Tag Archives: ECG

Evidence of Raised Intracranial Pressure on ECG

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Evidence of Raised Intracranial Pressure on ECG – A Resident Clinical Pearl

Robert Dunfield, PGY2 FMEM program,  Dalhousie University Saint John

Reviewed & Edited by Dr. Mandy Peach

Case

A 44 year old male presents to your trauma bay with progressive confusion and altered level of consciousness for the past three days. Collateral history reveals possible recent recreational methamphetamine use. No specific abnormal neurological features or findings on history and physical. A full workup is performed and investigations reveal a left frontal intracerebral hematoma with the following CT head (Figure 1) and ECG (Figure 2):

 

1. What clinical (history and physical) features suggest an elevated intracranial pressure? [4, 5]

On history, suspect an elevated intracranial pressure with:

• headaches
• vomiting
• altered mental status (ranging and alternating from drowsiness to coma)
• visual changes (blurred, diplopia, photophobia)
• history of malignancy, trauma

On examination, suspect an elevated intracranial pressure with:

• Cushing triad: hypertension, bradycardia and irregular respiration. This is a sign of impending brain herniation
• pupils unequal, unreactive
• disc edema
• optic atrophy
• bulging anterior fontanelle (in infants)
• evidence of trauma

 

2. What features on ECG are in keeping with an elevated intracranial pressure? [1, 2, 6]

Elevations in ICP or brain injuries are commonly associated with the following ECG changes:

• “Cerebral” T waves: widespread giant T wave inversion
• Flat T waves
• ST elevation/depression
• QTc prolongation
• Sinus bradycardia (if seen assess for other features of Cushing triad)
• Increased U wave amplitude
• Osborn (J) waves
• Other dysrhythmias: sinus tachycardia, junctional rhythms, premature ventricular contractions, atrial fibrillation, AV blocks

ECG changes are common with elevated ICP and intracranial hemorrhage. Approximately 56% of patients with intracranial hemorrhage have associated ECG changes.

Most importantly, recognize that these ECG changes can mimic acute coronary syndromes. This is potentially dangerous as a misdiagnosis of STEMI in a patient with an intracranial bleed could lead to unnecessary thrombolytics or PCI. For this reason, keep an elevated ICP in mind when identifying the above ECG changes.

 

3. What is a cerebral T wave? [1, 5]

Cerebral T waves are deep, symmetric, inverted T-waves seen on an ECG in patients with large intracranial bleeds. They are typically widespread

 

4. What other causes, other than elevated ICP, result in inverted T waves and should be kept on your differential? [2]

When analyzing an ECG it is important to recognize other causes of inverted T waves. The differential for inverted T waves includes:

• Myocardial ischemia and infarction
• Bundle branch block
• Ventricular hypertrophy
• Pulmonary embolism
• Hypertrophic cardiomyopathy

 

5. What is the pathophysiological cause for the ECG changes associated with an elevated ICP? [3, 4]

The full pathophysiology of ECG changes related to an elevated ICP is not fully understood.

ECG changes related to an elevation in ICP are thought to be related to neurogenic cardiac injury. This is mostly due to a surge of systemic catecholamines as a result of significant sympathetic activation from the central neuroendocrine axis and activation of the adrenal glands. Additionally, any injury to the hypothalamus or insula can cause dysfunction of the autonomic nervous system and a systemic inflammatory response.

Systemic catecholamine levels can be elevated for as long as 10 days. This prolonged exposure to catecholamines as well as the systemic inflammatory response can result in cardiac injury and dysfunction.

It is also possible for the heart to suffer from “neurogenic stunned myocardium syndrome” (NSM). This is reversible myocyte damage that results in ECG changes, in addition to other cardiac effects, due an excessive release of norepinephrine. The amount of cardiac damage caused by NSM correlates with the degree of brain injury. NSM can develop within four hours of brain injury. Other causes of NSM include pheochromocytoma, near drowning, and severe emotional experiences.

