Arrhythmias Flashcards
What is the pathophysiology of an arrhythmia
In disease (e.g. post-MI ventricular ischemia) cells in the myocardium outside the conduction system may inappropriately acquire the property of automaticity and contribute to abnormal depolarization. If these ectopic generators depolarize at a rate greater than the SA node, they assume pacemaking control and become the source of abnormal rhythm. Automaticity can be influenced by:
◆ neurohormonal tone (sympathetic and parasympathetic stimulation)
◆ abnormal metabolic conditions (hypoxia, acidosis, hypothermia)
◆ electrolyte abnormalities
◆ drugs (e.g. digitalis)
◆ local ischemia/infarction
◆ other cardiac pathology
■ this mechanism is responsible for the accelerated idioventricular rhythm and ventricular tachycardia that often occurs 24-72 h post MI
What are the normal pacemaking cells of the heart
SA node, AV node, and ventricular conduction system
What is a sinus arrhythmia
Normal P waves, with variation of the P-P interval by >120 msec due to varying rate of SA node
What are types of sinus arrhythmia
Respiratory SA
• Seen more often in young adults (<30 yr old)
• Normal, results from changes in autonomic tone during respiratory cycle
• Rate increases with inspiration, slows with expiration
Non-Respiratory SA
• Seen more often in the elderly
• Can occur in the normal heart; if marked may be due to sinus node dysfunction (e.g. in heart disease, or after digitalis toxicity)
• Usually does not require treatment
What is early afterdepolarization
- Early Afterdepolarizations
■ occur in the context of action potential prolongation
■ consequence of the membrane potential becoming more positive during repolarization (e.g. not returning to baseline)
■ result in self-maintaining depolarizing oscillations of action potential, generating a tachyarrhythmia (e.g new baseline voltage is greater than threshold, which automatically triggers a new action potential after the refractory period ends)
■ basis for the degeneration of QT prolongation, either congenital or acquired, into Torsades de Pointe
What are delayed afterdepolarizations
- Delayed Afterdepolarizations
■ occur after the action potential has fully repolarized, but before the next usual action potential, thus called a delayed afterdepolarization
■ commonly occurs in situations of high intracellular calcium (e.g. digitalis intoxication, ischemia) or during enhanced catecholamine stimulation (e.g. “twitchy” pacemaker cells)
What are re-entry circuits and how do they form
the presence of self-sustaining re-entry circuit causes rapid repeated depolarizations in a region of myocardium
◆ e.g. myocardium that is infarcted/ischemic will consist of non-excitable and partially excitable zones which will promote the formation of re-entry circuits
What is conduction block and how does it form
■ ischemia, fibrosis, trauma, and drugs can cause transient, permanent, unidirectional or bidirectional block
■ most common cause of block is due to refractory myocardium (cardiomyocytes are in refractory period or zone of myocardium unexcitable due to fibrosis)
■ if block occurs along the specialized conduction system distal zones of the conduction system can assume pacemaking control
■ conduction block can lead to bradycardia or tachycardia when impaired conduction leads to re entry phenomenon
What are bypass tracts in the heart
normally the only conducting tract from the atria to the ventricles is the AV node into the HisPurkinje system
■ congenital/acquired accessory conducting tracts bypass the AV node and facilitate premature ventricular activation before normal AV node conduction
Management for sinus bradycardia
Atropine
Pacing for sick sinus syndrome
First degree AV block definition
Prolonged PR interval (>200 msec)
Frequently found among otherwise healthy adults
Treatment for first degree AV block
No treatment required
2nd degree AV block Mobitz 1 definition
A gradual prolongation of the PR interval precedes the failure of conduction of a P wave (Wenckebach phenomenon)
2nd degree AV block in AV node (proximal) triggers
(usually reversible): increased vagal tone (e.g. following surgery), RCA-mediated ischemia
2nd degree AV block Mobitz 1 usual location
AV node
2nd degree AV block Mobitz 2 definition
The PR interval is constant; there is an abrupt failure of conduction of a P wave
2nd degree AV block Mobitz 2 location
AV block is usually distal to the AV node (i.e. bundle of His)
2nd degree AV block Mobitz 2 increases your risk of what
increased risk of high grade or 3rd degree AV block
3rd degree AV block definition
Complete failure of conduction of the supraventricular impulses to the ventricles; ventricular depolarization initiated by an escape pacemaker distal to the block
What is the pattern of intervals on ECG seen with 3rd degree AV block
Wide or narrow QRS, P-P and R-R intervals are constant, variable PR intervals; no relationship between P waves and QRS complexes (P waves “marching through”)
Presentation for SVT and pre-excitation syndromes
Palpitations, dizziness, dyspnea, chest discomfort, presyncope/syncope
What is a potential consequence of untreated tachycardias
untreated tachycardias can cause cardiomyopathy (rare, potentially reversible with treatment of SVTs)
Where do superventricular tacchyarrhthmias originate
tachyarrhythmias that originate in the atria or AV junction
Supraventricular tacchyarrhythmia definition
this term is used when a more specific diagnosis of mechanism and site of origin cannot be made
What is seen on ECG with supraventriular tachyarrhythmia
characterized by narrow QRS, unless there is pre-existing bundle branch block or aberrant ventricular conduction (abnormal conduction due to a change in cycle length)
Management of sinus tachycardia
Treat underlying cause
BB or CCB if BB is contraindicated
What is a premature atrial contraction and how can it be identified on ECG
Ectopic supraventricular beat originating in the atria
■ P wave morphology of the PAC usually differs from that of a normal sinus beat
What is a junctional premature beat and how can it be identified on ECG
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)
Junctional premature beat treatment
Usually not required
Atrial flutter origin
rapid, regular atrial depolarization from a macro re-entry circuit within the atrium (most commonly the right atrium)
Atrial flutter presentation
atrial rate 250-350 bpm
AV block usually occurs; it may be fixed (2:1, 3:1, 4:1, etc.) or variable
ECG: sawtooth flutter waves (most common type of flutter) in inferior leads (II, III, aVF); narrow QRS (unless aberrancy); commonly seen as 2:1 block with HR of 150
Atrial flutter etiology
CAD thyrotoxicosis mitral valve disease cardiac surgery COPD PE pericarditis
How to elicit flutter waves in 2:1 AV block
Carotid sinus massage (first check for bruits), Valsalva maneuver, or adenosine may decrease AV conduction and bring out flutter waves
Atrial flutter treatment
Acute and if unstable (e.g. hypotension, CHF, angina) electrical cardioversion
If unstable (e.g. hypotension, CHF, angina): electrical cardioversion
If stable:
- rate control: β-blocker, diltiazem, verapamil, or digoxin
- chemical cardioversion: sotalol, amiodarone, type I antiarrhythmics, or electrical cardioversion
■ anticoagulation guidelines same as for patients with AFib
Treatment of long-term atrial flutter: Antiarrhythmics Catheter radiofrequency (RF) ablation (success rate dependent on site of origin of atrial flutter – i.e. whether right-sided isthmus-dependent or leftsided origin)
What is multifocal atrial tachycardia (MAT)
irregular rhythm caused by presence of 3 or more atrial foci (may mimic AFib)
Presentation of MAT
atrial rate 100-200 bpm – 3 or more distinct P wave morphologies and PR intervals vary, some P waves may not be conducted
In what patients does MAT occur
occurs more commonly in patients with COPD, and hypoxemia
Less commonly in patients with hypokalemia, hypomagnesemia, sepsis, theophylline, or digitalis toxicity
MAT treatment
- Treat the underlying cause
calcium channel blockers may be used (e.g. diltiazem, verapamil)
β-blockers may be contraindicated because of severe pulmonary disease
• no role for electrical cardioversion, antiarrhythmics, or ablation
Rate vs rhythm control outcomes in A fib
No difference in mortality
Rate-control was as effective as rhythm-control in AF and was better tolerated. There were more hospitalization incidents in the rhythm-control group.
Atrial fibrillation symptoms
palpitations, fatigue, syncope, may precipitate or worsen heart failure
Atrial fibrillation classification
■ lone: occurs in persons younger than 60 yr and in whom no clinical or echocardiographic causes are found
■ nonvalvular: not caused by valvular disease, prosthetic heart valves, or valve repair
■ paroxysmal: episodes that terminate spontaneously
■ persistent: AFib sustained for more than 7 d or AFib that terminates only with cardioversion
■ permanent/chronic: continuous AFib that is unresponsive to cardioversion or in which clinical judgement has led to a decision not to pursue cardioversion
■ recurrent: two or more episodes of AFib
■ secondary: caused by a separate underlying condition or event (e.g. myocardial infarction, cardiac surgery, pulmonary disease, hyperthyroidism)
What does atrial fibrillation increase the risk of and how can you calculate that risk
■ may be associated with thromboembolic events (stroke risk can be assessed by CHADS2 score in nonvalvular AFib; CHA2DS2-VASc if the former gives a score of 0 or 1)
Source of atrial fibrillation
single circuit re-entry and/or ectopic foci act as aberrant generators producing atrial tachycardia (350-600 bpm)
impulses conduct irregularly across the atrial myocardium to give rise to fibrillation
in some cases, ectopic foci have also been mapped to the pulmonary vein ostia and can be ablated
Long term consequences of a fib
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
Consequences of a fib
The AV node irregularly filters incoming atrial impulses producing an irregular ventricular response of <200 bpm and the tachycardia leads to suboptimal cardiac output
fibrillatory conduction of the atria promotes blood stasis increasing the risk of thrombus formation – AFib is an important risk factor for stroke
CHADS risk prediction for non valvular a fib
Congestive heart failure Hypertension Age >75 Diabetes Stroke or prior TIA (2 points, all others 1 point)
A fib ECG findings
No organized P waves due to rapid atrial activity (350-600 bpm) causing a chaotic fibrillatory baseline
■ irregularly irregular ventricular response (typically 100-180 bpm), narrow QRS (unless aberrancy or previous BBB)
■ wide QRS complexes due to aberrancy may occur following a long-short cycle sequence (“Ashman phenomenon”)
■ loss of atrial contraction, thus no “a” wave seen in JVP no S4 on auscultation
Lenient vs strict afib rate control outcomes
Lenient control (resting HR<110) was equivalent to strict control (resting HR <80) for prevention of primary outcomes in patients with atrial fibrillation. Furthermore, lenient control was more easily achieved.
