Cardiology

One of the most important topics in emergency medicine. Chest pain is one of the most common chief complaints in the emergency department and having a broad differential diagnosis and a methodical approach to your evaluation is critical. Thankfully, because it is such a common complaint usually emergency medicine physicians are comfortable and are well trained to appropriately manage emergent cardiac complaints. This section is lengthy but we tried to include some of the high yield material.

STEMI

Important to know criteria in males vs females.

Pay attention to V2-V3, these are the leads with exceptions.

  • 1 mm elevation or more, in any contiguous leads, EXCEPT V2-V3

    V2-V3 EXCEPTIONS:

  • 1.5 mm elevation in FEMALES

  • 2 mm elevation in MALES 40 y.o. and older

  • 2.5 mm elevation in MALES less than 40 y.o.

ECG changes: early -> late

hyperacute T waves -> giant R waves -> ST elevation -> ST depression -> Q waves -> T wave inversions


Types:

Anterior (LAD) - elevation V1-V4, depression II, III, aVL

Lateral (LAD/Left Circumflex) - elevation I, aVL, V5-V6, depression V1

Inferior (posterior descending) - elevation II, III, aVF, depression V1-V4

Right ventricular (proximal right coronary) - elevation III > II, V1 > V2. Right sided leads w/ elevation in V4R, V5R.

Posterior (posterior descending) - depression in V1-V3, posterior leads w/ elevation of 0.5 mm


LBBB / Sgarbossa Criteria:

Concordant - 1 mm elevation (5pts) , 1 mm depression in V1-V3 (3pts)

Discordant - 5 mm elevation (2pts)

note, can be applied to paced rhythms

ST elevation ddx

 

acute MI

global ischemia (dissection, massive GI bleed, …)

early repol

myocarditis/pericarditis

vasospasm

ventricular aneurysm

LBBB/pacemaker

PE

high voltage (LVH, WPW, athletes…)

Na + channelopathies (TCA, hyperK, Brugada)

post cardioversion

hypothermia

takotsubo

intracranial abnormalities

hyperCalcemia

tPA

 

indications: PCI not available within 90 minutes or within 120 minutes with transfer

absolute contraindications: hx of brain bleed or known mass, ischemic stroke or TBI within 3 months, bleeding disorder, active bleeding, major surgery within 2 months, BP > 180/110 after treatment, suspect aortic dissection

tx: Over 67 kg: 100 mg administered as a 15 mg IV bolus followed by 50 mg infused over the next 30 minutes and then 35 mg infused over the next 60 minutes.

67 or less kg: 15 mg IV bolus, followed by 0.75 mg/kg (not to exceed 50 mg) infused over the next 30 minutes and then 0.5 mg/kg (not to exceed 35 mg) infused over the next 60 minutes.

Wellen’s Syndrome

early sign of proximal LAD lesion, may be asymptomatic, needs urgent cath

Type A

biphasic or deeply inverted T waves

Type B

symmetric T wave inversions in septal leads

 

De Winter pattern

STEMI equivalent, LAD/left anterior descending artery occlusion, needs emergent cath

 

upsloping ST elevation in aVR (0.5-1mm)

ST depressions and tall T waves in precordial leads

 

Post MI Complications

ruptured papillary muscle

Typically 2-7 days post MI, present with acute pulmonary edema, with new murmur. Tx nitroprusside, dobutamine, CT surgery

 

ventricular aneurysm

Persistent ST elevations > 2 wks after known MI and no reciprocal changes

 
 

dressler’s syndrome

2-10 wks post MI, low grade fever, chest pain, pericarditis/friction rub on exam, tx w/ ASA, ibuprofen, colchicine

Reading an ECG evaluate for all of the following

 

rate

Have a quick method of calculating the approximate heart rate. Rate of 300-150-100-75-60-50 corresponds to the number of large boxes between two consecutive QRS complexes, 1-2-3-4-5-6. If the rhythm is not regular then a quick method to get the approximate rate is to multiply the number of QRS complexes in a typical 10 second ECG by 6.

rhythm

Determine whether the rhythm is sinus, regular versus irregular. When a rhythm is initiated by the sinus node with every P wave followed by a QRS, it is known as sinus rhythm. Also, when the rhythm is initiated by the sinus node, the P wave will be upright in leads I, II, and III. P wave is usually best seen in lead II.

