Cardiovascular Emergencies Flashcards
What diseases are part of acute coronary syndrome?
- Unstable angina
- NSTEMI
- STEMI
What is the classic description of cardiac chest pain?
Intermittent substernal chest pressure, usually on the L side which radiates to the arm and neck, exacerbated with exertion and associated with SOB, diaphoresis, nausea, and palpitations
The classic description of cardiac chest pain is more often the exception than the rule. What are some aspects of more common presentations?
Pain can occur anywhere from the umbilicus to the neck, and to the back
Can be sharp or burning
People with diabetes and the elderly may have no chest pain
Women may present with fatigue, SOB, and generalized weakness
Physical exam findings in patients with ACS?
Highly variable
-Normal appearance to full cardiac arrest
-Diaphoretic, hypotensive or hypertensive, tachycardic or bradycardic, or dyspneic
May have normal heart sounds or a murmur from a ruptured papillary muscle or valve
+/- signs of heart failure (S3, JVD, pedal edema, pulmonary edema)
The high variability in presentation makes ruling out an ACS by secondary survey alone very difficult. Classic findings may lead you to increase your pre-test probability, but unless your evaluation leads you to another high probability diagnosis, be wary of removing ACS from your differential.
Yes.
Diagnostic criteria of an acute MI?
2 of the following 3:
- Consistent clinical history
- EKG changes
- Changes in cardiac enzymes
EKGs are an essential screening tool in anyone with chest pain. it can be diagnostic of acute MI if ___ are present, as they are in nearly 40% of cases. Interpret non-specific findings in the context of ___. Nearly ___% of patients with ACS initially have normal or non-diagnostic EKG. ___ tend to be more useful, and the majority of patients will show signs of ischemia.
ST elevations; old EKGs; 50; Serial EKGs
What location MIs are not measured by the traditional 12-lead EKG? What should be done in this situation?
Posterior and R-sided
Look for reciprocal changes (ST depressions in leads on the opposite side of the heart), then order appropriate extra leads (V7, V8, V9 for posterior, V4R for R)
List the 6 general MI locations.
- Anterior MI
- Septal MI
- Inferior MI
- Lateral MI
- Posterior MI
- R Ventricular MI
Location of ST elevations and reciprocal depressions in anterior MI
Elevations: V1-V6
Depressions: none
Location of ST elevations and depressions in septal MI?
Elevations: V1-V3
Depressions: none
Location of ST elevations and depressions in inferior MI?
Elevations: II, III, aVF
Depressions: I, aVL
Location of ST elevations and depressions in lateral MI?
Elevations: I, aVL, V5, V6
Depressions: II, III, aVF
Location of ST elevations and depressions in posterior MI?
Elevations: V7, V8, V9
Depressions: V1-V3
Location of ST elevations and depressions in R ventricular MI?
Elevations: V1, V4R
Depressions I, aVL
Artery affected in anterior MI?
Left anterior descending
Artery affected in septal MI?
Left anterior descending
Artery affected in inferior MI?
R coronary artery (80%), L circumflex (20%)
Artery affected in lateral MI?
L circumflex
Artery affected in posterior MI?
R coronary artery or L circumflex
Artery affected in R ventricular MI?
R coronary artery
List the 4 cardiac markers? Which is most sensitive?
Myoglobin
CK-MB
Cardiac Trop I*
Cardiac Trop T
Initial elevation, peak elevation, and return to baseline for myoglobin?
Initial: 1-4 hours
Peak: 6-7 hours
Return: 18-24 hours
Initial elevation, peak elevation, and return to baseline for CK-MB?
Initial: 4-12 hours
Peak: 10-24 hours
Return: 48-72 hours
Initial elevation, peak elevation, and return to baseline for cardiac trop I?
Initial: 3-12 hours
Peak: 10-24 hours
Return: 3-10 days
Initial elevation, peak elevation, and return to baseline for cardiac trop T?
Initial: 3-12 hours
Peak: 12-48 hours
Return: 5-14 days
In addition to EKG and serial troponins, what labs should be considered in chest pain?
- CBC (anemia may be a cause)
- CXR (may show pulmonary edema or other causes of chest pain)
- Electrolytes, BUN, creatinine, Mag (may effect Rx regimens)
- Echocardiogram (usually after admission to look for regional wall motion abnormality)
- Stress testing (either exercise or chemically-induced exertion to look for EKG changes and/or decreased radionuclide uptake in the ischemic region)
- Coags
+/- D-Dimer, BNP, T&S, LFTs, lipase
How is ACS diagnosed?