A fib management
major objectives (RACE): all patients with AFib (paroxysmal, persistent, or permanent), should be stratified using a predictive index for stroke risk and for the risk of bleeding, and most patients should receive either an oral anticoagulant or ASA (see below)
- Rate control: β-blockers, diltiazem, verapamil (in patients with heart failure: digoxin, amiodarone) – digoxin can be considered as a therapeutic option to achieve rate control in patients whose response to beta-blockers and/or calcium channel blockers is inadequate or contraindicated
2. Anticoagulation: use either warfarin or NOACs e.g. apixaban, dabigatran, rivaroxaban to prevent thromboembolism for patients with non-valvular AF (NVAF) oral anticoagulant (OAC) is recommended for most patients aged >65 yr or CHADS2 >= 1. ASA 81 mg is recommended only for patients with none of the risk outlined in the CCS algorithm (age <65 and no CHADS2 risk factors) who have arterial disease (coronary, aortic, or peripheral) Novel oral anticoagulant (NOAC) is to be used in preference to warfarin
- Cardioversion (electrical) –
if AFib <24-48 h, can usually cardiovert without anticoagulation
if AFib >24-48 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 – HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocarditis, ASD, postoperative PE, COPD, thyrotoxicosis, sick sinus syndrome, alcohol (“holiday heart”) – may present in young patients without demonstrable disease (“lone AFib”) and in the elderly without underlying heart disease
Rivaroxaban vs warfarin in a fib for stroke prevention
In patients with AFib, rivaroxaban is non-inferior to warfarin for stroke prevention and major and non-major bleeding
When should patients with a fib be cardioverted as soon as possible
Unstable patients
Many patients with a significant underlying structural heart lesion (e.g. valve disease, cardiomyopathy) will not tolerate AFib well (since may be dependent on atrial kick) and these patients should be cardioverted (chemical or electrical) as soon as possible
Management of newly discovered afib
anticoagulants may be beneficial if high risk for stroke
◆ if the episode is self-limited and not associated with severe symptoms, no need for antiarrhythmic drugs
◆ if AFib persists, 2 options
- rate control and anticoagulation (as indicated above)
- cardioversion (as above)
Management of recurrent afib
If episodes are brief or minimally symptomatic, antiarrhythmic drugs may be avoided; rate control and anticoagulation are appropriate
Patients who have undergone at least one attempt to restore sinus rhythm may remain in AFib after recurrence; permanent AFib may be accepted (with rate control and antithrombotics as indicated by CHADS2 score) in certain clinical stuations
if symptoms are bothersome or episodes are prolonged, antiarrhythmic drugs should be used
– no or minimal heart disease: flecainide, propafenone once proven to have no underlying CAD (usu. by exercise stress testing)
– LV dysfunction: amiodarone
– CAD: β-blockers, amiodarone
AVNRT definition
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 – cause is commonly idiopathic, although familial AVNRT has been reported
AVNRT presentation
- sudden onset and offset
- fast regular rhythm: rate 150-250 bpm
- usually initiated by a supraventricular or ventricular premature beat
- AVNRT accounts for 60-70% of all paroxysmal SVTs
- retrograde P waves may be seen but are usually lost in the QRS complex
AVNRT treatment
acute:
- Valsalva maneuver or carotid sinus pressure technique
- adenosine is first choice if unresponsive to vagal maneuvers
- if no response, try metoprolol, digoxin, diltiazem
- electrical cardioversion if patient hemodynamically unstable (hypotension, angina, or CHF)
long-term:
1st line – β-blocker, diltiazem, digoxin
2nd line – flecainide, propafenone
3rd line – catheter ablation
What are ventricular pre-excitation syndromes
refers to a subset of SVTs mediated by an accessory pathway which can lead to ventricular pre-excitation
What is Wolff-Parkinson White Syndrome
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 is the presentation of WPW syndrome
since the ventricles are activated earlier, the ECG shows early ventricular depolarization in the form of initial slurring of the QRS complex – the so-called “delta wave”
• atrial impulses that conduct to the ventricles through both the Bundle of Kent and the normal AV node/His-Purkinje system generate a broad “fusion complex”
• 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
Why does afib happen in WPW patients
rapid atrial depolarizations in AFib are conducted through the bypass tract which is not able to filter impulses like the AV node can
What is a common arrhythmia that occurs in WPW patients
A fib
What is the ECG presentation of afib in WPW patients
the ventricular rate becomes extremely rapid (>200 bpm) and the QRS complex widens because there is no filtration of impulses
Treatment of afib in WPW patients
electrical cardioversion, IV procainamide, or IV amiodarone
■ do not use drugs that slow AV node conduction (digoxin, β-blockers) as this may cause preferential conduction through the bypass tract and precipitate VF
■ long-term: ablation of bypass tract if possible
What are the supraventricular tacchyarrhythmias
- Sinus tach
- Premature beats (atrial, junctional)
- Atrial flutter
- MAT
- Atrial fibrillation
- AVNRT
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 accessory pathway and normal conduction system
- initiated by a premature atrial or ventricular complex
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
What is the treatment for AVRT
■ 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
■ drugs such as flecainide and procainamide can be used
What is a premature ventricular contraction or premature ventricular beat
QRS width >120 msec, no preceding P wave, bizarre QRS morphology
PVCs may be benign but are usually significant in the following situations
■ consecutive (≥3 = VT) or multiform (varied origin)
■ PVC falling on the T wave of the previous beat (“R on T phenomenon”): may precipitate ventricular tachycardia or VF
Accelerated idioventricular rhythm definition
ectopic ventricular rhythm with rate 50-100 bpm
• more frequently occurs in the presence of sinus bradycardia and is easily overdriven by a faster supraventricular rhythm
Accelerated idioventricular rhythm population
• frequently occurs in patients with acute MI or other types of heart disease (cardiomyopathy, hypertensive, valvular) but it does not affect prognosis
Accelerated idioventricular rhythm treatment
Usually not required
Ventricular tachycardia definition
3 or more consecutive ectopic ventricular complexes wide regular QRS tachycardia (QRS usually >140 msec)
■ rate >100 bpm (usually 140-200)
Ventricular flutter definition
if rate >200 bpm and complexes resemble a sinusoidal pattern
Sustained VT definition
lasts longer than 30 s
Monomorphic VT usual source and causes
identical complexes with uniform morphology
■ more common than polymorphic VT
■ typically result from intraventricular re-entry circuit
■ potential causes: chronic infarct scarring, acute MI/ischemia, cardiomyopathies, myocarditis, arrhythmogenic right ventricular dysplasia, idiopathic, drugs (e.g. cocaine), electrolyte disturbances
Polymorphic VT pattern
complexes with constantly changing morphology, amplitude, and polarity
Type of VT more frequently associated with hemodynamic instability
■ polymorphic VT more frequently associated with hemodynamic instability due to faster rates (typically 200-250 bpm) vs. monomorphic VT
polymorphic VT potential causes
■ potential causes: acute MI, severe or silent ischemia, and predisposing factors for QT prolongation
VT treatment
sustained VT (>30 s) is an emergency, requiring immediate treatment
■ hemodynamic compromise: electrical cardioversion
■ no hemodynamic compromise: electrical cardioversion, lidocaine, amiodarone, type Ia agents (procainamide, quinidine)
You have a wide complex tachycardia. How do you differentiate VT vs SVT with aberrancy
Presenting symptoms - not helpful
History of CAD and previous MI - VT
Physical exam
Cannon “a” waves, variable S1 - VT
Carotid sinus massage/adenosine terminates arrhythmia - SVT (can be VT if no structural heart disease)
AV dissociation - VT
Capture or fusion beats - VT
QRS width >140 msec - VT
Extreme axis deviation (left or right superior axis) - VT
Positive QRS concardance (R wave arss chest leads) - VT
Negative QRS conordance (S wave across chest leads) - may suggest VT
Axis shift during arrhythmia - VT (polymorphic)
Torsades de Pointes definition
a variant of polymorphic VT that occurs in patients with baseline QT prolongation – “twisting of the points”
• looks like usual VT except that QRS complexes “rotate around the baseline” changing their axis and amplitude
Torsades de Point rate
Ventricular rate >100 bpm, usually 150-300 bpm
Torsades de Point etiology
etiology: predisposition in patients with prolonged QT intervals ■ congenital long QT syndromes ■ drugs: e.g. class IA (quinidine), class III (sotalol), phenothiazines (TCAs), erythromycin, quinolones, antihistamines ■ electrolye disturbances: hypokalemia, hypomagnesemia ■ nutritional deficiencies causing above electrolyte abnormalitie
Torsades de Pointes treatment
IV magnesium, temporary pacing, isoproterenol and correct underlying cause of prolonged QT, electrical cardioversion if hemodynamic compromise
Arrhythmias that may present as a wide QRS tachycardia
- VT
- SVT with aberrant conduction (rate related)
- SVT with preexisting BBB or nonspecific intraventricular conduction defect
- AV conduction through a bypass tract in WPW patients during an atrial tachyarrhythmia (e.g. atrial flutter, atrial tachycardia) Antidromic AVRT in WPW patients
Assessment of the cardiac patient for fitness to drive and fly
following an appropriate shock these patients are at an increased risk to cause harm to other road users and therefore should be restricted to drive for a period of 2 and 4 mo, respectively. In addition, all ICD patients with commercial driving licenses have a substantial elevated risk to cause harm to other road uses during the complete follow-up after both implantation and shock and should therefore be restricted to drive permanently.
