Cardiology Flashcards
> Rapid rule-out protocols for ACS are now well-accepted
-ADAPT (incorporates TIMI score)
-HEART
-EDACS
These stratify patients to low enough risk to justify discharge for further outpatient evaluation
For intermediate risk patients (e.g. HEART score 4-6), admit/obs, get stress test or CCTA
For higher risk patients, admit for full workup and potential aggressive therapy
Chest Pain Evaluation
- Spectrum of disease due to myocardial ischemia
- Unstable angina to acute MI - Ischemic heart disease is the most common cause of death in the US
- 2 million MI and unstable angina patients each year
Acute Coronary Syndrome (ACS)
Usually due to atherosclerosis
Fixed lesion, critical stenosis
Plaque disruption, platelet aggregation, thrombus formation
Results in oxygen supply/demand imbalance leading to cardiac muscle damage
Causes of ACS
Trauma Connective tissue diseases (vasculitis) Metabolic diseases (thickening of vessels) Congenital anomalies Thrombus (DIC, TTP) Emboli (bacterial, non-bacterial) Thoracic aortic dissection Coronary artery dissection Drugs (cocaine) Infectious diseases
Non-Atherosclerotic Causes of ACS
4% of AMIs have normal EKG
Hyperacute T waves (early)
ST segment changes
1mm of elevation in two anatomically
contiguous leads
Elevation usually corresponds to areas of
involvement
Exception: AMI with LBBB
Depression over areas opposite injury
(reciprocal changes). Predictor of larger
MI, increased mortality
T wave inversion: within 4 hours is good
Px sign
Significant Q waves: 1 square wide, 1/3 of
height of R wave
AMI EKG Changes
Differential diagnosis of diffuse STE Acute MI (large one!) Prinzmetal's angina (vasospasm) Pericarditis Ventricular wall aneurysm Benign early repolarization
EKG - ST Elevation
Factors that increase the specificity
ST elevation (horizontal or convex upwards)
Follows coronary anatomy
Reciprocal ST depression
Changes over time (minutes to hours)
May see hyperacute T waves (early)
Q waves (start developing within a few hours)
ST Segment ElevationPredictors of MI
Convex or concave upwards morphology Transient over minutes More common in women Difficult to distinguish from true STEMI Generally underlying CAD is present Usually no reciprocal depression
Causes of ST Segment Elevation:Prinzmetal’s angina/spasm
Convex or concave upwards morphology Persistent ST elevation Large Q waves usually present Usually in anterior leads Easily seen on echo No reciprocal depression Look for old ECGs — no change No serial changes
Causes of ST Segment Elevation:Ventricular Aneurysm
Concave upwards morphology In many leads, maximal in mid-precordial leads with “fishhook” J-point Doesn't change over time No reciprocal depression Men > women, young > old No large Qs
Causes of ST Segment Elevation: “Early Repolarization”
Posterior MI
Usually accompanies inferior MI due to RCA…
But 4-10% will be isolated posterior MI
Look for large R waves with ST depressions in V1, V2 and upright Ts
R:S > 1 = “large R waves”
STEMI and STEMI EquivalentsPMI: ST-depression + tall R-waves in V1-2
EKG indications for emergent reperfusion
STE > 1 mm in 2 contiguous leads
Posterior MI (ST-depression with tall R-
waves and upright Ts in V1-2)
Left bundle branch block with
concordant Sgarbossa criteria
ST-segment elevation measuring ≥1
mm concordant with the QRS in any
lead.
ST-segment depression measuring
≥1 mm in any of the V1 through V3
leads (concordant with the QRS).