Cardiac catheterization
Features of the history that strongly suggest ACS?
Exertional pain or pressure Exertion shortness of breath History of vascular disease Strong cardiac family history Prior MI's
Features of the EKG that strongly suggest ACS?
ST elevation of 1+ mm in 2 contiguous limb leads (high lateral - I, aVL, inferior: II, III, aVF) or 2+ mm elevations in the precordial leads (anterior - V1, V2, V3, lateral - V4, V5, V6)
Rx ACS?
- ABC, IV access, O2, cardiac monitor
- Morphine, oxygen, nitroglycerin , aspirin, beta-blockers to control HR and blood pressure if needed
- If confirmed, given anti-thrombin therapy (heparin) and anti-platelet therapy (aspirin or IIb/IIIa inhibitor)
- If persistent ST-elevations -> revascularization (thrombolytics or angioplasty in cath lab)
- Without ST-elevations -> angiogram when appropriate
Cardiac enzyme testing will be negative in patients with angina. ___ is needed to discover any partially occluded coronary arteries.
Functional testing
What are the top 5 do-not-miss chest pain diagnoses?
- ACS
- PE
- Aortic Dissection
- Tension pneumothorax
- Esophageal rupture (Boerhaave’s syndrome)
Clinical features of tension pneumothorax?
JVD, tracheal deviation away from PTX, ipsilateral hyper-resonance to percussion/absent breath sounds, respiratory distress, hypotension
Rx tension pneumothorax?
Large bore needle (14 g) 2nd IC space midclavicular line for needle decompression -> convert to chest tube
Clinical features of esophageal rupture?
History of severe retching and vomiting followed by excruciating retrosternal chest and upper abdominal pain
SubQ emphysema, L PTX/pleural effusion, mediastinal widening/emphysema on CXR
Dx esophageal rupture?
Gastrograffin swallow/EGD/CT
Rx esophageal rupture?
IVFs
ABX
Surgical consult
Symptoms associated with ACS vs. CHF vs. PNA vs. PE vs. MSK
ACS: SOB, N/V (before or after CP), diaphoresis, palpitations
CHF: DOE, LEE, PND, orthopnea
PNA: cough, fever/chills
PE: calf pain/swelling, hemoptysis
MSK: trauma/heavy lifting, cough
Risk factors for cardiac problems?
CAD/PVD HTN DM HLD Smoking Family hx of early CAD (males 55 or earlier, females 65 or earlier) Cocaine use (previous or current)
Important physical exam steps in chest pain?
Neck: JVP, carotid bruit, carotid upstroke
Heart: S4, new MR murmur, rub, PMI
Lungs
Chest wall: reproducible pain, rashes/skin lesions
Abdomen
Extremities: edema, asymmetry, tenderness, distal pulses
Highest positive likelihood ratio (rule in) for acute MI?
CP radiating to R arm or shoulder
How is TIMI risk score used?
Primarily to determine aggressiveness of work-up, not discharge
MOA of aspirin in ACS + dosing/administration?
Irreversibly acetylates platelet cyclo-oxygenase
162-324 mg PO chewed to maximize bioavailability
MOA of nitroglycerin in ACS + dosing/administration?
Dilates coronary vessels to decrease preload and afterload (and thus decrease myocardial O2 demand)
Ask about Viagra/other PDE5 inhibitors (true contraindication)
Sublingual: 0.4 mg (=400 mcg) Q5 min x3 if SBP >100
Paste: 0.5-1 inch across chest
IV drip: 10 mcg/minute and titrate Q5-10 minutes to chest pain free or if SBP decreases to <100
When should you be cautious giving nitroglycerin in ACS?
Concern for inferior or RV infarct (pre-load dependent, can make someone unstable, though not an absolute contraindication)
When should beta-blockers be used in ACS?
Reasonable to give IV beta-blockers to patients who are hypertensive and without contraindications
Contraindications to beta-blockers in ACS?
CHF Low output state PR>0.24 2nd or 3rd degree AV block Reactive airway disease Increased risk for cardiogenic shock: age >70, SBP<120, HR< 60, sinus tachycardia >110
Dosing of beta-blockers in ACS?
Metoprolol 5 mg IV Q5min x3 -> 25-50 mg PO
Titrate to HR 55-60
MOA of plavix in ACS + dosing/administration?
Inhibitor of ADP-induced platelet aggregation
Loading dose of 300-600 mg PO
If pt needs CABG, recs are to hold Plavix for at least 5 days -> only give in conjunction with cardiologist
When should heparin or lovenox be considered in ACS?
