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
Avoid exertion (worsens obstruction and leads to arrhythmias) Negative inotropes (beta blockers, calcium channel blockers) to decrease obstruction Never use digoxin or positive inotropes (increased obstruction) Surgical myomectomy
Treatment of hypertrophic cardiomyopathy
Etiology Infectious Viral (most common) Bacterial TB Fungal Acute MI (Dressler's syndrome) Connective tissue disease Neoplasm Uremia Radiation
Pericarditis
Clinical manifestations
Chest pain (may radiate to trapezius ridge)
Chest pain increases with inspiration and swallowing
Dysphagia
Relief on sitting up, bending forward (and may hear the rub better in this position)
Fever, malaise, recent or current URI
Pericarditis
Physical exam
Rub (increased by leaning forward)
Tachycardia, pulsus paradoxus (an exaggerated BP response to breathing – BP goes down on inspiration and up on expiration)
Pericarditis
EKG: four stages
Stage 1: Diffuse ST elevation (does not correspond to coronary artery distribution) & PR segment depression
Stage 2: ST-segments and PR return to baseline
Stage 3: T wave inversions
Stage 4: Normalization of EKG
Pericarditis
CXR: usually normal Echocardiogram: pericardial effusion Complications Dysrhythmias (atrial) Large pericardial effusions, tamponade Residual pericardial constriction Treatment Treat underlying cause if possible ASA, NSAIDs, colchicine; no steroids in the ED
Pericarditis
Causes
Trauma, uremia, anticoagulation, neoplasm
Clinical signs
Beck’s triad: Hypotension, JVD, muffled heart sounds
Pulsus paradoxus
EKG
Electrical alternans (beat to beat alteration in the amplitude of the QRS complex), low voltage
ECHO findings
Effusion
RV diastolic collapse (specific for tamponade)
Pericardial Tamponade
Inflammation of the myocardium Often associated with pericarditis Etiology Idiopathic Infectious (usually viral, especially coxsackie B virus) Chemotherapy Connective tissue disease
Myocarditis
Clinical manifestations
“Flu-like” illness
Fever, sinus tach (out of proportion to fever)
Symptoms of CHF
Dysrhythmias (tachy or brady with AV blocks)
Emboli
Sudden death
EKG: anything! Non-specific, STE, ST depression, tachys, bradys and AVBs, etc.
CXR: possibly enlarged heart
Lab: elevated biomarkers
Myocarditis
ECHO: obtain to assess cardiac function, EF Natural history Most recover May have sudden death May have dilated cardiomyopathy Treatment Supportive care
Myocarditis
No signs or symptoms of acute organ damage
Acute intervention may be harmful
Behavior modification, initiation of therapy
Close follow up, e.g. in several days
Hypertensive urgency (DBP > 110)
Acute end-organ damage Brain (encephalopathy, stroke, IC bleed) Eyes (papilledema, hemorrhages) Heart (ACS) Lungs (pulm edema) Aorta (dissection) Kidneys (acute renal failure) Uterus (eclampsia) [Catecholamine crisis] Goal: rapid reduction in BP (reduce MAP 30%)
Hypertensive emergency
CNS: encephalopathy, hemorrhagic CVA
Nitroprusside
Labetalol
Ischemic stroke
Hypertension usually resolves within hours
Transient and cerebroprotective
Treatment: observe, labetalol, nicardipine
Hypertensive Emergencies
Cardiac: angina, CHF IV nitroglycerin Add nitroprusside or nicardipine if severely elevated BP
Aortic dissection
Need to decrease rate of rise of BP (dP/dT) to decrease shear forces on aorta
Beta blockers (esmolol, labetalol, propranolol), then nitroprusside or nicardipine
Hypertensive Emergencies
Alpha plus beta blocker is best
Do not use beta blocker alone (avoid unopposed alpha effect)
Labetalol plus phentolamine (alpha blocker)
