Cardiology Flashcards
The most common arrhythmias include
Premature atrial contractions (PACs), Premature ventricular contractions (PVCs)
Four categories of arrhythmias?
- Bradyarrhythmias
- Supraventricular tachyarrhythmias
- Pre-excitation Syndromes
- Ventricular Tachyarrhythmias
Etiology of palpitations?
- Arrhythmias
- Psychiatric causes: anxiety, panic disorders
- Drugs/medications: alcohol, caffeine, over-the-counter agents (e.g., digitalis, phenothiazine, theophylline, beta agonists), street drugs (e.g., cocaine)
- Nonarrhythmic cardiac causes: Atrial or ventricular septal defect, Cardiomyopathy, Congenital heart disease, Congestive heart failure, Mitral valve prolapse, Pacemaker-mediated tachycardia, Pericarditis, Valvular disease (e.g., aortic insufficiency, stenosis)
- Extracardiac causes: Anemia, Electrolyte imbalance, Fever, Hyperthyroidism, Hypoglycemia, Hypovolemia, Pheochromocytoma, Pulmonary disease, Vasovagal syndrome
What are the drugs/medications that can cause palpitations?
Prescription drugs (eg, antiarrhythmics, digoxin, beta-agonists, theophylline, and rate-limiting drugs); over-the-counter drugs (eg, cold and sinus drugs, dietary supplements containing stimulants), including alternative medicines; and illicit drugs (eg, cocaine, methamphetamines). Caffeine (eg, coffee, tea, numerous soft drinks and energy drinks)
What should be asked on history for palpitations?
History of present illness should cover the frequency and duration of palpitations and provoking or exacerbating factors (eg, emotional distress, activity, change in position, intake of caffeine or other drugs). Important associated symptoms include syncope, light-headedness, tunnel vision, dyspnea, and chest pain.
Examples of supraventricular arrhythmias?
- Sinus Tachycardia
- Premature beats: Atrial Premature Beat, Junctional Premature Beat
- Atrial Flutter
- Multi-focal atrial tachycardia
- Atrial Fibrillation
- Atrioventricular nodal reentrant tachycardia
Examples of ventricular tachyarrhythmias?
- Ventricular Premature Beat
- Ventricular arrhythmia
- Torsades de Pointes
- Ventricular Fibrillation
Physical exam for palpitations?
- General exam + vitals
- JVP + thyroid
- Cardiac exam: rate and regularity of the rhythm as well as any murmurs
What to consider when seeing paroxysm of high BP?
Pheochromocytoma
Investigations + labs for palpitations?
- ECG
- Holter monitoring for 24 to 48 hours may be appropriate in patients with daily palpitations
- Loop recorder - Patients with very infrequent symptoms that clinicians suspect represent a serious arrhythmia
Labs:
- CBC +lytes, Mg and Ca
- Troponin (chest pain)
- TSH (hyperthyroidism)
Patients with newly diagnosed arrhythmia, findings suggesting cardiac dysfunction or findings suggesting structural heart disease require ____?
Echocardiography and sometimes cardiac MRI
What is sinus bradycardia and marked sinus bradycardia?
Sinus rhythm < 60 beats/min, but marked sinus bradycardia if <50
Causes of sinus bradycardia
- Increased vagal tone or vagal stimulation; drugs (e.g. β-blockers, calcium channel blockers); ischemia/ infarction
- Age-related degeneration of SA node = Sick Sinus Syndrome - Often associated with sudden tachycardias arising from chaotic atrial rhythms -‘tachy–brady syndrome’
What is 1st degree AV conduction blocks and who are they found in?
1° = every P wave conducts, but >200ms delay between start P & QRS. Usually benign, found in healthy individuals
What is 2nd degree AV conduction blocks?
Only a proportion of P waves conducted by AV node (2 types)
Examples of bradyarrhythmias?
- Sinus Bradycardia
- AV Conduction Blocks
Examples of pre-excitation syndromes?
- Wolff-Parkinson-White Syndrome (WPW)
- AV Re-Entrant Tachycardia
What is Mobitz I = ‘Wenckebach’?
P-waves conduct with progressive increase in PR interval. Consequence of impaired conduction within the AV node
Hallmark of Wenckebach
Grouped beating
Causes of Mobitz I = ‘Wenckebach’
Can be sign of high vagal/parasympathetic tone (e.g. athletes), can be consequence of myocardial infarct
Treatment of Mobitz I = ‘Wenckebach’
Anti-cholinergic drug
What is Mobitz II?
No preceding PR prolongation, sudden blocked P, often, fixed ratio of P’s conduct: 2:1, 3:1, 4:1 etc.
Is Mobitz II caused due to conduction disturbance proximal or distal to the AV node?
Usually due to conduction disturbance below/distal the AV node (i.e. bundle of His)
Treatment of Mobitz II?
Treatment is usually required with a pacemaker.
Causes of Mobitz II?
Can be sign of high vagal /parasympathetic tone (e.g. athletes), can be consequence of myocardial infarct
What is sinus tachycardia?
Sinus P waves >100bpm w/ normal QRS.
What is 3rd degree AV conduction blocks?
3 ° = NO P waves conducted - need escape rhythm @ or below AVN
Totally dissociated P-waves / QRS’s, therefore no relationship between atrium and ventricle
Etiology of sinus tachycardia?
Occurs in normal subjects with increased sympathetic tone (e.g. exercise, anxiety, pain, pregnancy), alcohol use, caffeinated beverages, drugs (e.g. β-adrenergic agonists, anticholinergic drugs)
Treatment of sinus tachycardia?
Treat underlying disease; consider B-blocker if symptomatic, calcium channel blocker if B-blockers contraindicated
What are the two supraventricular tachyarrhythmias premature beats?
- Atrial Premature Beat
- Junctional Premature Beat
How do you treat the supraventricular tachyarrhythmias premature beats?
Simple reassurance is appropriate, sometimes a beta-blocker
What are atrial premature beats?
PACs are observed on the surface electrocardiogram as a P wave that occurs relatively early in the cardiac cycle (ie, prematurely before the next sinus P wave should occur) and has a different morphology and axis from the sinus P wave (inverted or biphasic).
What are junctional premature beats?
Ectopic supraventricular beat that originates in the vicinity of the AV node. P wave is usually not seen or an inverted P wave is seen and may be before or closely follow the QRS complex (referred to as a retrograde, or “traveling backward” P wave)
What is atrial flutter?
Rapid, regular atrial depolarization from a macro re-entry circuit within the atrium (most commonly right atrium)
The atria depolarize at a rate of 250 to 350 beats/minute (typically 300 beats/minute). Because the atrioventricular (AV) node cannot usually conduct at this rate, typically half of the impulses get through (2:1 block), resulting in a regular ventricular rate of 150 beats/minute.
ECG of atrial flutter?
Saw-tooth flutter waves
What can you do in atrial flutter with 2:1 block to make the waves more easily seen?
In atrial flutter with 2:1 block, carotid sinus massage (first check for bruits), Valsalva maneuver, or adenosine may decrease AV conduction and allow flutter waves to be more easily seen
Treatment of acute atrial flutter
- If unstable (e.g. hypotension, CHF, angina): electrical cardioversion
- If stable:
o 1. rate control: B-blocker, diltiazem, verapamil, or digoxin
o 2. chemical cardioversion: sotalol, amiodarone, type I antiarrhythmics, or electrical cardioversion - Anticoagulation guidelines same as for patients with AFib
Treatment of long-term AFib
AFib includes antiarrhythmics and radiofrequency (RF) ablation (success rate dependent on site of origin of atrial flutter)
What is multi-focal atrial tachycardia?