Consider in high risk ACS, EKG changes, or + cardiac enzymes
Positives and negatives of heparin?
+ Can turn off the drop, cheaper
- Less predictable, higher change of HIT
Positives and negatives of Lovenox?
+ More predictable, lower change of HIT, coags not needed
- can’t just turn it off, costs more
When would you consider a GP IIb/IIIa inhibitor?
High risk ACS, NSTEMI, or PCI
Goal door to drug time for thrombolytics in ACS if giving?
Within 30 minutes
Goal door to balloon time for primary PCI in ACS?
90 minutes
Pathogenesis of cocaine CP?
Increased O2 demand with limited O2 supply (increased HR/BP/contractility)
Coronary vasoconstriction (increased alpha-adrenergic stimulation)
May induce thrombus formation and accelerated atherosclerosis
Rx cocaine chest pain?
ASA, O2, NTG, benzodiazpines
Phentolamine 5-10 mg IV (non-specific alpha-adrenergic antagonist), CCBs
STEMI -> PCI>thrombolytics (hypertensive, increased risk of ICH)
Avoid beta-blockers, including labetalol
Because cocaine has sodium-channel blocking properties, it can cause ___.
Wide complex tachycardia (similar to TCA overdose)
Also at risk for aortic dissection
Rx wide-complex tachycardia 2/2 cocaine or TCA overdose?
Sodium bicarbonate
When does a single negative troponin rule out MI? What is an important caveat?
If patients arrive >8 hours after symptom onset
DOES NOT RULE OUT ACS -> provocative test still needed
Recent negative stress test should not obviate your concern if the HPI is concerning, as they are not perfectly sensitive and specific
If pre-test probability for PE is very high, what should be done?
Consider starting heparin/lovenox immediately if no contraindications
Consider thrombolytics (tPA 100 mg over 2 hours) if hemodynamically unstable or witnessed loss of vitals
What is the usual cause of death from PE?
Right-sided heart failure
Signs of R heart strain on physical and EKG?
Elevated JVP, TR murmur
S1Q3T3, new incomplete or RBBB, TW inversions V1-V4
If low/moderate pre-test probability for PE, what is the work-up?
D-Dimer rapid ELISA testing
If negative -> no further testing
If positive -> further work-up
What is the purpose of PERC rule?
Decrease over-testing with D-Dimer leading to false positives/overtesting
Overall approach to PE?
- If low pre-test proability/clinical gestalt –> PERC
- If PERC negative -> done
- If not PERC negative -> Wells criteria (4 or less) -> D-Dimer
- If D-Dimer negative -> done
- If D-Dimer positive -> diagnostic study
Diagnostic study options for PE?
- VQ scan (preferred in otherwise healthy patients with no underlying diagnosis, needs normal CXR
- CT angio (limited at sub-segmental level, IV contrast, radiation exposure)
- Pulmonary angiography (gold standard, invasive, significant morbidity and mortality)
- BLLE Doppler (plays a role) -> consider in pregnant patients
- Echo (shock of uncertain etiology, suspect PE, look for RV dysfunction)
- MRI - future potential
Next step based on VQ scan results?
Normal - done
High risk - treat
Low to intermediate risk - usually needs further assessment
Risk factors for aortic dissection?
HTN (most common)
M:F 2-3:1
Increasing age
Connective tissue disease (Marfan, Loeys-Dietz, Turner, Ehlers-Danlos vascular type)
Family history
Congenital aortic anomaly
Inflammatory vasculitis
Pregnancy (T3)
Trauma (blunt, AIBP, recent cardiac or aortic surgery)
Cocaine use
Pregnancy in women with chronic connective tissue disorders
Long-term exposure to steroids/immunosupressants
Presentation of aortic dissection?
“Chest pain + SOMETHING”
Excruciating pain, abrupt, maximal at onset, migrates as dissection propagates, tearing/ripping quality
Determine presence/strength of pulses in all 4 extremities + measure BP in bilateral upper extremities
Aortic insufficiency murmur
Hypertensive
Pericardial effusion/tamponade, AMI
CVA, visual changes, spinal cord defects (if carotid involvement)
Cold/pulseless extremity
Abdominal pain, flank/back pain, LE pain/weakness/paraplegia
Dx aortic dissection?
BP differential of >20 between UEs increases suspicion, but does not rule out or in
CXR - usually abnormal, but findings are non-specific/sensitive (widened mediastinum >8 cm, blurring of aortic knob, etc.)