A RBBB should not obscure the diagnosis
of an acute MI
STEMI and STEMI Equivalents
Predictors of reperfusion
Normalization of ischemia-related ST elevation
Failure to normalize may indicate the need for “rescue PCI”
Early T wave inversions can be highly specific markers of reperfusion
An accelerated idioventricular rhythm (rate 60-120) is also highly specific for reperfusion
Benign, don’t suppress it
Resolves within seconds to minutes
The EKG in AMI
1-2 hours (rises)
4-6 hours (peaks)
24 hrs (normalizes)
Myoglobin
3-6 hours (rises)
12-24 hours (peaks)
7-10 days (normalizes)
Troponin
3-4 hours (rises)
12-24 hours (peaks)
1-2 days (normalizes)
CK-MB
Advantage: early detection
Disadvantage: poor specificity, especially in trauma, renal failure, hemolytic syndromes
Myoglobin
more specific for AMI than CK-MB
High values predict complications and mortality
Troponin
Elevation without infarction (skeletal disease, muscle exertion, cocaine, renal failure)
Comparing MB to total CK improves specificity
CK-MB
Oxygen Nitrates (sublingual, topical, IV) Contraindicated if sildanefil (Viagra) etc. within 24 hours or if hypotensive Caution/avoid in RV MI Vasodilatation ASA (162-325 mg) ASA alone reduces mortality 23% Combined with thrombolytics, ASA reduces mortality 42% Morphine for persistent pain
Therapy of AMI
Heparin (Unfractionated or LMWH)
Beta blockers – early IV use is discouraged
Give within 24 hours orally but no rush
Contraindications (asthma, CHF, bradycardia, hypotension; caution in RV MI)
Addl. platelet inhibitors (in ED or cath lab)
GP Ilb/IIIa receptor antags IV
Clopidogrel, ticagrelor: can give oral load
Prasugrel 60 mg oral load at cath; avoid if history of TIA or stroke
Therapy of AMI
Thrombolysis vs. percutaneous coronary intervention
Outcomes have shown consistent benefit with PCI over thrombolytics
Guidelines recommend PCI if balloon inflation can be performed within 90 minutes
Window of benefit over lytics extended if chest pain > 6 hours or if cardiogenic shock
Therapy of AMI
Concerning Sx’s greater than 30 minutes but less than 12 hours, not relieved by nitroglycerin
EKG criteria of STEMI as previously discussed
STE in 2 contiguous leads
Posterior STEMI
[LBBB with Sgarbossa concordant criteria for EM boards]
PCI delayed greater than 90-120 minutes
Thrombolytic Therapy Indications
Absolute
PCI immediately available
Active bleeding from any site
CVA within 6 months or hemorrhagic CVA at any time in the past
Intracranial or intraspinal surgery or trauma within 2 months
Intracranial or intraspinal neoplasm, aneurysm or AV malformation
Suspected aortic dissection
Contraindications to Thrombolytic Therapy
Relative
History of GI bleed
Prolonged CPR
Surgical or invasive procedure within 3 weeks
Severe bleeding diathesis or thrombocytopenia
Uncontrolled hypertension (diastolic >120 after treatment)
Significant trauma within 4 weeks
Pregnancy or <10 days post- partum
Active cavitary lung disease
Known allergy to agent
Contraindications to Thrombolytic Therapy
Bleeding
Serious bleeding up to 5%
Intracranial hemorrhage: 0.5-1%. Higher risk with uncontrolled BP, age > 65, low body weight
Complications of Thrombolytic Therapy
Chest pain resolved
ST elevation resolved
Reperfusion dysrhythmias, T-wave inversions develop
Evidence of Reperfusion (within 90 min)
Arrhythmias with poor prognosis
2˚ Mobitz II (progress to 3˚)
3˚ AV block from anterior MI
Persistent sinus tach, A-fib
New BBB, bifascicular block (RBBB (RBBB + hemiblock)