Sudden cardiac arrest definition
unanticipated, non-traumatic cardiac death in a stable patient which occurs within 1 h of symptom onset
VFib is most common cause
Sudden cardiac arrest management
acute: resuscitate with prompt CPR and defibrillation
- investigate underlying cause (cardiac catheterization, electrophysiologic studies, echo)
- treat underlying cause
- antiarrhythmic drug therapy: amiodarone, β-blockers
- implantable cardioverter defibrillator (ICD)
- refer to ACLS guidelines
What are electrophysiology studies and what are they used for a
invasive test for the investigation and treatment of cardiac rhythm disorders using intracardiac catheters
- provide detailed analysis of the arrhythmia mechanism and precise site of origin when ECG data are nondiagnostic or unobtainable
- bradyarrhythmias: define the mechanisms of SA node dysfunction and localize site of AV conduction block
- tachyarrhythmias: map for possible ablation or to assess inducibility of V
Pacemaker indications
- SA node dysfunction (most common): symptomatic bradycardia ± hemodynamic instability
- common manifestations include: syncope, presyncope, or severe fatigue
- SA node dysfunction is commonly caused by: intrinsic disease within the SA node (e.g. idiopathic degeneration, fibrosis, ischemia, or surgical trauma), abnormalities in autonomic nervous system function, and drug effects
• AV nodal-infranodal block: Mobitz II, complete heart block
Pacemaker techniques
- temporary: transvenous (jugular, subclavian, femoral) or external (transcutaneous) pacing
- permanent: transvenous into RA, apex of RV, or both
- can sense and pace atrium, ventricle, or both
- new generation: rate responsive, able to respond to physiologic demand
- biventricular
What population should ICDs be used in
ICDs are safe and effective in reducing mortality in adult patients with LV systolic dysfunction but carry significant risks of inappropriate discharges. Differences between RCTs and observational studies show that improved risk stratification of patients may further improve outcomes and reduce adverse events.
• benefit seen in patients with ischemic and non-ischemic cardiomyopathy, depressed left ventricular ejection fraction (LVEF), prolonged QRS
What do ICDs do
sudden cardiac death SCD) usually results from ventricular fibrillation (VFib), sometimes preceded by monomorphic or polymorphic ventricular tachycardia (VT) • ICDs detect ventricular tachyarrhythmias and are highly effective in terminating VT/VFib and in aborting SCD • mortality benefit vs. antiarrhythmics in secondary prevention
What is radiofrequency ablation
radiofrequency (RF) ablation: a low-voltage high-frequency form of electrical energy (similar to cautery); RF ablation produces small, homogeneous, necrotic lesions
What is cryoablation and what are the pros and cons
New technology which uses a probe with a tip that can decrease in temperature to 20˚C and -70˚C. Produces small, necrotic lesions similar to RF ablation; when brought to -20˚C, the catheter tip reversibly freezes the area; bringing the tip down to -70˚C for 5 min permanently scars the tissue
■ advantage: can “test” areas before committing to an ablation
■ disadvantage: takes much longer than RF (5 min per cryoablation vs. 1 min per RF ablation)
Indications for catheter ablation
• paroxysmal SVT
■ AVNRT: accounts for more than half of all cases
• accessory pathway (orthodromic reciprocating tachycardia): 30% of SVT
■ re-entrant rhythm, with an accessory AV connection as the retrograde limb
■ corrected by targeting the accessory pathway
- atrial flutter: re-entry pathway in right atrium
- AFib: potential role for pulmonary vein ablation
- ventricular tachycardia: focus arises from the right ventricular outflow tract and less commonly originates in the inferoseptal left ventricle near the apex (note: majority of cases of VT are due to scarring from previous MI and cannot be ablated)
What is the pathophysiology of artherosclerosis
Hypertension, DM, smoking, dyslipidemia, RA –>
Endothelial injury –>
Monocyte recruitment
Enhanced LDL permeability –>
Monocytes enter into initial space and differentiate into macrophages - LDL is converted into oxidized LDL –>
Macrophages take up OX-LDL via scavenger receptors to become foam cells (‘fatty streak’ and lipid core of plaque) –>
Cytokine and growth factor signalling from damaged endothelium and macrophages promote medial smooth muscle cell migration into the intima, proliferation (intimal hyperplasia) and release of matrix to form the fibrous cap of plaque - rupture depends on balance of pro-and anti-proteases, magnitude of necrosis and location of plaque (bifurcation sites are exposed to greater shear stress) –>
Calcification -> increased vessel wall rigidity
Plaque rupture -> thrombosis
Hemorrhage into plaque -> lumen narrowing
Fragmentation -> emboli
Wall weakening -> aneurysm
What is the etiology of stable angina vs acute coronary syndromes
Chronic stable angina is most often due to a fixed stenosis caused by an atheroma
Acute coronary syndromes are the result of plaque rupture
CCS Classes
Class I: ordinary physical activity (walking, climbing stairs) does not cause angina; angina with strenuous, rapid, or prolonged activity
Class II: slight limitation of ordinary activity: angina brought on at >2 blocks on level or climbing >1 flight of stairs or by emotional stress
Class III: marked limitation of ordinary activity: angina brought on at <2 blocks on level or climbing <1 flight of stairs
Class IV: inability to carry out any physical activity without discomfort; angina may be present at rest
What are factors that decrease myocardial oxygen supply
■ decreased luminal diameter: atherosclerosis, vasospasm
■ decreased duration of diastole: tachycardia (decreased duration of diastolic coronary perfusion)
■ decreased hemoglobin: anemia
■ decreased SaO2: hypoxemia
■ congenital anomalies
What are factors that increase myocardial oxygen demand
■ increased heart rate: hyperthyroidism
■ increased contractility: hyperthyroidism
■ increased wall stress: myocardial hypertrophy, aortic stenosis
What is Levine’s sign
clutching fist over sternum when describing chest pain
Typical signs and symptoms of chronic stable angina
- retrosternal chest pain, tightness or discomfort radiating to left (± right) shoulder/arm/neck/jaw, associated with diaphoresis, nausea, anxiety
- predictably precipitated by the “3 Es”: exertion, emotion, eating
- brief duration, lasting <10-15 min and typically relieved by rest and nitrates
When should an ECHO be ordered in chronic stable angina
- to assess systolic murmur suggestive of aortic stenosis, mitral regurgitation, and/or HCM
- to assess LV function in patients with Hx of prior MI, pathological Q waves, signs or symptoms of CHF
Treatment of chronic stable angina
- General Measures
■ goals: to reduce myocardial oxygen demand and/or increase oxygen supply
■ lifestyle modification (diet, exercise)
■ treatment of risk factors: statins, antihypertensives, etc
■ pharmacological therapy to stabilize the coronary plaque to prevent rupture and thrombosis - Antiplatelet Therapy (first-line therapy)
■ ASA
■ clopidogrel when ASA absolutely contraindicated - β-blockers (first-line therapy – improve survival in patients with hypertension)
■ increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)
■ cardioselective agents preferred (e.g. metoprolol, atenolol) to avoid peripheral effects (inhibition of vasodilation and bronchodilation via β2 receptors)
■ avoid intrinsic sympathomimetics (e.g. acebutolol) which increase demand - Nitrates (symptomatic control, no clear impact on survival)
■ decrease preload (venous dilatation) and afterload (arteriolar dilatation), and increase coronary perfusion
■ maintain daily nitrate-free intervals to prevent tolerance (tachyphylaxis) - Calcium Channel Blockers (CCBs, second-line or combination)
■ increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)
■ caution: verapamil/diltiazem combined with β-blockers may cause symptomatic sinus bradycardia or AV block - ACE Inhibitors (ACEI, not used to treat symptomatic angina)
■ angina patients tend to have risk factors for CV disease which warrant use of an ACEI (e.g. HTN, DM, proteinuric renal disease, previous MI with LV dysfunction)
■ benefit in all patients at high risk for CV disease (concomitant DM, renal dysfunction, or LV systolic dysfunction) - Invasive Strategies
■ revascularization
Optimal medical therapy with or without PCI for stable coronary disease COURAGE trial
PCI as an adjunct in initial management in patients with significant stable coronary artery disease does not reduce mortality, MI, stroke, or hospitalization for ACS, but does provide angina relief and reduced risk of revascularization.
