Cardiovascular Medicine

CCU House Staff Handbook

2013

CCU Handbook 2

Thanks to all the faculty members who tirelessly contribute

to our education and to all the fellows who contributed to the

making of this handbook.

Written by: Revised & Designed by:

Mark McDonnell, MD Sarah Elsayed, MD Class of 2012 Class of 2015

Roy Lin, MD Class of 2016

Supervised by:

Ray Matthews, MD Cardiovascular Medicine Program Director

Faculty:

David Shavelle, MD Interventional Cardiology Program Director

Note to residents: The contents of this handbook are intended to help you

to successfully navigate this rotation and to begin the care process of the cardiology

patients you will encounter. The handbook is not a complete summary of cardiology

nor will mastering its contents ensure a high score on the ABIM board exam cardiology

section. Use the handbook as a guide to focus your reading on the topics covered

therein. This is a work in progress and we welcome your comments and suggestions.

Good Luck!

-May 2013-

CCU Handbook 3

Table of Contents

I. Introduction to CCU

a. Responsibilities

b. Sample Admission Note

c. Hints and Tips

d. Contacts and Extensions

e. Electrolyte replacement

II. Basics of ECGs

III. Arrhythmia

a. Narrow complex tachycardia

i. Irregular

ii. Regular

b. Wide complex tachycardia

i. PVC, V. Tach, Torsades de pointe, V fib

IV. Acute Coronary Syndrome

a. Acute management

b. Post-MI Complications

c. Chronic management

V. Heart Failure

a. Acute management

b. Chronic management

VI. Hypertensive Emergency

VII. Percutaneous Coronary Intervention

VIII. Pacermaker

IX. Landmark studies

X. Swan-Ganz Catheter Hemodynamics and different

types of Shock

XI. Vasopressors and Inotropes

XII. ACLS Algorithm

CCU Handbook 4

I. Introduction to CCU

Welcome

The CCU is a great rotation. It is a busy service with high turnover, but housestaff like

it because it is focused and there will be a great deal of teaching. You will learn a lot

this month. We act as a team and there is a lot of cross-coverage so you are expected to

know all the patients, not just your own. It is also expected that you will ask A LOT of

the questions. Your residents, fellows, and attending, are always available to you for

any questions. Also, the nurses in the CCU are an excellent resource, and it is

recommended that you use their knowledge and experience to your advantage.

Sample Daily Schedule

Until 7:45 am: Pre-rounding

8:15-9:00 am: FELLOW ROUNDS in 4D. All interns are expected to be present and

participate in rounds on all patients (not just their own) unless dealing with a sick

patient.

9:00-11:00 am: ATTENDING ROUNDS (will begin in 4D or conference room D)

11:00-noon: Get work done

12:00-1 pm: Noon lecture.

A. Responsibilities

Interns – Primary goal for a CCU intern is to be able to run through all pertinent

information for each patient without having to turn to the resident for answers. Please

know or have readily available all possible vitals, swan numbers, labs, imaging studies,

consult recommendations, etc.

- Obtain sign-out from post-call resident about any events on your patients

overnight

- Morning pre-rounds to be completed prior to 8:00 AM

- Fellow rounds starts at 8:00 AM

- Attending rounds start at 9:00 AM

- Develop a treatment plan for all patients to discuss on rounds.

- Interns and residents are expected to go to cardiology clinic on Mondays and

Wednesdays unless they are on-call, post-call, or have their own clinics.

Residents – Teach. Interns are a reflection of you. The more you teach and prepare

them, the smoother rounds will progress

- Review ECGs and other radiographic images with your interns during your

assessment of patients.

- Be sure to know your ACLS/BCLS

- Be able to interpret the following cardiology diagnostic testing procedures:

cardiac catheterization data, nuclear/stress test imaging data, and

echocardiogram

- Demonstrate understanding of risk factor modification for CAD (GRACE &

TIMI), management of patients with NSTEMI and STEMI, management of the

critically ill cardiac patient with decompensated heart failure, management of

cardiac arrhythmias, and interpretation of telemetry.

CCU Handbook 5

Reason to call

- Unstable patient that needs to be intubated or needs an urgent procedure

- Patient's condition is not improving or worsening

- New or worsening oliguria

- Recurrent angina or angina with EKG changes

- You will never be wrong by calling the resident, fellow or attending if you

have a question.

B. Sample Admission Note and Case Presentation

CC: What is the main reason this patient is here today?

HPI: Age, Ask about all major cardiac symptoms: chest pain, dyspnea, orthopena,

PND, ankle swelling, palpitation, dizziness/lightheadedness, presyncope, syncope,

exercise tolerance: must quantify walking distance (not time)

Chest pain: site, character, severity, onset, duration, progression, exacerbating factors,

relieving factors, associated symptoms, and radiation

Palpitations: onset, duration, frequency/pattern, # episodes per week or months or

year: regular or irregular

Syncope: when, where, duration, pre: chest pain or palpation, seizure, warning

symptoms, speed of recovery, any injury, witness reports; dates of first and most recent

episodes, total #

Pacemaker or ICD: ask for patient card to identify model; where, when implanted?

PMH: MI, HTN, dyslipidemia, DM, CVA, PVD, renal disease; other medical

conditions

PSH: cardiac or vascular surgeries or interventional procedures; other major surgeries

FH: CAD, HTN, DM, dyslipidemia, history of sudden cardiac death in family

Allergies: if allergic to meds and how

Medications: cardiac medication, other medication, supplement and junk meds

SH: employment, home city, mental status, place of birth; alcohol, tobacco, other

substances

RS: weight, height, HEENT, RESP, GI, GU, HEM, ENDO, NEURO, PSYCH,

MUSCUL

PE: VITAL SIGNS: HR (?reg or irreg), BP, RR, T, O2 Sat

General appearance

HEENT: any remarkable findings

Neck: JVD, carotids, thyroid

Chest: any scars pacers or ICDs, abnormalities of chest wall; back- kyphosis, scoliosis

CVS: PMI, S1S2, added sounds S3, S4, murmurs –systolic/diastolic, loudness; for

systolic murmurs – holosystolic vs ejection systolic – radiation to neck or axilla;

maneuvers and change in murmur

RS: auscultate lung fields – breath sounds, wheezes, crackles

ABD: hepatosplenomegaly, masses, aneurysms, renal or femoral bruits, bowel sounds

EXT: edema, pedal pulses (take off shoes & socks)

CNS: any major signs (i.e prior CVA)

CCU Handbook 6

EKG: rhythm, rate, axis, intervals, hypertrophy, ischemia or infarction, other findings

Other Test: holter, Event monitor, echo, stress test, cath, EPS

Labs: CXR, CT, MRI

Problem List: Primary problem – eg. Chest pain syncope, A.fib, VT

Underlying substrate - eg ischemia/dilated CM with EF (%)

Coronary artery disease – prior PTCA/stent or CABG

CHF – NYHA class I-IV and A-D.

Major valvular heart disease

Peripheral or cerebrovascular disease

Cardiac risk factors HTN, DM, dyslipidemia, renal disease, and other major

medical problems

Impression and Plan: Must develop primary diagnosis and differential diagnosis

Imaging – if any and why

Additional – lab test and why

Medication and why

Any medication or treatment to avoid and why

Procedure and why.