Irregular rhythm caused by presence of 3 or more atrial foci (may mimic AFib)
Multi-focal atrial tachycardia occurs more commonly in which patients?
Occurs more commonly in patients with COPD and hypoxemia
Treatment of multi-focal atrial tachycardia?
Calcium channel blockers may be used (e.g. diltiazem, verapamil), B-blockers may be contraindicated because of severe pulmonary disease
What causes the initiation of atrial fibrillation?
Single circuit re-entry and/or ectopic foci, mostly arising from the pulmonary veins, act as aberrant generators producing atrial tachycardia (350-600 bpm), which leads to multiple re-entry circuity (microreentry). Impulses conduct irregularly across the atrial myocardium to give rise to fibrillation
What causes the maintenance of atrial fibrillation?
Maintenance: The tachycardia causes atrial structural and electrophysiological remodelling changes that further promote AFib; the longer the patient is in AFib the more difficult it is to convert back to sinus rhythm
What is atrial fibrillation?
In atrial fibrillation, the atria do not contract, and the atrioventricular (AV) conduction system is bombarded with many electrical stimuli, causing inconsistent impulse transmission and an irregularly irregular ventricular rate, which is usually in the tachycardia rate range.
ECG of atrial fibrillation?
No organized P waves due to rapid atrial activity (350-600bpm) causing a chaotic fibrillatory baseline irregularly irregular ventricular response (typically 100-180 bpm), narrow QRS (unless aberrancy or previous BBB)
Treatment of atrial fibrillation?
RACE
- Rate control: Beta-blockers, Verapamil, Diltiazem, or Digoxin. In patients with heart failure: digoxin, amiodarone
- Anticoagulation: NOAC
- Cardioversion (electrical)
If AFib <48 h, can usually cardiovert without anticoagulation
If AFib >48 h, anticoagulate for 3 wk prior and 4 wk after cardioversion due to risk of unstable intra-atrial thrombus
If patient unstable (hypotensive, active angina due to tachycardia, uncontrolled heart failure) should cardiovert immediately
- Etiology
What usually initiates atrioventricular nodal reentrant tachycardia?
Usually initiated by a supraventricular or ventricular premature beat
What is atrioventricular nodal reentrant tachycardia?
Re-entrant circuit using dual pathways (fast conducting β-fibres and slow conducting α-fibres) within or near the AV node; often found in the absence of structural heart disease
Pathophysiology of atrioventricular nodal reentrant tachycardia?
Premature atrial beat might find fast pathway refractory - conduct down slow pathway - fires ventricle - now fast pathway recovered - retrograde conduction back up - fires atrium retrograde (hidden P’s) - repetitive ‘short circuit’
Etiology of Wolff-Parkinson-White Syndrome (WPW)?
Congenital defect
ECG features of WPW
- PR interval <120 msec
- delta wave: slurred upstroke of the QRS (the leads with the delta wave vary with site of bypass)
- widening of the QRS complex due to premature activation
- secondary ST segment and T wave changes
- tachyarrhythmias may occur - most often AVRT and AFib
What is Wolff-Parkinson-White Syndrome (WPW)?
- An accessory conduction tract (Bundle of Kent; can be in right or left atrium) abnormally allows early electrical activation of part of one ventricle
- Impulses travel at a greater conduction velocity across the Bundle of Kent thereby effectively ‘bypassing’ AV node
What initiates AV Re-Entrant Tachycardia?
Initiated by a premature atrial or ventricular complex
What is Orthodromic AVRT
Stimulus from a premature complex travels up the bypass tract (V to A) and down the AV node (A to V) with narrow QRS complex (no delta wave because stimulus travels through normal conduction system)
What is AV Re-Entrant Tachycardia?
Re-entrant loop via an accessory pathway
Treatment of AV Re-Entrant Tachycardia?
- Acute: similar to AVNRT except avoid long-acting AV nodal blockers (e.g. digoxin and verapamil)
- Long-term: for recurrent arrhythmias ablation of the bypass tract is recommended
What is Antidromic AVRT?
More rarely the stimulus goes up the AV node (V to A) and down the bypass tract (A to V); wide and abnormal QRS as ventricular activation is only via the bypass tract
Is antidromic AVRT or orthodromic AVRT more commonly associated with WPW syndrome?
Orthodromic AVRT comprises 95% of the reentrant tachycardias associated with WPW syndrome
What is ventricular premature beat?
Impulse travels from its ectopic site through the ventricles via slow cell-to-cell connections rather than through the normal rapidly conducting His– Purkinje system.
ECG of ventricular premature beat?
QRS width >120msec, no preceding P wave, bizarre QRS morphology
What is ventricular arrhythmia?
3 or more consecutive ectopic ventricular complexes. Often >160ms
What is ventricular flutter?
Ventricular flutter: if rate >200 bpm and complexes resemble a sinusoidal pattern
What is “sustained VT”?
“sustained VT” if it lasts longer than 30s
Favour Dx of VT
Left axis or right axis deviation, nonspecific intraventricular block pattern, monophasic or biphasic QRS in V1 with RBBB, QRS concordance in V1-V6
What is monomorphic VT?
Identical complexes with uniform morphology. Typically result from intraventricular re-entry circuit, may be idiopathic without any structural heart disease
Is monomorphic VT or polymorphic VT more common?
Monomorphic VT more common than polymorphic VT
What is polymorphic VT?
Complexes with constantly changing morphology, amplitude, and polarity
Treatment of ventricular arrhythmia?
- Sustained VT (>30 s) is an emergency requiring immediate treatment
- Hemodynamic compromise: electrical cardioversion
- No hemodynamic compromise: electrical cardioversion, amiodarone, type Ia agents (procainamide, quinidine)
Is monomorphic VT or polymorphic VT more frequently associated with hemodynamic instability
Polymorhpic VT is more frequently associated with hemodynamic instability due to faster rates (typically 200-250 bpm) vs. monomorphic VT
Treatment of Torsades de Pointes?
Treatment: IV magnesium, temporary pacing, isoproterenol and correcting the underlying cause of prolonged QT, electrical cardioversion if hemodynamic compromise
Sometimes an implanted defibrillator
Who is more predisposed to Torsades de Pointes?
Predisposition in patients with prolonged QT intervals
Causes of prolonged QT intervals
- Congenital long QT syndromes
- Drugs: e.g. class IA (quinidine), class III (sotalol), phenothiazines (TCAs), erythromycin, quinolones, antihistamines
- Electrolyte disturbances: hypokalemia, hypomagnesemia
- Nutritional deficiencies causing above electrolyte abnormalities
What is Torsades de Pointes?
A variant of polymorphic VT that occurs in patients with baseline QT prolongation – “twisting of the points”
ECG of ventricular fibrillation?
Ventricles look like a ‘bag of worms’
What is ventricular fibrillation?
Chaotic, random, colliding wave fronts of electrical activity CARDIAC ARREST
Treatment of ventricular fibrillation?
Only treatment = immediate electrical DEFIBRILLATION
Etiology for generalized edema?