Variant angina (Prinzmetal’s angina)
- myocardial ischemia secondary to coronary artery vasospasm, with or without atherosclerosis
- uncommonly associated with infarction or LV dysfunction
- typically occurs between midnight and 8 am, unrelated to exercise, relieved by nitrates
- typically ST elevation on ECG
- diagnosed by provocative testing with ergot vasoconstrictors (rarely done)
- treat with nitrates and CCBs
Syndrome X angina
- typical symptoms of angina but normal angiogram
- may show definite signs of ischemia with exercise testing
- thought to be due to inadequate vasodilator reserve of coronary resistance vessels
- better prognosis than overt epicardial atherosclerosis
Myocardial infarction diagnosis
evidence of myocardial necrosis
MI diagnostic criteria
Rise/fall of serum markers plus any one of:
◆ symptoms of ischemia (chest/upper extremity/mandibular/epigastric discomfort; dyspnea)
◆ ECG changes (ST-T changes, new BBB or pathological Q waves)
◆ imaging evidence (myocardial loss of viability, wall motion abnormality, or intracoronary thrombus)
◆ if biomarker changes are unattainable, cardiac symptoms combined with new ECG changes is sufficient
What is the difference in the diagnostic characteristics of NSTEMI vs STEMI
NSTEMI meets criteria for myocardial infarction without ST elevation or BBB
STEMI meets criteria for myocardial infarction characterized by ST elevation or new BBB
Unstable angina is clinically defined as any of the following
■ accelerating pattern of pain: increased frequency, increased duration, decreased threshold of exertion decreased response to treatment
■ angina at rest
■ new-onset angina
■ angina post-MI or post-procedure (e.g. percutaneous coronary intervention [PCI], coronary artery bypass grafting [CABG])
When should biomarkers for myocardial damage be drawn
immediately and then repeat 8 h later
When should serum lipids be drawn following MI
draw serum lipids within 24-48 h because values are unreliable from 2-48 d post-MI
Management of Acute Coronary Syndromes
- General Measures
■ ABCs, bed rest, cardiac monitoring, oxygen
■ nitroglycerin SL followed by IV
■ morphine IV - Anti-Platelet and Anticoagulation Therapy
- ASA chewed
-NSTEMI
◆ ticagrelor in addition to ASA or if ASA contraindicated, SC LMWH or IV UFH (LMWH preferable, except in renal failure or if CABG is planned within 24 h)
◆ clopidogrel used if patient ineligible for ticagrelor
■ if PCI is planned: ticagrelor or prasugrel and consider IV GP IIb/IIIa inhibitor (e.g. abciximab)
◆ clopidogrel used if patient ineligible for ticagrelor and prasugrel
◆ prasugel contraindicated in those with a history of stroke/TIA, and avoidance of or lower dose is recommended for those >75 yr old or weighing under 60 kg
■ anticoagulation options depend on reperfusion strategy:
◆ primary PCI: UFH during procedure; bivalirudin is a possible alternative
◆ thrombolysis: LMWH until discharge from hospital; can use UFH as alternative because of possible rescue PCI
◆ no reperfusion: LMWH until discharge from hospital
■ continue LMWH or UFH followed by oral anticoagulation at discharge if at high risk for thromboembolic event (large anterior MI, AFib, severe LV dysfunction, CHF, previous DVT or PE, or echo evidence of mural thrombus)
- β-blockers
■ STEMI contraindications include signs of heart failure low output states, risk of cardiogenic shock, heart block, asthma or airway disease; initiate orally within 24 h of diagnosis when indicated
■ if β-blockers are contraindicated or if β-blockers/nitrates fail to relieve ischemia, nondihydropyridine CCB (e.g. diltiazem, verapamil) may be used as second-line therapy in the absence of severe LV dysfunction or pulmonary vascular congestion (CCBs do not prevent MI or decrease mortality) - Invasive Strategies and Reperfusion Options
■ UA/NSTEMI: early coronary angiography ± revascularization if possible is recommended with any of the following high-risk indicators:
◆ recurrent angina/ischemia at rest despite intensive anti-ischemic therapy
◆ CHF or LV dysfunction
◆ hemodynamic instability
◆ high (≥3) TIMI risk score (tool used to estimate mortality following an ACS)
◆ sustained ventricular tachycardia
◆ dynamic ECG changes
◆ high-risk findings on non-invasive stress testing
◆ PCI within the previous 6 mo
◆ repeated presentations for ACS despite treatment and without evidence of ongoing ischemia or high risk features
◆ note: thrombolysis is NOT administered for UA/NSTEMI
■ STEMI
◆ after diagnosis of STEMI is made, do not wait for results of further investigations before implementing reperfusion therapy
◆ goal is to re-perfuse artery: thrombolysis (“EMS-to needle”) within 30 min or primary PCI (“EMS-to-balloon”) within 90 min (depending on capabilities of hospital and access to hospital with PCI facility)
◆ thrombolysis
– preferred if patient presents ≤12 h of symptom onset, and <30 min after presentation to hospital, has contraindications to PCI, or PCI cannot be administered within 90 min
◆ PCI
– early PCI (≤12 h after symptom onset and <90 min after presentation) improves mortality vs. thrombolysis with fewer intra-cranial hemorrhages and recurrent MIs
– primary PCI: without prior thrombolytic therapy – method of choice for reperfusion in experienced centres
– rescue PCI: following failed thrombolytic therapy (diagnosed when following thrombolysis, ST segment elevation fails to resolve below half its initial magnitude and patient still having chest pain)
TIMI (thrombolysis in myocardial infarction) risk score for UA and NSTEMI and interpretation
Historical Age ≥65 yr ≥3 risk factors for CAD Known CAD (stenosis ≥50%) Aspirin® use in past 7 d
Presentation
Recent (≤24 h) severe angina
ST-segment deviation ≥0.5 mm
Increased cardiac markers
Each is worth one point
If TIMI risk score ≥3, consider early LMWH and angiography
Diagnosis STEMI basic management/reperfusion strategy based on presentation time frame
See Tony’s C29
Absolute contraindications for thrombolysis in STEMI
Ischemic stroke (≤3 mo) Prior intracranial hemorrhage Known structural cerebral vascular lesion Known malignant intracranial neoplasm Significant closed-head or facial trauma (≤3 mo)
Active bleeding
Suspected aortic dissection
Relative contraindications for thrombolysis in STEMI
Chronic, severe, poorly controlled HTN Uncontrolled HTN (sBP >180, dBP >110)
Current anticoagulation
Noncompressible vascular punctures
Recent internal bleeding (≤2-4 wk)
Ischemic stroke (≥3 mo)
Prolonged CPR or major surgery (≤3 wk)
Pregnancy
Active peptic ulcer disease
When is risk of progression to MI or recurrence of MI or death highest
Within 1 month
Pre discharge workup following acute coronary syndrome
ECG and echo to assess residual LV systolic function
Long term management of ACS
drugs required in hospital to control ischemia should be continued after discharge in all patients other medications for long-term management of ACS are summarized below
- General Measures ■ education ■ risk factor modification
- Antiplatelet and Anticoagulation Therapy
■ ECASA 81 mg daily
■ ticagrelor 90 mg twice daily or prasugrel 10 mg daily (at least 1 mo, up to 9-12 mo, if stent placed at least 12 mo)
■ clopidogrel 75 mg daily can be used as alternatives to ticagrelor and prasugrel when indicated
■ ± warfarin x 3 mo if high risk (large anterior MI, LV thrombus, LVEF <30%, history of VTE, chronic AFib) - β-Blockers (eg metoprolol 25-50 mg bid or atenolol 50-100 mg daily)
- Calcium Channel Blockers (NOT recommended as first line treatment, consider as alternative to β-blockers) - Nitrates
■ alleviate ischemia but do not improve outcome
■ use with caution in right-sided MI patients who have become preload dependent - Angiotensin-Converting Enzyme Inhibitors
■ prevent adverse ventricular remodelling
■ recommended for asymptomatic high-risk patients (e.g. diabetics), even if LVEF >40%
■ recommended for symptomatic CHF, reduced LVEF (<40%), anterior MI
■ use ARBs in patients who are intolerant of ACEI; avoid combining ACE and ARB - ± Aldosterone Antagonists
■ if on ACEI and β-blockers and LVEF <40% and CHF or DM
■ significant mortality benefit shown with eplerenone by 30 d - Statins (early, intensive, irrespective of cholesterol level; eg. atorvastatin 80 mg daily)
- Invasive Cardiac Catheterization if indicated (risk stratification)
Most accurate clinical exam findings in MI
The most compelling features that increase likelihood of an MI are ST-segment and cardiac enzyme elevation, new Q-wave, and presence of an S3 heart sound.
In patients where the diagnosis of MI is uncertain, radiation of pain to the shoulder OR both arms, radiation to the right arm, and vomiting had the best predictive values, while radiation to the left arm is relatively non-diagnostic.
Complications of MI, when do they occur and what is the management
CRASH PAD Cardiac Rupture - 1-7 days, surgery 1. LV free wall 2. Papillary muscle (-> MR) 3. Ventricular septum (-> VSD) Arrhythmia - first 48h Shock (infarction or aneurysm) - within 48h, inotropes or intra aortic balloon pump Hypertension/Heart failure
Pericarditis - 1-7 days, ASA
Pulmonary emboli - 7-10 days, up to 6 months
Aneurysm
DVT - 7-10 days, up to 6 months
Dressler’s syndrome (autoimmune) - 2-8 weeks
Post MI risk stratification
Tony’s C30
LMWH vs UFH with fibrinolysis for STEMI
In patients with STEMI receiving thrombolysis, enoxaparin is superior to unfractionated heparin in preventing recurrent nonfatal MI and may lead to a small reduction in mortality.
Intensive vs moderate lipid lowering with statin therapy following ACS
In patients who recently experienced an ACS, high dose statin therapy provides greater protection against death and major cardiovascular events than standard dose therapy.
Treatment of NSTEMI
BEMOAN β-blocker Enoxaparin Morphine O2 ASA Nitrates
Management of chest pain
Tony’s C31
Indications for PCI
medically refractory angina
NSTEMI/UA with high risk features (e.g. high TIMI risk score, see sidebar C28)
primary/rescue PCI for STEMI
What is a major compliation of balloon angiography and what is done to prevent it
major complication is restenosis (approximately 15% at 6 mo), felt to be due to elastic recoil and neointimal hyperplasia
majority of patients receive intracoronary stent(s) to prevent restenosis
Complication of placing coronary stent
late stent thrombosis
What it the difference between bare metal and drug eluting stent and what is the benefit
coated with antiproliferative drugs (sirolimus, paclitaxel, everolimus)
reduced rate of neointimal hyperplasia and restenosis compared to BMS (5% vs. 20%)
Adjunctive therapies with coronary stenting
ASA and heparin decrease post-procedural complications
• further reduction in ischemic complications has been demonstrated using GPIIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban) in coronary angiography and stenting
• following stent implantation
■ dual antiplatelet therapy (ASA and clopidogrel) for 1 mo with BMS or ≥12 mo with DES
■ DAPT study showed benefit of dual antiplatelet therapy beyond 12 mo
■ ASA and prasugrel can be considered for those at increased risk of stent thrombosis
Duration of triple therapy in patients requiring oral anticoagulation after drug eluting stent implantation
Six weeks of triple therapy is not superior to 6 months. Physician should weigh trade-off between ischemic and bleeding risk when choosing shorter or longer duration of triple therapy
PCI vs CABG for severe coronary artery disease
In patients with three-vessel or left main coronary artery disease CABG is superior to PCI in preventing major adverse cardiovascular and cerebrovascular events within 12 mo of intervention.