 

6. What are the most common intracranial findings associated with ECG changes related to an increased ICP? [1, 3]

The most common causes of ECG changes related to an elevation in ICP involve massive intracranial hemorrhage, including subarachnoid hemorrhage (49 to 100% of cases)3 and intraparenchymal hemorrhage (57% of cases)1.

Less commonly, ECG changes are associated with massive ischemic stroke causing cerebral edema, traumatic brain injury, or less commonly cerebral metastases.

 

7. How long do ECG changes last with brain injuries related to elevated ICP, and what are the clinical implications for a finding of prolonged ECG changes? [3]

Normally, as brain injuries and elevated ICP resolve, so will ECG changes. Most ECG changes will resolve within three days but have been reported to last up to eight weeks from the etiology of the elevated ICP.

Some reports have shown that prolonged ECG changes are associated with an increased risk for ischemic neurological deficit, poor outcome, and death following a subarachnoid hemorrhage. Specifically, persistent prolonged QTc is associated with poor clinical outcomes and death, whereas recovery of QTc is associated with good clinical outcomes.

 

SUMMARY & KEY POINTS:

• Be aware of Cushing triad on clinical assessment of patients with potential elevation in ICP (sinus bradycardia, hypertension, and abnormal respiratory pattern).

• There are multiple nonspecific ECG changes associated with an elevation in ICP, including: cerebral T waves, ST elevation/depression, sinus bradycardia, increased U wave amplitude, J waves, and other dysrhythmias.

• The exact pathophysiology for the cause of elevated ICP causing ECG changes is complicated and not fully understood. It is thought to mostly be due to excess catecholamine and norepinephrine exposure, along with a dysregulated inflammatory reaction.

• Subarachnoid hemorrhage and intraparenchymal hemorrhage are the most common causes of ECG changes associated with elevated ICP.

• Be aware that ECG changes related to elevated ICP can mimic acute coronary syndrome, so keep intracranial pathologies on your differential when the above ECG changes are found.

 

Of note, the patient described in the clinical scenario was admitted to neurosurgery and observed for nearly two weeks. He recovered without operative management.

 

REFERENCES:

  1. Cadogan M. Raised Intracranial Pressure. Life in the Fast Lane 2020; Last updated: Nov. 3, 2020, Accessed: December 28, 2020. Available from: https://litfl.com/raised-intracranial-pressure-ecg-library/

  2. Gregory T and Smith M. Cardiovascular complications of brain injury, Continuing Education in Anaesthesia Critical Care & Pain. 2012; 12:2, 67–71. Available from: https://doi.org/10.1093/bjaceaccp/mkr058

  3. Levis JT. ECG Diagnosis: Deep T Wave Inversions Associated with Intracranial Hemorrhage. Perm J. 2017; 21:16, 049. doi:10.7812/TPP/16-049

  4. Pinto VL, Tadi P, Adeyinka A. Increased Intracranial Pressure. [Updated 2020 Jul 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482119/

  5. Tannenbaum L. ECG Pointers: Intracranial Hemorrhage. emDocs.net: Electrocardiography. 2018; Last updated: November 14, 2018. Accessed: December 29, 2020. Available from: http://www.emdocs.net/ecg-pointers-intracranial-hemorrhage/

  6. Yogendranathan N, Herath HM, Pahalagamage SP, Kulatunga A. Electrocardiographic changes mimicking acute coronary syndrome in a large intracranial tumour: A diagnostic dilemma. BMC Cardiovasc Disord. 2017;17(1):91. Published 2017 Apr 4. doi:10.1186/s12872-017-0525-2

 

 

 

 

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Syncope ECG – The ABCs

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ECG Interpretation in Syncope

Resident Clinical Pearl (RCP) – December 2018

Dr. Luke Taylor, FMEM PGY3 –  Dalhousie University, Saint John NB

Reviewed by Dr. David Lewis

 

What are you looking for on the ECG of the patient with syncope?

Quick review of frequently pimped question on shift!

