cardiology for primary care lois e - … for primary care lois e brenneman, msn, anp, ... aorta and...

© 2001 Lois E. Brenneman, MSN, CS, ANP, FNP

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CARDIOLOGY FOR PRIMARY CARE

Lois E Brenneman, MSN, ANP, FNP, C

CARDIAC ANATOMY AND PHYSIOLOGY

Anterior Heart Posterior Heart Internal Heart

ANATOMIC LOCATION

- Most of anterior surface of heart is right ventric le

- Right atrium forms narrow border from 3rd to 5th rib to right of sternum

- Left ventric le lies to the left and behind the right ventricle.

- Left ventric le apex is normally 5th ICS-MCL w apical impulse called PMI.

- Other chambers not ID on P /E

Anterior Position of Heart Posterior Position of Heart Pulmonary Circulation



CARDIAC LANDMARKS

- 2nd ICS to right and left of sternum called BASE .

- Left atrium: most posterior portion of heart; when enlarged, extends posteriorly and to the r ight .

- Tip of left ventricle is called APEX (5th ICS-MCL)

When left ventricle enlarges -> it extends laterally and downward hence PMI will no

longer be in 5th ICS-MCL but will be displaced (e.g CHF).

AUSCULTATION SITES

- Aortic: 2nd ICS, right sternal border (2ICS-RSB)

- Pulmonic: 2nd ICS, left sternal border (2ICS-LSB)

- Tricuspid: Left lower sternal border (LLSB)

- Mitral: Cardiac apex

- Erb's point: 3rd ICS os frequently the area to which pulmonic or aortic sounds

radiate.

Four classic auscultatory areas correspond to points over the precordium at which

events originating in each valve are best heard.

- Areas do not necessarily related to anatomic position of the valve

- Sounds heard in the area not necessarily directly produced by the valve that

names the area.

NEURAL STIMULATION OF THE HEART

- Sympathetic stimulation (norepinephrine) produces marked increase in HR and

contractility

- Parasym pathetic stimulation (acetylcholine) slows the heart (Vagus).

- Several receptors that provide circulatory info to medullary cardiovascular center

in brain

- Cardio-exc itatory and card ioinhibitory areas that regulate neura l output to sympathetic

and parasympathetic fibers.



Semilunar Valve Atrioventricular Valves

Valvular Stenosis

Heart Valves

CARDIAC VALVES

A-V valves: between atria and ventricles (1st sound)

Tricuspid (3 leaflets): right

Mitral (2 leaflets): left

Semilunar valves: between atria and arteries (2nd sound)

Aortic: aorta and L ventricle

Pulmonic: pulmonary artery and R

ventricle

COMPONENTS OF CARDIAC CYCLE

Isovolumetric contraction: Time between closure of AV

valve and opening of semilunar valve.

When pressure in RV exceeds diastolic press in PA:

pulmonic valve opens If stenotic hear pulmonic

ejection click.

When pressure in left ventricle exceeds the diastolic

pressure in aorta: aortic valve opens. If stenotic w ill

hear an ejection click.

Systolic period of ejection: time between opening and closing of semilunar valves

Point at which ejection is completed and the aortic and left ventricular curves separate is

called the incisura or dicrotic notch, and is simultaneous with the aortic component of S2

or closure of the aortic valve. (commonly written A2).



Pulmonic valve closes at the point when right ventricular pressure falls below the

pulmonary diastolic pressure and is the pulmonic component of S2 (commonly written

P2).

Isovolumetric relaxation: time between closure of semilunar valves and opening of

atrioventricular valves.

Tricuspid valve opens when pressure in right atrium exceeds right ventricular pressure.

Opening snap if tricuspid is stenotic.

Mitral valve opens when pressure in left atrium exceeds left ventricular pressure.

Mitral opening snap if mitral valve is stenotic.

Period of rapid filling of ventricles:

Occurs with opening of A-V valves; approximately 80% of ventricular filling

occurs at this time.