Advantages of PCI vs CABG
PCI -
Less invasive technique
Decreased periprocedural morbidity and mortality
Shorter periprocedural hospitalization
CABG -
Greater ability to achieve complete revascularization
Decreased need for repeated revascularization procedures
Indications for PCI vs CABG
PCI -
Single or double-vessel disease
Inability to tolerate surgery
CABG -
Triple-vessel or left main disease
DM
Plaque morphology unfavourable for PCI
Safety and efficacy of drug eluting vs bare metal stents
DES significantly reduces rates of target vessel revascularization compared to BMS. Although there is no difference in mortality or MI incidence as found by RCTs, observational studies suggest lowered mortality and MI rates in patients with DES over BMS.
CABG and antiplatelet regimens
Prior to CABG, clopidogrel, and ticagrelor should be discontinued for 5 d and prasugrel for 7 d before surgery
- dual antiplatelet therapy should be continued for 12 mo in patients with ACS within 48-72 h after CABG
- ASA (81 mg) continued indefinitely (can be started 6 h after surgery)
- patients requiring CABG after PCI should continue their dual antiplatelet therapy as recommended in the post-PCI guidelines
What is the pathophysiology of heart failure
most common causes are ischemic heart disease, hypertension and valvular heart disease
myocardial insult causes pump dysfunction/impaired filling leading to myocardial remodelling
■ pressure overload (e.g. AS or HTN) leads to compensatory hypertrophy (concentric remodelling) and eventually interstitial fibrosis
■ volume overload (e.g. AI) leads to dilatation (eccentric remodelling)
Either high output due to increased cardiac demand
Low output due to decreased cardiac output (systolic vs diastolic)
Both of these lead to increased cardiac workload that activates the SNS (tachycardia) and RAAS (increased Na and water retention, increasing preload and afterload) systems and increases cardiac demand and decompensation
The heart can either compensate (inc heart rate, contractility, blood volume) or decompensate (unable to maintain circulation)
Types of decompensation
- Left sided HF
Forward Failure
- Inability to maintain cardiac output
Backward Failure
- Elevated ventricular filling pressures
- Pulmonary vascular congestion
- Fluid accumulation in lungs, apnea, shortness of breath, fatigue, weakness - Right sided HF
Backward Failure
- Elevated ventricular filling pressures
- Vascular congestion in vena cava
- Fluid accumulation in lower extremities (edema in feet, ankles, legs, lower back, liver, abdomen), nausea - Biventricular HF
- Due to long-term left-sided failure leading to right-sided failure
- Disorders affecting entire myocardium
Grading heart failure based on ejection fraction
Grade I (EF >60%) (Normal)
Grade II (EF = 40-59%)
Grade III (EF = 21-39%)
Grade IV (EF ≤20)
NYHA functional classification of heart failure
Class I: ordinary physical activity does not cause symptoms of HF
Class II: comfortable at rest, ordinary physical activity results in symptoms
Class III: marked limitation of ordinary activity; less than ordinary physical activity results in symptoms
Class IV: inability to carry out any physical activity without discomfort; symptoms may be present at rest
5 most common causes of CHF
- CAD (60-70%)
- HTN
- Idiopathic (often dilated cardiomyopathy)
- Valvular (e.g. AS, AR, and MR)
- Alcohol (dilated cardiomyopathy)
What are things that can increase cardiac demand and cause high output heart failure
anemia thiamine deficiency (beriberi) hyperthyroidism A-V fistula or L-R shunting Paget’s disease renal disease hepatic disease
What is your diagnosis for precipitants of symptomatic exaerbations in heart failure
■ new cardiac insult/disease: MI, arrhythmia, valvular disease
■ new demand on CV system: HTN, anemia, thyrotoxicosis, infection, etc.
■ medication non-compliance
■ dietary indisretion e.g. salt intake
■ obstructive sleep apnea
or HEART FAILED Hypertension (common) Endocarditis/environment (e.g. heat wave) Anemia Rheumatic heart disease and other valvular disease Thyrotoxicosis Failure to take meds (very common) Arrhythmia (common) Infection/Ischemia/Infarction (common) Lung problems (PE, pneumonia, COPD) Endocrine (pheochromocytoma, hyperaldosteronism) Dietary indiscretions (common)
Acute treatment of pulmonary edema
• treat acute precipitating factors (e.g. ischemia, arrhythmias)
- L – Lasix® (furosemide) 40-500 mg IV
- M – morphine 2-4 mg IV: decreases anxiety and preload (venodilation)
- N – nitroglycerin: topical/IV/SL - use with caution in preload-dependent patients (e.g. right HF or RV infarction) as it may precipitate CV collapse
- O – oxygen: in hypoxemic patients
- P – positive airway pressure (CPAP/BiPAP): decreases preload and need for ventilation when appropriate
- P – position: sit patient up with legs hanging down unless patient is hypotensive
• in ICU setting or failure of LMNOPP, other interventions may be necessary
■ nitroprusside IV
■ hydralazine PO
■ sympathomimetics
◆ dopamine
– low dose: selective renal vasodilation (high potency D1 agonist)
– medium dose: inotropic support (medium potency β1 agonist)
– high dose: increases SVR (low potency β1 agonist) which is undesirable
◆ dobutamine
– β1-selective agonist causing inotropy, tachycardia, hypotension (low dose) or hypertension (high dose); most serious side effect is arrhythmia, especially AF
◆ phosphodiesterase inhibitors (milrinone) – inotropic effect and vascular smooth muscle relaxation (decreased SVR), similar to dobutamine
- consider pulmonary artery catheter to monitor pulmonary capillary wedge pressure (PCWP) if patient is unstable or a cardiac etiology is uncertain (PCWP >18 indicates likely cardiac etiology)
- mechanical ventilation as needed
• rarely used, but potentially life-saving measures:
■ intra-aortic balloon pump (IABP) - reduces afterload via systolic unloading and improves coronary perfusion via diastolic augmentation
■ left or right ventricular assist device (LVAD/RVAD)
■ cardiac transplant
Features of heart failure on CXR
HERB-B Heart enlargement (cardiothoracic ratio >0.50) Pleural Effusion Re-distribution (alveolar edema) Kerley B lines Bronchiolar-alveolar cuffing
Long term management
overwhelming majority of evidence-based management applies to HFREF
• currently no proven pharmacologic therapies shown to reduce mortality in HFPEF; control risk factors (e.g. hypertension)
• ACEI* • β-blockers* • ± Mineralocorticoid receptor antagonists* • Diuretic • ± Inotrope • ± Antiarrythmic • ± Anticoagulant *Mortality benefit
Non pharmacological management of heart failure
cardiac rehabilitation: participation in a structured exercise program for NYHA class I-III after clinical status assessment to improve quality of life (HF-ACTION trial)
Pharmacological management of heart failure
- Renin-angiotensin-aldosterone blockade
■ ACEI: standard of care – slows progression of LV dysfunction and improves survival
◆ all symptomatic patients functional class II-IV
◆ all asymptomatic patients with LVEF <40%
◆ post-MI
■ angiotensin II receptor blockers
◆ second-line to ACEI if not tolerated, or as adjunct to ACEI if β-blockers not tolerated – combination with ACEI is not routinely recommended and should be used with caution as it may precipitate hyperkalemia, renal failure, the need for dialysis
◆ combination angiotensin II receptor blockers with neprilysin inhibitors (ARNI) is a new class of medication that has morbidity and mortality benefit over ACEI alone; it has been recommended to replace ACEI or ARBs for patients who have persistent symptoms (PARADIGM HF)
- β-blockers: slow progression and improve survival
■ class I-III with LVEF <40%
■ stable class IV patients
■ carvedilol improves survival in class IV HF (COMET)
■ note: should be used cautiously, titrate slowly because may initially worsen CHF - Mineralocorticoid receptor (aldosterone) antagonists: mortality benefit in symptomatic heart failure and severely depressed ejection fraction
■ spironolactone or eplerenone symptomatic heart failure in patients already on ACEI, beta blocker and loop diuretic
■ note: potential for life threatening hyperkalemia
◆ monitor K+ after initiation and avoid if Cr >220 µmol/L or K+>5.2 mmol/L - Diuretics: symptom control, management of fluid overload
■ furosemide (40-500 mg daily) for potent diuresis
■ metolazone may be used with furosemide to increase diuresis
■ furosemide, metolazone, and thiazides oppose the hyperkalemia that can be induced by β-blockers, ACEI, ARBs, and aldosterone antagonists - Digoxin and cardiac glycosides: digoxin improves symptoms and decreases hospitalizations, no effect on mortality
■ indications: patient in sinus rhythm and symptomatic on ACEI, or CHF and AFib
■ patients on digitalis glycosides may worsen if these are withdrawn - Antiarrhythmic drugs: for use in CHF with arrhythmia
■ can use amiodarone, β-blocker, or digoxin - Anticoagulants: warfarin for prevention of thromboembolic events
■ prior thromboembolic event or AFib, presence of LV thrombus on echo
Resynchronization therapy in heart failure description and indications
resynchronization therapy: symptomatic improvement with biventricular pacemaker
- consider if QRS >130 msec, LVEF <35%, and persistent symptoms despite optimal therapy
- greatest benefit likely with marked LV enlargement, mitral regurgitation, QRS >150 msec
ICD description and indications
ICD: mortality benefit in 1° prevention of sudden cardiac death
■ prior MI, optimal medical therapy, LVEF <30%, clinically stable
■ prior MI, non-sustained VT, LVEF 30-40%, EPS inducible VT
What are procedural interventions that can be completed in heart failure