Left posterior hemiblock (large infarct size)
Increased risk of pump failure, mortality
High-grade blocks (i.e. Mobitz II, 3°AV block) seen in anterior MI due to structural loss of conduction tissue -> will need pacemaker
Early Complications of AMI (1)
Cardiogenic shock: usually >40% of LV muscle necrosed
High mortality
Treatment: fluids, inotropes, IABP (intra-aortic balloon pump) to increase coronary blood flow
Papillary muscle dysfunction
Acute mitral regurgitation (usually due to ischemic dysfunction of papillary muscles)
Recurrent chest pain, ischemia, re-infarction
Need immediate cath, possible CABG
Do not re-dose lytics
Early Complications of AMI
Right ventricular infarction
Associated with inferior MI
Do right sided chest leads (especially V4R) looking for ST elevation
Triad of hypotension, JVD and clear lungs
RV loses function, acts as conduit only (not pump)
Heart becomes very preload-dependent
Use NTG and morphine with caution (can drop BP precipitously)
Use fluids liberally (not pressors) to augment preload as long as lungs clear
Early Complications of AMI
Recurrent chest pain Embolism (from mural thrombus) Pericarditis Post-MI (seen 1-7 days after transmural infarct) Treatment: NSAIDs Dysrhythmias
Late Complications of AMI
pericarditis 2-8 weeks post-MI (probably a continuum with earlier pericarditis)
Fever, leukocytosis, friction rub, pericardial and
pleural effusions. Treatment: NSAIDs & + steroids
Dressler’s Syndrome
Myocardial rupture (1-2 weeks post-MI)
LV free wall: often results in acute tamponade, hypotension and death
Papillary muscle rupture (first week post-MI)
Results in acute MR and acute onset CHF
Septal wall rupture (7-10 days post-MI)
Results in acute VSD with acute onset CHF
Anterior or inferior MI
All seen in first 2 weeks post-MI
All need hemodynamic support, IABP, OR
Late Complications of AMI
Primary myocardial diseases (low output failure) Hypertension (most common cause) Coronary artery disease, MI Valvular heart disease Cardiomyopathy (i.e. ischemic)
Etiology of Heart Failure
Increased workload on heart (high output failure) Thyrotoxicosis Anemia A-V fistula Paget's disease of the bone Berry berry
Etiology of Heart Failure
Increased workload on heart (high output failure) Thyrotoxicosis Anemia A-V fistula Paget's disease of the bone Beriberi
Etiology of Heart Failure
Left-sided or right-sided systolic dysfunction
Impaired contractility low ejection fraction, low cardiac output (e.g. MI, dilated cardiomyopathy) high renin and angiotensin levels, high afterload
Classification of Heart Failure
Diastolic dysfunction
Impaired relaxation of heart in diastole leads to decreased LV filling and pulmonary congestion
May eventually lead to systolic dysfunction
Causes: ischemia, hypertrophy, amyloidosis
Classification of Heart Failure
Left sided failure Dyspnea Orthopnea Tachycardia S3 gallop
Pulmonary edema
Redistribution
Kerley B lines (Interstitial edema / lymphatic engorgement)
Alveolar edema
Presentation of Heart Failure
Acute right sided failure (uncommon)
Pulmonary embolism
RV infarction
Signs and symptoms
JVD early
Peripheral edema
Right upper quadrant pain (liver engorgement)
Pulsatile, enlarged liver
The most common cause of right sided failure is left sided failure
Longstanding heart failure is usually due to dysfunction of both ventricles
Presentation of Heart Failure
Treat underlying cause (remember ischemia!)
Symptomatic treatment with O2, CPAP, BiPAP
Noninvasive ventilation is the single best tx!
