PANCE PREP PEARLS V3 - PART A

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 Chapter 1 - Cardiovascular System
DILATED CARDIOMYOPATHY (DCMP

• Systolic dysfunction, l e a d i n g to a dilated, w e a k h e a r t .

• Most common type of Cardiomyopathy (95%).

RISK FACTORS
• Most common 20-60 years of age, men.

ETIOLOGIES

• I d i o p a t h i c m o s t c o m m o n c a u s e (may be familial).

• Infections: v i r a l m o s t c o m m o n (especially the e n t e r o v i r u s e s - C o x s a c k i e v i r u s B, Echovirus).

• postviral myocarditis, HIV, Lyme disease. Parvovirus B19, Chagas disease.

• Toxic: a l c o h o l a b u s e , cocaine, anthracyclines (eg, D o x o r u b i c i n ) , radiation.

• Pregnancy, autoimmune.
• Metabolic: eg, thyroid disorders, v i t a m i n B l ( t h i a m i n e ) deficiency.
CLINICAL MANIFESTATIONS
• Systolic h e a r t failure:
- Left-sided failure: L for Lung symptoms - dyspnea, fatigue.
- Right-sided failure: peripheral edema, jugular venous distention, hepatomegaly, GI symptoms.
- Embolic events, arrhythmias.

• Physical examination: S3 gallop h a l l m a r k (due to filling of a dilated ventricle). Mitral or tricuspid

regurgitation.

DIAGNOSTIC STUDIES
• E c h o c a r d i o g r a m : d i a g n o s t i c t e s t of c h o i c e - left v e n t r i c u l a r d i l a t i o n (large chamber), thin
ventricular walls, d e c r e a s e d ejection fraction, ventricular hypokinesis. Similar findings to Systolic
heart failure.

• Chest radiograph: c a r d i o m e g a l y , pulmonary edema, pleural effusion.

• ECG: may show sinus tachycardia or arrhythmias.

MANAGEMENT
• S t a n d a r d systolic h e a r t failure t r e a t m e n t :
Mortality r e d u c t i o n w i t h ACE i n h i b i t o r s , Beta b l o c k e r s (eg, Metoprolo!, Carvedilol), ARBs,
Spironolactone. S y m p t o m c o n t r o l w i t h d i u r e t i c s , Digoxin.

• Automated implantable cardioverter/defibrillator if ejection fraction < 35-30%.

 Chapter 1 - Cardiovascular System
STRESS (TAKOTSUBO) CARDIOMYOPATH

• Transient regional systolic dysfunction of the left ventricle t h a t can imitate Myocardial infarction,
but is associated with the a b s e n c e of significant obstructive coronary artery d i s e a s e or
e v i d e n c e of plaque rupture.
• Risk factors: p o s t m e n o p a u s a l w o m e n exposed to physical or emotional stress (eg, death of
relative, catastrophic medical diagnoses, acute medical illness).

PATHOPHYSIOLOGY
• Thought to be multifactorial, including catecholamine surge during physical or emotional stress,
microvascular dysfunction, and coronary artery spasm.

CLINICAL MANIFESTATIONS
• Similar to Acute coronary syndrome (ACS) - eg, substernal chest pain, dyspnea, syncope.

DIAGNOSIS
• ECG: ST elevations (especially in the anterior leads similar to anterior MI). May have ST depressions.
• Cardiac enzymes: often positive.
• Coronary angiography: a b s e n c e of acute plaque rupture or obstructive coronary disease. On
examinations, this is an "all the way question", meaning the diagnosis is considered in patients with
ACS with no evidence of obstructive coronary disease on coronary angiography.
• Echocardiogram: transient regional left ventricular systolic dysfunction, especially apical left
ventricular ballooning. Usually performed after ACS has been ruled out.

A) Echocardiograph showing dilatation of the left ventricle in the acute phase. (B) Resolution of left
ventricular function on repeat echocardiograph 6 days later.
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INITIAL MANAGEMENT
• Because the initial presentation of Takotsubo cardiomyopathy presents similar to ACS, patients a r e
treated as ACS with Aspirin, Nitroglycerin, Beta blockers, Heparin, and coronary angiography to rule
out obstructive coronary a r t e r y disease.

SHORT-TERM MANAGEMENT
• Because Takotsubo cardiomyopathy is a transient condition, conservative a n d supportive care is
t h e mainstay of t r e a t m e n t (eg, Beta blockers, ACE inhibitors for 3-6 m o n t h s with serial imaging t o
assess for improvement).
• Anticoagulation in some with severe LV dysfunction (eg, EF <30%) or if t h r o m b u s is present.
 Chapter 1 - Cardiovascular System
RESTRICTIVE CARDIOMYOPATHY (RCMP)
• Diastolic d y s f u n c t i o n in a n o n - d i l a t e d ventricle, which i m p e d e s v e n t r i c u l a r filling (decreased
compliance). The stiff ventricle fills with great effort.

ETIOLOGIES
• Infiltrative d i s e a s e : A m y l o i d o s i s ( m o s t c o m m o n ) , Sarcoidosis, H e m o c h r o m a t o s i s , Scleroderma,
Metastatic disease, endomyocardial fibrosis.

• Chemotherapy, radiation therapy.

CLINICAL MANIFESTATIONS
• R i g h t - s i d e d h e a r t failure > left-sided failure symptoms.
- Right-sided failure: eg, peripheral edema, jugular venous distention, hepatomegaly, ascites, GI
symptoms.

- Left-sided failure: L for Lung symptoms (eg, d y s p n e a m o s t c o m m o n c o m p l a i n t , fatigue).

• K u s s m a u l ' s sign: the lack of an inspiratory decline or i n c r e a s e in j u g u l a r v e n o u s p r e s s u r e w i t h

inspiration.

• Signs of h e a r t failure. S3 may be heard. Pulmonary hypertension.

DIAGNOSIS
• E c h o c a r d i o g r a m : d i a g n o s t i c t e s t of c h o i c e - n o n - d i l a t e d v e n t r i c l e s w i t h n o r m a l t h i c k n e s s (may
be slightly thick), d i a s t o l i c dysfunction, m a r k e d d i l a t i o n of b o t h a t r i a . Systolic function
generally preserved in early disease. Bright speckled myocardium in Amyloidosis.

• Chest radiograph: normal ventricular chamber size, enlarged atria. Pulmonary congestion.

• ECG: low voltage QRS, arrhythmias.

• Increased BNP.
• E n d o m y o c a r d i a l biopsy; definitive d i a g n o s i s (not used often).
- Amyloidosis associated with apple-green birefringence with Congo-red staining.