Resynchronization therapy
ICD
LVAD/RVAD
Cardiac transplantation
Valve repair if patient is surgical candidate and has significant valve disease contributing to CHF
Cardiomyopathy definition
intrinsic or primary myocardial disease not secondary to congenital, hypertensive, coronary, valvular, or pericardial disease
• functional classification: dilated, hypertrophic, or restrictive
Myocarditis definition
inflammatory process involving the myocardium ranging from acute to chronic; an important cause of dilated cardiomyopathy
Myocarditis signs and symptoms
- constitutional symptoms
- acute CHF - dyspnea, tachycardia, elevated JVP
- chest pain – due to pericarditis or cardiac ischemia
- arrhythmias
- systemic or pulmonary emboli
- pre-syncope/syncope/sudden death
Most common cause of myocarditis
Viral infection
Major risk factors for dilated cardiomyopathy
Alcohol
Cocaine
Family history
Dilated cardiomyopathy definition
unexplained dilation and impaired systolic function of one or both ventricles
Dilated cardiomyopathy signs and symptoms
■ CHF
■ systemic or pulmonary emboli
■ arrhythmias
■ sudden death (major cause of mortality due to fatal arrhythmia)
Hypertrophic cardiomyopathy definition
- defined as unexplained ventricular hypertrophy
* various patterns of HCM are classified, but most causes involve pattern of septal hypertrophy
Hypertrophic cardiomyopathy signs and symptoms
- clinical manifestations: asymptomatic (common, therefore screening is important), SOB on exertion, angina, presyncope/syncope (due to LV outflow obstruction or arrhythmia), CHF, arrhythmias, SCD
- pulses: rapid upstroke, “spike and dome” pattern in carotid pulse (in HCM with outflow tract obstruction)
- precordial palpation: PMI localized, sustained, double impulse, ‘triple ripple’ (triple apical impulse in HOCM), LV lift
- precordial auscultation: normal or paradoxically split S2, S4, harsh systolic diamond-shaped murmur at LLSB or apex, enhanced by squat to standing or Valsalva (murmur secondary to LVOT obstruction as compared to AS); often with pansystolic murmur due to mitral regurgitation
HCM ECG changes
LVH
High voltages across precordium
Prominent Q waves (lead I, aVL, V5, V6)
Tall R wave in V1
P wave abnormalities
HCM TTE and Echo Doppler changes
Asymmetric septal hypertrophy
Systolic anterior motion (SAM) of mitral valve and MR
LVOT gradient can be estimated by Doppler measurement
HCM Management
- Avoid factors which increase obstruction (ex. volume depletion) - aka avoidance of all competitive sports
- Medical agents - Beta blockers, disopyramide, verapamil (started only in monitored setting), phenylephrine (in setting of cardiogenic shock)
- For patients with drug-refractory symptoms
- Surgical myectomy
- Alcohol septal ablation - percutaneous intervention that ablates the hypertrophic septum with 100% ethanol via the septal artery - For patients with high risk of sudden death ICD
HCM Screening
First degree relatives should be screened (physical, ECG, 2D ECHO) q12-18 months during adolescence, then serially q5y during adulthood
Drugs to avoid in HCM
Nitrates
Diuretics
ACEI
These increase LVOT gradient and worsen symptoms
What is the major difference between restrictive cardiomyopathy and contrictive pericarditis
Present similarly but CP is treatable with surgery
HCM potential complications
Afib
VT
CHF
Sudden cardiac death 1% risk/year
What is the most common cause of SCD in young athletes
HCM
Major risk factors for SCD in HCM (consider ICD placement)
History of survived cardiac arrest/sustained VT
Family history of multiple premature sudden deaths
Syncope arrhythmic in origin, non sustained VT on monitoring, marked ventricular hypertrophy (30 mm +), abnormal BP in response to exercise in patients <40 years
Restrictive cardiomyopathy definition
Impaired ventricular filling with preserved systolic function in a non-dilated, non-hypertrophied ventricle secondary to factors that decrease myocardial compliance (fibrosis and/or infiltration)
RCM etiology
Infiltrative - amyloidosis, sarcoidosis
Non-infiltrative - scleroderma, idiopathic myocardial fibrosis
Storage diseases - hemochromatosis, Fabry’s disease, Gaucher’s disease, glycogen storage diseases
Endomyocardial - fibrosis, Loeffler’s endocarditis, eosinophilic endomyocardial disease, radiation heart disease, carcinoid syndrome (may have associated tricuspid valve or pulmonary valve dysfunction)
Constrictive pericarditis Key investigations
ECHO - may show respiratory variation in blood flow
CT - May show very thickened pericardium and calcification
MRI - best modality to directly visualize pericaridium and myocardium
RCM Clinical manifestations
CHF (usually preserved LV systolic function)
Atthythmias
Elevated JVP
Kussmaul’s sign
S3, S4, MR, TR
Thromboembolic events
RCM Investigations
ECG - low voltage, diffuse ST/T changes, non-ischemic Q waves
CXR - cardiac enlargement
ECHO - LAE, RAE, no respiratory variation on doppler
Cardiac cath - increased end-diastolic ventricular pressures
Endomyocardial biopsy - determine etiology for infiltrative
RCM Management
Exclude constrictive pericarditis
Treat underlying disease - control HR, anticoagulate if AFib
Supportive care and treatment for CHF, arrhythmias
Cardiac transplant might be considered for CHF refractory to medical therapy
RCM prognosis
Depends on etiology
IE prophylaxis
For patients with:
- Prothetic valve material
- Past history of IE
- Certain types of congenital heart disease
- Cardiac transplant recipients who develop valvulopathy
For the following procedures: ◆ dental ◆ respiratory tract ◆ procedures on infected skin/skin structures/MSK structures ◆ not GI/GU procedures specifically
Rheumatic Acute complications
• acute complications: myocarditis (DCM/CHF), conduction abnormalities (sinus tachycardia, AFib), valvulitis (acute MR), acute pericarditis (not constrictive pericarditis)
Rheumatic fever chronic complications
• chronic complications: rheumatic valvular heart disease – fibrous thickening, adhesion, calcification of valve leaflets resulting in stenosis/regurgitation, increased risk of IE ± thromboembolism
Rheumatic fever onset of symptoms
• onset of symptoms usually after 10-20 yr latency from acute carditis of rheumatic fever
Rheumatic fever most commonly affected valve
Mitral
Valve repair or replacement indications
indication for valve repair or replacement depends on the severity of the pathology; typically recommended when medical management has failed to adequately improve the symptoms or reduce the risk of morbidity and mortality
• pathologies that may require surgical intervention include congenital defects, infections, rheumatic heart disease as well as a variety of valve diseases associated with aging
Valve repair options
valve repair: balloon valvuloplasty, surgical valvuloplasty (commissurotomy, annuloplasty), chordae tendineae shortening, tissue patch
Valve replacement options
valve replacement: typically for aortic or mitral valves only; mitral valve repair is favoured in younger individuals; percutaneous techniques being established
Mitral valve repair vs replacement for severe ischemic mitral regurgitation outcome
No significant difference in left ventricular reverse modelling or survival at 12 mo between patients who underwent mitral valve repair or replacement Replacement provided more durable correction of mitral regurgitation, but there were no significant differences in clinical outcomes.
Mechanical valve characteristics
Good durability
Less preferred in small aortic root sizes
Increased risk of thromboembolism (1-3%/year) and requires long term antioagulation with coumadin
Target INR
Aortic valves 2-3
Mitral valves 2.5-3.5
Increased risk of hemorrhage 1-2% /year
Bioprosthetic valve characteristics
Limited long term durability (mitral < aortic)
Good flow in small aortic root sizes
Decreased risk of thromboembolism - long-term anticoagulation not needed for aortic valves
Some recommendation for limited anticoagulation for mitral valves
Decrease risk of hemorrhage
Aortic stenosis etiology
Congenital (bicuspid, unicuspid)
calfication
rheumatic disease
AS definition
Normal aortic valve area = 3-4 cm2 Mild AS >1.5 cm2 Moderate AS 1.0 to 1.5 cm2 Severe AS <1.0 cm2 Critical AS <0.5 cm2
AS pathophysiology
Outflow obstruction increased EDP concentric LVH LV failure CHF, subendocardial ischemia
AS symptoms
Exertional angina, syncope, dyspnea, PND, orthopnea, peripheral edema
AS physical exam
Narrow pulse pressure, brachial-radial delay, pulsus parvus et tardus sustained PMI
Auscultation: crescendo-decrescendo SEM radiating to R clavicle and carotid, musical quality at apex (Gallavardin phenomenon), S4, soft S2 with paradoxical splitting, S3 (late)
AS Investigations
ECG: LVH and strain, LBBB, LAE, AFib
CXR: post-stenotic aortic root dilatation, calcified valve, LVH, LAE, CHF
Echo: reduced valve area, pressure gradient, LVH, reduced LV function
AS treatment
Asymptomatic: serial echos, avoid exertion
Symptomatic: avoid nitrates/arterial dilators and ACEI in severe AS
Surgery if: symptomatic or LV dysfunction
Surgical options for AS
Valve replacement: aortic rheumatic valve disease and trileaflet valve
– prior to pregnancy (if AS significant)
– balloon valvuloplasty (in very young)
Interventional options for as
Percutaneous valve replacement (transfemoral or transapical approach) is an option in selected patients who are not considered good candidates for surgery
AR etiology
Supravalvular: aortic root disease (Marfan’s, atherosclerosis and dissecting aneurysm, connective tissue disease)
Valvular: congenital (bicuspid aortic valve, large VSD), IE