- Increased capillary hydrostatic pressure
- Increased plasma volume due to renal sodium retention
• Heart failure
• Reduced systemic vascular resistance (e.g., cirrhosis)
• Primary renal sodium retention (e.g., renal disease, drugs)
• Pregnancy
• Premenstrual edema
- Decreased arteriolar resistance (e.g., calcium channel blockers, idiopathic) - Decreased oncotic pressure (hypoalbuminemia)
- Protein loss (e.g., nephrotic syndrome)
- Reduced albumin synthesis (e.g., liver disease/cirrhosis, malnutrition) - Increased capillary permeability (e.g., burns, inflammation)
- Increased interstitial oncotic pressure (e.g., myxedema)
Etiology for localized edema?
- Venous insufficiency (including postphlebitic syndrome)
- Deep venous thrombosis (DVT)
- Trauma
- Lymphedema (e.g., malignancy, primary)
- Infection (cellulitis/soft tissue/bone)
- Inflammation (e.g., ruptured Baker cyst, chronic dermatitis)
What should be asked on history for generalized/localized edema?
- SOB (PE, HF), sx of hypothyroidism (slow mental and physical activity, weakness, or fatigue
- Meds
- PMHx: HTN, diabetes, thyroid disease, COPD, sleep apnea
- Social: alcohol use, liver disease
Signs and symptoms of generalized/localized edema?
- Unilateral or bilateral
- Dependency of edema
- Timing of edema
Bilateral (or, generalized edema) suggests ______
Systemic
Unilateral edema suggests _____ or _____ or _____
Local compression
Obstruction of vein
Lymphatic drainage
Edema that improves with limb elevation and worsens with dependency typically occurs with _____ and volume expansion
Venous insufficiency
Edema that does not worsen with dependency is associated with _____ found in conditions such as malabsorption, liver failure, and nephrotic syndrome
Decreased plasma oncotic pressure
Acute onset of edema (< 72 hours) in a limb with or without pain and erythema may suggest?
Deep venous thrombosis, cellulitis, ruptured popliteal cyst, acute compartment syndrome due to trauma, or use of a recent new medication (especially calcium channel blockers)
Peripheral edema occurs frequently in _____, often involves lower extremities, and typically begins during second trimester and is resolved during third trimester
Normal pregnancy
Chronic accumulation of generalized edema (> 72 hours) suggests onset or worsening of chronic systemic conditions such as?
CHF, renal disease, or hepatic disease
Physical exam findings for generalized/localized edema?
- Vitals: fever (cellulitis, hypotension (HF or cirrhosis, hypertension (renal disease), JVP (elevated = heart failure, constrictive pericarditis)
- Skin: Warmth (cellulitis), Signs of chronic venous insufficiency, Signs of myxedema
- HEENT: Nonpitting periorbital edema - myxedema (due to hypothyroidism) or nephrotic syndrome
- Cardiac: Valvular heart disease or S3 gallop indicative of low ejection fraction
- Lungs: SOB - pulmonary edema and/or heart failure
- Abdomen: Signs of liver failure
- Extremities: Pitting edema - found in dependent areas such as lower extremities (or sacrum if at bed rest). Nonpitting edema – lymphedema, myxedema, lipedema
Signs of chronic venous insufficiency
Brawny, reddish coloration of skin, especially at medial ankle/calf. Progression to lipodermatosclerosis, characterized by fibrosis, hemosiderin deposition, and/or ulceration or erosions (especially over malleolus)
Signs of myxedema
Due to hypothyroidism - generalized dry, thick skin, yellow to orange skin discoloration over knees, elbows, palms, and soles
Signs of liver failure
Enlarged or shrunken liver, which may suggest scarring. Other signs suggestive of cirrhosis such as jaundice, spider angiomata, and caput medusae. Presence of ascites may suggest advanced liver disease, right heart failure, or constrictive pericarditis
Investigations for generalized edema to rule out cardiac, liver and renal causes?
- Blood chemistry panel including serum creatinine and liver function tests to assess kidney and liver function
- Serum albumin to assess for nephrotic syndrome, liver disease, protein-losing enteropathy and malnutrition states
- Plasma B-type natriuretic peptide (BNP)
- Urinalysis to look for albuminuria and other signs of renal disease
- Chest x-ray to assess for heart failure and chronic obstructive pulmonary disease (COPD)
- Electrocardiogram to detect ischemic heart disease or pericardial disease
- Thyroid-stimulating hormone levels to rule out hypothyroidism
Investigations for acute localized edema?
D-dimer, duplex US
Investigations for generalized edema to rule out chronic venous insufficiency?
Chronic venous insufficiency: duplex ultrasonography, ankle-brachial index to evaluate for arterial insufficiency
Investigations for chronic localized edema?
- If patient has history of cancer, pelvic surgery, or trauma, perform pelvic magnetic resonance venography to detect tumor or obstruction
- If clinical exam suggests lymphedema, confirm with lymphoscintigraphy and/or T1-weighted magnetic resonance lymphangiography
Management of heart failure?
DDDD – Diet low salt < 2,000 mg/day, fluid restriction (1.5 2 L/day), diuretics (furosemide 20-80 mg/d), vasodilator (ACEi - first line therapy in HF and hypertension. ARB if ACEi not tolerated), B Blockers, digitalis digoxin
Strategies to reduce primary sodium retention and extracellular fluid volume include
- Dietary sodium restriction to < 2,000 mg/day
- Diuretics
• Loop diuretics (such as furosemide)
• Spironolactone commonly used in patients with cirrhosis who have secondary hyperaldosteronism
Management of chronic venous insufficiency?
- Leg elevation and exercise
- Compression stockings
Management of cirrhosis?
- Rapid diuresis should be avoided (500 mL per day is suggested), especially in those with primarily ascites (without much peripheral edema), to reduce risk of hepatorenal syndrome and hemodynamic collapse
- Large-volume paracenteses may be used to reduce need for high dose diuretics in selected patients
Management of deep venous thrombosis (DVT)?
- Treat acute thrombotic events with anticoagulation therapy (unfractionated or low molecular weight heparin or warfarin [Coumadin]) to prevent progression of clot or development of postthrombotic syndrome
- Consider thrombolysis in select patients
Management of lympedema?
- Maintenance treatment is compression stockings at 30-40 mm Hg
- Surgical debulking or bypass procedures should be limited to severe, refractory cases
A loud S1 can be heard if
Mild to moderate mitral stenosis, tachycardia or high cardiac output, shortened PR interval
When can you hear S1
Occurs just after the beginning of systole and is predominantly due to mitral closure but may also include tricuspid closure components
How can clicks be differentiated from S1 and S2?
Clicks occur only during systole; they are distinguished from S1 and S2 by their higher pitch and briefer duration.
A soft S1 can be heard if
Severe MS , severe AS , mitral regurgitation, prolonged PR interval
What can cause early systole clicks?
Early systole – Congenital aortic stenosis or pulmonic stenosis are thought to result from abnormal ventricular wall tension
When can you hear S2
Occurs at the beginning of diastole, due to aortic and pulmonic valve closure
_____ normally precedes pulmonic valve closure (P2)
Aortic valve closure (A2)
What can cause a loud S2?
Pulmonary hypertension (loud P2) or systemic hypertension (loud A2)
What can cause a widely split S2?
RBBB, pulmonary stenosis (PS), pulmonary hypertension
What can cause a fixed split S2?
Atrial septal defect, RV failure
When can you hear an S3
It occurs during passive diastolic ventricular filling and usually indicates serious ventricular dysfunction in adults
Characteristics of S3 and what can it suggest?