Third heart sound (S3) may be heard at end of this rapid filling period.

Ventricular filling.

Fourth heart sound (S4) may e heard at end of diastole during period of

Atrial contraction

HEART SOUNDS

- Normally only the closing of the heart valves can be heard .

- 1st heart sound: closing of A-V valves (mitral, tricuspid)

- 2nd heart sound: closing of semilunar valves (aortic, pulmonic).

- Opening of valves can be heard only if they are damaged.

- A-V valve (mitral or tricuspid) narrowed or stenotic: opening may be heard as an

opening snap (DIASTOLE).

Opening snap : refers to opening of a pathologically damaged A-V valve (mitral or

tricuspid) that occurs during diastole.

- Semilunar valve (aortic or pulmonic) stenosis : opening may be heard as an ejection

click (SYSTOLE).

Ejection click: refers to the opening of a damaged semilunar valve that occurs during

systole.

- Sequence of valves opening and closing:

Mitral valve close; tricuspid valve close (1st heart sound)

Pulmonic valve open; Aortic valve open

Aortic valve close; pulmonic vale close (2nd heart sound)

Tricuspid valve open; mitral valve open

- S1 (1st heart sound): closing of A-V valves (mitral, tricuspid)



- First heart sound heard loudest at APEX

- Splitting of first heart sound may be heard in tricuspid area.

- S2 (2nd heart sound): closing of semilunar valves (aortic, pulmonic)

- Heard loudest at base.

- A2 and P2 indicate the aortic and pulmonic component of S2, respectively. A2 normally

precedes P2 (aortic valve closes before pulmonic valve)

- With inspiration, intrathoracic pressure lowers thus drawing more blood from superior and

inferior venae cavae into right hear thus right ventricle enlarges and takes longer for all of blood to

be ejected into PA.

- Accordingly, pulmonic valve stays open longer and P2 occurs later in inspiration compared w

expiration causing a physiologic split of s2

- S3 (3rd heart sound) Period of rapid filling of ventricles:

- Normal only in children and young adults

- Occurs w opening of A-V valves (during period of rapid filling of ventricles) -

approximately 80% of ventricular filling occurs at this time.

- May be heard at end of this rapid filling period.

- It occurs 120-170 msec after S2; period same as it takes to say the "me" in "me too";

"me" = S2; "too" = S3.

- S3 normal in children and young adults; when present in individuals >30, signifies

volume overload to ventricle which could be secondary to valvular lesions and CHF

- S4 (4th heart sound): Atrial contraction (atrial kick)

- Normal only in children and young adults

- Occurs at end of diastole and is responsible for additional 20% of ventricular filling.

- May be heard at end of diastole during period of Atrial contraction

- Normal in children and young adults. When present in indiv iduals over the age of 30, it

indicates a noncompliant, or "stiff" ventricle. (e.g. HTN)

- The interval from S4 to S1 is approximately the time it takes to say "middle." The "m i"

is the S4 whereas the "ddle" is the S1. Note that "m i" is much softer than "ddle," quit

similar to the S4-S1 cadence.

- Pressure overload on a ventricle causes concentric hypertrophy, which produces a non-

compliant ventricle.

- CAD is a major cause of stiff ventricle.

- Gallop sounds or rhythms:

Presence of an S3 or S4 creates a cadence resembling the gallop of a horse called gallop

sounds or rhythms.



MURMURS GENERAL CONCEPTS

- Valves can only do two things: OPEN AND CLOSE.

- Normally open and close noiselessly

- MURMURS occur when there is valve malfunction -> turbulent blood flow

through a valve

- Most murmurs involve mitral and/or aortic valve

- Pulmonic and tricuspid valve murmurs are not common

- We can surmise what is going on the basis of when we hear the murmur (systole or diastole)

and where we hear the murmur (apex versus base).