MANAGEMENT
• No specific treatment.
• Treat t h e underlying disorder (eg, chelation for Hemochromatosis, Glucocorticoids for Sarcoidosis).
• Gentle diuresis for symptoms, vasodilators.

10
 Chapter 1 - Cardiovascular System
HYPERTROPHIC CARDIOMYOPATH

• Autosomal dominant genetic disorder of inappropriate LV a n d / o r RV hypertrophy with diastolic

dysfunction.
• Subaortic outflow obstruction due to asymmetrical septal hypertrophy and systolic anterior motion
of the mitral valve.
The obstruction w o r s e n s with
• Increased contractility (eg, exercise, Digoxin, beta agonists) a n d / o r
• Decreased LV volume (eg, dehydration, decreased venous return, Valsalva maneuver).

CLINICAL MANIFESTATIONS
• Dyspnea m o s t c o m m o n symptom, fatigue, angina (chest pain), pre syncope, syncope, dizziness,
arrhythmias. M a y b e asymptomatic initially.
• Sudden cardiac death, especially in adolescent or preadolescent children especially during t i m e s
of e x t r e m e exertion usually due to Ventricular fibrillation.

PHYSICAL EXAMINATION
• Harsh systolic murmur best heard at the left sternal border.
• Increased m u r m u r intensity with d e c r e a s e d v e n o u s return (eg, Valsalva, standing) or decreased
afterload (eg, Amyl nitrate).
• Decreased m u r m u r intensity with increased v e n o u s return (eg, squatting, supine, leg raise) or
increased afterload (eg, handgrip). Increased LV volume preserves outflow.
• May have loud S4, mitral regurgitation, S3, or pulsus bisferiens.

DIAGNOSIS
• Echocardiography: a s y m m e t r i c ventricular wall thickness (especially septal) 1 5 m m or greater,
systolic anterior motion of the mitral valve, & small LV chamber size.
• ECG: left ventricular hypertrophy, anterolateral & inferior pseudo q waves, enlarged atria.

MANAGEMENT
• Focus on early detection, medical management, surgical management, a n d / o r ICD placement.
• Medical: Beta blockers first-line medical m a n a g e m e n t
Alternatives include Calcium channel blockers & Disopyramide.
• Surgical: Myomectomy usually performed in young patients refractory to medical therapy.
• Alcohol septal ablation: an alternative to surgical myomectomy.
• Patients should a v o i d dehydration, e x t r e m e exertion, and exercise. Cautious u s e of Digoxin,
Nitrates, and diuretics (Digoxin increases contractility; Nitrates & diuretics decrease LV volume).

• EXAM TIP
• Aortic stenosis fAS) VS. Hypertrophic obstructive cardiomyopathy (HOCM)
• Both: angina, syncope, systolic murmur. Both m u r m u r s go in the same direction with afterload
maneuvers (eg, both increase with Amyl nitrate & both decrease with handgrip).
• HOCM: preload maneuvers t h a t decrease LV volume (eg, Valsalva, standing) will w o r s e n the
m u r m u r of HOCM w h e r e a s these maneuvers will decrease the intensity of most other m u r m u r s
(including AS). Increased LV v o l u m e (eg, squatting, leg raise) will d e c r e a s e t h e m u r m u r of
HOCM w h e r e a s these m a n e u v e r s will increase the intensity AS. No carotid radiation.

11
 Cardiomyopathy: disease of the heart muscle (myocardial tissue) with cardiac dysfunction NOT due to other heart diseases*
DILATED CARDIOMYOPATHY (95%) RESTRICTIVE CARDIOMYOPATHY (i%) HYPERTROPHIC CARDIOMYOPATHY ( 4 % ) 1
DEFINITION • SYSTOLIC DYSFUNCTION O ventricular • DIASTOLIC DYSFUNCTION • DIASTOLIC DYSFUNCTION due to impaired ventricular
dilation *$ "dilated, weak heart" -Ventricular rigidity impedes ventricular relaxation/ffUing.
filling (J.ventricularcompliance)
• SUBAORTIC OUTFLOW OBSTRUCTION:
-hvpertrophled septum
• Preserved contractility early on in-disease.
- svstolic anterior motion fSAM) of mitral valve & SAM
is increased with: O jcontractility (exertion) & ©
|LV volume (eg, ^decreased venous return,
dehydration).
ETIOLOGIKS •Idiopathic MC cause, autoimmune •Infiltrative diseases • Inherited genetic disorder of inappropriate LV and/or
•Viral myocarditis (eg, enteroviruses) - Amyloidosis most common (MC) cause RVhypertrophy (especially septal).
•Toxic: ETOH, cocaine, pregnancy -Sarcoidosis, Hemochromatosis
• XRT, doxorubicin, daunorubicin - Scleroderma, metastatic disease. Idiopathic
CLINICAL • Systolic heart failure symptoms •RIGHT SIDED FAILURE more > left sided • Dyspnea most common initial complaint (90%1.
MANIFESTATIONS - Dyspnea, edema, increased JVD failure. • Angina pectoris
• Embolic phenomena. Arrhythmias •Dyspnea most common symptom. • Arrhythmias AF: VT/VF (palpitations, svncope).
•Viral Myocarditis: viral prodrome ** signs •Poorly tolerated tachyarrhythmias • Sudden cardiac death: especially in
of heart failure or chest pain, +cardiac adolescent/preadolescent children (especially
enzymes, nonspecific ST-T changes. exertional) due to ventricular fibrillation.
PHYSICAL •I. heart failure •Kussmaul'ssign: t(VP with inspiration •Harsh svstoHc crescendo-decrescendo murmur <5>LLSB
-Pulmonary congestion: rales, tachycardia, - |murmur intensity: fvenous return (eg. squatting.
cough, pleural effusion lying supine) because |LV volume preserves outflow.
•R-sided heart failure Handgrip (increased afterload).
• R heart failure Peripheral edema, fJVP, hepatic congestion.
- Peripheral edema, |JVP, hepatic -tmurmur intensity: Jvenous return (Valsalva &
congestion • L-sided heart failure standing) & exertion - J.LV volume & ^contractility
Crackles (rales). will .[cardiac output Amyl nitrate (decreases
afterload).
• Usually no carotid radiation. Normal pulse, Loud Si. ± MR
DIAGNOSIS •Echocardiogram most useful test •Echocardiogram: •Echocardiogram:
- O left ventricular dilation: - Ventricles nondilated with normal wall - Asymmetric wall thickness (septal), SAM mitral valve.
thin ventricular walls thickness.
- © Rejection fraction f_EF) •ECG:
- © Regional or global LV hypokinesia. - MARKED DILATION OF BOTH ATRIA - Left ventricular hypertrophy, septal q waves
•OCR: -Diastolic dysfunction with normal or near
- Cardiomegaly, Pulmonary edema. normal systolic function. Avoid exertion. Implantable Defibrillator to prevent VF.
MANAGEMENT •Standard svstolic heart failure treatment •No specific treatment •Medical: BETA BLOCKERS*. Verapamil, DisoDvramide.
-ACEI, Beta blockers, Na restriction Treat underlying cause •Myomectomy, ETOH ablation
-Symptom control: diuretics, digoxin. •Cautious use of digoxin, nitrates & diuretics (digoxin j'es
- Implantable defibrillator if EF <35% contractility while nitrates & diuretics J. volume).
 Chapter 1 - Cardiovascular System
MYOCARDITIS
m
• Inflammation of the heart muscle. Most common in young adults.