Low-pitched, early diastolic sound, usually heard at apex (MON-TRE-al). Abnormal in most adults; suggest heart failure and/or volume overload.
S3 can be normal in ____ and ____.
May be normal in some children and pregnant woman
When can you hear an S4
Produced by augmented ventricular filling, caused by atrial contraction
What is a summation gallop?
A summation gallop occurs when S3 and S4 are present in a patient with tachycardia, which shortens diastole so that the 2 sounds merge. Loud S3 and S4 may be palpable at the apex when the patient is in the left lateral decubitus position
Characteristics of S4 and what can cause it?
Low pitched, late diastolic sound, usually heard at apex (tor-ON-to). Caused by atrial contraction into a non-compliant ventricle. Suggested ventricular hypertrophy. Almost always present in active myocardial ischemia or soon after myocardial infarction.
Definition of a murmur?
Murmurs are produced by blood flow turbulence and are more prolonged than heart sounds; they may be systolic, diastolic, or continuous. They are graded by intensity and are described by their location and when they occur within the cardiac cycle
Pathophysiology of mid systolic (ejection) murmurs?
Due to turbulent forward flow through narrowed or irregular valves or outflow tracts
Characteristics of mid systolic (ejection) murmurs?
Crescendo-diminuendo character that usually becomes louder and longer as flow becomes more obstructed. The greater the stenosis and turbulence, the longer the crescendo phase and the shorter the diminuendo phase.
Etiology of mid systolic (ejection) murmurs?
- Outflow obstruction (aortic sclerosis, aortic stenosis, coarctation of the aorta, hypertrophic cardiomyopathy, subvalvular stenosis, supravalvular stenosis)
- Dilation of ascending aorta (aneurysm of aorta, aortitis, atheroma )
- Dilation of pulmonary artery
- Increased blood flow across the aortic valve (aortic regurgitation, hyperkinetic states)
- Increased blood flow across the pulmonic valve (hyperkinetic states, left-to-right shunt due to atrial septal defect, ventricular septal defect)
- Pulmonic obstruction (infundibular stenosis, pulmonic stenosis, supravalvular pulmonary artery stenosis)
Etiology of mid-late systolic murmurs?
- Mitral valve prolapse
- Papillary muscle dysfunction
Etiology of pansystolic (regurgitant) murmurs
- Mitral regurgitation
- Tricuspid regurgitation
- Ventricular septal defect
Diastolic murmurs are always _____.
Abnormal
Etiology of early diastolic murmurs
- Aortic regurgitation
- Pulmonic regurgitation
Etiology of mid-diastolic murmurs
- Atrial ball-valve thrombi
- Increased blood flow across nonstenotic mitral valve (eg, mitral regurgitation, ventricular septal defect, patent ductus arteriosus, high-output states, complete heart block)
- Increased blood flow across nonstenotic tricuspid valve (eg, tricuspid regurgitation, atrial septal defect, anomalous pulmonary venous return)
- Left or right atrial tumors
- Mitral stenosis (eg, due to rheumatic fever, congenital stenosis, cor triatriatum)
- Tricuspid stenosis
Examples of continuous murmurs?
- Pericardial friction rub
- Patent ductus arteriosus - loudest in late systole obscuring obscuring S2, best heard in 2nd ICS LSB - sounds like ‘machinery’
- Venous hum - best heard in 1st or 2nd ICS
What is a pericardial friction rub?
A pericardial friction rub is caused by movement of inflammatory adhesions between visceral and parietal pericardial layers. It is a high-pitched or squeaking sound; it may be systolic, diastolic and systolic, or triphasic (when atrial contraction accentuates the diastolic component during late diastole).
What is the grading system for murmurs?
- Grade 1: very faint, heard only after ‘tuning in’, may not be heard in all positions
- Grade 2: quiet, but heard immediately after placing stethoscope on chest
- Grade 3: moderately loud without thrill
- Grade 4: loud, with palpable thrill
- Grade 5: very loud, with palpable thrill - may be heard when partly off the chest
- Grade 6: very loud, with palpable thrill - heard when completely off the chest
Causes of aortic stenosis?
- Degenerative calcification – wear and tear on normal valve
- Calcification of a congenital bicuspid aortic valve – fusion of two leaflets – most common cause under 65
- Rheumatic
Pathophysiology of aortic stenosis?
Increase LVP to drive blood across stenotic aortic valve results in hypertrophy (concentric) - increased LV wall thickness, LV cavity reduces (restores nearly normal afterload. However you have a price to pay - concentric LVH increases muscle stiffness, therefore LA pressures must increase to drive blood into LV and more oxygen supply. This increases the need of atrial kick. If they lose the atrial kick, they go into atrial fibrillation and require left atrium pressures more. End stage - increases LV wall tension = afterload - decreases LV systolic function (eventually) and thus the LV starts to enlarge (dilate) which increases the diastole LVP
Symptoms of aortic stenosis?
- Angina – Discomfort, usually squeezing, crushing, brought on by lack of O2 in cardiac tissue. Coronary Perfusion Pressure = Aortic P - LV P. In systole, LVP ~ AoP, therefore, it occurs in diastole. AS LVH - increasing the cardiac tissue to perfuse. The increase in LV diastolic pressure decreases the pressure gradient between aortic and LV
- Dyspnea – The increase in diastolic pressures can increase LA pressures, increasing pulmonary pressures = dyspnea
- Syncope – During exertion (decreased vascular resistance), the LV can’t increase CO because of the fixed stenotic aortic orifice with AS, no major increase output - decreases BP - decreases brain perfusion -syncope
Physical exam findings of aortic stenosis?
- LVH - apex usually still in normal position, when LV fails and dilates - diffuse, displaced apex
- Palpation (apical beat): Normal location, normal size, sustained apical beat >1/2 of systole
- Carotid pulse - ‘low and slow’ pulse (parvus et tardus)
- Peripheral pulses: Brachioradial delay
- JVP: Normal, A wave dominant in asymptomatic patient. Elevated only if decompensation of LV
- Aortic part of S2 (A2) may decrease intensity, or even disappear
- A2 comes later, even after P2 (pulmonic S2) = Paradoxical splitting of S2
- S4 - low-pitched sound made as increase atrial kick empties into stiff LV
Characteristics of aortic stenosis murmur?
Loudest RUSB, early systole, peaks later as AS progresses, holosystolic in severe AS. Crescendo-decrescendo, may radiate to clavicle or carotids
Investigation findings of aortic stenosis
- ECG – LVH
- Echo – examine leaflets
- Cardiac catheterization - can measure both LV and Ao pressures estimate severity of AS
Treatment of aortic stenosis
Only definitive treatment is valve replacement, can fix coronary disease at time of surgery
Causes of aortic regurgitation?
- Leaflet problems:
- Leaflets ↓ mobile = scarred, thickened = improper closing
- Bicuspid aortic valve - Leaflets fail to close / coapt well due to distorted cusps (predominates over AS)
- Leaflets normal mobility = perforated / eroded = leakage
- Leaflets ↑mobile / flail (partly detached) - Aortic annulus problems
- Support structures of leaflets abnormal = dilated aortic root - pulls leaflets open
- Hypertension
- Genetic defects - weak fibrous tissue in aorta
- Bicuspid aortic valve
Pathophysiology of acute aortic regurgitation?
