Idiopathic and Viral are the most common causes
Viral: Cox A & B, Echovirus, Adenovirus, HIV, EBV, Influenza, Hep B
Bacterial: Staph, Strep Pneumo, Mening., Mycobacterium, Rickettsia, Borrelia, Mycoplasma
Fungal: Histo, Blasto, Coccidiomycosis
Malignancies: Met from breast, lung, melanoma, leukemia, lymphoma or primary mesotheliomas
Presents with sharp substernal pain which can be pleuritic. Pain is increased when lying down and less when sitting up and leaning forward. Radiation to left or both trapezius ridge is almost pathognomonic
High pitched triphasic murmur is classic.
Diffuse ST elevations with reciprical decrease in AVR and V1, Concave upwards PR depression
Deep symmetric inverted Ts
Early post-mi pericardial effusions/pericarditis are possible
On occasion, however, the EKG may not be completely classic for MI or pericarditis. The clinician should be aware that the ratio of the ST-segment elevation (in millimeters) to T-wave amplitude (in millimeters) in excess of 0.24 in lead V6 strongly supports the diagnosis of pericarditis and this finding has been shown to reliably distinguish pericarditis from other repolarization abnormalities (1,2).References: (1) Lewis GD, et al. Case records of the Massachusetts General Hospital. Case 8-2007. A 48-year-old man with chest pain followed by cardiac arrest N Engl J Med 2007;356: 1153-62. (2) Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal variant: new electrocardiographic criteria Circulation 1982;65:1004-1009.
ECG evolution The electrocardiogram in acute pericarditis evolves through four stages [ 6,7]. (See “Electrocardiogram in pericarditis and pericardial effusion”).
- Stage 1, seen in the first hours to days, is characterized by diffuse ST elevation (typically concave up) with reciprocal ST depression in leads aVR and V1 ( show ECG 1). There is also an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST segments typically change in opposite directions, although the PR deviations, which are highly specific although not sensitive, are frequently overlooked.
- Stage 2 is characterized by normalization of the ST and PR segments.
- Stage 3 is characterized by the development of diffuse T wave inversions, generally after the ST segments have become isoelectric. However, this stage is not seen in some patients. In addition, patients with concomitant myocarditis may show ST and T changes resembling those with pericarditis alone or acute ischemia.
- In stage 4, the ECG may become normal or the T wave inversions may persist indefinitely (“chronic” pericarditis).
III. Pericarditis vs. Acute MI
Diffuse ST-segment elevation
May be localized rather than diffuse
But no reciprocal ST-segment depression! (except perhaps in aVR and V1)
ST-segment elevation is concave upwards
Beware that AMI may have similar ST-segment morphology
ST-segment elevation that is convex upwards or horizontal strongly favors
Additional pearl regarding ST-elevation
STE II > STE III strongly favors acute pericarditis
STE III > STE II very strongly favors acute MI
PR-segment depression (downsloping)
Primarily present in viral pericarditis
Often an early, transient finding
PR-segment elevation in aVR
May also be present in other diseases (e.g. AMI)
Often absent in constrictive pericarditis
Chest pain tends to be positional, pleuritic
Beware that 16% of AMIs may present with positional or pleuritic pain!
Factors strongly favoring acute pericarditis: pronounced PR-segment depression
(downsloping) in multiple leads; friction rub
Factors strongly favoring AMI: ST-segment elevation that is convex upwards;
reciprocal ST-segment depression (in leads other than aVR and V
1); known new Qwaves
(Amal Mattu, MD–Deadly Misdiagnoses in ECG Interpretation)
ESR will usually be elevated.
ASA 650 po Q6 or Motrin 600-800 PO Q6-8 or Indomethacin 50-75 mg po Q6-8 or Prednisone 60 mg po OD (only if others are contraindicated or fail. must rule out bacterial/tb cause before giving)
Consider adding Colchicine 0.6 mg BID to ibuprofen or ASA.
always add colchicine (Imazio M, Circulation 2005) for all pericarditis types
PREDICTING RISK IN ACUTE PERICARDITIS The decision as to whether or not to admit or discharge patients who present with acute pericarditis can often be a difficult one. An editorial in Heart provides some useful guidance about predicting risk. Features associated with high risk include the following: a pericardial effusion of more than 2 cm; anticoagulant therapy; malignancy; trauma; fever; subacute onset; immunosuppression; evidence of myopericarditis; atypical electrocardiogram evolution; pulsus paradoxus; raised acute phase reactants (Heart 2008;94:3989)
Typically, hospitalization is unnecessary for acute pericarditis unless poor prognostic indicators are identified. Name those indicators that mandate hospitalization.Myocarditis, cancer, conditions that confer a predisposition to tamponade (pericardial effusion > 2 cm, trauma, anticoagulation), and indicators of possible purulent pericarditis (fever, immunosuppression) (NEJM, vol. 356, pg. 1153 from emedhome).