- Diligent auscultatory characterization of heart murmurs and ancillary physical findings often

provide adequate basis for dx

STENOSIS: failure of valve to open completely

Significant problems when valve opening is reduced to ½ of normal

Degree of stenosis estimated by development of abnormal pressure gradient across

valve

Stenosis results in extra pressure work for heart

Blood must be forced thru high resistance of narrow opening

- Generally progresses s lowly over years to decade allowing heart to compensate

- Compensation via dilation and hypertrophy

Aortic Stenosis: Etiology:

- Post-inflammatory valvular scarring due to rheumatic heart disease (common)

- Valvular calcification with aging (common)

- Congenital anomaly: bivalve which is more susceptible than normal trivalve

REGURGITATION OR INSUFFICIENCY: inability of valve to close completely

- Allowing blood to flow in reverse direction

- May occur due to pathologic changes of valve or changes in supporting structures

around valve

- May develop suddenly due to valvular infection or rupture of supporting papillary

muscle.

- Sudden regurgitation is poorly tolerated due to no compensation

- Results in extra volume work for heart as more blood must be pumped to maintain

adequate forward flow

Diseased valves may have both stenosis and regurgitation: one problem usually predominates



SYSTOLIC MURMURS:

- Midsystolic ejection murmurs: produced by forward flow through the aortic and pulmonic valves

- Pansystolic regurgitant murmurs

Produced by backflow through the atrioventricular valves or flow from left to right ventric le

in a VSD

DIASTOLIC MURMURS

- Early diastolic: start w second heart sound

- Mid-diastolic: short pause after second sound

- Late diastolic or presystolic: due to atrial contraction

DESCRIPTION-GRADING OF MURMURS

- describe murmur: timing, radiation and point of intensity

- grade murmur: auscultatory characteristics

- differentiate: systolic vs diastolic

DESCRIBE MURMUR

:

Timing with respect to cardiac cycle, location, radiation, duration, intensity, pitch, quality,

relationship to respiration, relationship to body position .

Timing as to diastole and systole is paramount.

Systolic murmur begin w or after S1? end before or after S2? Entire systolic period

(holosystolic, pansystolic)? Systolic ejection murmur (begins after S1 and ends before

S2)? early-mid-late systolic murmur?

Holodiastolic : throughout diastole.

Best heard?

Radiation: axilla? neck? back?

GRADE MURMUR: Intens ity

I: Low intensity; often not heard by inexperienced

II: Low intensity, usually audible by inexperienced

III: Medium intensity without a thrill.

IV: Medium intensity with a thr ill.

V: Loudest murmur that is audible when stethoscope on chest; associated with a thr ill.

VI: Loudest intensity; audib le when stethoscope is removed from chest; assoc iated w a thrill

In general, intensity of a murmur tells you nothing about the severity of the clinical state!

Quality: rumbling, blowing, harsh, musical, machinery, scratchy.



CARDIAC RHYTHM AND RATE

- Sinus Arrhythmia: increase in heart rate w inspiration.

- NOT TRUE ARRHYTHMIA but physiologic response to decrease in left

ventricular volume during inspiration.

blood in right ventricle is pumped into large capacitance bed of lungs

therefore return of blood from lungs to heart is decreased and left atrium

and left ventricle become smaller.

- Atrial receptors trigger a reflex tachycardia that compensates for the decreased

left ventricular volume aka sinus arrhythmia.

- Timing the cardiac cycle: needed to interpret heart sounds

- To interpret heart sounds accurately, must time S1-S2

- Most reliable way of ID S1 and S2 is to palpate carotid artery.

- Use right hand to position stethoscope and left hand to palpate carotid artery

- The sound that preceded carotid pulse is S1; S2 follows pulse.

- Do not use radial pulse as time delay from S1 to radial pulse is significant and will result

in errors in timing.