C. Hints and Tips

- Things found in CCIS: Vitals, Basic labs in treatable form (CBC, Chem 10,

LFT's, blood gases, coags); Ins and Outs

- Past ECGs, Treadmill tests and Holters can be accessed on MUSEWEB

- Echocardiogram, stress test and cardiac cath reports on Affinity

- Imaging and nuclear stress test reports on Synapse

- Nurses are invaluable for events that occurred overnight

- Don’t forget overnight arrhythmias picked up on telemetry. Please print

pertinent strips to bring to rounds.

CCU Handbook 7

D. Contact Info and Extensions

Nuclear Med: x97468

Echo/Stress Labs: x97444, x97855

Vascular Lab: x94618

Cards Clinic: x93171

Anticoag Clinic: x95181

UR: Gloria 213-717-3289 (CCU)

UR: J 213-919-0428 (7200)

CTS consult: x97819

CTS NP: Cathy Andrews 213-717-3593

CTS Fellow: 877-424-7316

Helpful Numbers and Extensions

CCU 4D x97111

CCU 4M x97112, x97113

Echo reading room x97520

Echo front desk x97444

ECG tech on call x96705

Holter room x97442

Marci (nuclear) x97468

Janet (NP for stress lab/echos) x91799

Cath lab x97601

Cath recovery room x95284 (plavix check)

Cardiology clinic (Jay or Letty) x95442

Clinic appts for patients x95267

EP pacemaker clinic (323) 442-5689

Anticoagulation (323) 226-7606

CCU Handbook 8

E. Electrolyte Repletion Guide

For patients at risk for arrhythmias (post MI, low EF) and those being actively diuresed,

you will likely be checking K and Mg twice a day. Here is a rough guide to help you. If

the patient has a central line, write “mix for central line”. If they only have a peripheral,

try to give replacement PO, but be cautious on an empty stomach. Magnesium is not

absorbed well PO. The general rule of thumb is to divide the patient’s required

electrolyte need by their creatinine.

Example:

- K is 3.0 and Cr 1.6 100 mEq/1.6 give the patient 60 mEq.

- For normal renal function:

- K (goal _ 4.0): usually 10 mEq will give you a rise of 0.1 mEq/L; IV and PO

have an equivalent effect. Fastest infusion time is 10 mEq/hr through a

peripheral line, or 20 mEq/hr for a central line if on a monitored bed.

- Examples:

- 3.0 – 100mEq

- 3.5 – 60mEq

- 3.8 – 20mEq

- Mg (goal _ 2.0): usually 1 gm for each 0.1 mEq/L. Magnesium oxide can be

used PO (4 tabs being equal to 1 gm) but it is not absorbed well.

- Examples:

- 1.6 – 4 gm IV

- 1.8 – 2gm IV

- Phos (goal _ 3.0): can choose KPhos or NaPhos. If the patient needs K as well,

they will get 4.4 mEq of K for every 3 mmol of Kphos. Be careful in the

setting of hypercalcemia.

- Examples:

- >2.0 – oral neutraphos 2 tabs po TID x 3 doses

- 1.5- 2.0 – 0.08 mmol/kg IV over 6 hrs

- 0-1.5 – 0.16 mmol/kg IV over 6 hrs

- For decreased renal function: Always error on the side of UNDER

replacement. Calculate their requirement based on their creatinine (formula

above), and round downward if indicated. Patients on hemodialysis should

rarely require electrolyte repletion as they tend to increase. If dangerously low,

be cautious in repletion.

CCU Handbook 9

II. Basic ECG

A. Components of ECG

- P wave – Atrial depolarization

- QRS complex – Ventricular depolarization

- T wave – Ventricular repolarization

- U wave (normally not seen) – Possibly represents repolarization of the His-

Purkinje system

- PR interval – From the start of the P wave to the start of the QRS complex.

Represents AV conduction delay.

- QRS duration

- QT interval – From the start of the QRS complex to the end of the T wave

B. Approach to ECGs

• Rate • Axis • Rhythm • Conduction • Chamber enlargement/hypertrophy

• Ischemia/infarction • Miscellaneous

To determine the Rate

# of large boxes between

QRS complexes

Rate

1 300 bpm

2 150 bpm

3 100 bpm

4 75 bpm

5 60 bpm

6 50 bpm

CCU Handbook 10

To determine the QRS Axis

The QRS axis represents the average direction of the heart’s electrical activity.

This diagram displays the relationship of the grouped leads to which

corresponding region of the heart they represent:

To determine the Rhythm, ask the following questions:

1. Is the rate fast, slow, or “normal”?

Fast Increased/abnormal automaticity, or reentry

Slow Decreased automaticity, or conduction block

Rate of ~ 150 Suggests atrial flutter with 2:1 AV block

2. Is the rhythm regular?

Irregular Suggests atrial fibrillation, 2nd

degree AV block, multifocal atrial

tachycardia, or frequent PACs/PJCs/PVCs

3. Is the QRS complex narrow or wide?

Narrow Rhythm must originate from AV node or above

Wide Rhythm may originate from anywhere

4. Are there P waves?

Absent P waves Suggests atrial fibrillation, atrial flutter, junctional

rhythms, AVNRT, AVRT, or ventricular tachycardia

CCU Handbook 11

5. What is the relationship between P waves and QRS complexes?

More P waves than QRS complexes Suggests 2nd

or 3rd

degree AV block

More QRS complexes than P waves Suggests accelerated junctional or

ventricular rhythms

6. Is the onset/termination of the rhythm abrupt or gradual?

Abrupt onset/termination Suggests reentrant rhythms

Gradual onset/termination Suggests altered automaticity

To determine Enlargement/Hypertrophy

CCU Handbook 12

Romhilt-Estes Point System:

1. Amplitude – 3 points for any of the following:

a. Largest R or S wave in the limb leads > 20mm

b. S wave in V1 or V2 > 30mm

c. R wave in V5 or V6 > 30mm

2. ST depression and/or T wave inversion in lateral leads – 3 points (only 1 point

if patient is taking digitalis)

3. Left atrial enlargement – 3 points

4. Left axis deviation of greater than -30 – 2 points

5. QRS duration >.09 seconds, but <.12 seconds – 1 point

6. Intrinsicoid deflection in V5 and V6 >.05 seconds – 1 point

≥5 points LVH 4 points Suggestive of LVH

To determine Conduction

CCU Handbook 13

III. Arrhythmia

Quick Summary of Arrhythmia

1. For EP patients admitted post-ablation (e.g. for SVT), the most important

complication to watch for is AV blocks (second or third degree) due to

possibility of damage to the AV node during the procedure.

2. Patients with a pacemaker placed will usually be observed overnight for

complications and need follow-up in device clinic (call Susie Song for an

appointment) in 2 weeks after placement. The pacemaker will always be

interrogated by the company the day after placement (don’t need to contact-

standard procedure). Most of these patients will also be followed in the EP

clinic which occurs once a month.

