriate-synchronized DC cardioversion or defibrillation
Treat underlying cause

Narrow complex tachycardia, regular (QRS <120msec, rate >100)
Sinus tachycardia

Most common (usually rate does not exceed 160 bpm except in young patients)

Causes: hypoxia, hypovolemia, myocardial dysfunction, fever, anemia, medications (e.g. albuterol), hyperthyroidism, PE, pain, anxiety, drug or alcohol withdrawal, stimulants

Diagnosis: upright P waves in inferior leads (II, III, aVF) followed by QRS

Treatment: treat underlying cause
AVNRT (atrioventricular nodal re-entrant tachycardia)

Cause: dual AV pathways with differing refractory periods; rhythm often initiated by a PAC

Diagnosis: rate typically 150-250, inverted P (or pseudo S) in inferior leads (II, III, aVF) on EKG (with short R-P interval) (although P waves may not be visible if buried in QRS)

Treatment:
If unstable --> synchronized DC cardioversion
If no h/o CVA/TIA/carotid bruit --> carotid massage; other vagal maneuvers
(If patient does not have asthma) (Patient should be warned about symptoms first) Adenosine 6mg IVP, then 12mg IVP, then repeat 12 mg IVP (Make sure patient is on monitor, and record the rhythm). Push the adenosine fast and immediately chase it with a NS flush. Have atropine ready in case patient has a long pause. (rhythm can break with adenosine)
b-blocker-Metoprolol 5mg IV q5min x 3 (push over 2 min -> then flush)
Ca-channel blocker-Diltiazem 15mg IV, may repeat 15-20mg IV in 5min
Radiofrequency ablation
AVRT (atrioventricular re-entrant tachycardia)

Cause: re-entrant tachycardic circuit with conduction down AV node and back up over bypass tract

Diagnosis: retrograde P wave in inferior leads (II, III, aVF) (with long R-P interval)

Treatment: as for AVNRT above, and Procainamide (only in the setting of pre-excitation) (procainamide is really best used for Afib with pre-excitation. WPW patients show no pre-excitation during AVRT, since all ventricular activation is via the AV node.)
Atrial tachycardia

Cause: enhanced automaticity of atrial tissue or ectopic atrial pacemakers

Diagnosis: P wave precedes each QRS (usually with abnormal P wave axis, since atrial activation does not start at sinus node)

Treatment:
Beta-blocker
Ca-channel blocker
Class III antiarrhythmics
RF ablation
Atrial flutter with regular block

Causes: see Afib below

Diagnosis: flutter waves in inferior leads, ventricular rate is some division of 300 (think of flutter in HR=150, 100, 75); adenosine may help to reveal flutter waves

Treatment:
Rate control:
Digoxin
Beta-blocker
Ca-channel blocker
Cardioversion:
Synchronized DC cardioversion (50J, 100J, 200J, 300J, 360J)
Pharmacologic: Ibutilide (administered by EP, although Ibutilide is not often given for flutter and is administered as a one-time dose)
Anticoagulation:
IV Heparin or enoxaparin, then Coumadin (see Afib below)
Long term management:
Class IC or III drugs-requires very careful patient selection
Amiodarone and dofetilide are only antiarrhythmic shown not to increase mortality in patients with structural heart disease
Radiofrequency ablation (usually treatment of choice for flutter, since low risk and high effectiveness)

Narrow complex tachycardia, irregular (QRS<120 msec, rate >100)
Atrial fibrillation

Pulmonary disease

Idiopathic (common cause)/Ischemia (rarely causes Afib acutely)

Rheumatic heart disease (valvular disease)

Atrial myxoma (very rare cause of Afib)

Thyrotoxicosis

Ethanol

Sepsis (uncommon cause of Afib)
Hypertension (#1 cause)/CHF

Diagnosis:
Irregular ventricular rate in the absence of P waves or well-defined flutter waves in all leads
Check chemistry panel, thyroid function tests, cardiac enzymes in patients with known heart disease, echo to help determine cause and risk stratify

Treatment:
Rate control:
Digoxin: load 0.5 mg IV x 1, then 0.25mg IV q6h x 2, then 0.125mg PO/IV qd; check level; slow onset of action; adjust dose in renal failure, with amiodarone, etc.
Beta-blocker: Metoprolol 5mg IV q5min x3 (contraindicated in COPD and low EF)
Ca-channel blockers: Diltiazem 15mg IV, may repeat 15-20mg IV in 5min (can also be given as a continuous infusion until rate control is achieved)
Anticoagulation:
Any pt with Afib>48hours (or unknown) duration should be anticoagulated if no definitive contraindication (active hemorrhage, recent neurosurgery, recent hemorrhagic CVA, etc.) to prevent risk of thromboembolization
Start with Heparin drip (see protocol under Hematology), then Coumadin
Pt must be therapeutic (INR 2-3) for 3 weeks prior to attempt at cardioversion and must remain on anticoagulation for 1 month subsequent to successful cardioversion
Alternatively get TEE to r/o atrial appendage clot and proceed with earlier cardioversion, still need to anticoagulate for 4 or more weeks post cardioversion

Risk factors for thromboembolism: CHADS2 score (0-1 use ASA 325; if > 1 use Coumadin):
C = CHF (1 pt) EF < 45%, (1 pt) valvular heart disease
H = HTN (1 pt)
A = Age > 75 (1 pt)
D = Diabetes (1 pt)
S = Stroke/TIA in past (2 pt)
Cardioversion:
Synchronized DC (100J, 200J, 300J, 360J) OR pharmacologic:
Amiodarone 150 mg IV over 10min, then 1 mg/min x 6hrs, then 0.5 mg/min x 18 hrs to complete the load.
Procainamide: 1gm IV over 1 hour, then Procan SR 750mg PO QID; check for QT prolongation, QRS prolongation, hypotension; follow procainamide and NAPA (toxic metabolite) levels (total level of 10-20 is therapeutic); be sure to give AV nodal blocking agent (e.g. Digoxin) first
Ibutilide-risk of torsades; use with guidance of Cardiology attending or fellow only
Treat underlying cause:
Rarely possible (e.g. thyrotoxicosis)
Maintenance of sinus rhythm:
Complex problem! Choice of antiarrhythmic is dependent on pt's other medical problems (i.e. amiodarone is safest drug in patients with ischemic disease and/or low EF). Involve cardiology! Some commonly used antiarrhythmics:
Amiodarone
Sotalol
Propafenone (reserved for lone Afib, no structural heart disease)
Flecainide (reserved for lone Afib, no structural heart disease)
Dofetilide
Atrial flutter with variable block (see Aflutter/Afib above)
Multifocal atrial tachycardia

Causes: multiple ectopic pacemakers; often associated w/pulmonary disease, hypomagnesemia and hypokalemia

Diagnosis: three distinct P wave morphologies with three different PR intervals

Treatment: treat underlying cause (K > 4, Mg > 2, digoxin → not very effective, some data for ibutilide (EP-guidance)
Frequent premature atrial complexes (PACs)

Wide complex tachycardia, regular (QRS >120msec, rate >100)
Ventricular tachycardia (monomorphic): assume VT in all patients with heart disease!
See ACLS protocol. Synchronized shock for perfusing VT, and defibrillation for VF; Amiodarone (give 300 mg IV x 1 if in a code, if pt is not hemodynamically unstable → 300 mg IV over 10 min followed by (similar dosing to Afib) for stable patients
Check electrolytes
Ischemic disease predisposes to VT

EKG findings that favor VT:
Very wide QRS (>140msec)
Abnormal axis
AV dissociation
Fusion beats
Capture beats
SVT with aberrancy or over bypass tract
This is diagnosis of exclusion
Treat as SVT (AVNRT vs. AVRT), if appears as left bundle or right bundle morphology
Hyperkalemia (see Hyperkalemia → give calcium, insulin, D50W, etc.)