- LV volume increases and therefore diastolic pressure which backs up into the LA – backs up into the lungs – pulmonary edema
- There’s no time for the LV to dilate
Pathophysiology of chronic aortic regurgitation?
- Similar to MR, LV undergoes compensatory adaptation, chronic dilation – eccentric hypertrophy with some increased thickness
- Slight increase in LV diastolic pressure because of compliant LV. Decrease in aortic diastolic pressure
- Increased flow ejected needs increased LV systolic P = pressure load
- Long-standing LV volume / pressure load = slow decreased LV systolic function
- 5 x ↑↑↑ stroke volume = ↑↑ aortic systolic pressures (Aorta cannot stretch that much* with each systole!). Therefore, widened pulse pressure.
Symptoms of aortic regurgitation?
- Long asymptomatic time course
- Gradual onset of symptoms:
- Palpitations - common sensation of forceful heart beat and increased pulse pressure
- Angina – LVH, increased LV size, increased O2 demand. Due to the decreased aortic diastolic pressure and increased LV diastolic pressures results in decreased perfusion pressure which reduces myocardial oxygen supply.
- Dyspnea
Physical exam findings of aortic regurgitation?
- Vital Signs: BP may see wide pulse pressure, Resp (AR – pulmonary edema – dyspnea)
- Hands: May have signs of infective endocarditis, cyanosis, quincke’s sign, water hammer pulse (increase pulse pressure (systolic – diastolic BP))
- Face: de Musset’s sign, cyanosis
- Carotid: Pulsus bisferiens, hyperkinetic pulse and large pulse pressure
- Palpation: Systolic apical thrill (late AR). Apical beat: May be displaced inferolaterally, sustained, diffuse
- S3
- S4 = sign of high end-diastolic LV pressure, atrial ‘kick’ emptying into LV
Characteristics of the systolic flow murmur in aortic regurgitation?
Systolic Flow Murmur: RUSB, early-mid systolic, high (blowing), crescendo-decrescendo
Investigation findings of aortic regurgitation?
- ECG – may show LVH
- CXR – enlarged LV
- Echo - can define leaflet and root anatomy
Characteristics of the Austin flint murmur in aortic regurgitation?
- AR may hit anterior mitral leaflet - partially close the MV - functional mitral stenosis = Austin-Flint murmur
- Apex S, mid diastolic, low rumbling
Treatment of aortic regurgitation?
- BP drugs - lower BP - especially vaso-dilating calcium channel blocker = Nifedipine
- No beta-blockers
- Diuretics - may help alleviate heart failure symptoms from excessive LV volume loading
- Surgery once symptoms start and Asymptomatic patients with progressive bad LV dilation or dysfunction
Characteristics of the aortic regurgitation murmur?
L parasternal; 3rd-4th intercostal space, early diastolic, high, decrescendo, along L sternal border
Etiology of mitral regurgitation?
- Leaflet / Chords abnormal = 1° mitral valve problem
- Reduced mobility – rheumatic mitral valve, leaflets scar and can’t close properly
- Normal mobility – perforation almost always due to endocarditis
Increased mobility: Prolapse of leaflet = MVP, Flail leaflet due to rupture of chord - LV distorted - pulls mitral valve apart = 2° mitral regurgitation
- Ischemic papillary muscle - Papillary muscle fails to ‘pull’ on chords
- Ischemic scarred LV – scarred papillary muscle pulls leaflet open
- LV dilation – increase/dilates annulus
What is prolapse of leaflet (MVP)?
- Fibrous tissue (collagen) of the leaflets are replaced with myxomatous soft tissue
- Could be due to a genetic connective tissue disease
- Usually no symptoms, benign, could have vague chest pains, palpitations
What extra heart sound could an MVP have?
Produces a mid-systolic click:
- If volume in the LV decreases – click and murmur move closer to S1
- If volume in the LV increases – click and murmur move further from S1
Pathophysiology of acute mitral regurgitation?
- No time for LA or LV to dilate (still ‘stiff’)
- Since the LAP will increase dramatically, severe pulmonary edema and poor forward output
- Compensate - Since LA filled by MR and pulmonary veins, increase LV filling in diastole. LV accommodates by stretching its myofibers to increase stroke volume. However, the LV stiffness limits amount of increase in volume.
Pathophysiology of chronic mitral regurgitation?
- LA & LV dilate (decreases stiff) without increase pressure
- LV - accepts increases LV volume with no increase in diastolic LVP
- Compensate - Increase wall thickness – lengthening and thickening of fibers – eccentric hypertrophy
- Worsens with increase aortic BP, and aortic stenosis
Symptoms of mitral regurgitation?
- Long asymptomatic time course
- Increased back pressure will result in left heart failure
- Long-standing ↑↑LA back-pressure – atrial fibrillation
- Late – right heart failure – peripheral edema + ascites
Physical exam findings of mitral regurgitation?
- Carotid pulse: Severe MR - Hyperkinetic (but NO wide pulse pressure; normal diastolic P
- Severe MR - LV apex enlarged, displaced, diffuse, hyperdynamic
- Palpable MR ‘thrill’
- S1 variable, wide S2 split (A2 closes early)
- Chronic decompensated MR: L S3
- Acute MR: L S4
Characteristics of the acute MR murmur?
Apex, early-mid systolic, high-pitched blowing, decrescendo, radiates to L axilla
Characteristics of the chronic MR murmur?
Apex, holosystolic, high-pitched blowing, radiates to L axilla, isometric hand grip ↑intenisty
Investigation findings with MR?
- ECG – enlarged LV, LA
- CXR
Treatment of MR?
- Diuretics, could use rate-slowing drugs if a fib
- Timing of surgery – LV dysfunction – measure Ejection fraction (at rest or with exercise) or End-systolic volume. Once symptoms start or progressive LV dilation
What typically causes mitral stenosis?
Rheumatic fever
Pathophysiology of mitral stenosis?
Mitral valve is tight – increases LA pressure creates a backflow all the way to the systemic tissues
Symptoms of mitral stenosis?
- Dyspnea (especially during exercise), orthopnea, PND
- Hemoptysis (rupture of bronchial veins)
- Fatigue (pressure backs up into the RV which will dilate and fail causing insufficient forward input)
- Arrhythmias - increasing LA pressure – increases LA enlargement which increases likelihood of short circuits – fibrillation. The atrial doesn’t contract nicely (loss of atrial kick) and thus you need higher pressures to fill the LV. Creates sluggish flow resulting in blood clots – emboli (20%/yr in MS) – need to put on anticoagulant. almost always Afib - ↑↑HR (AV node filters out ~ 2/3rds of atrial signals bombarding it) - need HR control drugs
Physical exam finding of mitral stenosis?
- S1 will sound louder – thickened leaflets, however in late stage disease when rigid S1 intensity gradually decrease
- Opening snap – sound from MV opening, also disappears as valve becomes rigid. If it opens soon after S2, severity of MS increased
- RV overload - enlarged, hypertrophied RV causes palpable lift underneath sternum = ‘parasternal lift’ or ‘RV heave’
- Dilated RV = stretches tricuspid annulus leaky tricuspid valve = tricuspid regurgitation
Characteristics of the MS murmur?
Diastolic murmur – diastolic rumble – turbulent flow across the valve. the worse the MS, the longer into diastole the murmur lasts (longer time for pressure gradient to disappear). Presystolic accentuation
Investigation findings of mitral stenosis?