3. For bradyarrhythmias that are asymptomatic, just observe. If symptomatic,

have the nurse place the transcutaneous pacemaker pads on the patient first,

use your RICHMAN guide for additional management options, and call the

fellow.

4. Once a pacemaker is placed, do not worry about slowing the patient’s heart

rate with medications. The pacemaker is your built in protection and will pace

if the heart rate becomes too slow.

5. Atrial fibrillation:

a. Two questions: rate vs rhythm AND do they need anticoagulation

b. Use CHADS2 (CAD, hypertension, age > 75, diabetes, stroke or TIA

= 2 points, ) score (if >2 probably need Coumadin) to determine

anticoagulation versus aspirin.

Intracardiac conduction system

CCU Handbook 14

Clinical Approach to Arrhythmias

Supraventricular Tachyarrhythmia

Regular Narrow QRS (Supraventricular) Tachycardia

Figure. Atrial flutter Figure. Atrial fibrillation

Multifocal Atrial Tachycardia (MAT)

Irregular rhythm caused by presence of 3 or more atrial foci (may mimic AF)

Atrial rate 100-200 bpm; at least 3 distinct P wave morphologies

Occurs more commonly in patients with COPD, and hypoxemia; less

commonly in patients with hypokalemia, hypomagnesemia, sepsis,

theophylline or digitalis toxicity

Treatment: treat the underlying cause; calcium channel blockers may be used

(e.g. diltiazem, verapamil),

o Beta-blockers may be contraindicated because of severe pulmonary

disease

o No role for electrical cardioversion, antiarrhythmics or ablation

CCU Handbook 15

Atrial flutter

AV block usually occurs; it may be fixed (2:1, 3:1, 4:1, etc.) or variable

(classically Regular rhythm)

Atrial rate 250-350 bpm, usually 300 bpm

Rapid, atrial depolarization from a macro re-entry circuit within the atrium

(most commonly the right atrium)

Etiology: CAD, thyrotoxicosis, mitralvalvedisease, cardiacsurgery, COPD, PE,

pericarditis

ECG: sawtooth flutter waves (most common type offlutter) in inferior leads

(II, III, aVF); narrow QRS (unless aberrancy)

Treatment

o Acute:

If unstable (e.g. hypotension, CHF, angina): electrical

cardioversion

If stable

Rate control: beta-blocker, diltiazem, verapamil, or

digoxin

Chemical cardioversion: sotalol, amiodarone, type I

antiarrhythmics, or electrical cardioversion

o Anticoagulation guidelines same as for patients with AF

o Long-term: antiarrhythmics, catheter radiofrequency (RF) ablation

(success rate dependent on site of origin of atrial flutter)

Atrial Fibrillation

Most common sustained arrhythmia

Incidence increases with age (10% of population >80 yrs old)

Symptoms: palpitations, fatigue, syncope and may precipitate or worsen heart

failure

Classification:

o AF which develops in a patient with rheumatic mitral valve disease,

who has had a procedure to repair valves or has a prosthetic heart

valve is considered valvular AF.

o All remaining classes are considered nonvalvular AF

Associated with thromboembolic events (4%/yr in nonvalvular AF)

Initiation

o Single circuit re-entry and/or ectopic foci act as aberrant generators

producing atrial tachycardia (350-600 bpm)

o Impulses then conduct irregularly across the atrial myocardium to

give rise to fibrillation

o In some cases, ectopic foci have also been mapped to the pulmonary

vein ostia and can be ablated

Maintenance

o Tachycardia causes atrial structural and electrophysiological

remodelling changes that further promote AF; thus the longer the

patient is in AF, the more difficult it is to convert back to sinus

rhythm

CCU Handbook 16

Consequences

o AV node irregularly filters incoming atrial impulses producing an

irregular ventricular

o Response of <200 bpm and the tachycardia leads to suboptimal

cardiac output

o fibrillatory conduction of the atria promotes blood stasis increasing

the risk of thrombus formation - AF is an important risk factor for

stroke

Clinical Significance of Atrial Flutter and Fibrillation

Causes

Usually occur in setting of heart disease; but sometimes see “lone “ atrial

fibrillation

Hyperthyroidism (atrial fibrillation)

May acutely precipitate myocardial ischemia or heart failure

Chronic uncontrolled rates may induce cardiomyopathy and heart failure

Both can predispose to thromboembolic stroke, etc

Management

Major objectives (RACE)

1. Rate control: B-blockers, diltiazem, verapamil (in patients with heart

failure: digoxin, amiodarone)

2. Anti-coagulation: prevent thromboembolism

a. Assess stroke risk: determine CHADS2 score in patients with

nonvalvular AF

3. Cardioversion (electrical) a. If AF <24-48 h, can usually cardiovert without anticoagulation

b. If AF >24-48 h, anticoagulate for 3 wks prior and 4 wks after

cardioversion

c. If patient unstable (hypotensive, active angina due to

tachycardia, uncontrolled heart failure), should cardiovert

immediately

4. Etiology

a. HTN, CAD, valvular disease, pericarditis, cardiomyopathy,

myocarditis, ASD, post-operative, PE, COPD, thyrotoxicosis,

sick sinus syndrome, alcohol ("holiday heart")

b. May present in young patients without demonstrable disease

("lone AF") and in the elderly without underlying heart

disease

CCU Handbook 17

CHADS2 Risk Prediction for Non-Valvular AF

Vascular disease= prior MI, PAD, aortic plaque, CVA, TIA.

No difference in long-term survival when treating patients with a rhythm-

control versus rate-control strategy

CCU Handbook 18

However, many patients with a significant underlying structural heart lesion

(e.g. acute MI, history of congestive heart failure), valvular lesions (mitral

stenosis, mitral regurgitation, aortic stenosis), cardiac amyloid,

cardiomyopathies, pericardial disease and congenital heart lesions will not

tolerate AF well (since may be dependent on atrial kick) and these patients

should be cardioverted (chemical or electrical) as soon as possible

Newly Discovered AF

Anticoagulants may be beneficial if high risk for stroke

If the episode is self-limited and not associated with severe symptoms, no need

for antiarrhythmic drugs

If AF persists, 2 options:

o Rate control and anticoagulation

o cardioversion

Recurrent AF/Permanent AF

If episodes are brief or minimally symptomatic, antiarrhythmic drugs may be

avoided; rate control and anticoagulation are appropriate

Patients who have undergone at least one attempt to restore sinus rhythm may

remain in AF after recurrence: permanent AF may be accepted (with rate

control and antithrombotics as indicated by CHADS2 score) in certain clinical

situations

If symptoms are bothersome or episodes are prolonged, antiarrhythmic drugs

should be used

o No or minimal heart disease: flecainide, propafenone or sotalol

o LV dysfunction: amiodarone

o CAD: P-blockers, amiodarone

Regular Narrow QRS (Supraventricular) Tachycardia

Differential Diagnosis

• Sinus tachycardia

• Reentrant SVT incorporating AV nodal tissue

– AV nodal reentrant tachycardia

– Orthodromic AV reentrant tachycardia

• SVT mechanism confined to the atria

– Sinus tachycardia

– Atrial flutter

– Atrial tachycardia

- Short-RP favors AV node-dependent reentrant SVT

- Look for P-waves, Let the PR-RP relationship help

CCU Handbook 19

- Long RP tachycardia

o Sinus tachycardia

o Atrial tachycardia

o Some AVRTs

o Junctional tachycardia

o Aytypical AVNRT

- Short RP tachycardia

o Typical AVNRT

o Most AVRTs

o Atach with long PR interval

CCU Handbook 20

AVNRT

- Most common reentrant SVT

- May achieve rates >200 bpm

- Look for the psuedo-R’ in V1 or NO P wave AT ALL!