A Randomized Trial of Colchicine for Acute Pericarditis Massimo Imazio, M.D., Antonio Brucato, M.D., Roberto Cemin, M.D., Stefania Ferrua, M.D., Stefano Maggiolini, M.D., Federico Beqaraj, M.D., Daniela Demarie, M.D., Davide Forno, M.D., Silvia Ferro, M.D., Silvia Maestroni, M.D., Riccardo Belli, M.D., Rita Trinchero, M.D., David H. Spodick, M.D., and Yehuda Adler, M.D. for the ICAP Investigators N Engl J Med 2013; 369:1522-1528 It is good
Effusion-15 to 60 cc of fluid normally. Need 250 cc to produce megaly on C-XR
Pericardiocentesis-pericardial fluid does not clot. Put pt in LLR if possible.
Dresslers-late pericarditis post-mi. fever, pleuritis, leukocytosis, friction rub, effusion
Low voltage = I+II+III < 15 or V1,V2,V3<30
pts with viral or idiopathic pericarditis s effusion can go home
22% of pericarditis will have troponin abnormalities (Eur Heart J 2000;21(10):832)
Beck’s Triad: hypotension, JVD (originally an increased CVP), distant heart sounds
Narrow pulse pressure
Kussmaul’s=rise in CVP with inspiration
Dopamine or Dobutamine
Ultrasound sniff test, IVC normally collapses at least 50% when sharp inhalation is taken through nose. In tamponade, there will be no collapse.
Does this pt with an effusion have a tamponade (JAMA 2007;297:1810)
Does this pt have tamponade
diastolic collapse-right atrial is non-specific. In para-sternal or subcostal, use m-mode. from mitral opening to closing is diastole. if free wall of RV moves backwards, then tamponade physio exists.
transvalvular doppler inflow-apical view, tough without a good machine
IVC plethora-loss of resp variation
Does this patient have tamponade?(best review)
fluid loading (500 ml NS in this study) improved cardiac output in pericardial tamponade patients with shock (Circulation. 2008;117:1545-1549)
Low pressure tamponade occurs in patients who are intravascularly depleted (Circulation. 2006;114:945-952)
may present c same s/s as pericarditis
Troponin levels will be elevated
Can be viral, bacterial, parasitic, kawasaki’s, SLE, Sarcoid, sulfonamides, PCNs, methyldopa, Cocaine, Toluene
ABX if bacterial
High dose IVIG may be helpful
Avoid dig as myocardium will be sensitized to it
The patient presented on the previous page did well with a period of observation and a course of ibuprofen and metoprolol. His echocardiogram revealed mild left posterior wall hypokinesis and mildly decreased LV systolic performance. Cardiac MRI demonstrated inflammatory changes in the myocardium sparing the endocardium, thus confirming the diagnosis of myocarditis (with acute MI, there is involvement of the endocardium). Cardiac MRI is being used with increasing frequency as part of the evaluation of acute myocarditis; it has been shown to have sensitivities and specificities approaching 100% for the diagnosis.(Emedhome)
diseases of unknown etiology
Idiopathic Dilated Cardiomyopathy (IDC)
four chamber dilation and pump failure
Rx with diuretics, dig, vasodialators
Anticoagulate if intracardiac thrombi, systemic embolism, chronic A-Fib
predisposed to clots in either ventricle
consider ICD b/c of risk of dysrhythmia
ACEI re excellent, also consider b-blockade
Restrictive Cardiomyopathy (RC)
diastolic restriction of ventricular filling.
atria will enlarge greater than the ventricles
Hypertrophic Cardiomyopathy (HCM)
left ventricular hypertrophy which is asymmetrical with the septum being affected more. >50% of the time, there is autosomal dominant inheritance.
DOE, Ischemic chest pain, palpitations, syncope, sudden death.
Mid-systolic murmur which increases with valsalva or any other maneuver that decreases preload
Will see a prominent a-wave on neck exam.
You will see septal Q waves on ECG, looks like an old infarction without a history of infarction.
Shock any a-fib and then anticoagulate.
Do not give dig or nitrates/vasodilators as these will increase outflow obstruction.
Broken Heart Syndrome
Takotsubo cardiomyopathy is a transient cardiomyopathy with a presentation identical to that of an acute ST-segment elevation anterior MI – with cardiac biomarker release, chest pain, and myocardial dysfunction – with no evidence of angiographic disease on cardiac catheterization.