CARDIAC ARRHYTHMIAS

Rhythmicity (automaticity): intermittent spontaneous generation of action

potentials

Rate determined by relative influx of Na+ and Ca++ vs efflux of K+

Cell with the fastest rate of spontaneous depolarization becomes become

pacemaker for rest of heart - SA node in the normal heart (in right atrium)

Other myocardial cells capable of becoming pacemaker (spontaneous

depolarization) in certain circumstances (usually abnormal i.e. arrhythmias)

Rhythmicity influenced by drugs, electrolyte balance and autonomic nervous system

NORMAL CONDUCTION/CONTRACTION SEQUENCE

Conduction System: SA node -> spread contiguously cell to cell in atria -> bundle branches in atria

carry impulse more rapidly then other atrial cells -> av node * -> atrial contraction (when atria have

depolarized) -> slowing of impulse occurs after AV node -> Purkinje cells (fibers) where impulse travels

down intraventricular septum toward apex -> divides into right and left bundle branches which travel

down left and right side of intraventricular septum - > penetrate ventricular muscle mass from endocardial

side-> spread contiguously cell to cell through ventricle (toward epicardial surface) -> ventricular

contraction * at AV junction located in posterior septal wall of right atrium just behind ventricle

Note: fibrous skeleton which separates atria from ventricle thus prevents direct transmission of impulse

from atria to contiguous ventricular cells



P wave: Atrial depolarization

P-R interval: Atrial, AV node and Purkinje depolarization

Q wave: Septal depolarization

R wave: Apical depolarization

S wave: Depolarization of lateral walls (base)

T wave: Ventricular repolarization

SEQUELAE OF CARDIAC ARRHYTHMIAS

- Sudden death

- Syncope

- Heart failure

- Dizziness

- Palpitations

- Asymptomatic

Bradycardia (bradyarrhythmias) : heart rate < 60 bpm

Tachycardia (tachyarrhythmias): heart rate > 100 bpm

-Supraventricular tachycardia: arise from atria or AV junction

- Ventricular tachycardia: arise from ventricles

Ventricular arrhythmias tend to be more symptomatic (can be life-threatening)

MECHANISM OF ARRHYTHMIA

- Alteration of automaticity

- originate from single cell or abnormal interactions between cells

- can result in bradycardia or tachycardia

- Accelerated automaticity

- increasing rate of depolarization or changing threshold potential

- sinus tachycardias, escape rhythms and accelerated AV nodal rhythms

- Triggered tachycardia: oscillations of transmembrane potential at end of AP

- oscillations reach threshold and produce arrhythmia

- can be exaggerated via pacing or catecholamines/drugs (digoxin toxicity-> atrial tach)

- Re-entry (or circus movement): results in tachycardia

- wave of depolarization travels in 1 direction around a ring of cardiac tissue

- circus movement results where time to conduct around ring longer than recovery of any

tissue within ring

- Accounts for majority of paroxysmal tachycardias

NORMAL RHYTHM - Sinus Rhythm or NSR



ABNORMAL RHYTHMS

SINUS RHYTHMS: P waves upright in leads I and II of EKG; inverted in AVR and V1

- Sinus Arrhythmia: normal variation in children and young adults

- Fluctuations in autonomic tone -> phasic changes in sinus discharge rate

- Inspiration: parasym pathetic tone falls -> HR increases; expiration -> HR falls

- Sinus Bradycardia: less than 60 bpm day or 56 bpm night

- Usually asymptomatic unless very slow

- Normal in athletes and elderly

- Etiology

- Hypothermia, hypothyroidism, cholestatic jaundice, raised IC

- Beta blockers, digitalis, antiarrhythmic drugs

- Acute ischemia and infarction of sinus node

- chronic degenerative changes (fibrosis atrium, sinus node)

- TREATMENT:

- Acute symptomatic: atropine 600 ug

- Persistent irreversible: permanent pacemaker

- Sinus Tachycardia: greater than 100 bpm

- Etio logy:

Fever, exercise, emotion, pregnancy, anemia, cardiac failure wi com pensatory

sinus tachycardia, thyrotoxicosis, catecholamine excess, primary sinus

tachycardia (rare)