Two approaches – One using systematic ECG analysis, the other a mnemonic.

ECG Analysis (1)

Standard format of rate, rhythm, axis, and segments (PR, QRS, QT, ST).

Method of calculating heart rate (2)

Rate: Simple — Is the patient going too fast or too slow? *Remember this easy way to check:
Rhythm: Look at leads II, VI and aVR for P waves.
Ask yourself:
Are they upright in II/VI and inverted in aVR?
Does a QRS follow every P and a P before every QRS?

If so likely sinus rhythm.

In the setting of syncope we are looking to see if there is any signs of heart block – a P wave not conducted to a QRS, especially being sure not to miss a Mobitz type II block.

Axis: Axis comes in to play when looking for more extensive conduction disease. Is there axis deviation along with a change in your PR and BBB indicating something like a trifasicular block?

Segments:

PR interval— is it looooong (heart block) or short (reentrant)?
Long has already been discussed in looking for signs of heart block, but a short PR may be indicative of Wolf-Parkinson-White or Lown-Ganong-Levine syndromes.

WPW – look for short PR and delta wave
LGL – short PR but no delta wave due to its conduction being very close to or even through the AV node and not through an accessory pathway.

QRS Morphology analyzing this for signs of Brugada, HOCM, WPW, ARVD, pericardial effusion, and BBB.

ECG findings of Brugada (3)

Type 1: Coved ST segment elevation with T wav inversion
Type 2: Saddleback ST segment elevation and upright T waves
Type 3: either above without the ST elevation

QT interval — is it looooong (R on T) or short (VT/VF risk)?
Long is >450 men, 470 women
Short < 330ms – tall peaked T waves no ST segment
Pearl for long – should be less than half the RR interval. —>

Normal relationship of R-R and QT interval (4)

 

ST segment — think MI or PE (rare causes of syncope but need to be considered)
MI – elevations or depressions

PE – Tachycardia, RV strain, T-wave inversion V1-V3, RBBB morphology, S1Q3T3

 

Mnemonic (5)

ABCDEFGHII

A — Aortic stenosis
Go back to patient and listen!
B — Brugada
C — Corrected QT
D — Delta wave
E — Epsilon wave as in Arrhythmogenic Right Ventricular Dysplasia (ARVD)

Epsilon: Small positive deflection (‘blip’) buried in the end of the QRS complex (6)

F — Fluid filled heart
Pericardial effusion, electrical alternans, low voltage throughout
G — Giant PE
H — Hypertrophy
LVH in someone who shouldn’t have it
I — Intervals
PR, QRS, QT
I — Ischemia

 

Looking for a Basic ECG Guide? See our Med Student Pearl Here:

Basic ECG Interpretation

 

 

References

  1. CanadiaEM – ECGs in Syncope https://canadiem.org/medical-concept-ecgs-in-syncope
  2. https://en.ecgpedia.org/wiki/Rate
  3. ECG Waves https://ecgwaves.com/brugada-syndrome-ecg-treatment-management
  4. https://www.healio.com/cardiology/learn-the-heart/case-questions/ecg-cases/question-3-5
  5. Hippo EM Education Shorts https://www.youtube.com/watch?v=raTTYV7_Asl
  6. https://en.ecgpedia.org/index.php?title=Arrhythmogenic_Right_Ventricular_Cardiomyopathy

 

This post was copyedited by Dr. Mandy Peach

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Basic ECG Interpretation

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Bare Bones Basics of ECG Interpretation from a First Year Medical Student Perspective

Medical Student Clinical Pearl – October 2018

Victoria Kulesza – Med I Class of 2021, Dalhousie Medicine New Brunswick 

Reviewed and Edited by Dr. David Lewis

Physiology

Electrical Events and Corresponding Waves and Lines on a Standard ECG

Basic Interpretation

Common Arrhythmias

Summary

Suggested Resources

References

Physiology

Cardiac cells are electrically polarized in their resting state, with the inside holding a negative charge in comparison to the outside.1,3 Membrane pumps maintain this electrical polarity through the regulation of ions including potassium, sodium, chloride and calcium.1 Depolarization is the key electrical event of the heart that occurs spontaneously in some cells and is initiated by the arrival of an electrical impulse carrying positively charged ions in other cells.1 There are 3 key cells involved in the electrical and mechanical activities that occur within the heart:

 

The sequential depolarization of cells creates a wave of depolarization that transmits across the entire heart, representing a flow of electricity that can be detected by the electrodes placed on the surface of that patient’s body. The waveforms visible on the ECG represent the electrical activity of the myocardial cells, the cells making up the vast majority of the heart.1 At the end of the depolarization process, cardiac cells are repolarized through membrane pumps reversing the flow of ions. Both the depolarization and repolarization are represented as the wave forms on the ECG.1

Electrical Events and Corresponding Waves and Lines on a Standard ECG

P Wave

The heartbeat is initiated in the sinoatrial node located in the posterior wall of the right atrium.4 After the sinus node fires, the atrial myocardium is depolarized in a wave-like fashion causing the atrial contraction. This depolarization and contraction of the atrial myocardial cells results in the first P wave.1 The wave of depolarization does not immediately pass through to the ventricles, the atrioventricular node located at the floor of the right atrium, slows the conduction of the electrical impulse to allow the atria to fully complete their contraction. 1,4 The contraction of the atria forces blood from the atria through the atrio-ventricular valves, known as the tricuspid and mitral valves, into the ventricles.3

PR Interval

This interval is the time that is required for the electrical impulse to travel from the atria, through the AV node, bundle of His, bundle branches and Purkinje fibers to the point where the ventricular myocardium begins its depolarization.5 As blood flows through the AV valves the physiologic pause in electrical conduction is represented on the EKG as the flat line following the initial P wave. The ventricular conduction system is composed of 3 parts including the Bundle of His, Bundle Branches and the Terminal Purkinje Fibers.1 The ventricular depolarization is rapidly transmitted through the Bundle of His which emerges from the AV node and subsequently bifurcates into the left and right bundle branches which carry the impulse down the interventricular septum to their terminating fascicles in multiple Purkinje fibers.1,3 Once this current is delivered to the ventricular myocardium the depolarization causes ventricular contraction visible on the ECG as the QRS complex.1

PR Segment

A straight line between the end of the P wave and the start of the QRS complex reflects the time between the end of atrial depolarization and the start of ventricular depolarization.1

QRS Complex

The QRS complex consists of 3 individual waves in a normal conduction1,3:

  • Q Wave: first deflection downward
  • R Wave: first upward deflection
  • S Wave: first downward deflection subsequent to an upward deflection

A complete QRS complex represents ventricular depolarization as well as the initiation of ventricular contraction.1,3 The use of the term QRS Interval describes the duration of the QRS complex alone indicating the duration of ventricular depolarization specifically.1

ST Segment

A straight line between the end of the QRS complex and the beginning of the T wave known as the ST segment measures the time from the end of ventricular depolarization to the beginning of repolarization.1

T Wave

Following the depolarization of the myocardial cells, there is a short refractory period and subsequent recovery phase identified as the T wave on the ECG.1,3,5 This is phase of ventricular repolarization that begins after the QRS and is completed at the end of the T wave.3,5 Repolarization is a slower process than the depolarization which is illustrated by the broader nature of the T wave in comparison to the QRS.1,5

QT Interval

This interval includes the QRS complex, ST segment as well as the T wave which allows for the measurement of time between the beginning of ventricular depolarization to the end of ventricular repolarization.