These patients have profound and peculiar reversible cardiac wall motion abnormalities and dysfunction. In Japanese, “tako-tsubo” means “fishing pot for trapping octopus”. The heart’s appearance on a left ventriculogram in Takotsubo cardiomyopathy appears similar to this octopus jar: wide at the apex during end systole, with a narrowing where there is basilar hyperkinesis.
Almost invariably, Takotsubo cardiomyopathy is precipitated by acute emotional stress, hence, it is also known as “stress cardiomyopathy” or “broken-heart syndrome”. A preponderance of patients with this syndrome are postmenopausal females.
One case series reported that approximately 2.2% of ST-elevation acute coronary syndromes presenting to a referral hospital during 2002-2003 were consistent with Takotsubo cardiomyopathy (3). Current evidence suggests thrombolytics may only be harmful in these patients, with the inherent bleeding risks of the therapy without documented benefits.
References:(1) Kolkebeck TE, et al. Takotsubo cardiomyopathy: an unusual syndrome mimicking an ST-elevation myocardial infarction Am J Emerg Med 2007;25: 92-5. (2) Virani SS, et al. Takotsubo cardiomyopathy, or broken-heart syndrome Tex Heart Inst J 2007;34: 76-9. (3) Bybee KA. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome Am J Cardiol 2004;94:343346.
Takotsubo is Japanese for octopus bottle. During systole, the hearts akinetic apex balloons outward as the base of the heart contracts and it resembles the round bottle with a narrow neck that is used to trap octopi in Japan (Figure 4). This cardiomyopathy occurs in the absence of coronary artery disease. The etiology is unknown, but one hypothesis is that vasospasm of the microvasculature occurs due to elevated circulating catecholamines from a stressful event and the myocardium is stunned. It differs from the vasospam of Prinzmetals angina in that large vessel spasm cannot be provoked with ergonovine or acetylcholine. It is not clear why the cardiomyopathy is regionalized to the apex. Women are affected more often than men, particularly over the age of 60 years . In Japan, it has been estimated to account for 1% to 2% of patients provisionally diagnosed with ST elevation myocardial infarctions before catheterization, but is infrequently reported outside Japan (1). Significant emotional stress often involving loved ones usually precedes presentation, leading to the term broken heart syndrome. Increasingly, medical stressors are recognized as precipitants: surgery, medical procedures, acute abdominal pain, stroke, asthma flare, and severe alcohol abuse or withdrawal are the most commonly identified precursors (1, 2 and 3). The presenting symptom may be chest pain, dyspnea, or syncope. (75K) Figure 4. A takotsubo. Reprinted from American Heart Journal, 143, Kurisu S, Inoue I, Kawagoe T, et al. Takotsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction, Pages 44855 (8), Copyright 2002, with permission from Elsevier. Patients initially have regional ST elevations that progress over time to Q waves and inverted T waves. One small retrospective case series suggests that EKG criteria alone can distinguish between infarction and Takotsubo cardiomyopathy (4). Lack of inferior reciprocal changes, and ST segment elevation greater in leads V4V6 than leads V1V3 suggests Takotsubo cardiomyopathy. However, EKG criteria do not distinguish Takotsubo cardiomyopathy from infarction when the culprit lesion is distal to the left anterior descending artery, and no criteria distinguish Takotsubo from myocarditis (5). It is important to remember that this is a diagnosis of exclusion. Most patients will have elevated serum troponin, but fewer will have elevated serum creatinine kinase (6). Patients are at risk for ventricular rupture, dysrhythmia (polymorphic or monomorphic ventricular tachycardia, and ventricular fibrillation), and left ventricular mural wall thrombus formation and embolization (6 and 7). The mortality during the acute phase ranges between 2% and 4% (3). The EKG and echocardiogram completely normalize within 1050 days. Management focuses on the treatment of left ventricular failure, and hemodynamic support when necessary. This patient was started on a beta-blocker for suspected dysrhythmia, presumed to be the cause of the syncope, and placed on warfarin to prevent thrombus formation at the akinetic apex. Four weeks after the patients second ED visit, the echocardiogram and EKG had completely normalized. The patient is doing well and has contacted her family displaced by the hurricane. As exemplified by this case, patients with Takotsubo cardiomyopathy generally have an excellent outcome if supported through the acute phase of their disease (8).
Specific Heart Muscle Diseases
Toxins: ethanol, cobalt, cocaine, lithium, doxorubicin, daunorubicin, emetine, heavy metals, amphetamines
Nutritional Deficiencies: thiamine, Vit C, Vit B6, Selenium, Kwashiorkor
Metabolic: Hemochromatosis, Glycogen Storage, Hypothyroidism, Hyperthyroidism, Uremia, Pheo, Hypophos
Collagen Vascular Disease
Myocarditis: Viral, Bacterial, Chagas, HIV
| | |