Sick sinus syndrome clues to diagnosis
preceding fatigue or dizziness, sinus pauses on ECG
Advanced AV block clues to diagnosis
bifascicular block or prolonged PR interval on ECG, dropped QRS complexes on ECG
Torsades de pointes clues to diagnosis
no preceding symptoms, medications that prolong QT interval, hypokalemia or hypomagnesemia
V tach clues to diagnosis
no preceding symptoms, cardiomyopathy or previous MI
Aortic stenosis or HCM clues to diagnosis
exertional syncope, systolic murmur on PE
Treatment for hemodynamically unstable patients with torsades de pointes
immediate electrical defibrillation
Treatment for hemodynamically stable patients with torsades de pointes
IV magnesium sulfate
Treatment for cardiotoxicity due to hyperkalemia
calcium gluconate
First line therapy for monomorphic V tach
amiodarone
Treatment for acute termination of paroxysmal supraventricular tachycardia
adenosine
Wolff-Parkinson-White pathophys
ventricular preexcitation due to an accessory pathway that conducts depolarization directly from the atria to the ventricles; it competes with normal conduction through the AV node.
Most common arrhythmia seen with WPW
atrioventricular reentrant tachycardia
Procainamide
Class 1a antiarrythmic agent that inhibits cardiac sodium channels
Digoxin toxicity
atrial tachycardia due to increased automaticity of conduction in the atria
Mobitz type 1 AV block due to increased vagal tone causing slowed conduction through the AV node (you'll never see type 2 here)
Because digoxin competes with potassium to bind to the myocardium at the sodium-potassium ATPase
hypokalemia increases its binding and can worsen toxicity or cause it to occur at lower-than-expected serum levels
A wave
caused by right atrial contraction, closely followed by tricuspid valve closure
C wave
caused by right ventricular contraction against a closed tricuspid valve
V wave
representing the peak of right atrial filling, just prior to reopening of the tricuspid valve
Cannon A waves
intermittent prominent A waves caused by the surge in jugular venous pressure that occurs when the atria and ventricles happen to contract simultaneously; these waves can be seen with any arrhythmia involving atrioventricular dissociation, such as ventricular tachycardia, which is characterized by self-propagation within the ventricles without communication with the atria and is likely in a patient with recent MI. Can also be seen in complete AV block.
Symptoms associated with cannon A waves
headache, jaw pain, sensation of neck pulsation
Vasovagal syncope triggers
pain, anxiety, emotional stress, heat, prolonged standing
Situational syncope triggers
cough, micturition, defecation, eating, hair-combing
Vasovagal and situational syncope clinical presentation
prodome (warmth, pallor, nausea, diaphoresis)
rapid recovery of consciousness (<1-2 min)
Vasovagal and situational syncope diagnosis
mainly based on clinical history of event
upright tilt table testing sometimes indicated in uncertain cases
Vasovagal and situational syncope treatment
reassurance and avoidance of triggers
counterpressure techniques for recurrent episodes
Initial management of afib
usually focuses on rate control; a beta blocker (metoprolol) or nondihydropyridine calcium channel blocker (verapamil, diltiazem) is given initially. Emergency cardioversion is indicated only in patients who are hemodynamically unstab;e (severe hypotension)
First degree AV block
asymptomatic, PR interval prolongation, observation
Mobitz Type 1 second degree AV block
usually asymptomatic, progressive PR interval lengthening followed by dropped QRS complex, observation (rarely PPM placement)
Mobitz Type 2 second degree AV block
fatigue, light-headedness, syncope, constant PR interval with randomly dropped QRS complexes, PPM placement
Third degree (complete) AV block
fatigue-lightheadedness, syncope, complete dissociation of P waves and QRS complexes, PPM placement
Mobitz Type I AV block
level of block- AV node
ECG findings- progressive prolongation of PR interval followed by dropped QRS complex
QRS complexes- usually narrow
Decreased vagal tone (exercise, atropine)- block improves
Increased vagal tone (carotid massage/0- block worsens
Risk of complete block- low
Mobitz type II AV block