 

Basic Interpretation

The most effective way to ensure clinically significant abnormalities are not missed on ECG is to develop a consistent order of analysis. One suggested order is as follows:

 

A. Determine Rate:

  1. Sinus Tachycardia = >100 BPM
  2. Sinus Bradycardia = <60 BPM
  3. Three Ways to Determine Rate:
    • Identify an R wave that falls on or near one of the heavy lines of the ECG strip, count the number of large squares between this first R wave and the beginning of the subsequent wave. Divide 300 by the number of large squares between the R waves to determine the number of cardiac cycles per minute. Counting the number of small squares between R waves and dividing 1500 by this number would identify with greater accuracy the heart rate.1
    • Identify the series of small pink indicators above the rhythm strip that identify 3 second intervals and count the number of cycles between two 3 second intervals – multiply this number by 10 to identify the number of beats per minute.1
    • In the event of an irregular heartbeat identify the number of QRS complexes and multiply this number by 6. Each started ECG paper reads at 25mm/s therefore 1 ECG represents 10 seconds of activity.2

Thaler 2015

 

B. Intervals:

Identify the length of the PR and QT Intervals as well as the width of the QRS complexes

Normal Interval Lengths5:

  1. PR = 0.12 – 0.20 sec
  2. QT = varies with overall heart rate
  3. QRS = 0.05 – 0.10 sec

 

 

 

 

 

 

 

C. Rhythm5:

  1. P waves present and normal?
  2. QRS complexes wide or narrow? General pattern – regular, regularly irregular or irregularly irregular?
    1. Wide = >0.12 sec
    2. Narrow = <0.12 sec
  3. Relationship between P waves and QRS complexes
  4. Overall rhythm regular or irregular?

 

D. Axis

  1. The ECG electrodes record the average direction of flow of electrical current within the heart.
  2. Lead I is the zero reference point, any axis lying below is deemed positive while those lying above are deemed negative.
  3. When the wave of depolarization begins, any lead that views this wave as moving towards it will record this as a positive deflection on the ECG paper.
  4. Assessment of P Wave Axis:
    • Atrial depolarization begins at the sinus node in the right atrium and follows a right to left and inferior direction. This depolarization of the right to left atria should demonstrate a positive deflection in leads aVL, I, II and aVF.
  5. Assessment of QRS Complex Axis:
    • As the wave of depolarization moves through the interventricular septum the current moves in a left to right direction. This wave may not be visible on the ECG but when apparent appears as a negative deflection in leads I, aVL (V5 and V6). As a result of the increased size of the left ventricle in comparison to the right, the remainder of the QRS complex vector of flow is directed leftward and is demonstrated as the positively deflected R wave in most left lateral and inferior leads. The aVR lead will record a deep negative deflection based on the direction of flow being away from this lead.

 

 

Common Arrhythmias1

1. Sinus Tachycardia

  • HR >100 bpm
  • Can be normal or pathologic, strenuous exercise can cause HR above 100.

 

2. Sinus Bradycardia

  • HR <60 bpm
  • Can be normal or pathologic, many well-conditioned athletes maintain a resting HR below 60.

 

3. Paroxysmal Supraventricular Tachycardia

  • HR 150-250 bpm
  • Narrow complex QRS
  • Very common, sudden onset, sudden termination.
  • Clinical Symptoms: palpitations, shortness of breath, dizziness. Possibly induced by alcohol, caffeine or extreme excitement.

 

4. Atrial Flutter

  • P waves 250-350 bpm
  • Atrial depolarization occurs so rapidly that discrete P waves are indiscernible.
  • Leads II and III demonstrate a prominent saw-tooth
  • AV node cannot handle the number of atrial impulses therefore there is an unequal number of P waves to QRS complexes – some electrical impulses from the sinus node bump into a refractory node and go no further, this is called AV Block. 2:1 block is most common while 3:1 and 4:1 are also frequently observed.
  • Clinical Symptoms: shortness of breath, angina type discomfort.

 

 

5. Atrial Fibrillation

  • AV Node may receive >500 impulses per minute
  • More common than atrial flutter, most commonly sustained arrhythmia.
  • No true P waves are discernible, AV node allows occasional impulses to pass through to the ventricles, creating an irregularly irregular ventricular rate often in the range of 120-180 bpm.
  • Clinical Symptoms: some patients experience no symptoms, others experience shortness of breath, chest pain, palpitations and dizziness.