Acute Onset: IE, aortic dissection, trauma, failed prosthetic valve
AR pathophysiology
Volume overload LV dilatation increased SV, high sBP and low dBP increased wall tension pressure overload LVH (low dBP decreased coronary perfusion)
AR symptoms
Usually only becomes symptomatic late in disease when LV failure develops
Dyspnea, orthopnea, PND, syncope, angina
AR Physical exam
Waterhammer pulse, bisferiens pulse, femoral-brachial sBP >20 (Hill’s test wide pulse pressure), hyperdynamic apex, displaced PMI, heaving apex
Auscultation: early decrescendo diastolic murmur at LLSB (cusp pathology) or RLSB (aortic root pathology), best heard sitting, leaning forward, on full expiration, soft S1, absent S2, S3 (late)
AR investigations
ECG: LVH, LAE CXR: LVH, LAE, aortic root dilatation
Echo/TTE: quantify AR, leaflet or aortic root anomalies
Cath: if >40 yr and surgical candidate – to assess for ischemic heart disease
Exercise testing: hypotension with exercise
AR treatment
Asymptomatic: serial echos, afterload reduction (e.g. ACEI, nifedipine, hydralazine)
Symptomatic: avoid exertion, treat CHF
Surgery if: NYHA class III-IV CHF; LV dilatation and/or LVEF <50% with/without symptoms
AR surgical options
Valve replacement: most patients
Valve repair: very limited role
Aortic root replacement (Bentall procedure): – when ascending aortic aneurysm present valved conduit used
MITRAL STENOSIS etiology
Rheumatic disease most common cause, congenital (rare)
MITRAL STENOSIS definition
Severe MS is mitral valve area (MVA) <1.5 cm2
MITRAL STENOSIS pathophysiolgy
MS fixed CO and LAE increased LA pressure pulmonary vascular resistance and CHF; worse with AFib (no atrial kick) tachycardia (decreased atrial emptying time) and pregnancy (increased preload)
MITRAL STENOSIS symptoms
SOB on exertion, orthopnea fatigue, palpitations, peripheral edema, malar flush, pinched and blue facies (severe MS)
MITRAL STENOSIS physical exam
AFib, no “a” wave on JVP, left parasternal lift, palpable diastolic thrill at apex Auscultation: mid-diastolic rumble at apex, best heard with bell in left lateral decubitus position folowing exertion, loud S1, OS following loud P2 (heard best du ing expiration), long dastolic murmur and short A2-OS interval correlate with worse MS
MITRAL STENOSIS investigations
ECG: NSR/AFib, LAE (P mitrale), RVH, RAD
CXR: LAE, CHF, mitral valve calcification
Echo/TTE: shows restricted opening of mitral valve
Cath: indicated in concurrent CAD if >40 yr (male) or >50 yr (female)
MITRAL STENOSIS treatment
Avoid exertion, fever (increased LA pressure), treat AFib and CHF, increase diastolic filling time (β-blockers, digitalis) Surgery if: NYHA class III-IV CHF and failure of medical therapy
MITRAL STENOSIS invasive options
Percutaneous balloon valvuloplasty: young rheumatic pts and good leaflet morphology (can be determined by echo), asymptomatic pts with moderate-severe MS, pulmonary HTN
Contraindication: left atrial thrombus, moderate MR
Open Mitral Commissurotomy: if mild calcification + leaflet/chordal thickening – restenosis in 50% pts in 8 yr
Valve replacement: indicated in moderate-severe calcification and severely scarred leaflets
MR etiology
Mitral valve prolapse, congenital cleft leaflets LV dilatation/aneurysm (CHF, DCM, myocarditis), IE abscess, Marfan’s syndrome, HOCM, acute MI, myxoma, mitral valve annulus calcification, chordae/papillary muscle trauma/ischemia/rupture (acute), rheumatic disease
MR pathophysiolgoy
Reduced CO increased LV and LA pressure LV and LA dilatation CHF and pulmonary HTN
MR symptoms
Dyspnea, PND, orthopnea, palpitations, peripheral edema
MR physical exam
Displaced hyperdynamic apex, left parasternal lift, apical thrill
Auscultation: holosystolic murmur at apex, radiating to axilla ± mid-diastolic rumble, loud S2 (if pulmonary HTN), S3
MR investigations
ECG: LAE, left atrial delay (bifid P waves), ± LVH
CXR: LVH, LAE, pulmonary venous HTN
Echo: etiology and severity of MR, LV function, leaflets
Swan-Ganz Catheter: prominent LA “v” wave
MR treatment
Asymptomatic: serial echos
Symptomatic: decrease preload (diuretics), decrease afterload (ACEI) for severe MR and poor surgical candidates; stabilize acute MR with vasodilators before surgery
Surgery if: acute MR with CHF, papillary muscle rupture, NYHA class III-IV CHF, AF, increasing LV size or worsening LV function, earlier surgery if valve repairable (>90% likelihood) and patient is low-risk for surgery
MR surgical options
Valve repair: >75% of pts with MR and myxomatous mitral valve prolapse – annuloplasty rings, leaflet repair, chordae transfers/shorten/replacement
Valve replacement: failure of repair, heavily calcified annulus
Advantage of repair: low rate of endocarditis, no anticoagulation, less chance of reoperation
TS etiology
Rheumatic disease, congenital, carcinoid syndrome, fibroelastosis; usually accompanied by MS (in RHD)
TS pathophysiology
Increased RA pressure right heart failure decreased CO and fixed on exertion
tS symptoms
Peripheral edema, fatigue, palpitations
TS physical exam
Prominent “a” waves in JVP, +ve abdominojugular reflux, Kussmaul’s sign, diastolic rumble 4th left intercostal space
TS investigations
ECG: RAE
CXR: dilatation of RA without pulmonary artery enlargement
Echo: diagnostic
TS teatment
Preload reduction (diuretics), slow HR
Surgery if: only if other surgery required (e.g. mitral valve replacement)
TS surgical options
Valve Replacement:
– if severely diseased valve
– bioprosthesis preferred
TR etiology
RV dilatation, IE (particularly due to IV drug use), rheumatic disease, congenital (Ebstein anomaly), carcinoid
TR pathophysiology
RV dilatation TR further RV dilatation right heart failure
TR symptoms
Peripheral edema, fatigue, palpitations
TR physical exam
“cv” waves in JVP, +ve abdominojugular reflux, Kussmaul’s sign, holosystolic murmur at LLSB accentuated by inspiration, left parasternal lift
TR investigations
ECG: RAE, RVH, AFib CXR: RAE, RV enlargement Echo: diagnostic
TR treatment
Preload reduction (diuretics) Surgery if: only if other surgery required (e.g. mitral valve replacement)
TR surgical options
Annuloplasty (i.e. repair, rarely replacement
PS etiology
Usually congenital, rheumatic disease (rare), carcinoid syndrome
PS pathophysiolgoy
Increased RV pressure RV hypertrophy right heart failure
PS symptoms
Chest pain, syncope, fatigue, peripheral edem
PS physical exam
Systolic murmur at 2nd left intercostal space accentuated by inspiration, pulmonary ejection click, right sded S4
PS investigations
ECG: RVH
CXR: prominent pulmonary arteries enlarged RV
Echo: diagnostic
PS treatment
Balloon valvuloplasty if severe symptoms
PS surgical options
Percutaneous or open balloon valvuloplasty
PR etiology
Pulmonary HTN, IE, rheumatic disease, tetrology of Fallot (post-repair)
PR pathophysiology
Increased RV volume increased wall tension RV hypertrophy right heart failure
PR symptoms
Chest pain, syncope, fatigue, peripheral edema
PR Physical exam
Early diastolic murmur at LLSB, Graham Steell (diastolic) murmur 2nd and 3rd left intercostal space increasing with inspiration
PR investigations
ECG: RVH
CXR: prominent pulmonary arteries if pulmonary HTN; enlarged RV
Echo: diagnostic
PR treatment
Rarely requires treatment; valve replacement (rarely done)
PR surgical options
Pulmonary valve replacement
Mitral valve prolapse etiology
Myxomatous degeneration of chordae, thick, bulky leaflets that crowd orifice, associated with Marfan’s syndrome, pectus excavatum, straight back syndrome, other MSK abnormalities; <3% of population
Mitral valve prolapse pathophysiology
Mitral valve displaced into LA during systole; no causal mechanisms found for symptoms
Mitral valve prolapse symptoms
Prolonged, stabbing chest pain, dyspnea, anxiety/panic, palpitations, fatigue presyncope
Mitral valve prolapse physical exam
Auscultation: mid-systolic click (due to billowing of mitral leaflet into LA; tensing of redundant valve tissue); mid to late systolic murmur at apex, accentuated by Valsalva or squat-to-stand maneuvers
Mitral valve prolapse investigations
ECG: non-specific ST-T wave changes, paroxysmal SVT, ventricular ectopy
Echo: systolic displacement of thickened mitral valve leaflets into LA
Mitral valve prolapse treatment
Asymptomatic: no treatment; reassurance Symptomatic: β-blockers and avoidance of stimulants (caffeine) for significant palpitations, anticoagulation if AFib
Mitral valve prolapse surgical options
Mitral valve surgery (repair favoured over replacement) if symptomatic and significant MR
Etiology of acute pericarditis/pericardial effusion
• idiopathic is most common: presumed to be viral
• infectious
■ viral: Coxsackie virus A, B (most common), echovirus
■ bacterial: S. pneumoniae, S. aureus
■ TB • fungal: histoplasmosis, blastomycosis
- post-MI: acute (direct extension of myocardial inflammation, 1-7 d post-MI), Dressler’s syndrome (autoimmune reaction, 2-8 wk post-MI)
- post-cardiac surgery (e.g. CABG), other trauma
- metabolic: uremia (common), hypothyroidism
- neoplasm: Hodgkin’s, breast, lung, renal cell carcinoma, melanoma
- collagen vascular disease: SLE, polyarteritis, rheumatoid arthritis, scleroderma
- vascular: dissecting aneurysm
- other: drugs (e.g. hydralazine), radiation, infiltrative disease (sarcoid)
acute pericarditis/pericardial effusion signs and symptoms
- diagnostic triad: chest pain, friction rub and ECG changes (diffuse ST elevation and PR depression with reciprocal changes in aVR)
- pleuritic chest pain: alleviated by sitting up and leaning forward
- pericardial friction rub: may be uni-, bi-, or triphasic; evanescent and rare
- ± fever, malaise