PATHOPHYSIOLOGY
• Myocellular damage leads to myocardial necrosis & dysfunction, leading to Heart failure.

ETIOLOGIES

• Infectious: viral m o s t c o m m o n (especially the enteroviruses - Coxsackievirus B), bacterial.

• Autoimmune eg, Systemic lupus erythematosus, Rheumatoid arthritis.

• Uremia, medications (eg, Clozapine, Methyldopa, antibiotics, Isoniazid, Cyclophosphamide,

Indomethacin, Phenytoin, sulfonamides).

CLINICAL MANIFESTATIONS
• Viral p r o d r o m e - fever, myalgias, malaise for several days followed by s y m p t o m s of systolic
dysfunction (Dilated cardiomyopathy).

• Heart failure symptoms: dyspnea, fatigue, exercise intolerance, S3 gallop.

• Other: Megacolon, Pericarditis (pericardial friction rub, effusion).

DIAGNOSTIC STUDIES
• Chest radiograph: cardiomegaly classic.

• ECG: nonspecific - sinus tachycardia most common, normal or may show Pericarditis (eg, diffuse ST

elevations and PR depressions in the precordial leads).

• ^abs: may have positive cardiac enzymes, increased ESR.

• Echocardiogram: ventricular systolic dysfunction. Also helpful to rule out other causes.

• Endomyocardial biopsy: gold standard - infiltration of lymphocytes with myocardial tissue

necrosis. Usually reserved for severe or refractory cases.

MANAGEMENT
• Supportive mainstay of t r e a t m e n t - standard Systolic heart failure t r e a t m e n t (eg, ACE
inhibitors, diuretics, Beta blockers).

13
 Chapter 1 — Cardiovascular System
ECG CHEAT SHEET
STEP 1: DETERMINE THE RHYTHM
Regular or Irregular?
El Use Rhythm strip. Check R-R intervals. If < 0.12 second difference, consider it a regular rhythm.

STEP 2: DETERMINE THE RATE

If Regular rhythm •=> 1500/# of small squares OR 300-150-100-75-60-50 method between an R-R interval.
If Irregular rhythm => count the number of R waves in a 6 second strip & multiply that number by 10.

STEP 3: DETERMINE THE QRS AXIS

Normal
LAD RAD *ff Left Axis Deviation (LAD) based on I and aVF •=> check lead II.
• • n ^^M - If QRS is predominantly positive in lead II <* normal axis (0° to -30°)
^ B ^ H ^ ^ H • s -If QRS is predominantly negative in lead II => LAD (<-30°)

STEP 4: EVALUATE THE P WAVES/PR INTERVAL

(Look in Lead II and Vi for P wave morphology)
0 Sinus? If positive/upright in I, II, avF & negative in avR. Each P wave followed by QRS complex.
EI PR interval normal? Normal PRI = 0.12 - .20 sec (or 3-5 boxes). Prolonged (> .20); shortened (< .12)
0 Atrial enlargement?
LEFT ATRIAL ENLARGEMENT RIGHT ATRIAL ENLARGEMENT
• m-shaped P wave in Lead II tall P wave in Lead II >3 mm
> .12 seconds (3 boxes)
• Biphasic P in VI with larger Biphasic P in V1 with larger
terminal component initial component

STEP 5: EVALUATE THE QRS COMPLEX

0 Narrow v. Wide (normal < .12 seconds). If QRS is narrow, skip looking for bundle branch blocks.

0 Bundle Branch Blocks?

Left BBB Right BBB
1. Wide QRS > 0.12 seconds 1. Wide QRS > 0.12 seconds
2. Broad, slurred R in V5,6 2. RsR' in Vl,2
3. Deep S wave in VI 3. Wide S wave in V6
4. ST elevations V1-V3

0 Ventricular Hypertrophy
RIGHT VENTRICULAR HYPERTROPHY: look at V1: R>S in V1 or R >7 mm in height in V1

LEFT VENTRICULAR HYPERTROPHY:

Sokolow-Lvon criteria: S in V1 + R in V5 (or V6) >35 mm in men; >30 mm in women.

Cornell Criteria: R in aVL + S in V3 >28 mm in men; >20 mm in women.

0 Pathological Q waves? Q wave >1 box (in depth or width).

STEP 6: EVALUATE ST SEGMENT

0 ST depression or elevation >1 mm in depth/height?

STEP 7: EVALUATE T WAVES

0 Any T wave inversions (TWI); T wave flattening? Is the QT interval prolonged?
14
 Chapter 1 - Cardiovascular System

SUMMARY OF THE 12 LEADS AND THEIR RELATION TO THE HEART

Coronary Artery A n a t o m y The leads and their relation to the coronary arteries
Aortic Arch LEFT MAIN LEFT MAIN
CORONARY ARTERY CORONARY ARTERY

Left
Ventricle

LEFT
ANTERIOR
DESCENDING
Right Ventricle ARTERY Leads H, m, aVF V1-V4 Septal (VI A V2)
AREA OF INFARCTION Q WANES/ ARTERY INVOLVED 1
ST ELEVATIONS
ANTERIOR WALL VI through V4 Left Anterior Descending ("LAD)
- SEPTAL VI & V2 Proximal LAD
LATERAL WALL LaVL,V5,V6 Circumflex fCFX)
ANTEROLATERAL I, aVL, V4 + V5 + V6 Mid LAD +/- CFX
INFERIOR •"_._•_ II, III, aVF Right Coronary Artery f RCA")
POSTERIOR WALL ST DEPRESSIONS V1-V2 RCA, CFX
(really the reciprocal changes since
there are no "posterior" leads on a
standard 12 lead ECG)

QRS AXIS D E T E R M I N A T I O N

Axis: the general direction of t h e impulses through the heart. It is the summation of all the vectors.
Vectors move t o w a r d s hypertrophy & away from infarction. N o r m a l QRS a x i s is -30° t o + 9 0 °
PERPENDICULAR QUADRANT METHOD

1180° > | 0°

QUADRANT METHOD: If LAD (based on I and aVF) o check lead II. If QRS is predominantly negative in lead II <• LAD
Lead I I aVF •ETIOLOGIES_OF LEFT & RIGHT AXIS DEVIATION
© © Normal
© -ve LBBB, LVH, inferior MI, elevated diaphragm, L anterior hemiblock, WPW
-ve © RVH, lateral MI, COPD, Left posterior hemiblock
-ve -ve
LAD - vectors move t o w a r d s hypertrophy [LVH) or away from infarction (inferior MI ± cause LAD).
RAD - vectors move t o w a r d s hypertrophy (RVH) or away from infarction (lateral MI ± cause RAD).