Level of block- Below AV node (His bundle)
ECG findings- constant PR interval with randomly dropped QRS complexes
QRS complexes- narrow or wide
Decreased vagal tone (exercise, atropine)- block worsens
Increased vagal tone (carotid massage)- block improves
Risk of complete block- high (indication for PPM)
Class 1a antiarrythmics
quinidine, procainamide, disopyramide
Class 1a antiarrythmics ECG effects
pronlonged QRS and QT intervals
Class 1b antiarrythmics
lidocaine, mexiletine, tocainide, phenytoin
Class 1b antiarrythmics ECG effects
none
Class 1c antiarrythmics
flecainide, propafenone, moricizine
Class 1c antiarrythmics ECG effects
prolonged QRS
Class II antiarrythmics
metoprolol, atenolol, bisoprolol, esmolol, nadolol, propranolol, acebutolol, timolol
Class II antiarrythmics ECG effects
prolonged PR interval
Class III antiarrythmics
amiodarone, bretylium, dofetilide, dronedarone, ibutilide, sotalol
Amiodarone ECG effects
prolonged PR, QRS, and QT intervals
Sotalol ECG effects
prolonged PR and QT intervals
Other class III antiarrythmic ECG effects
prolonged QT interval
Class IV antiarrythmics
diltiazem, verapamil
Class IV antiarrythmics ECG effects
prolonged PR interval
Patients with prior MI complicated by left ventricular systolic dysfunction with EF no greater than 30% are at an increased risk of SCD due to
ventricular arrhythmia (v tach, v fib). Following a trial of optimal medical therapy, primary prevention with placement of an implantable cardioverter-defibrillator is indicated in these patients
Westermark sign
peripheral hyperlucency of the pulmonary arterial tree resulting from blood flow being cut off by the pulmonary embolism
Hampton Hump
peripheral, wedge-shaped lung opacity representing pulmonary infarction. An ipsilateral pleural effusion in also commonly present with this sign (pulm infarction is the typical cause of pulmonary embolism-associated pleural effusion)
Fleischner sign
enlargement of the pulmonary artery resulting from increased pressure proximal to the pulmonary embolism
Gold standard for ruling out or confirming pulmonary embolism
Chest CT angiography
Peptic ulcer perforation presents with
acute abdominal pain with radiation to the back or right shoulder and signs of peritonitis. Upright chest x-ray may reveal pneumoperitoneum with free air under the diaphragm
Vagal maneuvers (carotid massage, cold-water immersion of diving reflex, valsalva maneuver, eyeball pressure)
increases parasympathetic tone in the heart and result in a temporary slowing of conduction of the AV node and an increase in the AV node refractory period, leading to termination of AVNRT
Cardiac sarcoidosis should be suspected in any young patient younger than the age of 55 with
unexplained second or third degree heart block or when ECF changes occur in a patient with known or suspected systemic disease. A disease of noncaseating granuloma infiltration of the myocardium and can result in serious arrhythmia, cardiomyopathy, heart failure, and SCD
What should be used to reduce the risk of systemic thromboembolism in patients with afib and a high risk of thromboembolic events?
an anticoagulation agent, such as a direct oral anticoagulant (apixaban) or warfarin
Sick sinus syndrome clinical features
elderly patients
bradycardia: fatigue, dyspnea, dizziness, syncope
bradycardia-tachycardia syndrome: atrial arrythmias (afib), plapitations
Sick sinus syndrome ECG findings
sinus bradycardia, sinus pauses (delayed P waves), sinoatrial nodal exit block (dropped P waves)
Sick sinus syndrome treatment
pacemaker, +/- rate-control medication (if tachyarrhythmias)
Sick sinus syndrome
inability of the sinoatrial node to generate an adequate heart rate. Age-related degeneration of the cardiac conduction system with fibrosis of the sinus node is the most common cause.
IV adenosine
useful in the initial diagnosis and management of patients with narrow-QRS-complex tachycardia. It slows the sinus rate, increases atrioventricular (AV) nodal conduction delay, or can cause a transient block in AV node conduction. It can be useful in identifying P waves to clarify diagnosis or atrial flutter or atrial tachycardia. It can also terminate paroxysmal supraventricular tachycardias by interrupting the AV nodal reentry circuit.