ST

Don’t miss the STEMI.

 

intervals

Look at PR, QRS, and QT intervals in order. If any abnormalities are seen, think about the clinical picture, whether your patient has an AV block, electrolyte abnormalities, reason for syncope, WPW etc. A quick way to determine if QT interval is normal is to see if it is less then half the interval between two consecutive QRS complexes. This method can be used when rate is normal 60-100 bpm.

killers

HCOM - LVH, need-like Q waves

Brugada - pseudo RBBB, STE V1-V3, down sloping ST elevation followed by T wave inversion, or “saddle back” ST elevation. A sodium channelopathy.

WPW - delta wave, wide QRS, short PR

Prolonged QT - QTc is prolonged if > 440ms in men or > 460ms in women, QTc > 500 is associated with increased risk of torsades de pointes

ARVD - arrythmogenic right ventricular displaisa - epsilon wave in 30%, T wave inversions in V1-V3

atypical

Wellen’s

DeWinter

Posterior MI

 

Endocarditis

 

ss:

osler nodes, janeway lesions, roth spots, splinter hemorrhages, petechiae, new murmur

dx:

blood cx x3, echo/TEE is best, duke criteria

tx:

abx: vancomycin + gentamicin

 

Heart Failure

 

ss

cardiomegally

fluffy infiltrate

kerly B lines

pleural effusions

 

tx

BiPAP - start first

nitro

furosemide - diuresis

inotropes - norepinephrine, dobutamine

dx

diagnose with ECHO

S3 heart sound - 99% specific

JVD - 70% specific, 50% sensitive

dyspnea - 50% sensitivity and specificity

orthopnea - 80% specificity

 

misc

BiPAP - decreases work of breathing, decreases preload by positive pressure which increases intrathoracic pressure, decreases venous return

 

Murmurs

 

systolic

HOCM - probably most commonly tested, mid systolic, murmur increases valsalva/standing due to decrease in venous return/preload. Murmur decreases with increase in preload/venous return such as leg raise/squat, and also decreases with increased afterload such as hand grip.

MVP- mitral valve prolapse, mid systolic click with late systolic murmur. Maneuvers have same effect on murmur as with the HOCM murmur.

MR - mitral regurgitation, holosystolic murmur. Maneuvers have opposite effects on murmurs as with the HOCM murmur. (Therefore learn the HOCM murmur). MR decreases with valsalva/standing, increases with leg raise/squatting, and hand grip.

AS- aortic stenosis, crescendo-decrescendo systolic murmur. Same response to maneuvers as with MR, EXCEPT with HANDGRIP/increased afterload. With increased afterload, AS decreases, but MR increases.

diastolic

MS- mid diastolic murmur, loud at the apex, can be 2/2 rheumatic fever

AR- early diastolic murmur, wide pulse pressure, head bobbing, can be 2/2 rheumatic fever, bicuspid valve, endocarditis

 

Syncope

consider San Francisco Syncope Rules - admit pts w/ CHF, Hct < 30, EKG abnormal, SOB, SBP < 90, fam hx of sudden death, syncope w/ exertion, structural heart disease.

 

arrhythmias

consider arrhythmias, AV blocks, a-fib, VT, etc

structural

hypertrophic cardiomyopathy, aortic stenosis - especially when syncope with exertion

electrical

WPW, QT, Brugada, ARVD

 

PE

1/6 patient’s admitted for first episode of syncope workup found to have PE. (NEJM 10.1056/NEJMoa1602172) History, clinical judgement and ECG changes are key in considering PE as cause of syncope (S1Q3T3, new RBBB, ST wave changes/depressions/elevation, TWI).

MI

history/chest pain, ECG, hx of CAD, troponin

other

AAA, CVA, SAH, seizure, ruptured ectopic, GI bleed, orthostatic/ meds, vasovagal. Do not forget to check glucose.