Catecholamine crisis (pheochromocytoma, MAOI crisis, cocaine overdose)
Mode of action: arterial and venous dilatation
Onset of action: 1-2 minutes
Half life: 3-4 minutes
Metabolized to thiocyanate (cyanide) therefore do not use for long in renal or pregnant pts
Ideal medication for hypertensive emergencies (rapid onset, potent, short half life)
Can cause reflex tachycardia, therefore use with beta blocker
Sodium nitroprusside
Alpha and beta blocker (primarily beta) Onset of action: 5-10 minutes Half life: 5.5 hours No reflex tachycardia Low doses may lead to paradoxical hypertension due to predominant beta effect (unopposed alpha)
Contraindicated in bronchospasm, CHF,
AV-blocks
Labetalol
Venodilation primarily; arteriolar dilation at high doses
Limited utility with profound hypertension
Onset: immediate
Half life: 4 minutes
Tachyphylaxis
Ideal for cardiac emergencies such as CHF, MI
Side effects: headache and tachycardia
Nitroglycerin
Calcium channel blocker
Onset 5-15 min, duration 4-6 hrs
Theoretically reduces cardiac and cerebral ischemia
Nicardipine
Dopamine agonist, no alpha or beta effects
Onset 5 min, duration 30-60 min
Increases renal blood flow and sodium excretion
Might be preferred agent in the setting of renal dysfunction
Fenoldopam
Dihydropyridine calcium channel blocker
Elimination independent of liver or kidney
Onset within minutes, offset 5-15 min
Now priced similarly to nicardipine
Clevidipine
Direct arteriolar vasodilator
Onset: 10 min (IV)
Half life: 2-4 hours
Indicated in pregnancy-related hypertension, pediatric nephritis
Side effects include
reflex tachycardia (limits use in CAD, dissection)
Chronic use associated with “lupus-like” syndrome
Hydralazine
Dissection of intima from media
Depends on the rate of rise in blood pressure
Bimodal age distribution
Young with predisposing factors
Collagen vascular disorders such as Marfan’s
Pregnancy (especially third trimester)
Chest trauma, iatrogenic (cardiac catheterization)
Bicuspid aortic valve
Aortic coarctation
Elderly males with chronic hypertension
Atherosclerotic risk factors (smoking, hypertension, cholesterol, diabetes)
Aortic Dissection
Clinical presentation Abrupt tearing chest pain, radiation to back Maximal intensity at onset Migrating, dynamic pain pattern Aortic insufficiency Pulse deficits Syncope, decreased LOC, acute paralysis Physical exam Hypertension, normal BP or hypotension Asymmetric pulses, asymmetric BP (on boards) Acute aortic regurgitation Tamponade
Aortic Dissection
Type A: any dissection which involves ascending aorta (surgical treatment)
Type B: descending aorta only (primarily medical management)
Aortic Dissection
Stanford classification
EKG
May show acute MI if dissection is proximal and involves coronary ostia
Up to 8% with Type A will have ST elevations
CXR
Widened mediastinum in majority
Intimal calcium separation
Left pleural effusion
Aortic Dissection
MRI Very sensitive and specific Usually impractical due to inability to monitor patient and time constraints CT with contrast Now accepted as first-line test Shows thrombosed false lumen Requires dye load TEE (transesophageal echo) Very sensitive and specific best test if available Done in ED (safer for patient)
Aortic Dissection
Aortography
Higher risk, logistically difficult and expensive
Provides anatomy necessary for OR, including coronary involvement
False negatives possible (thrombosed false lumen)
Treatment
Beta blockers, then nitroprusside for both types
Stanford A: requires surgery
Stanford B: 1/3 will require surgery for complics.