- ECG – enlarged LA, RV hypertrophy
- CX – calcified MV, Kerley B lines
- Echo – see valve in action
Treatment of mitral stenosis?
- Diuretics, rate-slowing drugs, beta blockers, anticoagulant
- Balloon valvuloplasty – cracks open the fused MV
- Valve replacement – tissue or metal valve – clot risk (warfarin)
Etiology of anterior mediastinal masses?
“Four Ts” (Thymoma, Thyroid enlargement (goitre), Teratoma, Tumours (lymphoma, parathyroid, esophageal, angiomatous))
Etiology of middle mediastinal masses?
Pericardial cyst, bronchogenic cyst/tumour, lymphoma, lymph node enlargement (metastatic disease, SCLC), aortic aneurysm
Etiology of posterior mediastinal masses?
Neurogenic tumours, meningocele, enteric cysts, lymphoma, diaphragmatic hernias, esophageal tumour, aortic aneurysm. Mostly home of tumors of neural origin
Most frequently encountered anterior mediastinal mass?
Substernal thyroids
Study of first choice for thyroid masses?
Radioisotope thyroid scans are the study of first choice
The most common cause of a mediastinal mass overall?
Lymphadenopathy, whether from lymphoma, metastatic carcinoma, sarcoid, or tuberculosis
Mediastinal lymphadenopathy in Hodgkin lymphoma is usually _____ and _____
Bilateral and asymmetric
Most common primary neoplasm of the anterosuperior mediastinum in a patient over 40
Thymoma
Thymomas are associated with _____ about 35% of the time they are present
Myasthenia gravis
Young patient with uniform enlargement of the thymus compared to prior imaging. After chemo, radiation, steroids, stress (burns, injuries)
Thymic Hyperplasia
Mature teratomas have been associated with
Klinefelter syndrome
Signs and symptoms of mediastinal masses?
- 50% asymptomatic (mainly benign); when symptomatic, 50% are malignant
- Chest pain, cough, SOB, dyspnea, recurrent respiratory infections
- Hoarseness, dysphagia, Horner’s syndrome (ptosis, miosis, anhydrosis), facial/upper extremity edema (SVC compression)
- Paraneoplastic syndromes (e.g.myasthenia gravis [thymomas])
- Gynecomastia (teratoma), hypercalcemia sx (parathyroid adenoma), HTN (thyroid disorder)
Investigations for mediastinal masses?
- CXR (compare to previous)
- CT with contrast (anatomic location, density, relation to mediastinal vascular structures)
- MRI: specifically indicated in the evaluation of neurogenic tumours
- Radionuclide scanning: 131I (for thyroid), gallium (for lymphoma)
- Biochemical studies: thyroid function, serum calcium, phosphate, PTH, AFP, B-hCG
- Biopsy (mediastinoscopy, percutaneous needle aspiration)
Management of mediastinal masses?
- Excision - symptomatic benign mass that is enlarging or a mass with concerns for malignancy
- Resect bronchogenic cysts and localized neurogenic tumours via minimally invasive video assisted procedures
- Exploration via sternotomy or thoracotomy
- ± post-operative radiotherapy/chemotherapy if malignant
What is the DDx for chest pain?
Rifle approach – a bullet goes through all these layers:
- Skin - Bites, burns, Herpes, zoster
- Sub Q – cellulitis, abscess
- MSK - Sprains or strains, fractures, Costochondritis
- Pleura: Pneumothorax, Pneumonia, Pleural effusion, Pulmonary cancer, Pleurisy, PE
- Pericardium - Pericarditis
- Heart - MI, Myocarditis, stable angina, valvular heart disease
- Esophagus - GERD, esophagus spasm, mallory-weiss, esophagitis
- Trachea - perforation, tracheitis
- Aorta - Dissection, aneurysm
- Psych - Panic attack
What would be the signs/symptoms that would suggest pneumothorax as the cause of chest pain?
Sudden onset, sharp pleuritic pain, unilateral hyperresonance, decreased breath sounds
What would be the signs/symptoms suggestive of pericarditis?
Increased w/ respiration, decreased w/ sitting forward or sitting up +/- pericardial friction rub. Also radiates to trapezius
What would be the signs/symptoms suggestive of pleural effusion as the cause of chest pain?
Sudden onset pleuritic pain, increased RR and HR, decreased S2O2, ECG changes
What is the Diamond Forrester Classification for MI?
- Substernal Pressure 2. Exertional Chest Pain 3. Chest Pain relieved with rest (nitroglycerin).
- Typical Angina: 3 criteria from above
- Atypical Angina: 2 criteria from above
- Non-Anginal Chest Pain: 1 criteria from above
What would be the signs/symptoms suggestive of pneumonia as a cause of chest pain?
Pleuritic, dyspnea, fever, cough, sputum, increased RR, crackles, CXR infiltrate
If you suspect GI cause of chest pain, what should you give?
GI cocktail (Lidocaine)
What are the signs/symptoms of GERD as a cause of chest pain?
Substernal burning, acid taste in mouth, water brash. Increased with meals and recumbency, decreased by antacids
What are the signs/symptoms that would suggest aorta dissection as a cause of chest pain?
Sudden severe tearing pain +/- asymmetric BP, neurological symptoms (cerebral hypoperfusion or occlusion of carotid, vertebral, or spinal arteries)
What initial investigations should you order in a person presenting with chest pain?
- 12-lead ECG
- CXR, CT
- Troponin – At baseline and 3-6 h after symptom onset, repeat 6h later if clinical or ECG changes
- D-dimer (PE)
- BNP (acute heart failure)
- CBC (infections)
What are the common findings on ECG for PE?
The most common finding is sinus tachycardia. The classically described finding “S1Q3T3” (ie, prominent S wave in lead I, Q wave in lead III, and inverted T wave in lead III).
What should be on your focused history with a person presenting with chest pain?
- OPQRST
- Associated symptoms
- Pain quality and location
- Risk Factors (ACS, PE, pneumothroax)
What should be on your targeted physical exam in a person with chest pain?
- VS - BP in both arms (aortic dissection)
- Cardiac - Gallops (rapid rate of ventricular filling), murmurs (aortic insufficiency – aortic dissection), rubs (pericarditis), signs of vascular disease (carotid/femoral bruits, decreased pulses)
- Abdomen exam - epigastric tenderness (GI)
- MSK exam - Chest wall for reproducibility (costochondritis)
- Pulmonary - unilateral decreased breath sounds (pneumothorax), crackles (left ventricular dysfunction - ACS)
What are some risk factors for DVT and subsequent PE?
Recent history of prolonged immobilization (eg, long distance travel), surgery (particularly an orthopedic procedure of the lower extremity lasting more than 30 minutes), central venous catheterization, or trauma.
What are some risk factors for ACS?
Male sex, age over 55 years, family history of coronary artery disease, diabetes mellitus, hypercholesterolemia, hypertension, and tobacco use.
Compare the onset of pain between stable and unstable angina
- Stable angina, discomfort occurs only when activity creates an oxygen demand that outstrips supply limitations imposed by a fixed atherosclerotic lesion. This occurs at relatively predictable points and changes slowly over time.
- Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest.
What are the ECG findings suggestive of tamponade?
Low voltage and electrical alternans
What are the signs/symptoms of esophagus spasm as the cause of chest pain?
Intense substernal pain. Increased by swallowing, decreased by NTG.
What are the signs/symptoms that would suggest costochondritis as a cause of chest pain?