Hypertrophic cardiomyopathy pathophysiology
genetic mutations affecting cardiac sarcomere proteins, AD, variable phenotypic penetrance
Hypertrophic cardiomyopathy clinical features
many patients are asymptomatic, exertional dyspnea, fatigue, angina, light-headedness, syncope, systolic ejection murmur accentuated by decreased LV blood volume, diastolic dysfunction with audible S4, increased risk for afib and v tach
Hypertrophic cardiomyopathy diagnosis
ECG: left axis deviation, abnormalities of depolarization (Q waves) or repolarization (inverted T waves)
ECHO: septal LV hypertrophy, dynamic LVOT obstruction, LA dilation
Hypertrophic cardiomyopathy management
beta blocker or nondihydropyridine CCB (facilitate increased LV volume), avoidance of dehydration and vasodilators (avoid decreased LV blood volume), ICD placement for increased risk for SCD, septal ablation, cardiac transplantation
Where in the heart does afib come from?
pulmonary veins
Where in the heart does atrial tachycardia come from? (single focus)
ectopic pacemaker
Where in the heart does AVNRT come from?
atrioventricular node
Where in the heart does atrial flutter come from?
cavotricuspid isthmus
Where in the heart does WPW come from?
accessory pathway (bundle of kent)
Most common arrhythmia causing syncope
v tach
Conditions that increase risk of atrial fibrillation, triggers of increased automaticity
hyperthyroidism, excessive alcohol use, increased sympathetic tone: acute illness (sepsis, PE, MI), cardiac surgery, sympathomimetic drugs (cocaine)
Conditions that increase the risk of a fib (precipitants of atrial dilation and/or conduction remodeling
advanced age, systemic HTN, mitral valve dysfunction, left ventricular failure, coronary artery disease and related factors (DM, smoking), obesity and obstructive sleep apnea, chronic hypoxic lung disease (COPD)
Patients to screen for fibromuscular dysplasia
Women under age 50 with 1 of the following:
severe or resistant HTN, onset of HTN before age 35, sudden increase in BP from baseline, increase in creatinine after starting ACEI or ARB and without significant effect on BP, systolic-diastolic epigastric bruit
Clinical presentation of fibromuscular dysplasia
resistant HYN from renal artery involvement, cerebrovascular FMD with symptoms of brain ischemia (amaurosis fugax, Horner's syndrome, transient ischemic attack, stroke), nonspecific symptoms (headache, pulsatile tinnitus, dizziness) from carotid or vertebral artery involvement, can also involve iliac, subclavian, and visceral arteries
Diagnosis and follow up for fibromuscular dysplasia
noninvasive testing preferred (CT angiography, duplex US), catheter-based digital subtraction arteriography for pts with inconclusive noninvasive testing, medically treated patients need follow-up BP and creatinine every 3-4 months and renal US every 6-12 months
HTN-related clues to renovascular disease
resistant HTN (uncontrolled despite 3-drug regimen), malignant HTN (with end-organ damage), onset of severe HTN (>180/120 mmHg) after age 55, severe HTN with diffuse atherosclerosis, recurrent flash pulmonary edema with severe HTN
Supportive evidence of renovascular disease
PE- asymmetric renal size (>1.5 cm), abdominal bruit
Lab results- unexplained rise in serum creatinine (>30%) after starting aCEIs or ARBs
Imaging results- unexplained atrophic kidney
ADPKD clinical presentation
most patients asymptomatic until age 30-40, flank pain, hematuria, HTN, palpable abdominal masses (usually bilateral), CKD
ADPKD extrarenal features
cerebral aneurysms, hepatic and pancreatic cysts, mitral valve prolapse, aortic regurgitation, colonic diverticulosis, ventral and inguinal hernias
ADPKD diagnosis
US showing multiple renal cysts
ADPKD management
aggressive control of risk factors for CV and CVD, ACEIs preferred for HTN, hemodialysis, renal transplant for ESRD