 

6. Premature Ventricular Contractions

  • Most common ventricular arrhythmia.
  • Retrograde P wave or no P wave prior to the QRS.
  • Wide QRS of at least 0.12 seconds in majority of the leads often followed by a compensatory pause before the subsequent beat.
  • Often occur randomly and rarely require treatment unless an isolated PVC is noted in the setting of acute MI as it may trigger ventricular tachycardia or ventricular fibrillation.
  • When to worry:
    • Frequent PVCs
    • Consecutive runs, 3+ in a row
    • Multiform – demonstrating variation in the site of origin
    • Occurring on the T wave – “R-on-T” phenomenon
    • PVC in the setting of an acute MI

 

 

7. Ventricular Tachycardia

  • Rate 120-200 bpm
  • Wide complex QRS
  • A run of 3+ consecutive PVCs.
  • Prolonged ventricular tachycardia is an emergency requiring immediate treatment to prevent cardiac arrest.
  • May be uniform or polymorphic, uniform being more closely associated with healed infarctions and polymorphic waveforms more commonly associated with acute coronary events.

 

8. Ventricular Fibrillation

  • Spasmodic tracings or coarse ventricular fibrillation or fine ventricular fibrillation without any true QRS complexes.
  • Heart generates no cardiac output, CPR and defibrillation are required immediately.
  • Most common arrhythmia in adults who experience sudden death.
  • Common predisposing factors:
    • Myocardial ischemia/infarction
    • Heart failure
    • Electrolyte disturbances
    • Hypoxemia or hypercapnia
    • Hypotension or shock
    • Overdoses of stimulants especially when used in combination with others

 

 

Summary

 

 

 

 

Suggested Resources

Teaching Medicine – Rhythm Strip Interpretation Practice

ECG Guide Mobile Smartphone App

  • Available through itunes app store

The Only EKG Book You’ll Ever Need

  • PDF available online through Dalhousie Library

 

References

  1. Thaler, M. S. (2015). The Only EKG Book You’ll Ever Need (9th ed.). Lippincott, Williams & Wilkins.
  2. Andrade, J. (2013). ECG Guide [Mobile application software]. Retrieved from http://itunes.apple.com
  3. Dubin, D. (2000). Rapid interpretation of EKG’s: An interactive course (6th ed.). Tampa, Fla.: Cover Pub.
  4. McKinley, M. P., OLoughlin, V. D., Harris, R. T., & Pennefather-O’Brien, E. E. (2015). Human anatomy (4th ed.). New York, NY: McGraw-Hill Education.
  5. Khan, M. (2008). Rapid ECG interpretation (3rd ed., Contemporary cardiology (Totowa, N.J). Totowa, N.J.: Human Press.
  6. Thomas, V. (n.d.). Premature Ventricular Contractions Treatment Cape Town. Retrieved from https://cardiorhythm.co.za/premature-ventricular-contractions/
  7. https://inside.fammed.wisc.edu/medstudent/pcc/ecg/axis.html
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EM Reflections – April 2018

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Thanks to Dr. Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

 

 

Top tips from this month’s rounds:

 

Ondansetron (Zofran) and QTi

Globe Rupture

Ovarian Torsion

 

 

Ondansetron (Zofran) and QTi

  • Ondansetron prolongs QTi in a dose-dependent manner
  • Patient is most at risk for an arrhythmia when peak serum levels are reached
    • Largest difference in QTi was found at 15 minutes (IV), but has seen to persist up to 120 min in heart failure patients.
  • Arrhythmia after a single dose is EXCEEDINGLY RARE
    • No reports of arrhythmia after a single dose of oral ondansetron.
    • Consider ECG monitoring (or use another anti-emetic agent) in patients who are receiving IV ondansetron with other arrhythmogenic factors such as QTi prolonging agents or electrolyte abnormalities

Ondansetron and QTc Prolongation: Clinical Significance in the ED

 

 

Globe Rupture

  • When should you suspect?
    • Mechanism – severe blunt, penetrating, metal-on-metal
  • Signs of open globe include:
    • penetrating lid injury,
    • bullous subconjunctival hemorrhage
    • shallow anterior chamber
    • blood in the anterior chamber (hyphema),
    • peaked pupil
    • iris disinsertion (iridodialysis)
    • lens dislocation, and
    • vitreous hemorrhage. Loss of red reflex can indicate vitreous hemorrhage or retinal detachment.