Consider CT head if neurologic complaint. SAH for example can cause syncope however pt usually will have persistent HA, AMS.

Admit pt’s for echo, cath/holter monitor, EP study.

 

Heart Blocks

 
 
image.jpg

first degree

Prolonged PR greater than 200.

image.jpg

second degree

Two types.

Mobitz Type I - increasing PR then dropped beat. Wenckebach.

Mobitz Type II - prolonged PR then sudden dropped beat. Needs pacemaker.

third degree

Complete heart block, dissociation of P from QRS. Needs pacemaker.

 

Transvenous pacer placement

 

Cordis placement

 

First place a 5 or 6 French cordis, into the right IJ or left subclavian.

 

Insertion

 

Sterile: Make sure swan sheath and white proximal hub of the sheath is on the pacer wire before insertion into the cordis. Thread the pacer wire to 20 cm into the cordis. Inflate balloon with 1.5cc of air. Have Distal/negative port of the pacer connected to the V2 lead on the chest (this will be done by a non sterile assistant). Advance the pacer wire and watch the monitor until ECG changes resemble ventricular lead placement (Widened QRS, with ST changes/elevations).

Once confirmed ventricular placement, deflate the balloon.

 

Pacer Setup

 

You will need an assistant to set up the pacer with non sterile hands. Insert the Distal/negative port into the V2 lead on the chest, this will allow you to monitor ventricular pacer placement described above.

Once confirmed ventricular placement per steps above, connect the pacer ports into the pacing device. Negative (-) to (-), positive (+) to (+).

Set rate at 100 bpm

A output rate to 0 bpm

V output to 25mAmp/Max

Decrease V output until lose pacing

Set/lock pacing at 2x minimum V output mAmp

tachycardia ddx

 

Can be split into narrow and wide qrs complex tachycardia, regular and irregular.

 

Narrow/Regular

Sinus tachycardia

Atrial tachycardia

Atrial flutter

SVT: AVNRT/ orthodromic AVRT

Narrow/Irregular

Atrial fibrillation

Multifocal atrial tachycardia

Atrial flutter with varied conduction (regularly irregular)

Wide/Regular

VT

SVT with BBB

Antidromic AVRT

Wide/Irregular

torsades, polymorphic VT

wide complex tachycardia

 

ventricular tachycardia

On ECG you can find AV dissociation, QRS > 120/ wide, Heart rate > 100, fusion beats and capture beats.

If unstable but with a pulse -> synchronized cardioversion at 100J

SVT with BBB

Difficult to distinguish from VT. Look for previous ECG with evidence of BBB or history of SVT terminated by adenoside/vagal maneuvers. If in doubt treat like VT. Consider using Brugada algorithm in distinguishing between VT and SVT with BBB.

antidromic AVRT/ WPW

DO NOT USE: adenosine, amiodarone, beta blockers, calcium channel blockers.

 

treatment

If unstable but with a pulse, -> synchronized cardioversion @ 100J

procainamide: 17 mg/kg at a rate of 25-50 mg/min

amiodarone - loading dose of 150 mg IV over 10 minutes, followed by an infusion 1mg/min for 6 hours, then 0.5 mg/min for 18 hours.

misc

avoid AV nodal blockers such as adenosine, digoxin, diltiazem, verapamil

the rest

Bidirectional ventricular tachycardia, caused by digoxin toxicity.

Other Tox/drugs can cause wide complex arrhythmia: TCA’s

 

bradycardia ddx

After considering ddx, treatment’s include:

atropine 0.5mg IV for max of 3mg.

epinephrine 2-10 mcg/min

transcutaneous pacing

transvenous pacing

Cause specific treatment:

 

athlete - sinus bradycardia, asymptomatic/HDS -> no treatment needed

hypothermia - rewarm

hypoglycemia - D50

hypothyroid/myxedema coma - tx hemodynamics/ABC’s, abx, hydrocortisone 100mg IV, levothyroxine

hyperkalemia- calcium gluconate/chloride, insulin/D50, albuterool, HCO3 1amp IV, dialysis.