15
 BRADYCARDIA ALGORITHM TACHYCARDIA ALGORITHM

MCHEt Only 2 "shockable" rhythms using

dHfcjkf^tW
defibrillation (UNsynchronized
cardioversion) are:
O ventricular fibrillation &
© pulseless ventricular tachycardia*
UNSTABLE? JNSTABfcE T A C H Y A K R W H M M

Monitor and «- no yes 1CHI

Observe
(No acute medical Acute Heart Failure 'If regulaf, rlarrow QES"cornpleX|
treatment needed) 9
4 ffriayilftSliir.Adirlbsifte^
Or Symptomatic? d
i l Wide QRS Complex Tachycardia
" 1
'Antiarrhythmic: Amiodarom* 9
Atropine Inline* a
yes o
^Atropineppt^Iectivf <
O.IMfeconds (a
•iSrdialt>3ft&lt ** o
a
•TrYegufar, rrionomorpic,
r\im mtDsion z ^may/considpr. <
Transcutanepus Pacing,
i
o Vagal Maneuvers: Hold breath & bear
EXCEPTION TO SYMPTOMATIC/UNSTABLE BRADYARRHYTHMIA RULE? § down or carotid massage (make sure no
1. 3rd Degree heart block: transcutaneous pacing usually first line (ft regufar & n a r r o ^ M S ) * w
carotid bruits are present before performing)
followed by permanent pacemaker placement as definitive treatment. o
•Beta B|ocKer f orOa|ciyf| o
' leilfdck'efs 3
STABLE NARROW-COMPLEX TACHYARRHYTHMIAS:
S-B lockers: 1. ATRIAL FLUTTER OR A. FIB: Beta blocker or Calcium Channel Blocker 1st line.
Metoprolol, Esmolol, Propranolol 2. WOLFF-PARKINSON-WHITE fWPW): Procainamide preferred. Amiodarone. Avoid
ABCD if wide complex (Adenosine, Beta blockers, CCBs, Digoxin).
Calcium Channel Blockers
Non-dihydropyridines* 3. SVT: Vagal maneuvers. Adenosine first-line medical management
Diltiazem, Verapamil
4. Sinus arrhythmia: treat the underlying cause.
 Chapter 1 - Cardiovascular System

SINUS RHYTHMS I m p u l s e s originate at t h e SA (sinoatrial) node.

NORMAL SINUS RHYTHM fNSRI

• Every P wave is followed by a QRS complex.

• P waves a r e positive/upright in leads I, II, aVF, & negative in aVR.
• Rate 60-100 bpm.

SINUS ARRHYTHMIA
• Irregular rhythm originating from the sinus node.
• Normal variation of normal sinus rhythm (meets t h e r s a m e criteria except t h a t the rhythm is
irregular).
• More commonly seen in children, young adults and patients with Sinus bradycardia.

PHYSIOLOGY
• Beat to beat variations with respiration - rhythm increases w i t h inspiration and d e c r e a s e d w i t h
expiration, reflecting changes in stroke volume during respiration.

DIAGNOSIS
• ECG: normal-appearing P waves, beat to beat variation of the P-P interval (> .12 seconds), s h o r t e r
intervals during inspiration (increased rate) and longer P-P intervals during expiration (decreased
heart rate].

MANAGEMENT
• None n e e d e d in m o s t c a s e s (it is considered a normal variant).
• If symptomatic bradycardia occurs, Atropine is the first-line management.
• Transcutaneous pacing, Epinephrine, and Dopamine a r e second-line agents.

17
 Chapter 1 - Cardiovascular System
SINUS TACHYCARDL
• Increased h e a r t rate > 100 b p m originating from t h e sinus node.

ETIOLOGIES
• Physiologic: n o r m a l r e s p o n s e to exercise, emotional stress. Normal in y o u n g children & infants.
• Pathologic: fever, hypovolemia, hypoxia, pain, infection, h e m o r r h a g e , hypoglycemia, anxiety,
thyrotoxicosis, shock, s y m p a t h o m i m e t i c s (eg, d e c o n g e s t a n t s , cocaine).

DIAGNOSIS
• ECG: regular, rapid r h y t h m (> 100 b p m ) , n o r m a l - a p p e a r i n g P w a v e with every P followed by a
QRS complex.

MANAGEMENT
• T r e a t t h e u n d e r l y i n g c a u s e (first-line t r e a t m e n t ) .
• Beta blockers (eg, Metoprolol) u s e d in t h e m a n a g e m e n t of p e r s i s t e n t sinus tachycardia in t h e
setting of Acute c o r o n a r y a r t e r y s y n d r o m e .

SINUS BRADYCARDL
• Decreased h e a r t rate < 60 b p m originating from t h e sinus node.

ETIOLOGIES
• Physiologic: y o u n g athletes, vasovagal reaction, increased intracranial p r e s s u r e , nausea,
vomiting.
• Pathologic: Beta blockers, calcium channel blockers, digoxin, carotid massage, sinoatrial n o d e
ischemia, g r a m negative sepsis, & hypothyroidism.

DIAGNOSIS
• ECG: regular, s l o w , r h y t h m (< 6 0 b p m ) , n o r m a l - a p p e a r i n g P w a v e with every P followed by
a QRS complex
4-t
3

m 25
** *
•ft

MANAGEMENT
• Symptomatic or unstable: Atropine l^-line treatment.
E p i n e p h r i n e or t r a n s c u t a n e o u s pacing if n o t r e s p o n s i v e to Atropine.
• A s y m p t o m a t i c : n o t r e a t m e n t n e e d e d if p h y s i o l o g i c .
Observation o r cardiac consult m a y b e n e e d e d if pathologic.