- AV node dependent!

- Most common type (>90%) is the slow-fast variety (typical)

Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal

Conduction

• Vagotonic Maneuvers

– Carotid sinus massage

– Valsalva maneuver (bearing down)

– Facial ice pack (“diving reflex;” for kids)

• Adenosine (6-12 mg I.V.)

• SVT Responses to AV Nodal Depressant Maneuvers

• SVT termination

– AV nodal reentrant tachycardia

– Orthodromic AV reentrant tachycardia

• No SVT termination (despite maximal attempts)

– Sinus tachycardia

– Atrial flutter or fibrillation

– Most atrial tachycardias (a minority are “adenosine-sensitive”)

CCU Handbook 21

Wide Complex Arrhythmia

PVCs may be benign but are usually significant in the following situations:

- Consecutive (~3 = VT) or multiform (varied origin)

- PVC falling on the T wave of the previous beat ("R on T phenomenon"): may

precipitate ventricular tachycardia or VF

Ventricular Tachycardia (VT)

- 3 or more consecutive ectopic ventricular complexes

- Rate >100 bpm (usually 140-200)

- Ventricular flutter: if rate >200 bpm and complexes resemble a sinusoidal

pattern

- "Sustained VT" if it lasts longer than 30 sec

- ECG characteristics: wide regular QRS tachycardia (QRS usually >140

msec);AV dissociation; bizarre QRS pattern.

- Occasionally during VT supraventricular impulses may be conducted to the

ventricles generating QRS complexes with normal or aberrant supraventricular

morphology ("ventricular capture") or summation pattern ("fusion complexes")

- Monomorphic VT

o Identical complexes with uniform morphology

o More common than polymorphic VT

o Potential causes: chronic infarct scarring, acute Milischemia,

cardiomyopathies, myocarditis, arrhythmogenic right ventricular

dysplasia, idiopathic, drugs (e.g. cocaine), electrolyte disturbances

- Polymorphic VT

o Complexes with constantly changing morphology, amplitude, and

polarity

o Frequently associated with hemodynamic instability due to faster

rates (typically 200-250 bpm) vs. monomorphic VT

o Potential causes: acute MI, severe or silent ischemia, and

predisposing factors for QT prolongation

CCU Handbook 22

- Treatment

o Sustained VT (>30 s) is an emergency, requiring immediate treatment

o Hemodynamic compromise - electrical cardioversion

o No hemodynamic compromise - electrical cardioversion, lidocaine,

amiodarone, type Ia agents (procainamide, quinidine)

Causes of PVC’s and VT

• PVC’s are fairly common in normals but are also seen in the setting of heart

disease

• Monomorphic VT often implies heart disease, but can sometimes be seen in

structurally “normal” hearts

• Polymorphic VT can result from myocardial ischemia or conditions that

prolong ventricular repolarization

• Electrolyte derangements, hypoxemia and drug toxicity can cause PVC’s and

VT

Clinical Significance of PVC’s and VT

• Can be a tip-off to underlying cardiac, respiratory or metabolic disorder

• VT may (but need not invariably) lead to hemodynamic collapse or more life-

threatening ventricular tachyarrhythmias, increasing the risk of cardiac arrest

Clinical Clues to Basis for Regular Wide QRS Tachycardia

Regular wide QRS tachycardia: VT or SVT with aberrant conduction

• More R-Waves Than P-Waves Implies VT!

• REMEMBER: VT does not invariably cause hemodynamic collapse; patients

may be conscious and stable

• History of heart disease, especially prior myocardial infarction, suggests VT

• Occurrence in a young patient with no known heart disease suggests SVT

• 12-lead EKG (if patient stable) should be obtained

• Use Brugada criteria to help differentiate VT from SVT- see algorithm.

CCU Handbook 23

CCU Handbook 24

Torsades de Pointes

A variant of polymorphic VT that occurs in patients with baseline QT

prolongation - "twisting of the points"

Looks like usual VT except that QRS complexes "rotate around the baseline"

changing their axis and amplitude

Ventricular rate >100 bpm, usually 150-300 bpm

Etiology: patients with prolonged QT intervals are predisposed

o Congenital long QT syndromes

o Drugs - e.g. class IA (quinidine), class III (sotalol), phenothiazines

(TCAs), erythromycin,

o Quinolones, antihistamines

o Electrolyte disturbances - hypokalemia, hypomagnesemia

o Nutritional deficiencies causing above electrolyte abnormalities

Treatment: IV magnesium, temporary pacing, isoproterenol and correct

underlying cause of prolonged QT, electrical cardioversion if hemodynamic

compromise

Ventricular Fibrillation (VFib)

Chaotic ventricular arrhythmia, with very rapid irregular ventricular fibrillatory

waves of varying morphology

Terminal event, unless ACLS are promptly initiated to maintain ventilation and

cardiac output, and electrical defibrillation is carried out

Most frequent cause of sudden death

Refer to ACLS algorithm for complete therapeutic guidelines

CCU Handbook 25

IV. Acute coronary syndrome

CCU Handbook 26

Quick Summary of STEMI

1. In the event of a STEMI in the ER, a STEMI code will be called and the

patient is usually taken straight to cardiac catheterization.

2. Patient will be admitted to the CCU post-catheterization with post-cath orders

(will include aspirin, plavix, diet orders, fem-stop orders if used, and any drips

the cath team wants e.g. integrillin for 18 hours)

3. Draw troponins q8 to find peak level, as there is some prognostic value (and

also sometimes the ER does not draw troponin prior to STEMI activation)

4. Start patient post cath on meds as indicated above:

a. Theraputic heparin or fragmin is not indicated post cath and should be

D/Cd

b. Lipitor 80 mg po qHS irrespective of LDL

c. ACE (within 1st 24 hours)

d. Beta-blocker (PO in 1st 24 hours); avoid IV in most cases;

metoprolol if unknown EF

e. Aspirin 325 mg po daily (usually already in cath orders); duration of

high dose determined by type of stent

f. Plavix 75 mg Qday regardless of whether a stent was placed or not;

the patient was likely loaded with either 300mg or 600mg in cath lab.

If patient has three vessel disease and no stents were placed, no plavix

has been given and should not be given, as this will delay CABG 5-7

days. Duration determined by type of stent.

g. Nitroglycerin 0.4 mg SL q5 min prn chest pain (may repeat up to 3x);

long-acting nitrates should be reserved for patient with known CAD

and ongoing chronic chest pain

5. CXR if not already performed by ER

6. Draw A1c, fasting lipid panel (remember that lipids are lower post-MI than

actual)

7. Order TTE to evaluate for ejection fraction (even if left ventriculogram done

in cath lab)

8. Type of BB determined by EF (see above)

9. Consider aldosterone antagonist (see above)

10. Consider nutrition consult (especially for those with STEMI and no significant

PMHx which is quite frequent).