- TX: correct underlying cause; use of beta-blockers

PATHOLOGICAL BRADYCARDIAS

- Sick Sinus Syndrome (sick node disease): long intervals between p waves on EKG (> 2s)

Sinoatrial exit block: pause is exact multiple of basic sinus interval

Sinus arrest: interval is not multiple of basic sinus interval

Sinus pauses allow tachyarrhythmias to emerge

Tachybrady syndrome: combo of fast and slow supraventr icular rhythms

TREATMENT

:

- Permanent pacing w additional antiarrhythmic drugs (tachycardia)

- Anticoagulate (thromboembolism common) unless contraindication



ATRIOVENTRICULAR BLOCKS

First Degree AV Block : simple prolongation of PR interval to > 0.22 s; all p waves conduct but

delay in conduction to ventricles (no missing QRS complexes)

Second Degree (partial) AV Block: some p waves conduct; others do not - varying types

MOBITZ I BLOCK (WENCKEBACH PHENOMENON):

- progressive PR interval until p wave fails to conduct

- PR interval before blocked p wave much longer than PR interval after blocked p wave

MOBITZ II BLOCK: dropped QRS complex not proceeded by progressive PR interval prolongation

TREATMENT

:

- Wenckebach block is more benign vs other forms 2nd degree block

- Pts usually asymptomatic w 2nd degree b lock; monitor them closely

- No treatment required unless more serious block or symptomatic: then may need pacing



Third Degree AV Block:

- No p waves conduct to ventricles

- Life maintained via spontaneous escape rhythms

Associated with broad (> 0.12s) or narrow (< 0.12s) QRS complexes

NARROW COMPLEX ESCAPE RHYTHM : due to diseased AV node or proximal His bundle

- Occurs w adequate rate and relatively re liable

- Common etiologies- associations

Congenital heart d isease, isolated congenital problem, MI, diphtheria, rheumatic

fever, drug toxic ities (d igitalis, verapamil, BB), aortic calc ification, endocarditis

- TREATMENT: often unnecessary but can include

- correct drug toxic ity

- temporary or permanent pacing (esp for congenital AV block)

BROAD COMPLEX ESCAPE RHYTHM : due to disease of Purkinje system

- Rhythm is slow (15-40 bpm) and unreliable

- Dizziness and blackouts (Stokes-Adams attacks) common

- Etiology

- Elderly: degenerative fibrosis and calcification of

- distal conduction system (Lenegre’s disease)

- more proximal conduction system (lev disease)

- Younger pts: ischemic heart disease

- TREATMENT: permanent pacemaker (even if asymptomatic) considerable reduces

mortality

INTRAVENTRICULAR CONDUCTION DISTURBANCES

Intraventricular conduction system: His bundle, right and left bundle branches, anterio-superior

and posterio-inferior divisions of left bundle branch

His bundle delay: long PR internal but often too small delay to notice or surface EKG

Blocked His bundle conduction delay: AV block

Bundle branch conduction delay: tr ivial widening of QRS complex (to 0.11s) incomplete BBB

Com plete block of a bundle branch (BBB): wider QRS complex; shape (f) right or left BB

Bifascicular block: combination block of any two of the following:

- right bundle branch, left anterosuperior div ision and the left posteroinferior d ivision.

- block of remaining fascicle -> complete AV block

CLINICAL PRESENTATION

- Usually asymptomatic except for complete block of H is bundle

- L BBB may provoke chest pain

- Right BBB -> wide but physio logical splitting of 2nd heart sound

- Pts may complain of syncope (from intermittent complete HB or V tachyarrhythmias)



PATHOLOGICAL TACHYCARDIAS

Common Etiologies

- HTN, ischemic heart disease, rheumatic heart disease

- Thyrotoxicosis

- Cardiomyopathy, atrial septal defect

- Lone atrial fibrillation (no cause)

- Junctional tachycardia (Wolf-Parkinson-White Syndrome

- Pneumonia, carcinoma of the bronchus

- Pericarditis, pulmonary embolus

- Acute and chronic ETOH abuse

- Cardiac surgery

ATRIAL ECTOPIC BEATS

- Often asymptomatic; may be perceived as palpitations or heaviness of heart beat