Wide complex tachycardia, irregular (QRS >120msec, rate >100)
VT (polymorphic): see ACLS protocol and defibrillate
Torsades de pointes

Causes:
Medications: antiarrhythmic drugs that prolong QT, TCAs, phenothiazine, H1 blockers (astemizole, terfenadine), pentamidine, erythromycin, antifungal agents
Electrolyte abnormalities: hypokalemia, hypomagnesemia
Subarachnoid hemorrhage
Congenital long QT syndrome

Diagnosis:
Twisting QRS complex
Prior EKGs may show long QT (QTc = QT/√RR) (>450)

Treatment:
Magnesium sulfate 2gm IV over 1min
Isoproterenol infusion or temporary pacing to increase heart rate (involve Cardiology)
Treat underlying cause-stop precipitating medications, etc.
Atrial fibrillation with aberrancy or over accessory pathway
This is a diagnosis of exclusion
Treat as VT until proven otherwise

Hypertension
Do you believe the BP? Measure yourself manually with correct cuff size.
Differential Diagnosis
Alcohol withdrawal
Drug overdose (cocaine, amphetamines)
Drug withdrawal (alcohol, cocaine, amphetamines, narcotics, anti-hypertensive medications)
Drug interactions (MAO inhibitors + tricyclics/Demerol/antihistamine/foods)
Increased intracranial pressure (Cushing's reflex)
Renal failure and renal artery stenosis
Eclampsia
Coarctation of the aorta
Endocrine (thyrotoxicosis, Cushing's syndrome, pheochromocytoma)
Pain or Anxiety
Hypertensive Emergency
Exists when elevated BP (usually DBP>120) is associated with end-organ damage

Signs/Symptoms:
CNS: headache, mental status changes, seizure, stroke, irritability
Eyes: blurred vision, papilledema, exudates, flame hemorrhages
Cardiac: chest pain, EKG strain or ischemic changes, pulmonary edema
Vascular: aortic dissection
Renal: low urine output, edema, hematuria, azotemia

Management:
Hypertensive emergencies require admission to ICU with arterial line and reduction of BP, usually with IV medications, to reduce permanent organ dysfunction and death
IV Nipride 0.2-5 mcg/kg/min
1st line in most patients
Arteriolar and venous dilation
Toxicity with thiocyanate and cyanide metabolite must be considered with several days of therapy and with renal and hepatic insufficiency
IV Nitroglycerin 10-400mcg/min
First choice agent for patients with myocardial ischemia
Venous dilation
IV Labetalol (alpha1, beta1, beta2 antagonist) 20mg IV bolus, then 2mg/min
First choice agent for patients with myocardial ischemia or acute aortic dissection
Most potent adrenergic blocker.
Favorable response in hypertension associated with pregnancy.
Do not lower BP too abruptly as sudden drop in BP may lead to cerebral and other organ hypoperfusion; goal is 25% reduction in mean arterial pressure or to reduce DBP to no lower than 100-110mmHg in first 12-24 hrs.
Hypertensive Urgency
Exists when BP>220/120 without evidence of end-organ damage

Management (can usually be treated with short acting oral medications):
Clonidine: 0.2mg orally, followed by 0.1mg q hour to total of 0.8mg. Watch for sedation, bradycardia with AV nodal blockers. Onset in 30-60 minutes. Rebound hypertension if abruptly stopped.
Captopril 12.5-25mg orally works in 15-30 minutes with variable episodes of excessive response.
Metoprolol 12.5-100mg PO BID (ok to start titrating 25 mg p.o. q6hrs x 48 hrs -> then convert to BID). Try to avoid IV MTP as it lasts a short time. (2.5 mg PO MTP = 1 mg IV MTP)
Topical Nitropaste 1-2 inches to chest wall q6hr; wipe off for BP < (your parameter)

Hypotension
Do you believe the BP?
Re-check it yourself manually with correct cuff size.
If not audible, palpate radial pulse (present w/ SBP > 80) or carotid/femoral pulse (present w/ SBP > 60).

If pulse not found, ask for assistance and call CODE BLUE!
Continue assessment of ABCs and start CPR.
Is the hypotension relative? Check patient's baseline BP?
BP 100/50 is abnormal in pt whose usual BP is 160/80
BP 80/40 may be normal & represent a physiologic state like CHF or liver disease
Causes (see differential of shock in Pulmonary/Critical Care section)

Hypovolemia: hemorrhage (internal or external), vascular dissection, GI losses, over-diuresis, post-dialysis, third spacing

Cardiogenic: MI, valvular dysfunction, arrhythmia

Obstructive: PE, tamponade, tension pneumothorax, atrial myxoma

Distributive: sepsis, anaphylaxis, medications, neurogenic, adrenal insufficiency
Evaluation (do a focused history, PE, and chart review)
Any signs or symptoms of hypoperfusion or shock? (i.e. altered mental status, cool, clammy skin, diaphoresis, chest pain, decreased urine output, decreased peripheral pulses) If so, call for back up and begin initial management listed below.

Hypovolemia: volume status (mucous membranes, low JVP, skin turgor), post cath bleed, GI bleed, aortic dissection, LV free wall rupture s/p MI.

Cardiac ischemia: chest pain, SOB, history of CAD, EKG

Arrhythmia: pulse rate & rhythm, rhythm strip

Tamponade: pulsus paradoxus, distant heart sounds, JVD, electrical alternans on EKG

Pneumothorax: tracheal deviation, JVD, unequal breath sounds, hyperresonance

Pulmonary Embolism: dyspnea, hypoxia, JVD, loud P2, RV strain/S1Q3T3 pattern on EKG (sinus tachycardia occurs in 80% of the time)

Hemorrhage: GI, retroperitoneum, thigh, abdomen, pancreas, adrenal, hip or pelvic fracture

Anaphylaxis: stridor, wheezing, urticaria, flushed skin, pruritus, angioedema

Sepsis: fever or hypothermia, leukocytosis or leukopenia

Adrenal insufficiency: history of steroid use, hypopituitarism, adrenal hemorrhage/infection/trauma
Work-up
Determine likely cause(s) from your evaluation.
Review medication list (check for anti-hypertensives, diuretics, etc.)
Send indicated laboratory studies: Stat CBC and chemistry panel. Consider PT/PTT, UA, blood & urine cultures, CK, CK-MB, troponin, type & cross, BNP, lactate
EKG & CXR
Initial Management
Evaluate ABCs & confirm IV, O2, monitor in place
Place patient in Trendelenburg position
Stop anti-hypertensives. Wipe off nitropaste, take off the clonidine patch
Begin fluid resuscitation with 1L NS bolus if no clinical evidence of CHF. Continue with boluses and vigorous IV hydration as needed to replete intravascular volume depletion and maintain adequate BP. Remember only 1/10 of the bolus stays in the vessel, edema is only cosmetic. If the patient has adequate cardiovascular reserve and renal function one can continue giving fluids until O2 requirement begins to increase.
If exam or CXR suggests pulmonary edema/CHF or if volume status unclear, consider Swan-Ganz catheter to evaluate patient's hemodynamics (i.e. PCWP, SVR)-see table of hemodynamic parameters associated with specific shock states.
If hypotension persists after adequate fluid resuscitation, pressors may need to be started and you should consult your resident. Norepinephrine (Levophed) is typically initiated first if appears sepsis/hypovolemia. Other pressors include: dopamine, dobutamine, vasopressin, Phenylephrine (Neo-Synephrine), epinephrine. See the "Vasopressor & Vasodilator" chart below for guidance on dosing.
Specific Management

Cardiac ischemia: see acute MI protocol.