18
 Chapter 1 - Cardiovascular System
SICK SINUS SYNDROME ( b r a d v - t a c h v s v n d r o m e
• Dysfunction of t h e s i n u s n o d e t h a t leads to a combination of s i n u s a r r e s t w i t h a l t e r n a t i n g
p a r o x y s m s of atrial t a c h y a r r h y t h m i a s & b r a d y a r r h y t h m i a s .

ETIOLOGIES
• Sinus n o d e fibrosis ( m o s t c o m m o n ) , o l d e r age, corrective cardiac surgery, medications, systemic
diseases t h a t affect the h e a r t

CLINICAL MANIFESTATIONS
• I n t e r m i t t e n t s y m p t o m s of b r a d y c a r d i a & o r tachycardia: eg, palpitations, dizziness,
lightheadedness, angina, d y s p n e a on exertion, presyncope, o r syncope.

• T e l e m e t r y o r a m b u l a t o r y ECG m o n i t o r i n g m a y be n e e d e d to d o c u m e n t episodes.

MANAGEMENT
• Stable: may n o t r e q u i r e u r g e n t t h e r a p y as t h e s y m p t o m s a r e often t r a n s i e n t

• Hemodynamically unstable: Atropine first-line if m e d i c a t i o n s are needed. Dopamine,

epinephrine. T r a n s c u t a n e o u s pacing.

• Long-term: p e r m a n e n t p a c e m a k e r definitive. Addition of an a u t o m a t i c i m p l a n t a b l e c a r d i o v e r t e r

defibrillator if a l t e r n a t i n g b e t w e e n tachycardia a n d b r a d y c a r d i a .

19
 T R I O V E N T R I C U L A R C O N D U C T I O N BLOCKS

AV BLOCK: interruption of the normal impulse from the SA node to the AV node (AV node dysfunction).
PR I n t e r v a l (PR1) m o s t helpful in d e t e r m i n i n g t h e p r e s e n c e of AV c o n d u c t i o n blocks.
FIRST-DEGREE AV B L O C5
• AV node dysfunction leading to delayed but conducted impulses.

ETIOLOGIES
• Often a n o r m a l v a r i a n t (individuals with high vagal tone without structural h e a r t disease).
• Intrinsic AV node disease, acute myocardial infarction (eg, inferior wall MI), electrolyte disturbances
(eg, hyperkalemia), AV nodal blocking drugs (eg, Digoxin, Beta-blockers & Calcium channel
blockers), myocarditis due to Lyme, cardiac surgery.

CLINICAL MANIFESTATIONS
• Asymptomatic in most cases.
• If symptomatic, it is due to bradycardia-related decreased perfusion - fatigue, dizziness, dyspnea,
chest pain, syncope, or in severe cases (hypotension or altered mental status).

DIAGNOSIS
• ECG: all atrial impulses are delayed b u t conducted to the ventricles = p r o l o n g e d PR i n t e r v a l (> 0.20
seconds) + all P^vaves a r e followed b y QRS c o m p l e x e s .

MANAGEMENT
• A s y m p t o m a t i c : n o t r e a t m e n t , observation. Cardiac consult in some cases.
• S y m p t o m a t i c : A t r o p i n e first-line, epinephrine.
• Pacemaker definitive if persistently symptomatic & severe (PRI > 0.30 seconds).

SECOND DEGREE AV BLOCK

2 n d = not all of the atrial impulses are conducted to the ventricles.
This leads to some P waves that are not followed by QRS complexes ('dropped QRS').
M O B I T Z I - WENCKEBACH M O B I T Z I - WENCKEBACH
• PROGRESSIVE P R I LENGTHENING >^> d r o p p e d QRS.
Shortened R-R interval

MANAGEMENT
Symptomatic ^ A t r o p i n e . Epinephrine, ± pacemaker.
Asymptomatic ^observation. ± Cardiac consult.

MOBITZ II MOBITZ II; block commonly in the bundle of HIS.

• CONSTANT/PROLONGED P R I => d r o p p e d QRS.

MANAGEMENT: A t r o p i n e o r t e m p o r a r y pacing.
Progression to 3 rd degree AV block common so
p e r m a n e n t pacemaker is the definitive t r e a t m e n t

20
 Chapter 1 - Cardiovascular System
MOBITZ I SECOND DEGREE AV BLOCK ( W e n c k e b a c h )
• Interruption of electrical impulse at the AV node resulting in occasional non-conducted impulses.
• PATHOPHYSIOLOGY: AV node dysfunction (commonly above the bundle of HIS).

ETIOLOGIES
• Often a normal variant (individuals with high vagal tone without structural heart disease).
• Inferior wall MI (AV node ischemia), AV nodal blocking agents (eg, Beta blockers, Digoxin, Calcium
channel blockers), myocarditis due to Lyme, hyperkalemia, cardiac surgery.

CLINICAL MANIFESTATIONS
• Asymptomatic in most cases.
• Bradycardia-related decreased perfusion - eg, fatigue, dizziness, dyspnea, chest pain, syncope, or in
severe cases (hypotension or altered mental status).

DIAGNOSIS
• ECG: progressive lengthening of t h e PR interval until an occasional non-conducted atrial
impulse (dropped QRS complex).

MANAGEMENT
• Asymptomatic: n o treatment, observation. Cardiac consult in some cases.
• Symptomatic: Atropine first-line. Epinephrine.
• Pacemaker definitive if persistent.

MOBITZ II SECOND DEGREE AV BLOC"

• Interruption of electrical impulse at the AV node resulting in occasional non-conducted impulses.
• PATHOPHYSIOLOGY: AV node dysfunction (commonly at the bundle of HIS).

ETIOLOGIES
• Rarely s e e n i n patients without structural heart d i s e a s e (eg, myocardial ischemia, myocardial
fibrosis, myocarditis (eg, Lyme disease), endocarditis.
• Iatrogenic - AV nodal blockers, post-catheter ablation, post-cardiac surgery.

CLINICAL MANIFESTATIONS
• Asymptomatic in most cases.

• Symptomatic: due to bradycardia-related decreased perfusion - fatigue, dizziness, dyspnea, chest

pain, syncope, o r in severe cases, hypotension o r altered mental status.

DIAGNOSIS
• ECG: constant PR interval before & after the non-conducted atrial beat (dropped QRS complexes).

• If ischemia is suspected based on clinical picture, cardiac biomarkers, chest radiograph, and
electrolytes should be ordered.