Aortic Dissection
Pathophysiology
Increase in diameter >50% over normal artery
Due to medial degeneration (usually atherosclerosis)
Majority are infrarenal
Risk factors
Elderly male with atherosclerosis, hypertension
Connective tissue disease
Abdominal Aortic Aneurysm
Clinical Presentation Asymptomatic until bleed or rupture Abdominal, flank or back pain Most common misdiagnosis: renal colic Syncope More unusual presentations Erosion into duodenum aortoenteric fistula with massive GI bleed Erosion into IVC aortocaval fistula with embolization distally Distal embolization causing LE ischemia
Abdominal Aortic Aneurysm
Physical exam
Pulsatile mass is found in <50%
Abdominal or femoral bruits
Decreased femoral pulses
Diagnosis
Plain films: rule out calcified aneurysm
Abdominal cross table lateral
Lateral L-spine
Abdominal Aortic Aneurysm
Ultrasound
Excellent bedside screening tool
Very sensitive
Unable to determine leakage (unless free fluid)
May help to differentiate kidney stone (hydronephrosis, dilated ureter) from aneurysm
Abdominal Aortic Aneurysm
CT scan
Useful in stable patients
Able to visualize leakage into retroperitoneal space
Risky because patient is out of department
Abdominal Aortic Aneurysm
Management Hypotensive or unstable Priority is resuscitation and OR (multiple large-bore IVs, type and cross 10 units) Leaking: Emergent operation Asymptomatic: elective repair if >5 cm
Any back or abdominal pain in a patient known
to have an aneurysm must be presumed to be leaking or ruptured AAA until proven otherwise
Abdominal Aortic Aneurysm
Emboli Usually cardiac Mural thrombus from MI A-fib Endocarditis Arterial source Aneurysm Dissection Atherosclerotic disease Paradoxical embolus From venous emboli through septal defect
Acute Limb Ischemia
Embolus Sudden onset No previous arterial insufficiency Thrombus Etiology: atherosclerosis (most common) Low-flow states Develops slowly Past history of claudication Chronic arterial insufficiency
Acute Limb Ischemia
Signs of acute ischemia (6 P's) Pain Pallor Paresthesias (earliest Sx) Paralysis Pulselessness (late finding) Poikilothermia (polar, cold) Treatment of acute limb ischemia Vascular surgery consultation! Heparin (unless worried dissection/AAA) Embolectomy Bypass for atherosclerotic disease
Don’t forget to consider aortic
dissection or AAA
Acute Limb Ischemia
Pathogenesis (Virchow's triad) Stasis Hypercoagulability Endothelial damage Risk factors Immobilization Pregnancy Estrogen use Neoplasm Trauma
Deep Venous Thrombosis
Presentation Pain and swelling (unilateral) Erythema Low-grade fever Physical exam (e.g.Homans' sign) is insensitive
Deep Venous Thrombosis
Diagnosis
Duplex ultrasonography: very sensitive and specific for proximal thrombi
Venography: “gold standard” but invasive and has phlebitis as complication
D-dimer (if negative, rules out DVT in patients considered low risk by Wells or gestalt)
CT venography
Deep Venous Thrombosis
Treatment Heparin therapy initially Then oral anticoagulant for 3-6 months Caval filter when there is a contraindication to, or failure of, long-term anticoagulation Recurrent DVT Emboli
Deep Venous Thrombosis
Phlegmasia cerulea dolens and phlegmasia alba dolens
Uncommon, severe presentation of DVT
Massive iliofemoral DVT
Acute, severe, massive swelling
Cyanotic, congested extremity (cerulea)
Pale (alba) if arterial spasm causes “milk leg”
Increased compartment pressure, ischemia
May require surgery for compartment syndrome
Deep Venous Thrombosis
Defn. = Sudden, brief LOC and postural tone with spontaneous recovery due to a decrease in cerebral blood flow
Causes:
Neurally mediated (reflex-mediated HR or vascular tone changes):
Vasovagal (18%), situational (5%), carotid sinus (1%)
Psychiatric causes (2%)
Panic attacks, anxiety, somatization
Orthostatic hypotension (8%)
Syncope
Medications (3%)
Neurologic disease (10%)
Cardiovascular causes:
Organic heart disease (4%), arrhythmia (14%)
Vascular – subclavian steal (syncope associated with arm exercise)
Unknown (34%)
Tilt table tests suggest that most of these are neurally mediated
Syncope
No tests are routinely mandated except the ECG Let the hx and PE determine any other test-ordering What to look for on the ECG post-syncope Ischemia Dysrhythmias Intervals (long QT, short PR WPW) Hypertrophic cardiomyopathy Brugada syndrome
Syncope
Flat P waves Peaked T waves Wide QRS Prolonged QT (due to hypoCa) and PR Bradydysrhythmias and AV blocks Tachydysrhythmias Eventual sine wave and Vfib
EKG - Hyperkalemia
PVCs
U waves
Prolonged QT
ST segment depression
Hypokalemia
Shortened QT interval
Hypercalcemia
Prolonged QT interval
Hypocalcemia
Electrolyte abnormalities that prolong QT interval
Hypokalemia
Hypocalcemia
Hypomagnesemia
Prolonged QT leads to
ventricular tachydysrhythmias (torsade de pointes, Vfib)
Treatment Magnesium (will shorten QT interval) Overdrive pacing Isoproterenol Cardioversion/defibrillation Magnesium infusion for prophylaxis after conversion Do not use procainamide or amiodarone!