Tamponade: call CCU fellow for emergent echo and pericardiocentesis

Pneumothorax: don't wait for CXR; place 14 or 16 gauge needle into second intercostal space at midclavicular line ASAP. Call pulmonary fellow for chest tube placement.

Pulmonary Embolism: start thrombolytics/heparin. Dose: tPA: no loading dose, start 100 mg infuse over 2 hrs (ok to give w/ heparin), unless contraindications to tPA are present. Attain an echo to assess for RV function/strain. Please consult pulmonary fellow or attending prior to administration.

Bleeding: large bore IV, NS, blood product repletion, reverse any coagulopathy,

Anaphylaxis: epinephrine 0.1 mg (1cc of 1:10,000) slow IVP or 0.3 mg (0.3cc of 1:1,000) SQ

Sepsis: start broad spectrum antibiotics emergently (always double gram negative, and don't be afraid to give aminoglycosides) and pressors (Levophed > dopamine > vasopressin > Neo-Synephrine) as needed

Adrenal insufficiency: hydrocortisone 50mg IV q6hrs, after attaining the cosyntropin stim test; see Adrenal Testing in Endocrinology section.

Types of Shock
TYPES	CVP or RA (preload)	PA	PCWP	CO (pump function)	SVR (Afterload)	MAP
Hypovolemic	dn	dn	dn	dn	up	dn
Cardiogenic	up/dn	up	up	dn	up	dn
Tamponade	up	up	up	dn	up	dn
Constrictive Pericarditis	up	up	up	nl/dn	nl/up	nl/dn
RV Infarction	up	nl/dn	nl/up	nl/dn	up	nl/dn
Acute MR	nl/up	up	up	dn	nl/up	nl/dn
Massive PE	up	up	nl/dn	dn	up	dn
Acute LV Failure	nl	up	up	dn	nl/up	nl/dn
Sepsis (Early)	dn	dn	dn	up	dn	nl/dn

Vasopressors and Vasodilators (Adapted from Pressor Card, CCU)
Drug	a Vasoconstriction	b-1 Inotropy Chronotropy	b-2 Vasodilation	Drip
Dobutamine (500mg/250 D5W)	+	++++	++	2-20 mcg/kg/min
Epinephrine (2mg/250 D5W)	+++	++++	++	0.01-0.1mcg/kg/min 1-200mcg/min
Dopamine (400mg/250 D5W)	++++ >10 mcg/kg/min	+++ 5-10mcg/kg/min	++	2-20mcg/kg/min 2mcg/kg/min=renal dose
Norepinephrine (4mg/250D5W)	++++	+++	0	0.5-70mcg/min
Phenylephrine (50mg/250 D5W)	++++	0	0	40-200mcg/min
Isoproterenol (2mg/250 D5W)	0	++++ chronotropy	++++	2-10mcg/min
Milrinone* (20mg/100 D5W)	0	++++	++/+++	Load 50mcg/kg then maintenance doses: Min: 0.375mcg/kg/min Std: 0.5mcg/kg/min Max: 0.75mcg/kg/min
Nitroprusside$ (100mg/250 D5W)	0	0	++++	20-300mcg/min
Nitroglycerin$ (100mg/250 D5W)	0	0	++++	10-240mcg/min
Nesiritide^ (1.5mg/250 D5W)	0	0	++++	Initial 2mcg/kg bolus then 0.01mcg/kg/min, may increase by 0.005mcg/kg/min in 3 hour intervals (preceded by 1mcg/kg boluses) up to max of 0.03mcg/kg/min
*Vasodilation via phosphodiesterase (PDE) inhibition, not via b-2 receptor $Vasodilation via NO pathway, not via b-2 receptor ^Vasodilation via binding to guanylate cyclase receptor on VSMC activating cGMP, not via b-2 receptor

Vasopressors and Vasodilators (Adapted from Pressor Card, CCU)
Drug	BP Effects	Disadvantages	When To Use
Dobutamine (500mg/250 D5W)	No change since inc beta2 decreases SVR; may even lower BP.	Not for use as single agent in hypotension. Tachycardia.	1st line in low output cardiac failure and often needs support from concurrent pressor such as dopamine
Epinephrine (2mg/250 D5W)	Increases BP at all dosing range	Tachyarrhythmias (Atrial and Ventricular) Coronary ischemia, ischemic limb, renal, and bowel	Incredibly potent generally used as the LAST RESORT vasopressor for any type of shock
Dopamine (400mg/250 D5W)	Increases BP at all dosing range	Tachyarrhythmias (AF, SVT, and Ventricular) Ischemic limb necrosis	1st line in cardiogenic shock and distributive shock; also used concurrently in low output cardiac failure with dobutamine
Norepinephrine (4mg/250D5W)	Increases BP at all dosing ranges	Bowel / renal / limb hypoperfusion	Considered 1st line alternative in septic shock
Phenylephrine (50mg/250 D5W)	Increases BP at all dosing ranges	Reflex bradycardia, peripheral hypoperfusion	1st line in distributive shock other than anaphylaxis
Isoproterenol (2mg/250 D5W)
Milrinone* (20mg/100 D5W)	inc CO + dec SVR tends to drop blood pressure	Hypotension, thrombocytopenia	2nd line agent in cardiogenic shock from low-output state
Nitroprusside$ (100mg/250 D5W)
Nitroglycerin$ (100mg/250 D5W)
Nesiritide^ (1.5mg/250 D5W)	No change since inc beta2 decreases SVR; may even lower BP.	Not for use as single agent in hypotension. Tachycardia.	1st line in low output cardiac failure and often needs support from concurrent pressor such as dopamine

Chest Pain
Differential Diagnosis

Life threatening Causes:
MI: consider in all patients, especially the elderly, those with cardiac risk factors; pain is often pressure like, associated with SOB, diaphoresis, nausea; may radiate to jaw/arm
Aortic dissection: consider in patients with HTN, smoking; often tearing pain radiating to back, unequal pulses
Pneumothorax: consider in patients with COPD, trauma, on mechanical ventilation; look for decreased breath sounds, hyperresonance, deviation of trachea away from side with pneumothorax, hypoxia - not responding to 100% oxygenation
PE: consider in all hospitalized patients; pain may be pleuritic; pt is often dyspneic, hypoxic, may have hemoptysis; A-a gradient may be increased

Other Causes:
Pericarditis
Pneumonia/Pleurisy
Stable angina
GERD
PUD
Esophageal spasm
Esophagitis (candida, herpes)
Varicella zoster (shingles)
Costochondritis
Anxiety (diagnosis of exclusion!)
Evaluation
Check vital signs immediately, including O2 sat and BP in both arms
Focused H&P to distinguish between the life-threatening causes
Check EKG, compare to previous
Consider ABG, CXR, other tests as indicated by H&P

Risk Stratification
TIMI Score can be used to stratify chest pain patients
One point for each of the following:
Age over 65
3 or more risk factors for CAD [Diabetes, cigarette smoking, HTN (BP 140/90 mm Hg or on antihypertensive medication), dyslipidemia, Family history of premature CAD (CAD in male first-degree relative 55 or younger, CAD in female first-degree relative 65 or younger, Age (men 45 years; women 55 years)]
Established CAD (Angiographic stenosis of >= 50%)
2 or more angina episodes in past 24 hours
ASA use in the last 7 days
Elevated cardiac enzymes
ST depression >= 0.5 mm

TIMI Scale
0-2 = low risk
3-4 = intermediate risk
5-7 = high risk
GRACE (Global Registry of Acute Coronary Events)
http://www.outcomes-umassmed.org/GRACE/acs_risk.cfm
Variables at admission to determine risk:
Age
Heart rate
SBP
Creatinine
CHF Class
Cardiac Arrest?
ST-deviation (elevation or depression)
Elevated cardiac enzymes

Fundamentals of Stress Testing
(Adapted from Dr. Michelle Kittleson's Stress Test Lecture October 2008)
Indications: Why should I order a stress test?

