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Quick Case #04

September 4, 2013 By Christopher Partyka Leave a Comment

the case.

An 85 year old female is bought to ED with right hip pain. She was found outside after unfortunately spending the night on the ground.

This is her ECG. [Read more…]

Filed Under: #FOAM, ECG Tagged With: ECG, hypothermia, J waves, osborne waves, QRS notching, shivering artefact, sinus bradycardia

palpitations & presyncope…

August 20, 2013 By Christopher Partyka Leave a Comment

the case.

A 54 year old female presents to ED with an ‘odd sensation’ in her chest. This has been occurring intermittently for 2 months but has now increased in frequency & severity. She reports 3 episodes earlier today associated with nausea, clamminess & presyncope. [Read more…]

Filed Under: Cardiology, ECG Tagged With: arrhythmogenic right ventricle, ARVD, broad complex tachycardia, ECG, inferior axis, LBBB, monomorphic VT, palpitations, right ventricular outflow tract, RVOT VT, ventricular tachycardia

a game changer…

June 28, 2013 By Christopher Partyka Leave a Comment

The case.

A 76 year old female presents to ED after being repeated assaulted by her aggressive, demented husband, including punches, kicks and attempted strangulation. She has a past medical history of hypertension & GORD and takes telmisartan, amlodipine & pantoprazole.

On examination, she is alert and oriented with a patent airway, complaining of central chest pain and jaw pain. There are ligature marks over the anterior neck, but no haematoma, subcutaneous emphysema or hoarseness of voice. She has significant bruising (of various ages) over her maxilla, mandible, chest wall and thigh.

E-FAST reveals trace free-fluid in the Pouch of Douglas only, so with her normal vital signs she is booked for a CT pan-scan….

Whilst you are writing your notes, the Resus nurse hands you her ECG…

Assault ECG01 - June 18 @ 946pm

… it appears to be a game-changer ! Suddenly your team questions everything !!

What’s your interpretation ?!

    • Sinus rhythm at 88 bpm. 1x junctional ectopic (5th complex).
    • Normal axis.
    • PR 200msec, QRS 80-90msec, QTc 485msec (Bazett)
    • Widespread ST-segment elevation
        • Concave up.
        • Predominately inferolateral leads (V4-6, I, II, III, aVF – up to 4.5mm)
        • Associated ST depression & PR elevation aVR. Suggestion of PR depression along rhythm strip (II).

Differential Diagnoses.

    • Acute Coronary Syndrome (STEMI).
    • Pericarditis
    • Myocardial injury/contusion ?

What else should we consider ??

Differential Diagnosis of ST-Segment Elevation

      • Acute Coronary Syndrome / AMI
      • Acute Pericarditis
      • Bundle Branch Block (left & right)
      • Benign Early Repolarisation
      • Ventricular escape/paced rhythm.
      • LVH
      • LV aneurysm.
      • Cardiomyopathy / Myocarditis
      • Myocardial contusion.
      • Post-defibrillation
      • Hyperkalaemia
      • Hypothermia (Osborn J-waves)
      • Channelopathies (eg. Brugada)
      • Preexcitation Syndrome (eg. WPW)
      • Intracranial/CNS Injury (eg. SAH)

What do you do next ?!

      • Bedside ECHO:
          • No pericardial effusion.
          • LV apex is hypokinetic.
      • Do you give aspirin ?? What about other ischaemic meds ??
          • Is this a true AMI ??
          • She could have traumatic intracranial pathology.

The story continues…

Whilst the team is concerned about her ECG changes, it is decided that she should have her neuroimaging prior to administration of antiplatelet therapy. She is rushed off to CT…

The findings;

      • CT Brain – Small acute left subdural haematoma with minimal mass effect with tiny focus of subarachnoid blood in the left parietal lobe.
          • Remainder of CT is negative for traumatic pathology.
      • HS-Troponin is elevated @ 1161 ng/L (delta Trop returns at 1365 !!)
      • Formal Cardiology ECHO (1150pm!!) shows moderate systolic impairment with apical & periapical hypokinesis.
      • Decision made to give 300mg of aspirin and head to the CATH lab for angiography…
      • Angiogram showed only minor coronary disease. No culprit lesion identified. No ventriculogram performed.

The Diagnosis???

TAKOTSUBO CARDIOMYOPATHY

aka. Stress-induced cardiomyopathy, Apical ballooning syndrome, Broken-heart syndrome.