11. Aggressive risk factor modification (smoking cessation, diabetes, cardiac

rehab)

12. Sudden cardiac risk based on EF <35% and cannot be determined until 40

days post MI

Quick Summary of NSTEMI

CCU Handbook 27

1. Troponin positive with convincing story or EKG changes (ST depression, T

wave changes)

2. Start heparin drip/fragmin SubQ (hold heparin 2 hours before cath or dose of

fragmin prior to cath)

3. Optimize medical management

a. BP control with beta blocker and ACE (both PO within 1st 24 hours)

b. Aspirin 325 mg po daily prior to cath, 81mg Qd if medical

management only. ASA dose post cath will be determined by type of

stent if one placed (see stents vs CABG)

c. Lipitor 80 mg po qHS irrespective of LDL

d. NTG gtt can be started for ongoing chest pain/HTN or both prior to

cath

4. Integrillin drip, plavix, or both can be started prior to cath if continued chest

pain despite maximal medical therapy (discuss with your fellow)

5. Draw A1c, fasting lipid panel

6. Order TTE to evaluate for EF if none recently

7. Type of BB determined by EF (see above)

8. Consider aldosterone antagonist (see above)

9. Consider nutrition consult (especially for those with no significant PMHx

which is quite frequent).

10. Aggressive risk factor modification (smoking cessation, diabetes, cardiac

rehab)

11. Sudden cardiac risk based on EF <35% and cannot be determined until 40

days post MI

High Risk Features of NSTEMI patients: (clues that pt. not doing well- call

Fellow):

CCU Handbook 28

- Pathogenesis: > 90% - plaque disruption with platelet aggregation intracoronary

thrombus

Consequences of Coronary Thrombosis

CCU Handbook 29

Progression of STEMI:

CCU Handbook 30

Progression of NSTEMI:

Summary of ACS:

CCU Handbook 31

CK-MB is a more useful marker for tracking ongoing infarction than

troponins, given their shorter half-life.

o Rising and falling CK-MB levels suggest infarct expansion or

recurrent infarction.

o Elevations of CK-MB greater than or equal to 50% more than a

previous nadir are diagnostic for reinfarction.

CCU Handbook 32

Steps in ACS and Subsequent Treatments:

UA/NSTEMI

- NSTEMI is distinguished from UA by presence of elevated serum levels of cardiac

biomarkers.

- EKG – serial to eval for ACS

- TWI, ST dep, transient ST elev

- TWI alone generally not predictive of adverse ischemic events

- ST dev or preexisting LBBB at increased risk for death or MI at 1 year

- Note: 20% of NSTEMI does not have ischemic ECG changes

- NSTEMI predicts poorer prognosis, elevated cardiac biomarkers are independently

predictive of morbidity and mortality

- Clinical risk classification via TIMI risk Score

CCU Handbook 33

TIMI Risk Score:

- Be aware of Braunwald classification and GUSTO risk score

- Echocardiogram

- High-risk patients: Early invasive approach with cardiac catheterization with plans for

revascularization

(Table risk stratification)

- Primary goal of revascularization is not acute reperfusion as in STEMI but

minimization of subsequent morbidity and mortality

Therapy

- Antiplatelets: ASA (decrease death or nonfatal MI by 50%) and clopidogrel (faster

onset versus other thienopyridines)

- Antianginal: nitrates (contra in sildenafil use) and beta-blocker (cardioselective

metoprolol or atenolol with goal HR 50-60)

- Anticoagulation: UFH (reduces death or nonfatal MI by 33% versus ASA alone),

LMWH (Enoxaparin shown in some study to be superior to UH), direct thrombin

inhibitor or factor Xa inhibitor

- glycoprotein IIb/IIIa inhibitor in high-risk patients or those undergoing early PCI

(intravenous as oral forms have not been shown to be beneficial and may increase

mortality)

CCU Handbook 34

Post-MI Complications

“ACT RAPID”

Arrhythmias

Congestive Heart Failure

Tamponade / Thromboembolic disorder

Rupture (Ventricle, septum, papillary muscle)

Aneurysm (Ventricle)

Pericarditis

Infection

Death / Dressler’s Syndrome

Arrhythmic

- most common complication after acute MI. It is related to the formation of re-

entry circuits at the confluence of the necrotic and viable myocardium.

- PVCs ~ 90%

- Vfib ~ 2 - 4%

- Supraventricular ~ 10%

- Bradyarrhythmias – common with inferior MI

- Complete AV Block ~ 20% with RV infarct

Ischemic

- infarct extension or post MI angina usually have continuous or recurrent chest

pain, with protracted elevation in creatine kinase (CK) and occasional new ECG

changes.

Mechanical

- Papillary Muscle Rupture : 13 hours post MI

- Acute Mitral Regurgitation

- Ventricular Septal Rupture : 2-5 days post MI

- Free Wall Rupture : within 2 weeks post MI

- Left Ventricular Failure and Cardiogenic Shock

CCU Handbook 35

- Right Ventricular Failure

- Ventricular Aneurysm

Embolic

- The incidence of clinically evident systemic embolism after MI is less than 2%.

This figure increases in patients with anterior wall MIs. The overall incidence of

mural thrombus after MI is approximately 20%. Large anterior MI may be

associated with mural thrombus in as many as 60% of patients

Inflammatory / Immunologic

- Pericarditis : 1-8 weeks post MI in 10%

- Postural Chest Pain

- Aspirin is the therapy of choice for post-MI pericarditis in doses of 650 mg every

4 to 6 hours. NSAIDS and corticosteroids should be avoided for 4 weeks after the

acute event. These agents may interfere with myocardial healing and contribute to

infarct expansion.

- Dressler’s Syndrome : weeks to months in 1-3% of post MI patients

- Postcardiac injury syndrome (PCIS)

Summary of Post-MI Complications

CCU Handbook 36

On Discharge

- Patients should not be discharged from the hospital (including chest pain,

unstable angina, acute myocardial infarction, cardiac catheterization, angioplasty,

coronary bypass, and ischemic heart failure hospitalizations) without initiation of

definitive atherosclerosis treatment.

- Discharge medications:

o ASA; clopidogrel

o Beta blocker

o ACE inibitor

o Warfarin as indicated

o PRN Nitrates

o Statins with goal LDL < 70 mg/dL (Secondary goal HDL > 40

mg/dL, Triglycerides < 150 mg/dL)

o HbA1C <7.0% Diabetes management, tight control in diabetics

o Exercise prescription (30-60 min, daily Physical activity)

o Low fat diet

o Smoking Cessation

CCU Handbook 37

V. Heart Failure

Quick Summary of CHF exacerbation

1. Often patients will be admitted to the CCU for better dieresis (i.e. a lasix drip

(usu. start at 5 mg/hr))

2. Patients may also be on nitroglycerin gtt to help decrease preload, which is

very useful if CHF is caused by CAD, in which case you get the coronary

vasodilatory effects as well as synergistic diusresis.