Diagnosis CAD:
Ischemia
Viability

Assessing Functional Capacity:
Ischemia
Valvular Heart Disease (e.g. AS,AR)
Hypertrophic Cardiomyopathy
Cardio vs. Pulmonary Disease

Risk Stratification Post MI
Submaximal Stress 3 to 7 days post MI to assess need for Cath
Symptom-Limited Stress 2 to 6 weeks post MI to assess activity level
Assess efficacy of medical therapy
Afib (HR control)
Post MI (BP,HR control)
CONTRAINDICATIONS: Why shouldn't I order a stress test?

Complications
Death: 1 in 10,000 patients
Cardiac Arrest: 2 in 10,000 patients

Absolute Contraindications
Severe/Symptomatic AS
Acute MI (within 2 days)
Unstable Angina
Decompensated HF
Unstable Arrhythmias
Acute PE
Suspected Aortic Dissection

Relative Contraindications
Left Main CAD
Moderate AS
HOCM
Electrolyte Abnormalities
Afib with RVR
3rd degree AV block
Resting BP > 200/110
TYPES OF STRESS TESTS: Which test should I order?

Exercise
EKG (ECHO or Nuclear)
o Advantages
* stress of choice
* cheap
* no needed IV's
* added information on functional capacity
o Disadvantages
* Lower sensitivities/specificities
* Can't use with abnormal baseline EKGs
LBBB
Vpaced
LVH with strain pattern
Digoxin associated ST depressions

Pharmacological
Dobutamine (ECHO or Nuclear): Mechanism: beta-1 agonist (increase HR and contractility)
o Advantages:
* Assess Wall Motion and Valvular function
* Can do rapidly ( 30 -45 minutes)
* More Specific
* Cheaper, NO IV's, NO radiotracers
o Disadvantage:
* Possible side effects: Palpitations, Tachyarrythmias
* Pt can not take beta blockers night prior to test
* Contraindications (False Positive 2/2 to abn septal wall motion)
LBBB
Vpacing
Symptomatic Aortic aneurysms
Adenosine (Nuclear only): Mechanism: Vasodilator
o Advantages:
* Assess Radiotracer Uptake and Blood Flow
* More Sensitive
o Disadvantage
* Possible side effects: hypotension, chest pain, flushing, wheezing
* Test takes 2-4 hours, tracer last 2 days
* Radioactive tracers, need for IV
* Caffeine, Theophylline decrease sensitivity
o Contraindications:
* Bronchospasm (pts with severe COPD/Asthma)
* Heart Block
* Severe AS

Interpretation: What does this mean for my patient?
Treadmill
o Stress Test is only negative if patient reaches target heart rate
o Target Hear Rate = 0.85 * (220 - age)
o Hold Beta Blocker for assessing for ischemia
o Exercise time is prognostic
o DUKE Treadmill Score:
* Duration of Exercise - 5 X max ST deviation - 4 X treadmill angina index ( 0, none till 2, limiting angina)
* Scores
Low-risk - score >=+5 ( 99% 4 yr survival)
Moderate-risk - score from -10 to +4 (95% 4 yr survival)
High-risk - score <=-11 (79% 4 yr survival)

Post Catheterization Groin Checks
NEVER PULL A FEMORAL SHEATH, THIS IS DONE BY THE CATH FELLOWS.
Check the patient's skin, color, temperature and peripheral pulses below the puncture site.
If bleeding occurs at the site, apply direct manual pressure to the site and notify resident and/or cardiology fellow.
Complications
Hematoma, uncontrolled oozing, unpalpable or undopplerable pulses on either foot, signs of retroperitoneal bleed, pseudoaneurysms, vasovagal response.

Management
If suspect angina/MI: give ASA, Metoprolol, sublingual NTG or nitropaste, Heparin and see acute MI below
If suspect aortic dissection: begin IV labetalol, transfer to ICU, arrange for emergent CT or TEE and call vascular surgery
If suspect pneumothorax: call surgery or pulmonary for emergent chest tube placement; if suspect tension pneumothorax, do NOT wait for CXR-->place needle or Angiocath into 2nd intercostal space at midclavicular line on side of pneumothorax
If suspect pulmonary embolism: see Pulmonary/Critical Care section

Acute Myocardial Infarction
Adapted from Fonarow, GC. "UCLA Clinical Practice Guideline for Acute Myocardial Infarction,"1994 and "UCLA Acute Myocardial Infarction Program: The CLOT Team Protocol-97/98." For further details refer to www.med.ucla.edu/champ.
Definition

Acute ST elevation MI requires two of the following:
Chest pain or chest pain-equivalent (indigestion, SOB, dizziness, etc.)
EKG with >= 1mm ST elevation in >= 2 contiguous leads
Left bundle branch block, not known to be old
Patients with sustained symptoms in absence of diagnostic EKG should have repeat EKG in 30mins
Patients who have symptoms associated with an EKG showing ST depression unrelieved within 30 minutes of initiating medical therapy should be considered to have refractory unstable angina.

As the CCU resident, call CCU fellow (#94228) immediately if called for suspected AMI patient (meeting above criteria); perform a brief evaluation of all chest pain/rule out MI patients and review EKG within 10 minutes of being informed of admission; call CCU fellow if any question on EKG.
Assessment

Rapid assessment is key! Patients who are revascularization candidates should receive an EKG within 10 minutes of arrival, then either:
Direct catheterization and angioplasty (within 90 minutes of arrival), OR
Thrombolytics within 30 minutes of arrival in ER

Focused H&P:
Current symptoms: onset, duration, and quality; exacerbating/alleviating factors; associated symptoms.
Prior ischemic disease? CHF? Arrhythmia? Other cardiac disease?
Cardiac risk factors: Age, HTN, DM, PVD, CVD, hyperlipidemia, family history of premature CAD, smoking
Other medical problems: renal failure, bleeding disorders, GI bleeds
Assess vital signs-look for signs of cardiogenic shock or CHF; BP in both arms, JVP, murmurs (MR, VSD, etc)

Diagnostic tests:
EKG: (with rapid interpretation) call CCU fellow with any questions; repeat EKG in 30mins, in 6 hrs, or if any recurrent symptoms, then QD x 2d and on day prior to discharge; in reperfusion patients, check at end of therapy and repeat in 4-6hrs, then as above
Labs: CBC with platelets, Chem 7, PT/PTT, nonfasting lipid panel; others as indicated (ABG for respiratory insufficiency, hypoxia, etc.)
CXR
Cardiac enzymes: STAT troponin, CK, CK-MB immediately; repeat troponin, CK, CK-MB in 6hrs. If first trop (-) but symptoms/EKG worrisome, can get cardiac enzymes in 3 hrs.
Echocardiography: indicated acutely if you suspect pericarditis, aortic dissection (TEE), tamponade, acute MR; also useful to assess LV dysfunction, size, location and severity of regional wall motion abnormalities, valvular abnormalities
Acute coronary angiography: for urgent reperfusion by angioplasty or CABG, or localization of lesions for further management
Right heart catheterization: for complicated MI-hypotension, oliguria, CHF, cardiogenic shock.
Initial Therapy (Use in ST elevation AMI, non-ST elevation AMI, and unstable angina)

ASA: 325mg chewed immediately
Contraindications:
Active hemorrhage
Severe aspirin allergy
Note that heme positive stool, non-melenic stool, peptic ulcer disease are NOT contraindications