Preload reduction with Nitrates Diuretics (after afterload reduction) Nesiritide (?? utility in the ED) Morphine (doubtful) Phlebotomy (decrease circulatory volume, best with renal failure)
Treatment of Acute Heart Failure
Afterload reduction with High-dose IV nitroglycerin ACE inhibitors Nitroprusside Inotropes if very low EF or acute MI + AHF in presence of borderline BP Dobutamine
If too hypotensive to tolerate the above, use vasopressors, intra-aortic balloon pump
Treatment of Acute Heart Failure
Risk factors for infective endocarditis (IE) Rheumatic or congenital heart disease Prosthetic valves IVDA Acquired valvular disorders (e.g. AS) Mitral valve prolapse (small risk) Cardiac pacemakers Prior history of endocarditis Recent major GI, GU, dental procedures Median age is increasing More prosthetic heart valve survivors
Infective Endocarditis
Valvular involvement (MATP) Mitral > aortic > tricuspid (IVDA) > pulmonic
IVDA Most have normal valves (75%) Tricuspid valve most common (50%) Staph. aureus is the most common pathogen Prosthetic valves Staph. aureus
Infective Endocarditis
Acute IE Younger, normal valves in half the cases Virulent strains Higher morbidity and mortality Staph. aureus
Subacute IE
Older, abnormal valves
Anemia of chronic disease
Strep. viridans (50-60%)
Infective Endocarditis (3) Types
Left sided IE S. viridans, S. aureus Gram negatives (IVDA or contaminated catheters) Cause of death is heart failure Emboli: CNS and systemic infarction Right sided IE IVDA, indwelling catheters S. aureus, S. pneumoniae, gram negatives Emboli: pulmonary infarction & infection Less heart failure, mortality rate lower
Infective Endocarditis (4) Types
Prosthetic valve IE
Most common during first two months post-op
S. epidermidis, S. aureus
Late causes similar to native valve endocarditis
S. viridans, Serratia, Pseudomonas
Infective Endocarditis (5) Types
Findings of IE
Fever, chills, “flu-like” illness, back pain
Heart murmur
Valvular incompetence (the most common cause of acute AR)
Infective Endocarditis
Embolic and vasculitic components
Osler nodes: tender nodules on the tips of the fingers and toes (Osler = Ow!)
Janeway lesions: nontender, hemorrhagic plaques on the palms and soles
Roth spots: retinal hemorrhages with central clearing
Petechiae and splinter hemorrhages
Infective Endocarditis
Laboratory
Three blood cultures: 90% rate of diagnosis of the causative bacteria
Anemia and elevated ESR
Diagnosis: ultrasound (TEE) for vegetations
Treatment: penicillins or vancomycin, and add aminoglycoside
Add rifampin for prosthetic valves
Infective Endocarditis
Prophylaxis High-risk cardiac conditions Prosthetic cardiac valve History of infective endocarditis Congenital heart disease (CHD) Cardiac transplantation recipients with cardiac valvular disease
Infective Endocarditis
Group of diseases directly altering cardiac structure, impairing myocardial function Three types Dilated cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy
Cardiomyopathy
Idiopathic (most common) Alcohol Peripartum Viral (myocarditis) End-stage CAD Hypothyroidism
Dilated cardiomyopathy
Pathophysiology Decreased contractility dilatation of all chambers decreased output -Clinical presentation CHF (biventricular failure) Emboli Dysrhythmias Sudden death -CXR Globular heart CHF -EKG LVH LAE Conduction defects A-fib
Dilated Cardiomyopathy
Treatment Largely supportive Diuretics Afterload reduction Anticoagulation Antidysrhythmics Transplantation
Dilated Cardiomyopathy
Often familial autosomal dominant
Asymmetric thickening of septum causing two problems
Noncompliant ventricle with decreased diastolic filling
Dynamic obstruction of LV outflow (with mitral valve leaflets blocking outflow tract)
Hypertrophic Cardiomyopathy
Clinical manifestations Exertional syncope Sudden death Cardiac ischemia Dysrhythmias
Hypertrophic Cardiomyopathy
Physical exam
Harsh, mid-systolic murmur at LLSB
Murmur louder with decreased preload (hypovolemia, standing, Valsalva, amyl nitrite, beta agonists)
Murmur decreased with increased afterload (squatting, Trendelenburg, hand grip, volume expansion, alpha agonists)
CXR: nondiagnostic
EKG: large amplitude QRS complexes, often with deep narrow Qs esp. in lateral leads
Hypertrophic Cardiomyopathy