The EyeRounds.org website has some useful tutorials.

 

Management 

  • Stop Examination
  • NO PATCH – Use Eyes Shield
  • Consult Ophthalmology immediately
  • NPO, Tetanus, IV Antibiotics, analgesia and antiemetics

Download (PDF, 181KB)

 

 

Ovarian Torsion

  • Uptodate:  “It is one of the most common gynecologic emergencies and may affect females of all ages”
  • Most common ages 20-50 years
  • Acute onset pain with adnexal mass
  • As size of mass increases, risk of torsion increases
    • #1 RF is ovarian mass >5 cm
    • benign > malignant
  • Increased risk during pregnancy, fertility treatments
  • U/S test of choice, although normal doppler does not rule out torsion
  • CT not diagnostic, although if you had a CT that didn’t show an ovarian mass of >5cm, unlikely it was torsion…
  • 86-95% of patients with torsion have a mass (exception – pediatric population – more likely to have torsion with normal ovaries)
  • Pediatric patients – early surgical detorsion more likely to be successful
  • >36 hours – non-viable

A useful recent review can be viewed here

CoreEM provides another useful summary (as well as a huge amount of other EM Topics)

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Nar’ pump, mo’ problems

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Nar’ pump, mo’ problems, a case on cardiogenic shock

Resident Clinical Pearl (RCP) – June 2017

Mandy Peach, R2 FMEM, Dalhousie University, Saint John, New Brunswick

Reviewed/Edited by Dr. David Lewis and Dr. Kavish Chandra

It’s 11 pm, you’re doing the overnight shift and EMS calls in to report a patient with an ETA of 3 minutes: “80 yo female, found on floor in apartment by husband after reportedly feeling unwell for 2 days. Decreased LOC but arousable and responding appropriately. BP 82/36, HR 120, RR 22, Afebrile, oxygen sat 86% on 6L nasal cannula.”

You hear the vitals, and many differentials run through your mind – PE, sepsis, hemorrhage, tamponade. Your main concerns are: this person needs more airway support and they are in shock, and when you think shock you think ‘fluids’.

EMS rolls in with your patient and she looks awful – pale, mottled extremities and drowsy. She is being re-assessed, RT is present to switch to a face mask, IV access is being established and you’re about to pound her with fluids when you are handed her ECG:

1https://lifeinthefastlane.com/ecg-library/basics/inferior-stemi/

This lady clearly is having an inferior STEMI – there is marked ST elevation in II, III and aVF with early Q wave formation.

 

Take home point #1: In any Inferior STEMI, you must suspect RV involvement

Look for ST elevation in V1 and depression in V2, or ST elevation in lead III > lead II. If these are present – get a 15 lead ECG.1

On closer look at our patient’s ECG there is ST elevation in V1-V2 and the elevation in lead III is indeed larger than lead II. You order the 15 lead.

2 https://lifeinthefastlane.com/ecg-library/right-ventricular-infarction/

Look for ST elevation in right sided leads V3-V6, but the money is on V4R – ST elevation in this lead has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% for RV infarction2. Our patient does have RV infarction seen by ST elevation in V4R.

 

Take home point #2: RV involvement is associated with increased risk of cardiogenic shock and death with a mortality of 50% within the first 48 hours3. If there is RV involvement, giving nitroglycerin for chest pain is CONTRAINDICATED

Due to a poorly functioning RV, patients are pre-load sensitive2. If you decrease the pre-load then they have even less to pump, further worsening the hypotension.