acute pericarditis/pericardial effusion investigations
- ECG: initially diffuse elevated ST segments ± depressed PR segment, the elevation in the ST segment is concave upwards → 2-5 d later ST isoelectric with T wave flattening and inversion
- CXR: normal heart size, pulmonary infiltrates
- Echo: performed to assess for pericardial effusion
acute pericarditis/pericardial effusion treatment
- treat the underlying disease
- anti-inflammatory agents (high dose NSAIDs/ASA, steroids use controversial), analgesics
- colchicine reduces the rate of incessant/recurrent pericarditis (ICAP N Engl J Med 2013; 369:1522-1528
acute pericarditis/pericardial effusion complications
• recurrent episodes of pericarditis, atrial arrhythmia, pericardial effusion, tamponade, constrictive pericarditis
Acute pericarditis triad
Chest pain
friction rub
ECG changes
Pericardial effusion etiology
• transudative (serous) • CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism
• exudative (serosanguinous or bloody)
■ causes similar to the causes of acute pericarditis
■ may develop acute effusion secondary to hemopericardium (trauma, post-MI myocardial rupture, aortic dissection)
• physiologic consequences depend on type and volume of effusion, rate of effusion development, and underlying cardiac disease
Pericardial effusion signs and symptoms
- may be asymptomatic or similar to acute pericarditis
- dyspnea, cough
- extra-cardiac (esophageal/recurrent laryngeal nerve/tracheo-bronchial/phrenic nerve irritation)
- JVP increased with dominant “x” descent
- arterial pulse normal to decreased volume, decreased pulse pressure
- auscultation: distant heart sounds ± rub
- Ewart’s sign
Pericardial effusion investigations
• ECG: low voltage, flat T waves, electrical alternans (classic, but not sensitive to exclude effusion)
■ be cautious in diagnosing STEMI in a patient with pericarditis and an effusion - antiplatelets may precipitate hemorrhagic effusion
- CXR: cardiomegaly, rounded cardiac contour
- ER: bedside ultrasound with subxiphoid view showing fluid in pericardial sac
- Echo (procedure of choice): fluid in pericardial sac
- pericardiocentesis: definitive method of determining transudate vs. exudate, identify infectious agents, neoplastic involvement
Pericardial effusion treatment
- mild: frequent observation with serial echos, treat underlying cause, anti-inflammatory agents
- severe: treat as in tamponade
What is Ewart’s sign
Bronchial breathing and dullness to percussion at the lower angle of the left scapular in pericardial effusion due to effusion compressing left lower lobe of lung
Cardiac tamponade etiology
- major complication of rapidly accumulating pericardial effusion
- cardiac tamponade is a clinical diagnosis
- any cause of pericarditis but especially trauma, malignancy, uremia, proximal aortic dissection with rupture
Cardiac tamponade pathophysiology
high intra-pericardial pressure → decreased venous return → decreased diastolic ventricular filling → decreased CO → hypotension and venous congestion
Cardiac tamponade signs and symptoms
- tachypnea, dyspnea, shock, muffled heart sounds
- pulsus paradoxus (inspiratory fall in systolic BP >10 mmHg during quiet breathing)
- JVP “x descent only, blunted “y” descent
- hepatic congestion/peripheral edema
Cardiac tamponade investigations
- ECG: electrical alternans (pathognomonic variation in R wave amplitude), low voltage
- echo: pericardial effusion, compression of cardiac chambers (RA and RV) in diastole
- cardiac catheterization
Cardiac tamponade treatment
- pericardiocentesis: Echo-guided
- pericardiotomy
- avoid diuretics and vasodilators (these decrease venous return to already under-filled RV → decrease LV preload → decrease CO)
- IV fluid may increase CO
- treat underlying cause
Cardiac tamponade classi quartet
Hypotension
Increased JVP
Tachycardia
Pulsus paradoxus
What is Beck’s triad
Hypotension
Increased JVP
Muffled heart sounds
Constrictive pericarditis etiology
- chronic pericarditis resulting in fibrosed, thickened, adherent, and/or calcified pericardium
- any cause of acute pericarditis may result in chronic pericarditis
- major causes are idiopathic, post-infectious (viral, TB), radiation, post-cardiac surgery, uremia, MI, collagen vascular disease
Constrictive pericarditis signs and symptoms
- dyspnea, fatigue, palpitations
- abdominal pain
• may mimic CHF (especially right-sided HF)
■ ascites, hepatosplenomegaly, edema
- increased JVP, Kussmaul’s sign (paradoxical increase in JVP with inspiration), Friedreich’s sign (prominent “y” descent)
- BP usually normal (and usually no pulsus paradoxus)
- precordial examination: ± pericardial knock (early diastolic sound)
Constrictive pericarditis investigations
- ECG: non-specific – low voltage, flat T wave, ± AFib
- CXR: pericardial calcification, effusions
- echo/CT/MRI: pericardial thickening, ± characteristic echo-Doppler findings
- cardiac catheterization: equalization of end-diastolic chamber pressures (diagnostic)
Constrictive pericarditis treatment
- medical: diuretics, salt restriction
- surgical: pericardiectomy (only if refractory to medical therapy)
- prognosis best with idiopathic or infectious cause and worst in post-radiation; death may result from heart failure
DDX of pulsus paradoxus
Constrictive pericarditis (rarely)
Severe obstrcitve pulmonary disease
Tension pneumothorax
PE
Cardiogenic shock
Cardiac tamponade
Constrictive pericarditis characteristics vs cardiac tamponade
JVP
y>x vs x>y
Kussmaul’s sign
present vs absent
pulsus paradoxus
uncommon vs always
pericardial knock
present vs absent
hypotension
variable vs severe
ACEI examples
enalapril (Vasotec®), perindopril (Coversyl®), ramipril (Altace®), lisinopril (Zestril®)
ACEI MOA
Inhibit ACE-mediated conversion of angiotensin I to angiotensin II (AT II), causing peripheral vasodilation and decreased aldosterone synthesis
ACEI indications
HTN, CAD, CHF, post-MI, DM
ACEI contraindications
Bilateral renal artery stenosis
pregnancy
caution n decreased GFR
ACEI side effects
Dry cough
10% hypotension
fatigue
hyperkalemia
renal insufficiency
angioedema
ARB examples
candesartan, irbesartan, valsartan
ARB MOA
Block AT II receptors, causing similar effects to ACEI
ARB indications
Same as ACEI, although evidence is generally less for ARBs; often used when ACEI are not tolerated
ARB contraindications
Same as ACEI
ARB side effects
Similar to ACEI, but do not cause dry cough
Direct renin inhibitors (DRIs) examples
aliskiren
Direct renin inhibitors (DRIs) moa
Directly blocks renin thus inhibiting the conversion of angiotensinogen to angiotensin I; this also causes a decrease in AT II
Direct renin inhibitors (DRIs) indications
HTN (exact role of this drug remains unclear)
Direct renin inhibitors (DRIs)contraindications
Pregnancy, severe renal impairmen
Direct renin inhibitors (DRIs) side effects
Diarrhea, hyperkalemia (higher risk if used with an ACEI), rash, cough, angioedema, reflux, hypotension, rhabdomyolysis, seizure
BBlockers examples
β1 antagonists - atenolol, metoprolol, bisoprolol
β1/β2 antagonists - propranolol
α1/β1/β2 antagonists - labetalol, carvedilol
β1 antagonists with intrinsic sympathomimetic activity - acebutalol
BBlockers moa
Block β-adrenergic receptors, decreasing HR, BP, contractility, and myocardial oxygen demand, slow conduction through the AV node
BBlockers indications
HTN, CAD, acute MI, post-MI, CHF (start low and go slow), AFib, SVT
BBlockers contraindications
Sinus bradycardia,
2nd or 3rd degree heart block
hypotension
WPW
Caution in asthma, claudication, Raynaud’s phenomenon, and decompensated CHF
BBlockers side effects
Hypotension
fatigue
lightheadedness
depression
bradycardia
hyperkalemia
bronchospasm
impotence
depression of counterregulatory response to hypoglycemia
exacerbation of Raynaud’s phenomenon, and claudication
CCB examples
Benzothiazepines Phenylaklylamines (non dihydropyridines) - diltiazem, verpamil
Dihydropyridines - amlodipine (Norvasc), nifedipine (Adalat), felodipine (Plendil)
CCB moa
Non- dihydropyridines - Block smooth muscle and myocardial calcium channels causing effects similar to β-blockers Also vasodilate
Dihydropyridines - Block smooth muscle calcium channels causing peripheral vasodilation
CCB indications
Non - DH - HTN, CAD SVT, diastolic dysfunction
DH - HTN, CAD
CCB contraindications
Non-DH - Sinus bradycardia, 2nd or 3rd degree heart block, hypotension, WPW, CHF
DH - Severe aortic stenosis and liver failure
CCB side effects
Non-DH - Hypotension, bradycardia, edema Negative inotrope
DH - hypotension, edema, flushing, headache, light-headedness
Thiazide diuretics examples
hydrochlorthiazide, chlorthalidone, metolazone
Thiazide diuretics moa
Reduce Na+ reabsorption in the distal convoluted tubule (DCT)
Thiazide diuretics indications
HTN (drugs of choice for uncomplicated HTN)
Thiazide diuretics contraindications
Sulfa allergy, pregnancy
Thiazide diuretics side effects
Hypotension, hypokalemia, polyuria
Loop diuretics examples
furosemide
Loop diuretics moa
Blocks Na+/K+-ATPase in thick ascending limb of the loop of Henle
Loop diuretics indications
CHF, pulmonary or peripheral edema
Loop diuretics contraindications
Hypovolemia, hypokalemia
Loop diuretics side effects
Hypovolemia, hypokalemic metabolic alkalosis
Aleosterone receptor antagonists examples
spironolactone, eplenerone
Aleosterone receptor antagonists moa
Antagonize aldosterone receptors
Aleosterone receptor antagonists indications
HTN, CHF, hypokalemia
Aleosterone receptor antagonists contraindications
Renal insufficiency, hyperkalemia, pregnancy
Aleosterone receptor antagonists side effects
Edema, hyperkalemia, gynecomastia