MANAGEMENT
• Initial: t r a n s c u t a n e o u s pacing o r Atropine for s y m p t o m a t i c bradycardia with p e r m a n e n t
pacemaker long-term management. These patients often do not respond to Atropine.

• Definitive: p e r m a n e n t p a c e m a k e r required in m a n y patients because it often progresses to third

degree AV block and is associated with complications of hypotension, and cardiac arrest.

21
 Chapter 1 - Cardiovascular System
THIRD DEGREE AV BLOC
• AV dissociation = no atrial impulses reach the ventricles, so the atrial activity is independent of the
ventricular activity.
• This leads to an escape rhythm from below the block.

ETIOLOGIES
• Myocardial ischemia (inferior wall MI), AV nodal blocking a g e n t s (eg, Beta-blockers, Digoxin,
Calcium channel blockers), endocarditis, myocarditis due to Lyme, cardiac surgery.
• Increased vagal tone, hypothyroidism, hyperkalemia, myocarditis.

CLINICAL MANIFESTATIONS
• M a y b e asymptomatic.
If symptomatic, it is due to b r a d y c a r d i a - r e l a t e d decreased perfusion especially during exertion (eg,
fatigue, dyspnea, dizziness, chest pain, syncope) or in severe cases, hypotension or altered mental
status.

DIAGNOSIS
• ECG: shows regular P-P intervals & regular R-R intervals but they are n o t related to each other.
5
atients are often bradycardic.

t*_4

MANAGEMENT
• Acute or symptomatic: transcutaneous pacing often followed by p e r m a n e n t pacemaker
placement

• Definitive: p e r m a n e n t pacemaker p l a c e m e n t

HEART BLOCKS - REVIEW

ST
1 DEGREE:
• Prolonged PRI, every P followed by QRS (all conducted)

2 nd degree = dropped QRS

(some NOT conducted)
• MOBITZ 1: Progressive lengthening PRI - dropped QRS

• MOBITZ 2: Same length (may be prolonged) +

Occasional dropped QRS

3RD DEGREE
AV Dissociation (NONE are conducted)

22
 TRIAL DYSRHYTHMIAS

ATRIAL FLUTTEi
• 1 irritable atrial focus firing at a fast rate (atrial rate usually around 300 beats/min).
• Similar to Atrial fibrillation, there is an increased risk of atrial thrombus formation that can lead
to cerebral & / o r s y s t e m i c embolization (eg, stroke).
• It may occur alone or be an interval rhythm between sinus tachycardia and atrial fibrillation.

CLINICAL MANIFESTATIONS
• Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain.
• Unstable: are due to hypoperfusion and can include refractory chest pain, h y p o t e n s i o n (eg, systolic
BP in double digits) or altered mental status.

DIAGNOSIS
• ECG: flutter ("sawtooth" atrial w a v e s usually around 300 beats per minute (250-350 normal
e P waves. The flutter waves a r e identical (1 ectopic atrial focus).

MANAGEMENT
• Stable: Vagal maneuvers. Rate control with Beta blockers (eg, Metoprolol, Atenolol or Esmolol) OR

non-dihydropyridine Calcium channel blockers (eg, Diltiazem, Verapamil).

• Unstable: direct current (synchronized) cardioversion.

• Anticoagulation: similar criteria (eg, CHA2DS2-VASc) for nonvalvular atrial fibrillation in patients at
risk for embolization.
• Reversion to normal sinus rhythm:
- Radiofrequency catheter ablation (definitive management).
- Direct current cardioversion.
- Class IA, IC, or III antiarrhythmics (eg, Ibutilide).

23
 Chapter 1 - Cardiovascular System
ATRIAL FIBRILLATION fAF
• Multiple i r r i t a b l e a t r i a l foci fire at fast rates.
• Similar to Atrial flutter, there is an i n c r e a s e d r i s k of a t r i a l t h r o m b u s f o r m a t i o n t h a t c a n l e a d t o
c e r e b r a l & / o r s y s t e m i c e m b o l i z a t i o n (eg, stroke).
• Atrial fibrillation is the most common chronic arrhythmia. Most patients are asymptomatic.

ETIOLOGIES
Cardiac disease, ischemia, pulmonary disease, infection, cardiomyopathies, electrolyte imbalances,
idiopathic, endocrine or neurologic disorders (eg, thyroid disorders), increasing age, genetics,
hemodynamic stress, medications, drug or alcohol use. Men > women; Whites > blacks.

TYPES
- Paroxysmal: self-terminating within 7 days (usually <24 hours). ±Recurrent.
- Persistent: fails to self-terminate, lasts >7 days. Requires termination (medical or electrical).
- Permanent: persistent AF >1 year (refractory to cardioversion or cardioversion never tried).
- Lone: paroxysmal, persistent or p e r m a n e n t without evidence of heart disease.

CLINICAL MANIFESTATIONS
• Symptomatic: palpitations, dizziness, fatigue, & dyspnea.
• U n s t a b l e : are due to hypoperfusion and can include h y p o t e n s i o n (eg, systolic BP in double digits),
a l t e r e d m e n t a l s t a t u s , & r e f r a c t o r y chest pain.

DIAGNOSIS
ECG:
Irregularly irregular rhythm with fibrillatory
w a v e s (no discrete P waves).
Often atrial rate >250 beats per minute.
The AV nodal refractory period determines the
Ashman's p h e n o m e n o n (seen here on 2 nd &
ventricular rate.
8th beat)
± Ashman's phenomenon: occasional aberrantly
conducted beats (wide QRS) after short R-R
cycles.

• Cardiac monitoring: a Holter monitor or telemetry can be used if Atrial fibrillation is not seen on an
ECG but is suspected.

MANAGEMENT
Stable:
• Rate control with Beta b l o c k e r s (eg, Metoprolol, Atenolol, or Esmolol) OR non-dihydropyridine
Calcium c h a n n e l b l o c k e r s (eg, Diltiazem, V e r a p a m i l ) .
• Digoxin may be used when Beta blockers or calcium channel blockers are contraindicated (eg, CHF or
severe hypotension).
Unstable:
• Direct c u r r e n t (synchronized) cardioversion.
Long-term:
• Rate control usually preferred over rhythm control for long-term management.
• Direct current (synchronized cardioversion) or pharmacologic cardioversion.
• Radiofrequency catheter ablation or surgical "MAZE" procedure.
• Anticoagulation: similar criteria (eg, CHA2DS2-VASc) for nonvalvular atrial fibrillation in patients at
risk for embolization.