Torsade de Pointes
Regular, narrow complex tachycardia
Rate 150-200
Absent or retrograde P waves
Treatment: vagal maneuvers, adenosine, calcium channel blockers (diltiazem, verapamil)
Supraventricular tachycardia
Etiologies AMI, HTN, RHD Thyrotoxicosis Digoxin toxicity Chronic obstructive pulmonary disease Pericarditis PE, hypoxia WPW Electrolyte abnormalities
Atrial Fib / Flutter
Regular, narrow complex with atrial rate 250-350
Ventricular rate usually blocked (2:1, 3:1, 4:1)
Sawtooth baseline (flutter waves)
Atrial flutter
Irregularly irregular rhythm with undulating baseline (associated with thyrotoxicosis, CAD, CHF, PE, sepsis, alcohol)
Atrial fibrillation
Treatment: rate control (chemical, electrical)
Stable: diltiazem, beta blockers, amiodarone, digoxin
Unstable
Atrial flutter: synchronized cardioversion (start at 50 J)
A-fib: synchronized cardioversion (start at 200 J)
Anticoagulation for long term A-fib
Atrial Fib / Flutter
Treatment: rhythm control (chemical, electrical) For patients with AF < 48 hours duration Electrical Pharmacologic Amiodarone Ibutilide Flecainide Propafenone Procainamide
Atrial Fib / Flutter
Classic findings: - Regular, narrow complex with atrial rate = 250-350 - Ventricular rate usually blocked - 2:1, 3:1, 4:1 - Sawtooth baseline (flutter waves)
Atrial Flutter
Classic findings: - Irregularly, irregular rhythm
Atrial Fibrillation
Irregularly irregular narrow complexes, rate >100 At least 3 different P wave morphologies Variable PR intervals Associated with Hypoxia COPD Theophylline toxicity Treat underlying condition MgSO4 may be helpful; no shocks!
Multifocal atrial tachycardia
Classic findings: - Irregularly irregular with narrow complex, rate >100 - At least 3 different P wave morphologies, Variable PR
Multifocal Atrial Tachycardia
Indications for emergency pacing
Hemodynamically unstable bradycardia
Overdrive pacing of refractory tachy (e.g. torsades)
Pacing of asystole no longer recommended
Indications for “Standby” pacer
Mobitz II or CHB that is stable (for now!)
New BBB in symptomatic patient
Apply magnet over PM to turn off sensing function temporarily converts PM from demand to fixed rate
Allows assessment of whether PM function is intact, whether capture is present, and if battery is working
Assess for electrolyte abnormalities
Pacemaker failure
Prior VT/VF cardiac arrest VT in assn. with structural heart dis. History of syncope with unstable VT Non-sust. VT with significant CAD LV EF < 30% after MI/PCI/CABG Signs/Sxs of VT/VF in cardiac transplant candidates Inherited conditions with high risk for VT/VF (e.g. HCM, long QT syndrome, ARVC) Brugada syndrome Syncope with advanced structural HD Etc.
AICDs indications
Assess for concerns of ACS or arrhythmia based on history and exam
Check lytes
If no concerns identified, patients can be discharged to close followup
AICDs single discharge
For multiple discharges
Mandates interrogation
If continuing discharges, use magnet to inactivate AICD
Cardiac arrest: no change in protocols is needed
Place your own pads (A-P), 8-10 cm away from AICD
AICDs (3)
Infection
Early infection clinical findings of redness, tenderness, etc.