3. Can consider addition of nesiritide instead of NTG (see above), but discuss

with your fellow before starting. Is effective but also very expensive. Addition

of zaroxylin (2.5 or 5mg 30 minutes prior to lasix bolus or anytime if on gtt is

also effective).

4. Do not order another TTE in a patient with known CHF and an obvious reason

for exacerbation (dietary or medication noncompliance) if an echo has been

performed in the last year.

5. Optimize CHF meds as detailed above.

6. If patient has never had a cath it is recommended to r/o CAD if EF <40%. This

is debatable in patients with a clear global hypokinesis on echo and obvious

nonischemic etiology (heavy EtOH or methamphetamine use).

7. Cath should be done after adequate dieresis and right and left heart cath is

usually ordered.

HF with systolic dysfunction

- Impaired contractility of the left ventricle, there is discordance between symptom

presentation of heart failure and degree of cardiac dysfunction

- Major pathologic precss is cardiac remodeling

- Note not all HF have signs and symptoms of congestion

- HF is a bedside diagnosis that is defined by clinical assessment

- Acute decompensation – many etiology (dietary indiscretion, medical

noncompliance, arrhythmia

- Primarily a clinical diagnosis but additional information via other diagnostics can

be beneficial

Classification

- NYHA functional classification

- Killip classification for post ACS

- AHA ABCD classification

CCU Handbook 38

Signs and symptoms:

- PE important to identify signs of volume overload, peripheral perfusion, pulsus

alternans, VS

- BNP and pro-BNP in HF, only used in aid of diagnosis

o Variation exist between gender, age, medication, BMI, renal function,

concomitant diseases.

o BNP< 100 pg/mL proBNP <125pg/ml if age < 75, and <450pg/mL if

age >= 75 years. RECOMMENDS a diagnosis of HF.

o High negative predictive value (up to 90%) useful in rule out of cardiac

etiology. Important to note BNP in acute exacerbation may not rise until

a few hours later.

o MONITORING: BNP parallels changes in symptoms and treatment, but

are only complementary to clinical assessment.

o PROGNOSIS: higher BNP or pro BNP values consistent with higher

mortality.

- Other labs: mainly to identify reversible causes: TSH, H/H

Etiology

- Dilated (congestive) cardiomyopathy is a group of heart muscle disorders in

which the ventricles enlarge but are not able to pump enough blood for the body's

needs, resulting in heart failure. (Example - CAD, myocarditis, EtOH, HIV)

- Hypertrophic cardiomyopathy includes a group of heart disorders in which the

walls of the ventricles thicken (hypertrophy) and become stiff, even though the

workload of the heart is not increased. (Example – congenital HOCM, or

acquired)

CCU Handbook 39

- Restrictive (infiltrative) cardiomyopathy includes a group of heart disorders in

which the walls of the ventricles become stiff, but not necessarily thickened, and

resist normal filling with blood between heartbeats. (Example – radiation,

amyloidosis)

Management: it is important to understand the difference of acute and chronic therapy.

- ACUTE medical management – main goal is short-term hemodynamic

stabilization and optimization of tissue perfusion

o Maximizing oxygenation: upright position, supplemental oxygen,

mechanical ventilation should be considered, anemia corrected

(carefully as patient are very sensitive to increased intravascular

volume)

o Vasodilator: first-line drug therapy for those not in cardiogenic shock.

Nitroglycerin, nitroprusside, nesiritide

o Diuretics: Interestingly, in addition to reducing intravascular volume

diuretics have immediate vasodilator effect. Ptients with long-term

furosemide usually need an IV bolus dose at least equivalent to their

oral dose. (Monitor for BP, hypoK, hypoMg, hypoCa)

o Inotropic: used temporary for hemodynamic support and have not

been shown to improve survival. Without significant hypotension:

dobutamine and milrinone (extreme caution in pt with ischemia and

preexisting arrhythmia; both cause hypotension). Significant

hypotension, dopamine, norepinephrine and phenylephrine

o Positive airway pressure ventilation

o Ultrafiltration

CCU Handbook 40

- CHRONIC medical management – main goal is to prolong survival and improve

symptoms and functional status

o ACEI – established to reduce morbidity and mortality in patients with

systolic heart failure, related to attenuation of neurohormonal

response by RAAS.

o ARBs

o hydralazine and isosorbide dinitrate: improve mortality and morbidity

in African American with NYHA class III-IV; indicated when

patients unable to tolerate ACEI or ARBs

o beta-blockers: first-line therapy for symptomatic patients (NYHA

class II or III); only carvedilol, bisoprolol, and metoprolol succinate

have been approved for CHF (no evidence support for atenolol and

metoprolol tartrate)

o Aldosterone receptor antagonist: spironolactone indicated in patients

with recent or current HYHA class III or IV, LVEF <=35%) already

treated with ACEI and beta-blockers without significant renal

dysfunction (Cr > 2.5 or K>5)

o diuretics: used to maintain euvolemia and improve symptoms; lowest

possible dose of diuretic needed to prevent substantial volume

overload

o digoxin: commonly used to treat patients with heart failure and

concomitant atrial fibrillation; safe and significantly reduces

hospitalization for HF. (note level of 1.2 nmol/L is desirable (contrary

to range indicated on laboratory “normal” level)

o CRT (cardiac resynchronization therapy): indicated in patients with

LVEF < 30%, advanced HF (symptomatic despite maximal therapy),

QRS duration more than 130 ms

o Anticoagulation in setting of systolic heart failure is controversial,

however general rule is that warfarin indicated in setting of

ventricular thrombi, h/o atrial fibrillation, PE or chronic DVT, post

large transmural anterior wall MI with large akinetic/dyskinetic wall.

Interestingly, recent study in HF with sinus rhythm reveal similar

morbidity/mortality with either ASA or warfarin.

o Antiarrhythmic: amiodarone appears not to be harmful in pt with

systolic HF and frequent PVC, may reduce the incidences of

arrhythmic death; ICDs in pt with h/o MI and systolic HF (EF<35%)

CCU Handbook 41

VI. Hypertension Emergency

Hypertensive emergencies are common

Occurs in 1-2% of the hypertensive population

But, 50 million hypertensive Americans

500,000 hypertensive emergencies/year

Defined by severe HTN (SBP>180mmHg or DBP >120mmHg) with evidence of

acute end organ damage

Quick Summary of Hypertensive Emergencies

1. Usually ER/consult service will have already started a drip to control blood

pressure (frequently nitroglycerin).

2. It is important to know that patients can become resistant to the effects of nitro

fairly quickly, so this medication is useful only in the acute setting.

3. If nitroglycerin alone not controlling blood pressure, can consider switching to

nitroprusside (which is a venous and arterial dilator) but know your renal and

hepatic function prior to starting to avoid toxicity. Esmolol can also be an

effective gtt in the acute setting that is easily titratable.

4. The reason for starting with one of these drips is their short half-life and rapid

onset allows you to closely monitor the degree of blood pressure drop in the

first 6-12 hours after presentation. Your goal is to decrease the mean BP by no

more than 20% in first hour and down to 160/110 mm Hg in first 2-6 hours.