CTA chest - quick, non-invasive, good sensitivity, but must leave ED, needs IV contrast, may miss a dissecting flap if moving quickly
MRI (last resort in stable patients and with direct unput from CT surgery, distance, length of time, metal implants)
TEE - stays in ED, evaluates coronary arteries/pericardium/valves, no IV contrast, operator dependent
TTE - effusion, wall motion abnormalities
D-Dimer? Limitations, need more studies.
Management of aortic dissection?
- Control the forces that propagate the dissection HR, SBP, rate of elevation of aortic pulse pressure)
A. IV beta-blockers FIRST (esmolol) to blunt reflex tachycardia
B. Then IV vasodilators: nitroprusside; alternative - nicardipine (vascular selective CCB)
Alternative single agent - labetalol drip
Goals: SBP 100-120, HR 60-80
- Surgical if Stanford A (proximal/ascending), medical without complications if Stanford B (distal/descending)
- Pain control
Thoracic aortic dissection should be considered for every patient presenting to the ED with what CC?
Chest pain or back pain, particularly if accompanied by neurologic signs or symptoms
___% of patients with a type A thoracic aortic dissection die within 24-48 hours without appropriate treatment. With surgical management, mortality may exceed ___%.
50; 25
DeBakey classification of aortic dissection?
Type I - both ascending and descending aorta
Type II - ascending aorta only
Type III - descending aorta only
Approximately 2/3 of aortic dissections are classified as ___.
Type A
Define acute vs. chronic dissection.
Acute - <14 days elapsed since dissection occurred
Chronic - 2+ weeks
DDx of aortic dissection?
ACS Aortic aneurysm Cardiac tamponade Esophageal rupture Pneumonia Pnuemothorax PE Stroke/TIA
List the actions to take for unstable patients in whom thoracic aortic dissection is highly suspected based on initial H&P.
ABCs
2 Large-bore IVs (18g or larger)
Un-crossmatched blood to the bedside (give if hypotensive/shock)
Monitoring
EKG
Portable CXR
Bedside US for pericardial effusion and systolic function
Labs - CBC, CMP, PT/PTT, type and cross, troponin, lactate
Page CT surgeon
Compare the differences in presentation in Type A vs. B dissections.
A - more likely to cause chest pain or syncope, more likely to be hypotensive
B - more likely to cause back or abdominal pain, more likely to be hypertensive (150+)
List some non-specific findings of dissection on CXR.
-Widened mediastinum (>8 cm at aortic knob)
-Abnormal aortic or cardiac contour
-Displaced intimal calcification
-Widened R paratracheal strip (5+ mm)
Tracheal deviation (usually rightward)
Opacified aortopulmonary window
Pleural effusion (usually L)
NYHA CHF classification scheme?
Class I - ordinary activity not limited by symptoms
Class II - ordinary activity leads to dyspnea, fatigue, etc.
Class III - marked limitation of ordinary activity
Class IV - symptoms at rest or with any physical activity
What is systolic dysfunction?
Impaired contractility, often with a dilated L ventricle, typically due to ischemia, infarction, cardiomyopathy, myocarditis, or dysrhythmia
What is diastolic dysfunction?
L ventricle intact and normal in size, but with impaired ability to relax
What is low outpatient heart failure?
Decreased CO 2/2 myocardial damage, such as with ischemia, dilated cardiomyopathy, valvular disease, or chronic HTN
What is high output heart failure?
High or normal CO, but insufficient to meet O2 demands, as in hyperthyroidism, pregnancy, anemia, AV fistulas, beriberi, or Paget’s disease
Symptoms of R-sided heart failure?
Congestion of pressure and fluid into the R ventricle -> hepatic enlargement, increased JVD, dependent edema
Symptoms of L-sided heart failure?
Congestion or pressure and fluid into the left ventricle -> pulmonary congestion
DDx - CHF
COPD PE PT Anaphylaxis Asthma Pneumonia Foreign body obstruction ACS
Initial actions and primary survey in CHF?
ABCs
Monitor, pulse oximetry, IV access with 2 large bore IVs
If hypoxic, give O2 via 100% NRB facemask and consider more invasive methods of oxygenation (CPAP, BiPAP, intubation)
Elevate the head of the bed +/- dangle legs over stretcher to reduce venous return and decrease preload
If CP, EKG +/- nitroglycerin
CXR
CBC with diff, CMP, troponin, PT/PTT, BNP, +/- lactate and BCx x2 if febrile
Presenting symptoms of CHF?
Dyspnea, especially on exertion (100% sensitive, 17% specificity)
Orthopnea (88% sensitive, 50% specificity)
PND (39% sensitive, 80% specificity)
Cough with sputum that is pink and frothy
Lewer extremity swelling
Physical exam findings in CHF?
