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