Late infection subtle findings, may only manifest pain
Low threshold for ultrasound to assess for pocket infection
AICDs
Bypass tract joining atria to ventricles with no conduction delay (short PR interval)
Delta wave when conduction is through bypass tract during NSR
Delta wave is not reliably seen in tachyarrhythmias
Wolff-Parkinson-White Syndrome
Treatment is based on QRS width Narrow-complex regular tachycardia Treat like SVT Wide-complex regular tachycardia Treat like VTach A-fib with QRS complexes that change width and have rates > 200-250 Procainamide, cardioversion Do not use AVN blockers: digoxin, CCBs, BBs, adenosine, amiodarone
Wolff-Parkinson-White Syndrome
Regular, wide-complex, rate >120 (usually >150)
Associated with
Underlying heart disease (CAD, cardiomyopathy, MVP)
Electrolyte disturbances
Toxic ingestions
If stable: procainamide > amiodarone > lidocaine,
If unstable: sync cardioversion
Ventricular Tachycardia
Regular wide complex with rate > 120 (usually >150)
Ventricular Tachycardia
Primary: no preceding hemodynamic compromise
Secondary: prolonged LV dysfunction, shock
Structural heart disease, ischemia
Totally disorganized, non-perfusing rhythm
Associated with CAD, MI, toxic ingestions, electrolyte disturbances
Treatment: defibrillation (ACLS protocols)
Ventricular fibrillation
Totally disorganized, non-perfusing rhythm
Ventricular Fibrillation
Premature, wide complex, no preceding P wave (compensatory pause)
Unifocal or multifocal
Associated with
Normal heart, alkalosis, CHF, MI, hypokalemia, hypoxia, cardiomyopathy, drugs, digoxin toxicity
Premature ventricular contractions (PVCs)
PVCs in acute MI
Indicate electrical instability
Prophylactic treatment not proven to decrease mortality
Treatment
Treat underlying cause (e.g. electrolytes, ischemia, hypoxia)
Consider magnesium, beta blockers
Treat sustained VT (> 30 seconds or if hemodynamic instability develops)
Premature Ventricular Contractions
Wide complex regular rhythm with rate 40-120 Runs may last few minutes Associated with acute MI and reperfusion Treatment: observe! Is self-terminating, NOT destabilizing
Accelerated idioventricular rhythm (“slow Vtach”)
PR > 200 ms Look for underlying cause Medications, congenital Common in elderly In itself it is not an acute concern No specific treatment unless also bradycardic
First Degree AV Block
Progressively longer PR and shorter RR until a P-wave is non-conducted, then starts over
Causes: same as 1st degree block, common with inferior MI, often transient; treatment if hemodynamic instability
Atropine or transcutaneous pacemaker usually sufficient
Mobitz I (Wenckebach)
Constant PR interval and non-conducted P-waves
Associated with anterior MI and destruction of conduction tissue
Usually associated with bundle branch block
May progress to complete heart block
Temporary pacer often needed in the setting of AMI
Mobitz II
AV dissociation: no relation between P and QRS PR interval changes randomly
Junctional (narrow QRS’s) or ventricular (wide QRS’s) escape beats
Associated with anterior MI and destruction of conduction tissue
Narrow complex: may be temporary due to vagal tone
Wide complex: usually requires transvenous pacer
Third degree AV block (complete heart block)
- AV dissociation no relation between P and QRS
- PR interval changes randomly
Third Degree AV Block
Syncope or sudden death in young patients with a structurally normal heart resulting from polymorphic VT venticular fibrillation Often occurs during high vagal tone (night, early morning, after meals) Familial autosomal dominant Particularly common in SE Asian males Pseudo-RBBB pattern ST elevations in V1 and V2 Test of choice: EP study Implantable defibrillator is treatment
Brugada Syndrome
AV dissociation (“cannon” A waves in neck, variable intensity S1, variable pulse amplitude beat-to-beat) Fusion beats QRS >14 ms Elderly patients History of CAD or MI
VTach findings
QRS in same direction as baseline QRS
Always assume a regular WCT on the boards is Vtach
SVT with aberrant conduction findings
Bystander/lay rescuer CPR in out-of-hospital cardiac arrest (JAMA 2010)
Chest compression alone > conventional CPR
Post-arrest care
Ventilation goals: normoxia (pox low-mid 90s) and normocarbia
Hypotension is bad (target MAP > 65 mm Hg)
Therapeutic hypothermia is good (goal temp??)
Urgent PCI for STEMI is good, consider for NSTEMI as well