 

The Basics.

    • An increasingly reported syndrome.
        • May account for ~2% of suspected STEMIs.
    • Characterised by transient systolic dysfunction of the apical &/or mid-segments of the left ventricle.
        • “Takotsubo” – Japanese for an octopus trap, the shape resembling that of the apical ballooning configuration of the left ventricle.
    • Mimics acute myocardial infarction, but there is absent obstructive CAD.
    • Most common in post-menopausal women.

Stress-cardiomyopathy

 

The Pathophysiology.

    • Poorly understood.
        • Suggested mechanisms include; catecholamine excess, coronary artery spasm or microvascular dysfunction.
        • Potential role for plaque rupture & coronary thrombosis (with spontaneous thrombolysis).
    • Frequently but not always triggered by an acute medical illness or intense, emotional or physical stress [unexpected family death, domestic violence, financial stress, natural disasters].
    • Physical or emotional stress.
        • ?Diffuse catecholamine-induced microvascular spasm [“myocardial stunning”]
        • ?Direct catecholamine-associated myocardial toxicity.
    • Critical illness.
        • A “not uncommon” diagnosis in the medical ICU population, even among patients with non-cardiac diagnoses and no prior history of cardiac disease.

Clinical Features.

    • The presentation is similar to that of AMI.
    • Most common symptom is acute, substernal chest pain.
        • Associated dyspnoea, syncope, shock and ECG abnormalities.
    • Acute complications include;
        • Heart failure
            • More common when age > 70, physical stressor present & LVEF < 40%
        • Tachy & bradydysrhythmias
        • Mitral regurgitation
            • Secondary to acute LV outflow tract obstruction (a result of LV basal hyperkinesis)
        • Cardiogenic shock

Investigations.

    • ECG abnormalities include;
        • ST-segment elevation (most common in precordial leads)
        • Deep T-wave inversion
        • Prolonged QT
        • Abnormal Q-waves
        • Can be normal…
    • Troponin.
        • Usually elevated (typically mild).
    • ECHO & Ventriculography.
        • Characteristic apical ballooning with akinesis/dyskinesis of the apical 1/2 to 2/3’s of the LV.
        • Systolic function is reduced.
        • Wall motion abnormalities may involve the distribution of more than one coronary artery.

Diagnosis.

    • This should be suspected in postmenopausal women who present with ACS following intense psychological stress in whom clinical and ECG abnormalities are out of proportion to the degrees of troponin elevation.
    • Coronary angiography typically shows either normal vessels or mild-moderate coronary atherosclerosis.
    • Cardiac MRI can provide additional information.
    • The Mayo Clinic diagnostic criteria require all of the following to make the diagnosis.
        • Transient hypokinesis, akinesis or dyskinesis of the LV mid-segments with or without apical involvement.
        • Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
        • New ECG abnormalities (ST-elevation or TWI) or modest troponin elevation.
        • Absence of phaeochromocytoma or myocarditis.

Management.

    • A patient with chest pain and ST-elevation should be managed as though they have acute myocardial ischaemia.
        • Cardiac catheterisation if available, otherwise suspicion of stress-induced cardiomyopathy is not a sufficient reason to withhold fibrinolytic therapy.
    • Takotsubo cardiomyopathy is a transient disorder managed with supportive therapy.
    • Standard therapy for patients with LV impairment have been suggested.
        • Eg. ACE inhibitors, beta-blockers and diuretics.
        • Typically continued until there is resolution of LV function (usu. 1-4 weeks).
    • Aspirin for those with co-existing coronary atherosclerosis.
    • Hypotension/Shock.
        • Urgent ECHO for LVOT obstruction.
            • Treated w/ beta-blockers & fluid resuscitation.
        • Absence of LVOT obstruction.
            • Cautious use of inotropic agents (remember this is a condition of catecholamine excess).
        • Consideration of IABP counterpulsation.
    • Thromboembolic prophylaxis.
        • Intraventricular thrombus formation and embolisation are potential sequelae.
        • Data is limited on use of anticoagulation.
            • Suggested for those with identified LV thrombus, or for those with severe LV dysfunction (until akinesis/hypokinesis resolves).

The finale…

    • Troponin peaked 6 hours into admission.
    • Further headache during day one of admission with CT showing slight progression of SDH. She did not require neurosurgical intervention.
    • She remained haemodynamically stable and was started on bisoprolol and ramipril. Subsequent ECHOs showed some improved in LV function.
    • She was discharged home on Day 10 with outpatient Cardiology followup.