AV blocking meds - CCB OD: high dose insulin, Calcium gluconate/chloride. BB OD: Glucagon 3mg IV. Digoxin OD: Digibind

sick sinus syndrome - pace

OSA - hemodynamics

heart block - pace

MI/ischemia - treat MI/cath lab?

CHA2DS2VASc

Score used to determine need for anti-coagulation in patient’s with Atrial Fibrillation. If score of 0, start ASA or no AC at all. Score of 1, consider AC. Score of 2 start AC.

Low risk - 0, Medium risk - 1 , High risk - 2 or greater points. As you can see below, many people will need anti-coagulation.

CHF - 1

HTN - 1

Age >75 - 2

DM - 1

Stroke - 1

Female - 1

ACLS

Evaluate for pulse first. If no pulse, then look at the rhythm and determine if rhythm is shockable or not shockable.

Remember that good CPR is what saves lives.

200J for defibrillation of shockable rhythms.

 

asystole / PEA

not shockable

CPR pulse check q2 min, and epinephrine q3-5 min

evaluate reversible causes, H’s/T’s


VT / V-fib

shockable, defibrillate at 200J

CPR pulse check 2min, epinephrine q3-5 min

amiodarone 300mg -> 150mg or lidocaine 1-1.5mg/kg


tx for reversible causes

hypoglycemia

acidosis

hyperkalemia

hypomagnesemia

tPA

H’s and T’s

 
  • hypoxia

  • hypovolemia

  • hypo/hyperKalemia

  • hypo/hyperThermia

  • H+ acidosis

  • Thrombosis/ MI

  • Thromboembolism / PE

  • Tension PTX

  • Tamponade

  • Toxins

Hypertension treatment, JNC 8 Recommendations

 

Asymptomatic Hypertension

If a patient is symptomatic from hypertension, presenting with HA, blurred vision or other end organ damage, then a completely different approach is used and is not addressed here. However in patients with hypertension greater than 180 mm Hg systolic, and 120 mm Hg diastolic, who are NOT symptomatic i.e. no signs of end organ damage, starting someone on anti-hypertensives is recommended. If BP is less then 180/120 mm Hg in patient’s who are asymptomatic, it is reasonable to have then follow up with their PCP for management of their blood pressure.

Patient’s need to follow up with their PCP for further management, recheck renal function, electrolyte levels.


African Americans

Thiazide / HCTZ - start with 12.5 mg daily

Calcium channel blocker / amlodipine - start with 2.5 mg once daily

Non African Americans

Thiazide / HCTZ - start with 12.5 mg daily

ACE-i or ARB - lisinopril start with 10 mg daily (In all races start ACE-i or ARB as initial therapy in CKD patients)

CCB / amlodipine - start with 2.5 mg once daily

LVAD labs

 
  • LDH

  • free hemoglobin

  • haptoglobin

  • cbc, cmp

  • troponin, bnp

  • PT/PTT/INR

Pulmonary Embolism

 

Massive PE

Hypotension with SBP < 90 for at least 15 minutes. Hypotension not due to other causes such as sepsis, arrhythmia, hypovolemia.

Persistent bradycardia, HR < 40 with signs of sock.

Tx: with tPA


Submassive PE

Acute PE without hypotension, SBP > 90, but with RV strain or dysfunction. Elevated Troponin, BNP.

Tx: anticoagulation, consider embolectomy, consider tPA?

PE

HDS, normal BP, no RV strain, normal troponin/BNP.

Tx: anticoagulation

ddx list

Just a salad of tested diagnoses and key facts about each.

 

Ebstein anomaly

apical displacement of tricuspid valve

 

Commotio cordis

v-fib after getting struck in the chest by an object

 

Coarctation of the aorta

typically pediatric presentation, tx with prostaglandin E1. Remember PGE1 can cause apnea so you will need to intubate the pediatric patient first.

 

Eisenmenger syndrome

VSD/left to right shunting progressing to right to left shunting

 
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