Clopidogrel: 600mg orally (eight 75mg tablets)
No dose adjustment is required in elderly or renal insufficiency
Contraindications:
Severe thrombocytopenia (platelets < 20,000)
Active pathological hemorrhage
History of intracranial hemorrhage or hemorrhagic stroke
Severe uncontrolled hypertension
Known hypersensitivity to drug

IV Heparin or Low Molecular Weight Heparin: Unfractionated Heparin 71U/kg IV bolus followed by continuous infusion 14U/kg/hr with goal PTT 1.8-2.5x control (see Heparin protocol). Alternatively Enoxaparin 1mg/kg SQ q12hrs. Use in all patients regardless of treatment plan (cath vs. thrombolytics vs. medical management).
Studies have shown Lovenox and Arixtra to be superior to heparin gtt, however, most interventional cardiologists at UCLA prefer heparin gtt, therefore in majority of the cases heparin gtt is started
Contraindications:
Hemorrhage
Pericarditis
Aortic dissection

Beta-blockade: Metoprolol 5mg IV q2-5mins x 3, followed by 25 mg p.o. q6hrs x 48hrs--> 50mg PO BID begin 30-60mins after IV infusion.
Contraindications:
Cardiogenic shock
Hypotension (SBP < 80 mmHg)
Decompensated heart failure (crackles > 1/3 the way up from the bases)
Symptomatic bradycardia
2^nd or 3^rd heart block without a pacemaker
Active wheezing

Direct Angioplasty:
Preferred reperfusion therapy in patients presenting <24hrs after onset of symptoms
Indications:
Need for rapid, successful (95%) reperfusion (symptoms <1-2 hrs with large infarct)
Cardiogenic shock with single vessel disease
Glycoprotein IIb/IIIa (abciximab, eptifibatide, or tirofiban) are decided upon in the cath lab

Thrombolytic therapy:
Commonly used as 1st line reperfusion at other institutions
Indications:
Symptoms <12hrs, EKG with ST elevation in >= 2 contiguous leads, or LBBB, not known to be old
Symptoms >6hrs but <12hrs with Q wave development
Contraindications:

Absolute: Cardiogenic shock, active bleeding, recent surgery (<1wk), h/o CNS hemorrhage, tumor, aortic dissection, acute pericarditis

Relative: prior MI with LV dysfunction, moderate-severe CHF, remote GI bleeding, bleeding diathesis, uncontrolled hypertension in elderly, pregnancy
Dosing: (do NOT initiate without discussing w/CCU attending)
Tissue plasminogen activator: front-loaded, weight adjusted regimen

Acute CABG:
Indicated in cardiogenic shock with left main or multivessel disease

Intra-aortic balloon pump:
May be necessary, in setting of cardiogenic shock, as bridge to CABG/other reperfusion or post-revascularization

Nitroglycerin:
Indicated for symptom control of ischemia and to prevent vasospasm after direct angioplasty.
Sublingual NTG (400mcg) q5 min PRN chest pain, repeat PRN up to 3 doses and topical Nitropaste (1-2 inches to chest wall)
If pain unrelieved by above, or pain recurs, begin IV NTG drip (20-200mcg/min)
Contraindications:
Use of sildenafil/tadalafil/vardenafil
Hypotension
Severe anemia
Cerebral hemorrhage
Increased intracranial pressure

Oxygen:
Indicated for treatment of hypoxia

Analgesia:
Consider morphine (venodilation--> decrease PCWP) in patients whose symptoms are not relieved with nitroglycerin and beta-blockers while you prepare for reperfusion
Sub-Acute Therapy

Monitoring: cardiac monitoring for arrhythmias and silent ischemia for 48-72hrs in uncomplicated MI

ASA: 81-325mg PO QD should be continued long term in all patients without contraindications; clopidogrel 75mg PO QD or warfarin to INR 2-3.5 can be used in patients with contraindications to ASA.

Clopidogrel: 75mg PO QD should be continued for at least 6mos or indefinitely based on physician discretion; patients undergoing stenting for acute coronary syndrome should receive therapy for at least 1 month (Bare-metal stents), and 1 year or longer (Drug-eluting stent).

Heparin or Low Molecular Weight Heparin: continue for 48hrs or until revascularization is performed; indications beyond 48hrs include Afib or LV thrombus; consider long-term (3mos) SQ heparin for large anterior MI or anticoagulation with warfarin. If no intervention, ok to stop heparin once troponin trends down or 48hrs.

b-blockade: continue Metoprolol 50-100mg PO BID long-term in all patients without contraindications. The benefit of b-blockers occurs once the HR reaches 55-60, make sure to aggressively titrate up the b-blocker.

ACE-inhibition: long term use in all patients; begin within 12-24 hrs of AMI onset; start at low dose and titrate to target doses

HMGCo-A Reductase Inhibitors (statins): indicated in all patients with atherosclerosis; check nonfasting lipid panel on admit (within 6-12 hours of onset of AMI; acute phase reaction beginning at 12-24 hours will lower LDL levels by 25-50% for up to 6wks) and start statin; aim for dose that will achieve LDL<70 see CHAMP card; if baseline LDL is pending or not known, empiric doses may be used: pravastatin 40mg PO QHS, simvastatin 40mg PO QHS, or atorvastatin 80 mg PO QHS (anti-inflammatory affect). Baseline LFTs should be checked upon admission and at 6 weeks to screen for statin-induced hepatitis.

Goal Lipid Levels by CAD Risk
Risk Factor(s)	LDL goal (mg/dl)
No DM or CAD, but 0-1 risk factor(s)$	<160
No DM or CAD, but 2 or more risk factors$	< 130
DM and/or CAD, PVD	< 70
$Age (male>45yo, female>55yo or premature menopause without HRT), Tobacco, HTN, HDL<35 (subtract one risk factor if HDL>60), family history of premature CAD (male<55yo, female<65yo)

Warfarin: indicated for Afib, LV thrombus; consider in pts unable to take ASA post-MI

Antiarrhythmics: only amiodarone is safe post-MI; all others substantially increase risk of sudden death and overall mortality

Exercise: begin ambulation by day 2-3; give instructions for minimum of 30-60 mins of moderate intensity activity 5-7 times per week aerobic exercise program

Smoking Cessation: give patients written information re outpatient programs, nicotine replacement therapy and bupropion or varenicline.

Diet: patient and family should receive counseling about National Cholesterol Education Program Step 2 Diet

Follow-up: set up appointment with cardiologist in 2-6 weeks.
Risk Assessment

Inpatient or outpatient stress or modified stress test: risk stratify if ruled out for MI or in patients with uncomplicated MI not undergoing direct catheterization where information about residual ischemia would alter therapy or follow-up (Inpatient Echo lab x66701)

Electrophysiology study: consider if cardiac monitoring or 24 Holter demonstrate NSVT > 24hrs after MI onset in patients with LVEF< 35%; if pt is inducible, ICD placement

EKG Diagnosis in Ischemia, Infarction and Injury
Adapted from Dr. Henry Honda's handout, November 6, 2000.
In patients with ischemic chest pain symptoms, sensitivity of EKG for diagnosis of all MIs is ~50% with a specificity of ~90%

Rough Angiographic Correlation of EKG diagnosis of MI
Location	Leads	Culprit Vessel
Septal	V1-2(3)	LAD (if +I +aVL, prox to D1)
Anterior	V(2)3-4	LAD (distal to S1)
Anterolateral	I, aVL, V3-6	LCx
Lateral	V5-6 +/- I, aVL	LAD
High lateral	I, avL	OM or MR
Inferior	II, III, avF	RCA (90%) or LCx (esp if +lat)
Posterior	V1-2 (large R)	PDA
RV	V4R	RV branches from RCA