5. You should then start the PO meds before titrating off the drips.

6. Once patients are off drips with stable blood pressure, they can be transferred

to medicine if there are no other significant issues.

CCU Handbook 42

Acute management (see figure): - immediate parenteral blood pressure control

- BP reduced in controlled predictable manner because of the lower limit of

autoregulation . BP be reduced initially by no more than 25% of MAP over

minutes to hours. Further reduction over days to weeks. Exception includes aortic

dissection, LV failure and pulmonary edema

- Sodium nitroprusside is DOC

- Nitroglycerin DOC for HTN in setting of myocardial ischemia, acute MI and

congestive heart failure. Primary vasodilator. Directly increases CBF, raises ICP

and not used in setting initially characterized by high ICP

- Labetalol

- Fenoldopam

- Hydralazine

- Nicardipine

- Enalaprilat

CCU Handbook 43

CCU Handbook 44

VII. Percutaneous Coronary Intervention

Coronary Angiography

- Coronary vasculature accessed via the coronary ostia contraindicated with severe

renal failure (due to contrast agent toxicity), must check renal status

- Primary PCI is the preferred treatment strategy for patients presenting with

STEMI less than 12 hours from symptom onset (or more than 12 hours with

persistent symptoms), provide that door-to-balloon time is anticipated to be <

90minutes

Diagnostic Catheterization

- Outcomes related to complications for diagnostic catheterization approximately

<1%

- Procedure related complications: vascular injury, renal failure, stroke, MI

- Mortality rate 0.1-0.2%

- Fluid loading may unmask latent pericardial constriction

- Afterload reduction or inotropic stimulation may be used to increase the outflow

tract gradient in HCM

- Coronary vasoreactive agents (e.g. methylergonovine, acetylcholine)

- variety of pulmonary vasoreactive agents in primary pulmonary HTN (e.g.

oxygen, calcium channel blockers, adenosine, nitric oxide, or prostacyclin)

Note: Hemodynamically significant stenosis is defined as 70%or more narrowing of

the luminal diameter.

ACC/AHA 2002 Recommended Indications for Coronary Angiography

- Disabling (CCS classes Ill and IV)

- Chronic stable angina despite medical therapy

- High-risk criteria on clinical assessment or non-invasive testing

- Serious ventricular arrhythmia or CHF

- Uncertain diagnosis or prognosis after non-invasive testing

- Inability to undergo non-invasive testing

CCU Handbook 45

- Invasive catheters are introduced percutaneously into arterial and venous

circulation under conscious sedation and contrast is injected

- Arterial access most commonly through the femoral artery; radial approach

gaining favour especially for obese patients and outpatients dependent on driving

and ambulation

- Venous access through the femoral vein or internal jugular vein

- catheterization permits direct measurement of intracardiac pressures,

transvalvular and mean

- Peak pressure gradients, valve areas, cardiac output, shunt data, oxygen

saturations, and visualization of coronary arteries, cardiac chambers and great

vessels

- Angiography may provide valuable information regarding lesion severity,

complexity, location and prognosis

Left Heart Catheterization

- Systolic and end-diastolic pressure tracings recorded; LV size, wall motion and

ejection fraction can be assessed by injecting contrast into the left ventricle (left

ventriculography)

- Cardiac output (measured by the Fick oxygen method or the indicator dilution

method)

Right Heart Catheterization (Swan-Ganz catheter)- see later

- Right atrial, right ventricular, pulmonary artery pressures are recorded

- Pulmonary capillary wedge pressure (PCWP) obtained by advancing the catheter

to wedge into the distal pulmonary artery

- Records pressures measured from the pulmonary venous system

- In the absence of pulmonary venous disease, will reflect left atrial pressure

Post Catheterization Groin Check

- Assess the 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.

*Never pull a sheath unless it has been discussed with the fellow and the attending.

CCU Handbook 46

VIII. Pacemaker

Summary of Arrhythmia-Related Indications for Pacemaker Placement

Class I

- Sinus node dysfunction with documented symptomatic bradycardia

- Symptomatic chronotropic incompetence (failure to increase HR with exercise or

increased metabolic demand)

- 3° and advanced 2° AV block at any anatomic level, associated with any of the

following:

o Symptomatic bradycardia

o Arrhythmias that require drugs resulting in symptomatic bradycardia

o Sinus pauses > 3 seconds

o Asymptomatic escape rate < 40bpm while awake

o Post-op AV block, not expected to resolve after surgery

o Neuromuscular disease with AV block, regardless of presence or

absence of symptoms (there may be an unpredictable progression of

AV conduction disease)

- 2° AV block, regardless of type or site of block, with associated symptomatic

bradycardia

- Type II 2° AV block with wide QRS, regardless of symptoms or escape rate

Class IIa

- Syncope of unexplained origin when major abnormalities of sinus node function

are discovered or provoked during EP studies.

- Asymptomatic 3° AV block with an awake ventricular rate > 40bpm

- Asymptomatic type II 2° AV block

- Asymptomatic type I 2° AV block at intra or infra-His levels

- 1° or 2° AV block with symptoms suggestive of pacemaker syndrome

Transvenous Pacemakers

Transvenous pacemakers are only one form of temporary cardiac pacing, but are the

form most likely to be encountered outside the cardiac surgery setting. (Other forms

include epicardial, transesophageal, and transcutaneous pacing.) Transvenous pacers

are typically placed under fluoroscopic guidance, but can be also placed via a balloon-

tipped catheter via the right internal jugular or left subclavian veins. Although some

Swan-Ganz catheters are equipped with pacing ability, they are less stable than other

endocardial leads, and should be avoided in patients who are pacemaker dependent.

Situations in which a temporary pacemaker (transvenous or epicardial) may be

preferred over a permanent implantable pacemaker:

Injury to the conduction system during CABG (frequently improves

over time)

Lyme disease

Temporary SA node injury following heart transplantation

Cardiac trauma

Reverisble toxic/metabolic conditions (hyperkalemia, digoxin

toxicity, beta blocker overdose)

CCU Handbook 47

To establish the possible benefit from a permanent pacemaker in a

patient with sinus bradycardia or AV block when the cause of

symptoms is unclear

Symptomatic bradycardia or new bifascicular block during an acute

MI

Patient with an indication for a permanent pacemaker, but also with

an active systemic infection

Transvenous pacemakers typically consist of a single ventricular lead, which both

senses and paces, however temporary dual chamber AV sequential pacing all exists.

Serious complication from transvenous pacemakers are generally rare, but include:

Local bleeding

Pneumothorax

Thrombophlebitis

Air embolism

Infection

Cardiac perforation and subsequent

tamponade

Induction of ventricular arrhythmias

Catheter knotting

Subdiaphragmatic stimulation

CCU Handbook 48

IX. Landmark Studies

A. Ischemia and MI:

1. COURAGE Trial. NEJM 2008; 358:1887-98

* Demonstrated that as an initial management strategy in patients with stable

coronary artery disease, PCI does not reduce the risk of death, myocardial

infarction, or other major cardiovascular events when added to optimal

medical therapy. Only noted difference was reduction in symptoms of angina.