So we have diagnosed this lady with cardiogenic shock secondary to AMI (the most common cause of cardiac related shock) and we determined she has RV involvement. We know we can’t give her nitroglycerin. Let’s reassess her status – the basic ABC’s.

Airway & Breathing – the RT has since advanced her to a non-rebreather with a sat level in the high 80’s. You suggest trying Optiflow or BiPAP as a temporizing measure – this lady is going to need to be intubated.

 

Take home point #3: Positive pressure ventilation requires a stable, cooperative patient – which is often not the case in cardiogenic shock

Positive pressure can decrease pre-load and potentially worsen hypotension3. It is a temporizing measure only. The majority will require endotracheal intubation to maintain their saturation as their work of breathing is a large expenditure of energy.

You successfully complete a RSI and the saturation improves to 94-98%.

Circulation – Repeat BP is 82/36. You complete a cardiac point-of-care-ultrasound (PoCUS) and see poor contractility, but no pericardial effusion or large clots suggesting chordae or papillary rupture. IVC is > 50% collapsible.

 

Take home point #4: On PoCUS, heart failure caused by acute ischemia will show a large RV and small LV secondary to low filling pressures, which is best seen on the apical 4 chamber view3

Your patient continues to be hypotensive – you give a small 500 cc bolus; you don’t want to overload a poorly pumping heart with fluid it can’t handle. However you anticipate that this will not be enough to improve her BP, and as she continues to be hypotensive her myocardial ischemia worsens, which subsequently worsens her pump dysfunction in a vicious cycle. She needs pressure support.

 

Take home point #5: Cardiogenic shock requires vasopressor support

If systolic BP > 90: Start with dobutamine for inotropy. Double up on agents – likely will need to add a vasoconstrictor. Dopamine is usually the next to add.

If systolic BP < 90: Can still use dobutamine, but need to add norepinephrine for vasoconstriction. Dopamine alone will worsen BP as it is a vasodilator.

3Tintinalli’s Comprehensive Guide to Emergency Medicine.

You start dobutamine and dopamine peripherally with the intention of obtaining central venous assess once stabilized.

In the meantime, cardiac labs and portable CXR are pending, you treat this patient as any other STEMI in terms of dual anti-platelet and anti-coagulation loading.

 

Take home point #6: Do not give beta blockers

Do not give beta blockers in RV infarcts as high risk of bradycardia and AV block due to ischemia of the AV nodal artery3.

You consult cardiology to activate the cath lab.

 

Take home point #7: Early revascularization in ischemic related cardiogenic shock is key

Early revascularization has a long term mortality benefit, preferably if done within 6 hours4.  Catheterization or CABG is the preferred method over thrombolytic therapy.

You consult cardiology to activate the cath lab.

Back to our patient –

This lady did go on to the cath lab and had stenting of her RCA, however her infarct likely occurred > 48 hours before presentation. Unfortunately, despite aggressive vasopressor therapy and revascularization, she coded immediately after the procedure and resuscitation attempts were unsuccessful, emphasizing the poor prognosis associated with ischemia related cardiogenic shock.

 

Bottom line for cardiogenic shock: fluid bolus 500 cc 0.9% NaCl, vasopressor support and RSI. Early revascularization is key – catheterization is preferred. Despite these interventions, the diagnosis portends a poor prognosis.

 

References

  1. Inferior STEMI – Life in the Fast Lane https://lifeinthefastlane.com/ecg-library/basics/inferior-stemi/
  2. Right Ventricular Infarction – Life in the Fast Lane https://lifeinthefastlane.com/ecg-library/right-ventricular-infarction/
  3. Tintinalli, JE. (2016). Cardiogenic Shock (8th ed.) Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (pages 349-352). New York: McGraw-Hill.
  4. Cardiogenic Shock – Literature Summary – Life in the Fast Lane https://lifeinthefastlane.com/ccc/cardiogenic-shock-literature-summaries/

 

This post was copyedited by Kavish Chandra @kavishpchandra

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