Diagnosis of MI in presence of bundle branch block:
No change in criteria in setting of RBBB, RBBB+LASH and RBBB+LPHB
In LBBB, normally ST-T wave changes are in opposite direction of QRS
Acute MI:
>= 1mm concordant ST elevation, or
>= 1mm ST depression in V1-3
> 5mm discordant ST elevation
Q waves in I, aVL, V5-6 suggestive of Q wave infarction

Congestive Heart Failure
Adapted from Fonarow, GC. "UCLA Heart Failure Clinical Practice Guideline and Summary," 1996, 1998, 2000.
Definition
Congestive heart failure is inadequate blood supply to maintain normal function.
Heart failure may be due to systolic dysfunction (LVEF<50%) or due to isolated diastolic dysfunction (LVEF>50%).
Goals of treatment for heart failure due to systolic dysfunction should be diuresis, afterload reduction and inotropy.
Goals of treatment for diastolic dysfunction should be improved ventricular filling with rate control.
Etiology
Coronary artery disease
Hypertension
Idiopathic dilated cardiomyopathy
Valvular heart disease
Drugs (i.e. alcohol, cocaine, methamphetamine)
Diastolic dysfunction
Less common: congenital, infiltrative cardiomyopathy (amyloid, sarcoid), hemochromatosis, thyroid disease, pheochromocytoma, chronic renal disease, HIV and viral cardiomyopathy
Factors Contributing to CHF Exacerbation
Ischemia
Arrhythmia
Cardiovascular stress (infection, anemia, pregnancy, stress, hyperthyroidism)
Pulmonary embolism
Medical noncompliance
Dietary indiscretion
Diagnosis

History:
Focus on distinguishing between possible reasons for exacerbation and for symptoms of volume excess (decreased exercise tolerance, SOB, DOE, PND, weight gain, edema, RUQ tenderness) and/or low cardiac output (fatigue, malaise, decreased appetite)

Physical:
Look for signs of left and/or right sided failure, cardiogenic shock, and hypoperfusion
Left sided signs: rales, tachypnea, S3
Right sided signs: elevated JVP, hepatojugular reflux, ascites, peripheral edema, enlarged liver
Low cardiac output signs: cachexia, muscle loss, cool extremities, tachycardia, S3

Tests:
Labs: Chem 7, CBC, TSH, FT4, FT3, LFTs, Lipid panel, Urinalysis, trop, CK, CK-MB x 2
B-type natriuretic peptide (BNP)
Neurohormone secreted by cardiac ventricles as a response to ventricular volume expansion and pressure overload
BNP levels <100 pg/ml essentially excludes heart failure as a cause of a patient's symptoms or physical exam
BNP that is elevated (>100 pg/ml) suggests possible CHF
BNP levels are NOT influenced by HTN, diabetes, mild renal insufficiency, or COPD
Dialysis patients may have increased BNP levels reflecting increased ventricular filling pressures
12 lead EKG, CXR
Echo or cath report describing ejection fraction, systolic vs. diastolic dysfunction
Hemodynamic monitoring with Swan-Ganz catheter indications:
Hypoperfusion: narrow pulse pressure, altered mental status, declining renal function despite adequate volume status
Congestion in presence of angina, baseline renal insufficiency, or hemodynamic intolerance of ACE inhibitors
Persistent congestion despite salt and fluid restriction, high dose loop diuretics and metolazone
Management

Antagonism of Neurohormonal Activation:
ACE-inhibitor: first line therapy for afterload reduction in all pts with reduced EF (because heart failure is characterized by systemic vasoconstriction)
Target doses: Captopril 50mg PO TID, Enalapril 10mg PO BID, Benazepril 40mg PO QD, Lisinopril 40 mg p.o. daily.
Beta-blocker: indicated in all classes of heart failure once clinically stable; start at low dose-Carvedilol 3.125mg PO BID, titrate up to target 25mg PO BID, Toprol-XL 12.5 QDAY and titrate up. Carvedilol was superior to MTP BID in pt with EF < 40%.
Spironolactone: aldosterone antagonism; start at 12.5 mg or less, goal 25mg PO QD; adjust loop diuretic and potassium supplementation; must check chemistry panel within 7 days; closely monitor K, BUN, Cr.
Contraindications: Male Cr > 2.5, Female Cr > 2.0. Only benefit patients with Class III-IV HF (EF < 40%), ischemic etiology

Volume Excess: for diuresis in acute CHF with adequate BP, consider the mnemonic below:

Lasix: add PRN metolazone

Morphine: for comfort and vasodilation

Nitrates: for preload reduction

Oxygen

Position: head up will improve oxygenation

Vasodilators: Add hydralazine up to 100mg p.o. QID, Isordil up to 80mg TID if patient's BP remains high despite maximum dose of ACE-I. Also if pt is intolerant to ACEI/ARB due rise in Cr, regimen provides good afterload reduction.

Inotropes: necessary in patient with evidence of systemic hypoperfusion (that has not responded to afterload reduction). Prior to starting, please call the CCU fellow. (Usually requires central access)

Other: Maintain strict I/Os, daily weights, 2g Na diet, 2L fluid restriction, frequent electrolyte checks
ACE Protocol
UCLA's heart failure guideline for hemodynamic optimization of patients with NYHA Class III or IV symptoms. Refer to ACE protocol guidelines for details; brief review follows.
CCU fellow to place Swan-Ganz catheter to determine patient's filling pressure, cardiac index, and SVR; patient should be admitted to COU or CCU, depending on acuity
Goals: RA < 7mmHg, PCWP < 15mmHg, SVR < 1200, and SBP >= 80mmHg. Optimal filling pressure (PCWP) is the lowest one that can be maintained without a fall in cardiac index and/or blood pressure
If elevated filling pressures (PCWP > 20 and/or RA > 10), diurese with IV Lasix until PCWP is as low as possible while maintaining SBP >= 80. Follow K and Mg.
If elevated SVR > 1300, begin afterload reduction with nitroprusside 20mcg/min, titrate to max 300mcg/min to keep SVR < 1200, RA < 7, PCWP < 15, while maintaining SBP >= 80. When optimal hemodynamics have been achieved and maintained for 2-6hrs, add oral captopril at 6.25mg PO, doubling dose q2hr to target 50mg PO q6hr while weaning off nitroprusside. For additional vasodilation, add Isordil when captopril has been titrated up to 25mg (especially in patients with CAD).
If patient has low cardiac index (< 1.2), consider inotropic agent such as dobutamine (if BP can tolerate, because dobutamine can decrease the BP), ok to start with dopamine to increase BP, then add dobutamine to increase CI.
Check patient's Swan tracings, Is/Os, and electrolytes several times per day and adjust medications accordingly; keep K >= 4, Mg >= 2
D/C Swan after 4-8 hours of optimal hemodynamics (by two sets of readings) on final oral regimen.