May be hypertensive and diaphoretic
Increased JVD >4cm (highly specific for CHF 98%, 17% sensitive)
Rales 2/2 alveolar edema (29% sensitive, 77% specific)
Wheezing 2/2 peribronchial edema
May have tachycardia, S3 gallop (99% specificity, 24% sensitivity)
Lower extremity edema (pitting)
Findings of CHF on CXR?
Cardiomegaly (CT ratio >50% diameter)
Pleural effusions
Peribronchial cuffing (thickened bronchial walls 2/2 edema)
Perihilar congestion (large hila with indistinct margins suggesting pulmonary vascular edema)
Cephalization (redistribution of blood flow to upper lobes)
Kerley B lines (dilated lyphatic channels)
May lag by 12 hours from onset of symptoms, findings may persist for several days despite clinical improvement
20% have no pulmonary congestion on CXR
May have normal heart size in diastolic failure
How is BNP helpful in diagnosing CHF?
90% sensitive and 76% specific
<100 unlikely CHF
100-500 potentially CHF, could be PE, pulmonary HTN, ESRD, cirrhosis, HRT
>500 most likely CHF
Release stimulated by high ventricular filling pressures
Has a diuretic effect and antihypertensive effect by increasing sodium in urine
EKG findings of CHF? How is a normal EKG helpful?
May show underlying cardiac ischemia, dysrhythmias, LVH, or heart block
High negative predictive value for systolic dysfunction
Echocardiogram findings in CHF?
Ejection fraction changes Ventricular size Wall abnormalities Valvular pathologies Pericardial thickening Tamponade Constrictive pericarditis
ED treatment for normotensive patients with CHF
Give rapid acting nitrates to vasodilate
IV morphine for chest pain and to increase vasodilation
IV diuretics to increase urine output
ED treatment for hypertensive patients with CHF
Add nitroprusside IV drip for severe, persistent hypertension
ED treatment for hypotensive patients with CHF
Avoid nitrates and morphine (will drop BP more)
Instead, increase contractility with dopamine, dobutamine, norepinephrine, amrinone, or milrinone
ED treatment for severe or chronic low output CHF
ACEIs to increase hemodynamic stability and exercise capability
ED treatment for diastolic CHF
CCBs may help, but DO NOT USE in patients with concurrent, depressed LV function (can increase mortality and recurrence)
What surgical therapies may be needed as CHF becomes more advanced?
Automatic internal cardiac defibrillator (AICD)
Left ventricular assistance device (LVAD)
Heart transplant
Who should get an AICD?
Patients with previous MI, EF <35%, non-sustained VT, and inducible VT unresponsive to procainamide -> placement reduces sudden death by 54% at 2 years
Who should get an LVAD?
Definitive treatment if not a transplant candidate or temporizing measure until transplant can be performed
Veins in the deep venous system of the lower extremities?
Calf veins (anterior tibial, posterior tibial, peroneal veins) Popliteal veins Femoral veins External iliac veins Superficial femoral vein
Initial actions and primary survey for PE?
ABCs
Monitor, IV access, supplemental O2 as needed
EKG and CXR (r/o DDx items)
Classic presentation of DVT?
May be subtle and non-specific
General leg pain, cramping sensation, fullness in the calf, swelling, edema, or tenderness on palpation
Unilateral swelling or edema of the extremity, tenderness to palpation, and a palpable venous “cord”
DDx - DVT?
MSK strain or tear Cellulitis Superficial thrombophlebitis Venous insufficiency Lymphedema Popliteal cyst
Classic presentation of PE?
SOB, CP, vague complaints of general malaise or functional deterioration, syncope, possible pleuritic chest pain, unilateral leg symptoms, signs of R heart failure (JVD, edema), tachycardia with normal pulse ox (typically seen)
Dx testing for PE?
CXR (r/o other diagnoses) EKG (findings usually non-specific) D-Dimer Duplex US (test of choice for DVT, classic finding is the inability to fully compress the vein in the deep venous system) VQ scan CTPA +/- CT venography if needed
What is D-Dimer and what causes it to be elevated?
Protein-derived enzymatic breakdown product of a cross-linked fibrin; indicate clot formation in the body
Elevated in many diseases, including malignancy, infection, inflammation, MI, strokes, advanced age, pregnancy
Rx PE or DVT
Anticoagulation - either unfractionated heparin or LMWH (enoxaparin for example)
IVC filter if contraindication to anticoagulation
Thrombolytics (controversial, usually indicated if massive PE)