Localized sharp pain, increased w/ movement. Reproduced with palpation
Most common cause of chest pain in ER
Costochondritis
The discomfort of ____ is classically positional: worse when lying supine and relieved somewhat when leaning forward. It may also worsen with deep inspiration
Pericarditis
Coronary Disease = __ reduction in lumen diameter
> 70%
Define angina?
Discomfort/chest pain associated with disturbance in myocardial function but without necrosis. 70% stenosis – inadequate coronary vasodilation reserve if over-exert – myocardial ischemia – sensation of angina
What is included in the framingham risk score and what does it predict?
Predicts 10yr risk of non-fatal MI or coronary death (age, FHx, gender, smoking, HDL level, systolic BP, DM)
Findings on resting ECG for stable Coronary Artery Disease
No critical blockage during rest and therefore normal ECG
Finding on stress ECG for stable Coronary Artery Disease
Exercise causing stress and perhaps ischemia of myocardium (usually sub-endocardium) ST depression
- If seen on BOTH stress & rest = scar = infarct
- If defect with stress, OK rest = reversible = ischemia
Indications for invasive testing (Angiography)?
- High risk EST (Exercise Stress Test)
- High clinical suspicion with equivocal non-invasive testing
- Unresponsive to maximal medical therapy
- Heart failure with ischemia
- Multiple ischemic areas on myocardial perfusion scanning
- Gold standard for diagnosing where / how bad coronary stenoses are + Identifies patients who may benefit from revascularization
Stable CAD treatment
- Coronary balloons/stents using PCI
- Balloon angioplasty
- Stents: Bare metal Stents, Drug-eluting stents - Anti-proliferative drug inside stent - prevents intimal scarring. Cuts re-stenosis rate > 50% compared to similar bare metal stent. However, it impairs endothelial healing, or ‘chew away’ at underlying vessel wall tissue and increases risk of clots
- CABG: Long patency with IMA, saphenous vein not as good patency
Stable angina treatment
BB (best option), CaCB, nitrates
MI prevention, when to use antiplatelets?
- Stable CAD aspirin 81mg forever – secondary prevention
- Unstable CAD add P2Y12 receptor antagonist (eg Clopidogrel, Ticagrelor) for 1 year if not longer
- Bare metal stent – ASA + Clopidogrel for 1 month then ASA forever
- Drug eluting stents - ASA + Clopidogrel for at least 3 months, (at least 12-36 months in ACS) then ASA forever.
- Never stop the dual therapy!
MI prevention?
- Antiplatelets
- ACEi
- B Blockers: First line chronic therapy for acute coronary syndrome and LV dysfunction, decrease the rates of recurrent infarction
- CaCB: slow heart rate, decrease BP, and dilate coronary arteries
- Blood Pressure Control: <140/90 mm Hg or <130/80 mm Hg (perhaps lower) if patient has diabetes or chronic kidney disease
- Cholesterol Management: Consider statin therapy for all CAD patients–high potency, even if low LDL. Target: LDL-C ≤ 2.0 mM (or at least 50% decrease in LDL)
- Diabetes Management: NO TZD medications (pioglitazone) s/e increases Na reabsorption
- Diet
- Exercise
- End Pain: Discontinue all COX-2 inhibitors and NSAIDs, EXCEPT aspirin or Acetaminophen
- Vaccines: Annual influenza + pneumococcal polysaccharide vaccinations (prevent complications
When to use ACEi as an MI prevention?
Heart failure, or LVEF ≤ 40%, large myocardial infarcts, diabetes, severe left ventricular hypertrophy
Pathophysiology of acute coronary syndrome?
If plaque ruptures–>blood meets cholesterol–> thombrogenic stimuli–> clots–> ischemia. Includes STEMI, NSTEMI and unstable angina
Clinical presentation of unstable coronary artery disease
- Onset – typically gradual in onset
- Provocation and palliation – Ischemic pain is generally provoked by an activity, such as exercise, which increases cardiac oxygen demand. Ischemic pain does not change with respiration or position. It may or may not respond to nitroglycerin and, if there is improvement, this may only be temporary.
- Quality – Ischemic pain is often characterized more as a discomfort than pain
- Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw).
- Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. In comparison, patients with an acute coronary syndrome (ACS) may have chest pain at rest, and the duration is variable but generally lasts longer than 30 minutes.
- Associated symptoms: The most common is shortness of breath, which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction. Other symptoms may include belching, nausea, indigestion, vomiting, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue.
Define unstable angina?
When the chest pain occurs at rest, is new, is increasing in frequency, or when its onset is triggered with a lower level of exertion. Unstable angina is caused by an unstable plaque that has ruptured and caused a non-occlusive thrombus
- NO myocardial damage ie. necrosis (no rise in blood enzymes)
What is variant angina?
Non-exertional, often early morning angina, from spontaneous severe coronary vasospasm - major drop in O2 supply. Classically without major coronary plaques. Treatment = very high dose anti-spasm drugs
Define NSTEMI
Myocardial Infarct = severe enough mismatch in myocardial blood / O2 supply relative to demands - myocardial necrosis = myocardial death. No ST elevation - usually NOT transmural ischemia
Define STEMI
Myocardial Infarct = severe enough mismatch in myocardial blood / O2 supply relative to demands - myocardial necrosis = myocardial death. ST elevation - usually transmural ischemia. Usually 100% blockage for 100% of time! After 6 hrs you’ll get full thickness necrosis
AMI initial management (orders)?
- Admit: to CCU
- Diagnosis: acute myocardial infarction
- Diet: cardiac diet (<2g Na/d)
- Activity: bed rest (with bathroom privileges)
- Vitals: CCU vitals
- Ins/Outs: fluid restriction if CHF
- IV: TKVO DK5 or SL IV
- Investigations
- Drugs (MONA + DVT Prophylaxis + Other): morphine 4mg IV q4h PRN + oxygen by nasal prongs (2-4L) to bring saturation >92% + nitroglycern 0.4mg SL q5min x 3 + ASA 325mg chewed STAT then 81-325mg PO OD + LMWH IV to keep PTT at 1.5-2x normal + metoprolol or atenolol 5mg IV q5min x 3 doses (not in HR < 50, SBP < 90, CHF, severe asthma/COPD, 2nd or 3rd degree heart block
Initial investigations for AMI?
Continuous cardiac monitoring + ECG qdaily and PRN with chest pain + CXR + Cardiac Enzymes (CK + Troponin + CK-MB q8h x 3) + Fasting Lipids (total cholesterol, LDL-C, HDL-C, TG) + Fasting Glucose + (CBCd + Urea + Creatinine + INR/PTT) qDaily + Echocardiogram + Exercise Tolerance Test or MIBI +/- Angio)
Acute management of STEMI
- Select reperfusion strategy: Primary PCI for pt <12 hours chest pain, especially for high risk patients with cardiogenic shock, heart failure, late presentation, or contraindications to fibrinolysis.
- Activate cardiac catheterization team as indicated. For patients with symptoms of >12 hours, fibrinolytic therapy is NOT indicated, but emergent PCI may be considered, particularly for patients with evidence of ongoing ischemia or those at high risk of death.