Pulmonary Artery (Swan-Ganz) Catheter Tracing
Normal Values for Hemodynamic Monitoring

Central venous pressure (CVP)/Right atrial pressure (RA): 1-7 mmHg

Right ventricular (RV) systolic pressure: 15-25 mmHg

Right ventricular (RV) diastolic pressure: 0-8 mmHg

Pulmonary artery (PA) systolic pressure: 15-25 mmHg

Pulmonary artery (PA) diastolic pressure: 8-15 mmHg

Pulmonary capillary wedge pressure (PCWP)/Left atrial (LA) pressure: 6-12 mmHg

Cardiac output (CO): 3.5-5.5 L/min

Systemic vascular resistance (SVR): 900-1200 dyne/sec/cm²

MVO2: Mixed venous partial pressure of oxygen. Goal 70-75%. Drawn from end of PA catheter. Value holds true as long as there is no shunt present.
Calculated Hemodynamic Variables

CO = HR x SV

Cardiac index (CI) = CO / body surface area (BSA)

Mean arterial pressure (MAP) = (SBP + DBP x 2) / 3

SVR = (MAP-CVP) / CO x 80

Trans-pulmonary gradient = Mean pulmonary artery pressure (MPAP) - PCWP
If transpulmonary gradient > 15 (intrinsic pulmonary vascular disease, patient needs lung/heart transplant)

Early Pacemaker Complications
Pneumothorax (check CXR)
Hematoma formation (especially if patient on anticoagulation)
Lead perforation of RA or RV (suspect if hemodynamically unstable)
Lead dislodgment or pacemaker failure (suspect if failure to sense or capture)

Chronic Valvular Disease
Chronic Aortic Stenosis

Clinical signs: systolic murmur heard best at RUSB, crescendo-decrescendo, transmitted to carotids, A2 decreased; paradoxical splitting of S2; narrow pulse pressure; pulses parvus et tardus.
Mean gradient and valve area (normal is 3-4 cm²)

Mild: < 25 mmHg, > 1.5 cm²

Moderate: 25-50 mmHg, 1.0-1.5 cm²

Severe: > 50 mmHg, < 1.0 cm²

Critical: > 80 mmHg, < 0.7 cm²
AV replacement should be considered in symptomatic patients. Patients should NOT be treated on the basis of a determination of valve area alone.

Clinical symptoms predict survival: mnemonic "Aortic Stenosis Failure or ASF 5,3,2 Rule." In the setting of the following symptoms, without AVR, 50% survival rates are as follows:

Angina 5 years

Syncope 3 years

Failure < 2 years
Chronic Aortic Regurgitation

Clinical signs: diastolic blowing murmur heard best at LUSB; wide pulse pressure, Quincke's sign (capillary pulsations at fingertips), De Musset's sign (bobbing head), Müller's sign (pulsing uvula), Corrigan's pulse (water hammer).

Indications for operation:
NYHA functional class III or IV
Severe LV dilatation: LV end diastolic dimension > 75mm, LV end systolic dimension >55mm
Mild to moderate LV dysfunction with EF < 50%
Concomitant angina and severe AR
Progressive LV dilatation, declining LVEF or exercise tolerance
Chronic Mitral Stenosis

Clinical signs: low rumbling diastolic murmur heard best at apex; opening snap may be heard.
Mean gradient and valve area

Mild: < 5 mmHg, > 1.5 cm²

Moderate: 5-10 mmHg, 1-1.5 cm²

Severe: > 10 mmHg, < 1 cm²
Indication for MV repair or balloon valvuloplasty: NYHA class III-IV symptoms, moderate or severe MS (MVA < 1.5 cm²), and valve morphology favorable for repair.
Chronic Mitral Regurgitation

Clinical signs: loud, holosystolic, high-pitched, heard best at apex and transmitted to axilla, soft S1.

Surgical indications: NHYA class III or IV, LV end-systolic dimension > 45mm, LV end-systolic volume index > 50ml/m², LVEF < 60 and progressive declining.
Mitral valve REPAIR should be preferred over mitral valve REPLACEMENT whenever possible. However, mitral valve repair is LESS favorable in cases that are a) rheumatic, b) ischemic, c) infective, d) anterior or bileaflet prolapse, and e) significant calcification present.

Syncope
Major Causes of Syncope

Neurologic: vertebrobasilar TIA, subclavian steal syndrome, normal pressure hydrocephalus, seizure disorder

Metabolic: hypoxia, hypoglycemia, hyperventilation

Psychiatric: panic disorder, hysteria

Mechanical cardiac disease: aortic stenosis, mitral stenosis, pulmonary stenosis, global ischemia, aortic dissection, obstructive cardiomyopathy, left atrial myxoma, prosthetic valve dysfunction, pulmonary embolus, pulmonary hypertension (careful cardiac auscultation and obtain ECHO)

Cardiac arrhythmias:
Bradyarrhythmia
Sinus node dysfunction
AV conduction disease
Tachyarrhythmia
Supraventricular arrhythmia

Ventricular arrhythmia (MOST important one to exclude risk of sudden cardiac death in patients with history of cardiac disease)

Vasodepressor syncope (most common) AKA "vasovagal syncope," "cardioneurogenic syncope," and "reflex syncope"

Mechanism:
Stimulation of medullary vasodepressor region of brainstem via afferent pathways from:
Gastrointestinal & genitourinary mechanoreceptors: micturition, postprandial, defecation, peptic ulcer
Cerebral cortex: panic, fright, pain, noxious stimuli
Cranial nerve: glossopharyngeal neuralgia, oculovagal
Cardiopulmonary baroreceptor: carotid sinus, tussive
Cardiac C fibers: Valsalva, upright tilt, jacuzzi, weight lifting, trumpet playing, post-exercise, volume depletion, pacemaker syndrome, supraventricular tachycardia.
Brainstem vasodepressor region generates efferent signals that cause increase vagal tone via vagus nerve (bradycardia) and vasodilation via unclear pathway (decrease cardiac filling and blood pressure).
Both bradycardia and vasodilation lead to syncope.

Diagnosis: tilt table testing

Treatment: b-blocker and avoidance of precipitating factors. Hypersympathetic tone is necessary to engage cardiac C fiber and therefore beta-blocker can inhibit this step in the beginning, however the benefit is marginal.

Preoperative Clearance For Noncardiac Surgery
Adapted from Eagle, K. "Guidelines for Perioperative Cardiovascular Evaluation for Noncardiac Surgery." Circulation. 2002;105:1257-1267.
What are the cardiac complications of noncardiac surgery?
Death, MI, CHF, arrhythmia
Step1: What is the urgency of surgery?
If emergent, patient must go to OR regardless of cardiac risk. Perioperative optimization with beta blockers may be indicated
Step 2: Has patient been revascularized in past 5 years?
If patient has had PTCA or CABG in past 5 years and no change in symptoms, no further evaluation is necessary.
Step 3: Has patient had coronary evaluation in past 2 years?
If yes with favorable prognosis and no new symptoms, and intermediate or low risk procedure, no further evaluation is necessary.
Step 4: Does patient have unstable heart disease?
Step 5: Does patient have intermediate predictors of coronary risk?
Consider functional capacity (see below)
Clinical Features for Risk Stratification

Functional capacity: MET = metabolic equivalent of O₂
1 MET: ADLs, walk around block
4 METs: climb flight of stairs with load

Risk class:
High (worst prognosis): < 4 METs
Intermediate: 4-6 METs
Low: > 6 METs

Predictors of Risk:
Major (consider angiography or delay elective surgery):
Recent MI (< 1 month)
Unstable angina or severe angina (class III or IV)
Decompensated CHF
Significant arrhythmia (high degree AV block, symptomatic VT, SVT with uncontrolled ventricular rate)
Severe Valvular disease especially obstructive lesions (AS, MS, HOCM and LVH ) as one cannot compensate with increase cardiac output
Intermediate:
Mild angina
Previous MI or pathologic Q waves on EKG
Compensated or previous CHF
DM
Renal Insufficiency
Minor:
Advanced age
Abnormal EKG (LVH, LBBB, ST-T wave changes)
Rhythm other than sinus
Low functional capacity
History of CVA
Uncontrolled HTN

Risk by type of surgery:
High risk (>5% risk MI or death):
Emergency procedures, particularly in the elderly
Vascular (AAA, PVD)
Prolonged procedures with large fluid shifts/blood loss (Whipple)
Intermediate risk (<5% risk MI or death):
CEA
Head and neck
Intraperitoneal/Intrathoracic
Orthopedic
Prostate
Low risk (<1% risk MI or death):
Cataract
Breast
Endoscopy
Decision-Making
If minor or intermediate predictors with moderate to excellent functional capacity and:
Intermediate or low risk procedure®OR without further testing
High risk procedure®pursue noninvasive testing
If operation is not urgent and pt is felt to have significant risk as defined above, then it is prudent to first perform further cardiac testing (treadmill, angiography, etc.)
Most hospitalized patients requiring surgery are in an urgent situation
For example, delay in surgical repair of a hip fracture affects functional recovery and is optimally done within 48 hours of admission. Therefore, medically optimizing risk is preferred over further cardiac evaluation.
Stress Testing
Treadmill (85% sensitive): do not use if LBBB, WPW, paced rhythm, or other EKG abnormalities that will make it uninterpretable-use imaging (i.e. stress echocardiogram or adenosine Myoview in these cases)