- Early abnormal p waves usually but not always followed by QRS

- Treatment only if symptomatic and often with BB

ATRIAL TACHYCARDIA: uncommon; most associated with heart disease

- Paroxysm al tachycardia

- incessant tachycardia (young children w no obvious heart disease)

- atrial tachycardia w AV block (digitalis toxicity)

TREATMENT: class Ia, Ic or III antiarrhythmics

ATRIAL FLUTTER: usually associated with organic heart disease; 280-350 bpm (300 common)

- Symptoms (f) degree of AV block; most often every second beat conducted -> HR 150

- Occasionally every beat conducted

- More often and esp w tx: conduction block reduces to HR 75 bpm

- EKG shows classic sawtooth-like atrial flutter wave (f waves) between QRS complexes

Atrial Flutter w 2:1 AV Block

TREATMENT

:

- electrical cardioversion and Class III drugs; prophylaxis w Ia, Ic or III

- AV nodal blocking drugs may control ventricular rate (II, IV, digitalis)

- radiofrequency catheter ablation: virtual cure for persistent flutter



ATRIAL FIBRILLATION: continuous rapid (400 bpm) activity; only proportion of impulses conducted

- Multiple meandering wavelets; atria respond electrically but no coordinated action

- Common; occurs in 5-10% of patients over 65 yrs

- Paroxysm al form occurs in younger pts

- Etio logy:

- Raised atrial pressure, increased atrial muscle mass, atrial fibrosis,

inflammation and infiltration of atrium

- Includes most cardiac disorders - some cases no cause (lone atrial fibrillation)

- Thyrotoxicos is: a-fib may be only feature in the elderly (‘masked’ hyperthyroid)

- Thyroid function testing mandatory for unexplained a-fib

CONDITIONS ASSOCIATED WITH ATRIAL FIBRILLATION

CARDIAC

- Acute MI

- Cardiac Sx

- Cardiomyopathy

- Congestive

- Hypertrophic

- CHF

- CAD

- HTN

- Valvular Disease

- Mitral annular calcification

- Rheumatic m itral stenosis

NONCARDIAC

- Acute ETOH intoxication

- Acute pulmonary embolism

- Cholinergic drug use

- Hyperthyroidism

CLINICAL PRESENTATION

- highly variable: asymptomatic to emergency hospital presentation

- Signs and Symptoms

- Dizziness - Palpitations

- Dyspnea - Presyncope

- Fatigue - Syncope

- usually deterioration of exercise capacity or well-being (may be subtle)

- pt has very irregular pulse (irregularly irregular)

- EKG: no p-waves, irregular QRS w tachycardia (120-180)

- Tachycardia responds well to treatment

MANAGEMENT

- Tx underlying cause where possible: thyroid, ETOH, chest infection, etc.

- Ventricular rate control (pharmacologic) or cardioversion (+/- anticoagulation)

Do not cardiovert chronic/long standing -> thromboemboli

- Spontaneous cardioversion is not uncommon



CARDIOVERSION: Can be electrical (DC shock) or pharmacologic

- IV infusion of antiarrhythmic drug of class Ia, Ic or amiodarone

- AV nodal blocking drugs to control ventricular response rate (goal < 90)

- Most common is digoxin

- Verapamil and BB also used

- Adenosine: no role due to transient duration of action

OTHER TREATMENT OPTIONS

- Other treatment options used in some instances

- permanent pacemaker (control rate during a-fib)

- Catheter ablation of AV node w pacemaker implantation

ANTICOAGULATION:

- Essential: a-fib in association with valvular heart disease, left ventricular

dysfunction, old age (> 75 yrs) or HTN

- Advised: previous thromboembolus, left atrium hypertrophy, poor LV function

- ASA: appropriate for most other pts

- Lone AF (< 65 w no heart disease) may not require anticoagulation

SPECIAL TX REQUIRED FOR WOLF-PARKINSON-WHITE SYNDROME

- avoid digoxin, adenosine, CaCh blockers, BB -> V-fib

- refer to cardiology: IV procainamide; electrical cardioversion

JUNCTIONAL REENTRANT TACHYCARDIA

- Intra-AV nodal re-entry tachycardia (AVNRT)

- Atrioventricular re-entry tachycardia (AVRT)

- Often strikes suddenly w/o provocation

- Certain factors may aggravate or induce: caffeine, ETOH, exertion

- Rhythm: rapid and regular (140-280)

- May resolve spontaneously or require medical intervention

- Palpitations is most prominent symptom; chest pain, polyuria, dyspnea, syncope

- Normal QRS complex w rate of 140-280; sometimes BBB

WOLF-PARKINSON-WHITE SYNDROME (congenital condition)

- Caused by abnormal myocardial connection between atrium and ventricle (Bundle of

Kent)

- Impulse travels over this abnormal connection to depolarize part of ventricles

abnormally

-Typical EKG pattern: sort PR interval, wide ORS complex w sigma wave

- Results in two types of tachycardia

- Atrioventricular reentry: treat with adenosine

- Atrial fibrillation: treat with radio-frequency ablation of abnormal pathway



VENTRICULAR TACHYARRHYTHMIAS

- 4 types: VPCs, V-tach, V-fib, torsades de pointes (twisting of points)

- Most caused by CHD, HTN or cardiomyopathy

- Torsades arises when ventricular repolarization is greatly prolonged

VENTRICULAR PREMATURE BEATS (VPCs OR PVCs)

- May be uncomfortable; pt may complain of extra beats, heavy beats or missed beats

- Bigemini, trigemini - may be felt at radial pulse

- TX advised if symptomatic or w structural heart disease; otherwise not treated

- TX w I, II, III

VENTRICULAR TACHYCARDIA

- 3 or more ventricular bears occurring at a rate of 120 bpm

- often hypotensive or ill but some v-tach is well tolerated

- pulse 120-220; clinical signs of AV dissociation

- EKG: rapid ventricular rhythm w broad ORS (often > 0.14s)

- Dissoc iated p waves may be seen; supraventricular tach w BBB may mimic

- treatment is urgent

- emergency cardioversion if low output/hypotension

- IV class I antiarrhythmics if output maintained: lidocaine is first-line

- prophylaxis against re lapse is important: BB, class I, class II

- most antiarrhythmics cannot be used prophylactically if severe LV dysfunction

Use amiodarone or mexiletine instead



VENTRICULAR FIBRILLATION: rapid irregular ventricular activation w no mechanical effect

- patient is pulseless and rapidly unconscious -> respiratory arrest

- EKG; shapeless, rapid oscillations; no hint of organized complexes

- Usually provoked by ventricular ectopic beat (esp in acute MI), ventricular tach or

torsades de pointes

- Rarely reverses spontaneously - electrical defibrillation indicated

- Advanced life-support; occasionally IV bretylium used

- Prophylaxis: antiarrhythmics (amiodarone, BB) or implantable defibrillator

TORSADES DE POINTES

- short duration and spontaneously reverts to SR

- causes syncope, presyncope and occas ionally V-fib/sudden death

- EKG:

- rapid, irregular sharp complexes

- continuously change from upright to inverted position

- prolonged QT interval between spells of tachycardia (> 0.44s)

- sometimes precipitated by commonly used drugs

CLASSIFICATION OF ANTIARRHYTHMIC DRUGS (Vaughan W illiams’)

Class Ia: quinidine, procainamide, disopyramide

Class Ib: Lidocaine, mexiletine, tocainide

Class Ic: Flecainide, propafenone

Class II: BB

Class III: Amiodarone, sotalol, bretylium, ibutilide, dofetilide

Class IV : Verapamil, diltiazem

other: adenosine, digoxin

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