- Treat with fibrinolysis within 30 min of first medical contact, symptoms <12 hours, and no contraindications – use if delay to cath >90min of ECG diagnosis
- Give antiplatelet (clopidogrel 300mg PO x1 dose, or 75mg if age >75) and anticoagulant (ASA 160) therapy to all patients
- Morphine for pain control
Absolute Contraindications of fibrinolysis
Absolute Contraindications of fibrinolysis – prior intracranial hemorrhage, recent stroke or head trauma <3months, head trauma, active internal bleeding, aortic dissection
Acute management of unstable angina or non-STEMI?
- Give antiplatelet and anticoagulant therapy to all patients (aspirin)
- Enoxaparin 1mg/kg SC BID for 48 hours
- BB, nitrates (if current pain), statins, heparin
- Cardiac cath and revascularization
Post-MI medications?
ABCN: ASA (81mg PO OD) + ACEi (Ramipril 2.5-5mg PO OD) + Beta Blocker (Carvedalol 6.25mg PO BID) + Cholesterol Drug (Lipitor 10mg PO OD) + Clopidogrel (Plavix 75mg PO OD) + Nitroglycerin 0.3mg SL q5min x 3 PRN
Definition of cardiac arrest?
Cardiac arrest is the cessation of cardiac mechanical activity resulting in the absence of circulating blood flow. Cardiac arrest stops blood from flowing to vital organs, depriving them of oxygen, and, if left untreated, results in death
Etiology categories of cardiac arrest?
- Coronary artery disease
- Cardiac conduction abnormalities
- Myocardial abnormalities
- Non-cardiac causes (e.g., pulmonary embolus)
Ddx of coronary artery disease for cardiac arrest
- Ischemia secondary to atherosclerotic heart disease
- Anomalous coronary circulation
- Coronary vasospasm
- Ischemic cardiomyopathy
Ddx of cardiac conduction abnormalities for cardiac arrest
- Congenital long QT syndrome
- Acquired long QT syndrome
- congenital short QT syndrome
- Brugada syndrome
- catecholaminergic polymorphic ventricular tachycardia (CPVT)
- Wolff-Parkinson White (WPW) syndrome
- idiopathic ventricular tachycardia
Ddx of myocardial abnormalities for cardiac arrest
- dilated cardiomyopathy
- hypertrophic cardiomyopathy
- takotsubo cardiomyopathy
- infiltrative, such as cardiac sarcoidosis, amyloid heart disease
- arrhythmogenic right ventricular cardiomyopathy
- left ventricular noncompaction
- myocarditis
Ddx of non-cardiac causes of cardiac arrest
- Metabolic imbalance causes include: hyperkalemia, hypokalemia, hypocalcemia, hypomagnesemia, severe acidosis
- Neurological causes include: intracerebral hemorrhage, epilepsy
- Massive pulmonary embolism (PE)
- Opioid overdose
- Other noncardiac causes include: digoxin, antiarrhythmic drugs, antidepressants, drugs prolonging QT interval
Mechanism for cardiac arrest with cardiac etiology
- Trigger catalyzes an anatomic or electrophysiological substrate (can be genetic or acquired) and results in ventricular fibrillation or ventricular tachycardia that degenerates to ventricular fibrillation
- Ventricular fibrillation results in hemodynamic collapse, cessation of cardiac mechanical activity, and loss of cerebral perfusion
Asystole or pulseless electrical activity following acute event (PE)
Physical exam for cardiac arrest?
- General physical: unresponsiveness and absence of blood pressure, pulse, and/or breathing
- Skin: pallor, mottling, or cyanosis
- HEENT: look for vomitus or blood, dilated and unresponsive pupils
- Cardiac: absent heartbeat
- Lungs: absent or agonal breathing
- Extremities: absent pulses
History asked for cardiac arrest?
o Obtain detailed history from both patients (post arrest history) and any witnesses as patient often has retrograde amnesia and unable to recall event
o Ventricular fibrillation most common initial rhythm when cardiac disease is cause of arrest
o Ask about possible exertion trigger event, if applicable, including less common inherited conditions that are triggered by exertion
o Medication history
o Past medical history (PMH): chest pain, syncope, chronic ischemic heart disease, myocardial infarction, hypertrophic cardiomyopathy, ventricular tachycardia, long QT syndrome
o Family history (FH): sudden cardiac arrest or death
Investigations for cardiac arrest?
- 12-lead electrocardiogram (ECG)
- echocardiography
- coronary angiography in patients with ischemic electrocardiogram (ST-elevation or ST-segment depression with T-wave inversion), history of chest pain, or known coronary artery disease risk factors
- Stress testing
- Cardiac magnetic resonance imaging
- Blood tests: obtain blood gases (VBG), pH, and electrolytes
- Measure markers of cardiac injury (cardiac troponins) and screen for toxins and/or drugs
What are the steps to BLS?
Step 1: Assess scene safety.
Step 2: Assess patient responsiveness -shake shoulders
Step 3: Call for help – 911, retreieve AED
Step 4: Assess for signs of life - Check pulse and respiration simultaneously - Head-tilt/chin-lift maneuver, jaw-thrust maneuver. Start CPR immediately if any of the following are identified: No palpable pulse, Apnea, Agonal respirations
Step 5: Perform CPR and defibrillate as needed.
- Single-rescuer CPR
- Perform 30 chest compressions followed by two rescue breaths (30:2) per cycle
- Compression-only CPR is reasonable if mouth-to-mouthbreathing is deemed too risky and BMV equipment is unavailable.
AED
When should cardiac magnetic resonance imaging for cardiac arrest be performed?
Consider advanced imaging in patients with nondiagnostic electrocardiogram, coronary angiography, and echocardiography if suspect any
- arrhythmogenic right ventricular dysplasia
- cardiac sarcoidosis
- myocarditis
- myocardial injury from coronary spasm
What are the steps to ACLS?
- Priority 1: CPR: Perform CPR for at least 2 minutes before the first rhythm check. Do not interrupt CPR, except for rhythm and pulse checks
- Priority 2: Rhythm and pulse check.
- If either of the following shockable rhythms is identified, proceed first to “Priority 3”: Ventricular fibrillation, Ventricular tachycardia
- If either of the following nonshockable rhythms is identified, proceed directly to “Priority 4”: PEA, Asystole - Priority 3: Defibrillation (shockable rhythms only): Deliver shock as soon as a shockable rhythm is recognized (do not defibrillate nonshockable rhythms).
- Priority 4: Resuscitation Medications
- Priority 5: Hs and Ts
- Treat Hs and Ts
- IV fluids
- Rewarming
- Medications: e.g., calcium chloride,
- Thrombolytics
Resuscitation medications for nonshockable rhythms?
Epinephrine 1 mg IV/IO as soon as possible; repeat every 3-5 minutes as needed
Resuscitation medications for shockable rhythms?
- After 2nd cycle of defibrillation: epinephrine 1 mg IV/IO
- After 3rd unsuccessful cycle of defibrillation
- Amiodarone 300 mg IV/IO; then 150 mg IV/IO once after 3-5 minutes
OR - lidocaine 1-1.5 mg/kg IV/IO once, then 0.5-0.75 mg/kg IV/IO once after 3-5 minutes
- Repeat epinephrine every 3-5 minutes as needed
What are the reversible causes of cardiac arrest?
Hs
- Hypovolemia
- Hypoxia
- Hypokalemia
- Hyperkalemia
- Hydrogen ion (acidosis)
- Hypothermia
Ts
- Tension pneumothorax
- Tamponade (cardiac)
- Toxins
- Thrombosis (pulmonary embolism)
- Thrombosis (myocardial infarction)