Positive stress test:
> 1 mm ST depression horizontal or downsloping 2 boxes beyond J point in 2 consecutive leads
> 2 mm ST depression rapidly upsloping 2 boxes beyond J point in 2 consecutive leads
Any ST elevation necessitates urgent cardiac cath
Hypotension or typical angina at low workload

Contraindications to stress testing:
Absolute: aortic dissection, critical AS
Relative: left main disease, moderate AS
Minimizing perioperative risk

Perioperative beta-blockade: decreased mortality in patients receiving atenolol or bisoprolol before and after surgery during perioperative period-goal HR<60
Restart aspirin early postoperatively (or continue throughout perioperative period if bleeding risk is acceptable)
Antibiotic prophylaxis if indicated (see Infectious Disease section)

Minimizing long term risk: ensure initiation, reinitiation or continuation of CHAMP medications (ASA, beta blocker, ACE-I, statin) postoperatively in all patients with established CAD, CVD, PVD and/or diabetes unless contraindicated or intolerance exists.
Revised Goldman Cardiac Risk Index (RCRI) Stratification
Adapted from Auerbach A, Goldman L. "Assessing and reducing cardiac risk of noncardiac surgery." Circulation. 2006;13:1361-1376.

Revised Goldman Cardiac Risk Index (RCRI)
Patient is at risk if he or she has any one of the following:
1.	High-risk surgical procedure: thoracic, abdominal, pelvic vascular (i.e. aorta, renal, mesenteric)
2.	Ischemic heart disease: history of myocardial infarction, history of or current angina, use of sublingual nitroglycerin, positive exercise test, Q waves on ECG, patients who have undergone PTCA or CABG and who have chest pain presumed to be of ischemic origin
3.	Heart failure: left ventricular failure by physical examination, history of paroxysmal nocturnal dyspnea, history of pulmonary edema, S3 or bilateral rales on physical examination, pulmonary edema on chest x-ray
4.	Cerebrovascular disease: history of transient ischemic attack or history of cerebrovascular accident
5.	Insulin-dependent diabetes mellitus
6.	Chronic renal insufficiency with baseline creatinine ³ 2.0 mg/dl

Dosing of Common Cardiovascular Drugs
Drug	Dose
Adenosine	6 mg rapid IV, may repeat with 12 mg rapid IV, 12 mg may be repeated once
Atropine*	Arrest: 1 mg IV, may repeat q 3-5 min, max 0.04 mg/kg Bradycardia: 0.5 mg IV, may repeat q 3-5 min, max 0.04 mg/kg
Bretylium	Arrest: 5 mg/kg IV, Repeat in 5 min 10 mg/kg to total of 30 mg/kg Stable: 5-10 mg/kg over 10 min, may repeat in 10-30 min, max 30 mg/kg per 24h
Diltiazem	0.25 mg/kg IV, may repeat in 5 min 0.35 mg/kg. Maintenance drip 5-15 mg/h
Dobutamine	2-20 mcg/min IV (250 mg in 250 ml D5W or NS)
Dopamine	2-20 mcg/kg/min IV (400 mg in 250 ml D5W or NS)
Epinephrine*	Arrest: 1 mg IV (10 cc 1:10,000) q3-5 min. May increase doses Bradycardia: 2-10 mcg/min (1mg in 500 ml NS) Anaphylaxis: 0.1 mg (I cc of 1:10,000) slow IV OR 0.3 mg (0.3 cc of 1:1,000) SQ
Furosemide	0.5-1 mg/kg IV
Isoproterenol	2-10 mcg/min titrate to heart rate; use with caution
Lidocaine*	Arrest: 1.5 mg/kg q 3-5 min, max 3 mg/kg Drip: 2-4 mg/min
Magnesium Sulfate	1-2 g IV
Morphine Sulfate	1-3 mg slow IV, may repeat to desired response
Naloxone*	0.8-4 mg IV
Nitroglycerin	Sublingual: 0.4 mg SL, may repeat q 3-5 min Drip: 10-20 mcg/min (50 mg in 250 ml D5W), titrate to response, watch BP
Nitroprusside	0.1-5 mcg/kg/min (50mg in 250 ml D5W), titrate to BP
Norepinephrine	0.5-30 mcg/min IV, (4mg in 500cc D5W), titrate to BP
Procainamide	Arrest: 20-30 mg/min IV, max 17 mg/kg, watch QT interval
Sodium Bicarbonate	1 mEq/Kg IV
Verapamil	2.5-5 mg IV, may repeat 15-30 min 5-10 mg IV
*Denotes medications that may be given by endotracheal tube. Dose should be 2-2.5 x IV dose

Cardiac Transplant Basics
Indications: Severe heart disease despite adequate medical therapy.
Dilated cardiomyopathy
Ischemic cardiomyopathy
Congenital heart disease for which no conventional therapy exists or that conventional therapy has failed
Ejection fraction less than 25%
Intractable angina or malignant cardiac arrhythmias for which conventional therapy has been exhausted
Pulmonary vascular resistance of less than 2 Wood units (160 dyn*s/cm5 ) or Transpulmonary gradient >15
Contraindications
Fixed pulmonary vascular resistance of greater than 3 Wood units (240 dyn*s/cm5)
Active systemic infection
Active systemic disease such as collagen vascular disease , myopathic disease, or sickle cell disease
Active malignancy: Patients with malignancies who have demonstrated a 3- to 5-year disease-free interval may be considered, depending upon the tumor type and the evaluating program.
An ongoing history of substance abuse (eg, alcohol, drugs, tobacco)
Psychosocial instability
Inability to comply with medical follow-up care
Criteria for Transplant Listing at UCLA: Patients are listed with UNOS (United Network for Organ Sharing).
(Adpated from Goldhaber et al)
Status 1A or IB-top priority for transplant
Status lB's are allowed to be at home
Status 2-at home waiting
Status 7-temporarily inactive
Patients who wait for transplant dependent on:
Height and Weight
Blood Type
Status
Time spent waiting on the list
ABO Compatibility- most important
UCLA's alternate list:
Developed for patients that are not acceptable for the regular list.
Main reason for to be on the alternate list are patients older than 70 years of age.
Also patients who have risk factors making them unacceptable for the regular list, but without absolute contraindications.
Patients listed as an alternate will not be eligible for status one listing if they deteriorate. Nor will they be candidates for a VAD.

Goal Immunosuppression Levels
Months after transplant	Tacrolimus	Cyclosporine
0-1	10-15	250-350
2-3	8-12	200-300
>3	5-10	150-250
>6	5-10	100-200

Cardiac transplant medications
Tacrolimus=Prograf=FK506
Cellcept=Mycophenolate mofitil=MMF
Rapamune=Sirolimus
Cyclosporine=CSA (note, different brands of "cyclosporine" have different bioavailabilities; therefore use the same brand the patient gets as an outpatient.
Cylex test=immune cell function (measures how much ATP a patients WBCs are using as a surrogate marker of level of immune function.
Very immunosuppressed: <225 (i.e. patient at risk of infection)
Goal immunosuppression: 270-300 depending on type of organ transplant.
Poor immunosuppression: >525 (i.e. patient at risk of rejection)