24
 Chapter 1 - Cardiovascular System

CARDIOVERSION
• Direct current (synchronized cardioversion) or pharmacologic cardioversion. Cardioversion is most
successful when performed within 7 days after the onset of Atrial fibrillation.
• Echocardiogram is n e e d e d prior to cardioversion to ensure there are no atrial clots.
• AF greater than 4 8 hours undergoing elective cardioversion, anticoagulation for at least 3 w e e k s
before cardioversion or a transesophageal echocardiography guided approach with abbreviated
anticoagulation.
• AF < 4 8 hours undergoing elective cardioversion, anticoagulation prior is recommended.
• Anticoagulation m u s t b e continued for 4 w e e k s after cardioversion. With effective
anticoagulation the stroke risk is decreased 3-fold after 4 weeks of anticoagulation.

CANDIDATES FOR ANTICOAGULATION WITH NONVALVULAR AF

• CHA2DS2-VASc score for nonvalvular Atrial fibrillation assess patients' risk for embolization.
Chronic oral anticoagulation (eg. Warfarin or Novel oral anticoagulants) is r e c o m m e n d e d for
m o d e r a t e t o high risk (score of 2 or greater).
• The use of anticoagulant therapy has been shown to reduce embolic risk by 70%.

ANTICOAGULATION RISK STRATIFICATION IN NONVALVULAR ATRIAL FIBRILLATION

CHA7DS7- VASc CRITERIA POINTS RECOMMENDED T H E R A P Y
Congestive Heart Failure > 2 = Moderate to high risk:
Hypertension chronic oral anticoagulation recommended.
&ge > 75y
Diabetes Mellitus 1 = low risk:
S21 Stroke, TIA, thrombus Based on clinical judgment, consideration of risk to
Vascular disease (prior MI, benefit assessment & discussion with patient
aortic plaque, peripheral Anticoagulation may be recommended in some cases.
arterial disease")
Age 65 - 74y 0 = very low risk:
Sex (female] No anticoagulation needed.
MAXIMUM SCORE May be recommended in some (based on clinical
judgment & consideration of risk to benefit ratio).

ANTICOAGULANT AGENTS:
1. Non-vitamin K antagonist oral anticoagulants fNOAC): usually now preferred over Warfarin in
most cases due to similar or lower rates of major bleeding as well as lower risk of ischemic stroke,
convenience of not having to check the INR, & less drug interactions.
- Dabigatran: direct thrombin inhibitor (binds & inhibits thrombin).
- Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors.

2. Warfarin:
Indications: may be preferred in some of the following patients - some with severe chronic
kidney disease, contraindications to the NOAC (eg, HIV patients on protease inhibitor-based
therapy, on CP450-inducing antiepileptic medications such as Carbamazepine, Phenytoin etc),
patients already on Warfarin who prefer not to change, cost issues (Warfarin is less
expensive). Warfarin usually bridged with heparin until Warfarin is therapeutic.
Monitoring: International Normalized Ratio (INR) goal of 2-3. Prothrombin Time (PT).

3. Dual antiplatelet therapy: (ex. Aspirin + Clopidogrel). Anticoagulant monotherapy is superior to dual
antiplatelet therapy. Dual antiplatelet therapy may be reserved for patients w h o cannot be
treated with anticoagulation (for reasons OTHER than bleeding risk).

25
 Chapter 1 - Cardiovascular System
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)
Any tachyarrhythmia originating above the ventricles (either an atrial or atrioventricular nodal
source).
SVT is an umbrella term when a more specific t e r m cannot be applied to a tachyarrhythmia originating
above the ventricles.

PATHOPHYSIOLOGY: reentry circuits

• AV n o d e re-entrant tachycardia: two pathways (1 normal and 1 accessory pathway both within
the AV n o d e ) . Most c o m m o n type.
• AV reciprocating tachycardia: t w o pathways (1 normal and 1 accessory pathway outside of the AV
node) - eg, Wolff-Parkins on-White (WPW) & Lown-Ganong-Levine syndrome (LGL).

CLINICAL MANIFESTATIONS
• Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain.
• Unstable: hypoperfusion can cause hypotension (eg, systolic BP in double digits), altered mental
status, & refractory chest pain.

ECG
Orthodromic (95%): regular, narrow-complex tachycardia (no discernable P w a v e s due to the
rapid rate) - "If you can't tell if the b u m p is a P or a T, then it must be SVT!"
Antidromic f5%1: regular, w i d e - c o m p l e x tachycardia (mimics ventricular tachycardia).
Heart rate >100 bpm.
• Rhythm usually regular with narrow QRS
complexes.
• P waves hard to discern due to the rapid rate.

MANAGEMENT
• Stable (regular, narrow complex"): Vagal maneuvers.
- AV nodal blockers - A d e n o s i n e first-line medical m a n a g e m e n t .
- Second-line: Calcium channel blockers (eg, Diltiazem); Beta blockers (eg, Metoprolol); Digoxin.
• Stable (wide complex): antiarrhythmics (eg, Amiodarone). Procainamide if WPW suspected.
• Unstable: direct current (synchronized) cardioversion.
• Definitive: radiofrequency catheter ablation.

WANDERING ATRIAI MAKER fWAPl & MULTIFOCAL ATRIAL TACHYCARDIA fMATl

WANDERING ATRIAL PACEMAKER:

• Multiple ectopic atrial foci generate impulses that are conducted to the ventricles.
• ECG: heart rate < 1 0 0 b p m & £ 3 P w a v e morphologies.

MULTIFOCAL ATRIAL TACHYCARDIA:

• Same as wandering atrial pacemaker except the heart rate is >100 bpm.
• ECG: heart rate > 1 0 0 b p m & S3 P w a v e morphologies.
• MAT classically associated with s e v e r e COPD (chronic obstructive pulmonary disease).
Difficult to treat: Calcium channel blocker (eg, Verapamil) or (3-blocker used if LV function is preserved.

26
 X
Chapter 1 - Cardiovascular System
WOLFF-PARKINSON-WHITE fWPWI
• Preexcitation syndrome that is a type of AV reciprocating tachycardia (AVRT).

PATHOPHYSIOLOGY
• Accessory pathway (Bundle of Kent) outside of the AV node "preexcites" t h e ventricles (directly
connects the atria & ventricles, bypassing the AV node), leading to a delta w a v e (slurred, wide QRS).

CLINICAL MANIFESTATIONS
• Most patients are asymptomatic b u t they are prone to the development of tachyarrhythmias.
• Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain.
• Unstable: are due to hypoperfusion and can include h y p o t e n s i o n (eg, systolic BP in double digits),
altered mental status, & refractory chest pain.