2. PROVE IT-TIMI 22 Trial. NEJM 2004; 350:1495-1504

* Demonstrated that among patients hospitalized for ACS, high-dose

atorvastatin 80mg/day reduced all-cause mortality, Ml, unstable angina,

revascularization, and stroke compared with pravastatin 40mg/qday. It

revealed that intensive lipid-lowering regimen had added benefits compared to

standard therapy.

3. JUPITER Trial. NEJM 2008; 359:2195-2207

*In apparently healthy people without hyperlipidemia (LDL <130) but with

elevated high-sensitivity C-reactive protein levels (hsCRP >2), rosuvastatin

20mg reduced both LDL and hsCRP levels and significantly reduced mortality

and the incidence of major cardiovascular.

4. HOPE Trial. NEJM 2000; 342:154-60

*In high-risk patients without low LVEF or CHF, ramipril reduced rates of

death, Ml, stroke, revascularization, new diagnosis of diabetes and

complications due to diabetes. Vitamin Ehad no effect on outcomes.

5. CURE Trial. NEJM 2001; 345:494-502

* Clopidogrel has beneficial effects in patients with acute coronary syndromes

without ST-segment elevation in addition to aspirin. However, the risk of

major bleeding is increased among patients treated with clopidogrel, but risk

of fatal bleeding is not increased.

6. SYNTAX Trial. NEJM 2008; 360:961-972

*CABG has lower rate of major cardiac or cerebrovascular events. The rate

of stroke was increased with CABG, whereas the rate of repeat

revascularization was increased with PCI

7. ARMYDA-2 Study. Circ 2005;111:2099-2106

*Pretreatment with high loading dose of clopidogrel 600mg when given 4 to

8hrs prior to PCI is safe and superior compared to 300mg loading dose. This

dose significantly reduced periprocedural MI in patients undergoing PCI; it

was associated with a 50% risk reduction of MI.

CCU Handbook 49

Heart Failure:

1. COMET Trial. Lancet 2003; 362:7-13

*This study demonstrated that in subgroup of CHF patients with EF of <35%,

Carvedilol more significantly reduced all-cause mortality and conferred a

survival benefit when compared to Metoprolol.

2. RALES Trial. NEJM 1999; 341 :709-17

*Among patients with NYHA class III or IV heart failure and EF<35%, the

addition of Spironolactone to standard therapy decreased mortality by 30%

and hospitalization by 35%. Standard therapy included an ACEI, loop diuretic

and in most cases digoxin.

3. MERIT-HF Trial. Lancet 1999; 353:2001-7

Metoprolol CR/XL daily in addition to optimum standard therapy improved

survival in clinically stable patients, equating to prevention of 1 death per 27

patients treated per year

4. A-HeFT Trial. NEJM 2004; 351:2049.

* Addition of a fixed dose of isosorbide dinitrate plus hydralazine to standard

therapy for heart failure demonstrated a 40% decrease in mortality in blacks.

5. SCD-HeFT Trial. NEJM 2005; 352:225-237

* This study demonstrated that In patients with NYHA class II or III CHF and

LVEF of 35 percent or less, amiodarone had no favorable effect on survival,

but single-lead shock-only ICD reduced overall mortality by 23 percent.

Arrhythmia:

1. AFFIRM Trial. NEJM 2002; 347:1825-33

*Rhythm-control strategies in atrial fibrillation offer no survival advantage

over the rate-control strategies. Moreover, there are additional advantages of

lower risk of adverse drug effects with rate-control.

2. CARE-HF Trial. NEJM 2005;352:1539-49.

*In subgroup of patients with HF due to left ventricular systolic dysfunction

with NHA class III-IV and cardiac dyssynchrony, cardiac resynchronizations

(biventricular pacing) along with medical therapy illustrated 36% decrease in

mortality, improved EF, and improved quality of life compared to medical

therapy alone. It should be considered if patients have refractory HF, EF </=

35% and QRS >/= 120ms, and if there is evidence of dyssynchrony on

echocardiography.

CCU Handbook 50

X. Swan-Ganz Catheter Hemodynamics and Different Types of Shock

CCU Handbook 51

CCU Handbook 52

XI. Vasopressors and Inotropes

Receptors 1 vascular smooth muscle cells vasoconstriction increase SVR

1 calcium mediated actin/myosin binding etc enhanced myocardial

contractility

2 vascular smooth muscle cells vasodilation

D1/D2 dopaminergic receptors in kidney and splanchnic vasculature renal and

mesenteric vasodilation

Medications

1. Dopamine - Immediate precursor to norepinephrine

- Acts on D and adrenergic receptors based upon dose:

0.5 to 3 mcg/kg/min D1/D2 vasodilation and increased renal blood flow

3 to 10 mcg/kg/min 1 NE release increased cardiac contractility and HR

10- 20 mcg/kg/min 1 vasoconstriction

2. Dobutamine

- Synthetic catecholamine

- Affinity for both 1 and 2 receptions in ration of 3:1 (1 > 2)

- Mainly an inotrope via 1 but also mild vasodilation

- Dose 1 to 15-20 mcg/kg/min; > 20 mcg/kg/min more vasoconstriction

- Increases myocardial oxygen consumption

- Tolerance can develop after several days of therapy

- Can precipitate ventricular arrhythmias

- Caution if on Beta blocker at high dose when starting

3. Norepinephrine (Levophed) - Potent 1 adrenergic receptor agonist with modest agonist activity

- Main action is powerful vasoconstrictor with less direct inotropic activity

- Increases systolic, diastolic and pulse pressure; minimal net impact on CO

- Dose 0.01 to 3 mcg/kg/min

4. Epinephrine (Adrenalin) - Endogenous catecholamine with high affinity for 1, 1 and 2 receptors in cardiac and

vascular smooth muscle

- effects more pronounced at low doses; 1 effects at higher doses

- Dose 0.01 to 0.1 mcg/kg/min

- Can give boluses to start – 1 mg IV every 3-5 mins

CCU Handbook 53

5. Isoproterenol (Isuprel) - Potent, non selective adrenergic agonist with low affinity for receptors

- Powerful chronotropic and inotropic properties

- Useful for bradycardia

- Dose 2 to 10 mcg/min

6. Phenylephrine (neo-synephrine) - Potent adrenergic activity with virtually no activity

- Pure vasoconstrictor useful for immediate correction of severe hypotension

- Useful for patients taking sildenafil and nitrates (Acute MI patients)

- Useful to decrease outflow tract gradient with HCM

- No HR effects

- Dose bolus 0.1 to 0.5 mg IV; 0.4 to 9 mcg/kg/min

7. Vasopressin (Pitressin) - Stored in the posterior pituitary gland – released after hypotension and increased

plasma osmolality

- Effects via V1 (vascular smooth muscle cells) and V2 (renal collecting duct system)

- Less direct coronary and cerebral vasoconstriction compared to catecholamines

- Neutral effect on CO, dose dependent increase in SVR

- Pressor effects preserved during hypoxic and acidotic conditions (useful during shock)

- Dose bolus 40-U IV; 0.01 to 0.1 U/min (most use 0.04 U/min)

CCU Handbook 54

XII. ACLS Algorithm

CCU Handbook 55

We wish you the best learning experience and hope to

contribute to making you a well prepared physician.