ECG: 3 components "WPW"

• ^ a v e - delta w a v e (slurred QRS upstroke)
• £R interval that is short
• Mflde QRS complexes (> 0.12 seconds)

iTnTT
Delta waves (arrows)

MANAGEMENT
Stable (wide c o m p l e x ! tachycardia:
• Antiarrhythmics - Procainamide preferred. Amiodarone.
• Avoid AV nodal blocking agents ABCD if w i d e QRS c o m p l e x e s (Adenosine, Beta blockers. Calcium
channel blockers, Digoxin) because they can lead to preferential conduction d o w n t h e Bundle of
Kent, worsening the tachycardia.
Unstable:
• Direct current (synchronized) cardioversion.
Definitive:
• Radiofrequency catheter ablation definitive m a n a g e m e n t - electrically destroys the abnormal
pathway. May be indicated if patients experience recurrent, symptomatic episodes.

V JUNCTIONAL DYSRHYTHMIAS

AV node/junction becomes the dominant pacemaker of the heart in AV junctional rhythms.

Etiologies: sinus disease, coronary artery disease, most common rhythm seen with Digitalis toxicity,
Myocarditis. May be seen in patients without structural heart disease.
ECG: Regular rhythm. P w a v e s inverted (negative) if p r e s e n t in leads w h e r e they a r e normally
positive (I, II, aVF) or are n o t seen. Classically associated with a n a r r o w QRS (± wide).
Junctional Rhythm: heart rate is usually 40-60 bpm (reflecting the intrinsic rate of the AV junction).
Accelerated Junctional: h e a r t rate 60-100 bpm.
lunctional Tachycardia: h e a r t rate > 1 0 0 b p m .
Junctional rhythm with inverted P waves Junctional rhythm with absent P waves
*w*» Hinimnwimiiwii imoiii

27
 Chapter 1 - Cardiovascular System
VENTRICULAR DYSRHYTHMIAS

P R E M A T U R E VENTRICULAR COMPLEXES fPVC]

J i .jK • --U- v us
-i'V.*}.1 >^f-U

Unifocal (one morphology) Multifocal (>1 morphology) Bigeminy (every other beat is a PVC) Couplet (two PVCs in a row]
- PVC: p r e m a t u r e beat originating from the ventricle => wide, bizarre QRS occurring earlier than
expected. With a PVC, the T w a v e is in the o p p o s i t e direction of the QRS usually. Associated with
a compensatory p a u s e = overall rhythm is unchanged (AV node prevents retrograde conduction].

MANAGEMENT
- No t r e a t m e n t usually n e e d e d (common finding on ECG).
- Most ventricular arrhythmias occur after a PVC.

VENTRICULAR TACHYCARDIA
• Defined as 3 or more consecutive PVCs at a rate >100 beats p e r minute (usually between 120-300].

CLASSIFICATION
• Sustained VT = duration at least 30 seconds. Non-sustained if > 30 seconds.
• Monomorphic (same QRS morphology) or Polymorphic.
• Torsades d e p o i n t e s : a variant of polymorphic VT (waxing and waning QRS amplitude on ECG)

ETIOLOGIES:
• Underlying h e a r t disease: ischemic heart d i s e a s e m o s t c o m m o n (eg, post MI), structural heart
defects, cardiomyopathies.
• Prolonged QT interval, electrolyte abnormalities (eg, Hypomagnesemia, hypokalemia,
hypocalcemia), Digoxin toxicity.

CLINICAL MANIFESTATIONS
• Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain.
• Unstable: a r e due to hypoperfusion and can include h y p o t e n s i o n (eg, systolic BP in double digits),
altered m e n t a l status, & refractory chest pain.

ECG
• Regular, w i d e c o m p l e x tachycardia with no discernable P waves.

MANAGEMENT OF ACUTE TACHYARRHYTHMIAS

Stable s u s t a i n e d VT Antiarrhythmics (Amiodarone, Lidocaine, Procainamide).
U n s t a b l e VT w i t h a n u l s e Direct current (Synchronized) cardioversion.
VT ( n o p u l s e ) - Defibrillation (Unsynchronized cardioversion) +
CPR (treat similar to Ventricular Fibrillation).
Torsades de pointes IV Magnesium. Correct electrolyte abnormalities.

28
 Chapter 1 - Cardiovascular System
TORSADES DEPOINTES
• A variant of polymorphic Ventricular tachycardia (waxing and waning cyclic alterations of the QRS
amplitude on ECG).

PATHOPHYSIOLOGY
• Prolonged repolarization and early afterdepolarization + triggered activity.

ETIOLOGIES
• Prolonged QT interval, electrolyte abnormalities (eg, Hypomagnesemia, hypokalemia,
hypocalcemia), females > males. Congenital long QT syndrome.
• Medications: Digoxin, class IA antiarrhythmics (eg, Quinidine, Procainamide, Disopyramide), class III
antiarrhythmics (Sotalol, Ibutilide), antibiotics (eg, Macrolides), antipsychotics, antidepressants, &
antiemetics.

CLINICAL MANIFESTATIONS
• Symptomatic: palpitations, dizziness, fatigue, dyspnea, & chest pain.

DIAGNOSIS
• ECG: polymorphic Ventricular tachycardia (cyclic alterations of t h e QRS amplitude o n ECG
around the isoelectric line) aka sinusoidal waveform.
• Labs: rule out Hypomagnesemia and hypokalemia.

MANAGEMENT
• IV Magnesium sulfate first-line (suppresses early afterdepolarizations, terminating t h e
arrhythmia). Magnesium is effective in both terminating and preventing r e c u r r e n t TdP. Correct
electrolyte abnormalities.
• Discontinue all QT prolonging drugs.
• Isoproterenol and transvenous overdrive pacing may be used in refractory cases.

VENTRICULAR FIBRILLATION
• A type of cardiac death associated with ineffective ventricular contraction.

ETIOLOGIES
• Underlying h e a r t disease: ischemic heart d i s e a s e m o s t c o m m o n (eg, post MI), structural h e a r t
defects, cardiomyopathies, sustained Ventricular tachycardia.

CLINICAL MANIFESTATIONS
• Unresponsive, p u l s e l e s s patient, syncope.

ECG
• Erratic pattern of electrical im pulses, no P waves.
Tn ft** Tr rtr tut ffH •+ffjstt$
«2 SJ~ \i It"
t*J TTTt 5 : ^•-^N*- Tp fir •H1 fikr-fr BltttiH
IT ffi H ±32ttbr:UliUI xt
Co ars e v ent ric ula.rfi )n lation Fin e ventr cular fib rillatio

MANAGEMENT
• Unsynchronized cardioversion (Defibrillation) + CPR (initiate ACLS)

29