References.

  1. UpToDate. “Stress-induced (takotsubo) cardiomyopathy”
  2. Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.

Filed Under: Cardiology, ECG, ECHO Tagged With: apical ballooning, cardiomyopathy, catecholamine, chest pain, ECG, ST elevation, ST segment, stress cardiomyopathy, Takotsubo

eh-vee-arrr

December 29, 2012 By Christopher Partyka Leave a Comment

The Case.

A 38 year old male presents to your ED with left sided chest heaviness which radiates to his left shoulder & down the arm. He has associated dyspnoea, nausea & vomiting. He looks unwell.

He underwent a CT-Coronary Angiogram 4 months earlier showing a Calcium-Score of 450 !! (‘Extensive plaque burden’. 8x increase in Framingham predicted risk). However, a Sestamibi study performed at the same time showed no evidence of inducible ischaemia.

This is his ECG…

38yo ECG01

What’s your interpretation ?

my take…

  • Sinus tachycardia at ~ 100bpm.
  • Normal axis. Normal intervals.
  • ~1.5mm STE in aVR, with widespread ST depression (V2-5, II, III, aVF).
  • DDx. Left main ischaemia vs triple vessel disease !!

He was treated aggressively with aspirin, GTN infusion & heparin.
I elected to withhold clopidogrel (a decision backed by Cardiology).

As his pain settled the following ECGs are taken…

38yo ECG02 38yo ECG03

Is it significant ???

For me this case was all about…..

aVR

The right-ward facing unipolar lead.

Obtains information about the right, upper side of the heart including the right ventricular outflow tract and basal septum.

Why is it important ??

Toxicology (particularly Na-channel blockade), dysrhythmias (P-wave configuration, identification of AV dissociation etc.) & ischaemic chest pain ….

In the setting of cardiac ischaemia, ST-segment elevation in aVR can indicate left main coronary artery stenosis.

      • Significant mortality (~70%)
      • Medical therapy not helpful –> patients need cardiac catheterisation
      • Other ECG features:
          • Concurrent STE in aVL
          • STE in aVR > STE in V1.
      • The greater the ST-elevation, the greater the mortality !!

It may also indicate proximal LAD occlusion or triple-vessel disease.

Where do we go from here ??

A recent post by Dr Smith on aVR has bought to my attention this important paper…

An Early and Simple Predictor of Severe Left Main and/or Three-Vessel Disease in Patients With Non–ST-Segment Elevation Acute Coronary Syndrome

Am J Cardiol. 2011 Feb 15;107(4):495-500

This study demonstrates that  ST-segment elevation >1 mm in lead aVR and positive troponin on admission are highly suggestive of severe LMCA or triple vessel disease (the converse is also true). The negative predictive value of STE > 1mm in aVR was 98% !! The authors (as well as Dr Smith) suggest that with the subsequent increased need for CABG, these patients would benefit from withholding clopidogrel (reducing the risk of intra-operative bleeding).

The Follow-up.

  • Patient is transferred pain-free to Coronary Care on GTN & Heparin infusions.
  • HS-Troponins 8 –> 12 –> 24 (Normal < 5).
  • The following morning he has an angiogram demonstrated significant 3-vessel disease.

He is now awaiting bypass-grafts….

References

References.

  1. Gorgels AP, Engelen DJ, Wellens HJ. Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography. J Am Coll Cardiol. 2001 Nov 1;38(5):1355-6.
  2. Kosuge M et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500
  3. Dr. Smith’s ECG Blog: ST elevation in aVR, with widespread ST depression
  4. Life in the Fast Lane: Another Widow Maker.
  5. EMRAPTV Episode 68: aVR – Gets No Respect!

Filed Under: Cardiology, ECG Tagged With: aVR, CABG, cardiac ischaemia, ECG, electrocardiogram, left main coronary, LMCA, ST elevation, triple vessel disease

another ECG case…

October 21, 2012 By Christopher Partyka Leave a Comment

The Case.

I was superficially involved in this case of a 32 year old suicidal patient who ingested two full packets of Solian (amisulpride) (~ 24 grams) approximately 90 minutes prior to arrival to ED.

On initial assessment he was GCS 12/15 & had a systolic BP of 115 mmHg.

This is his ECG….

amisulpride ECG

Amisulpride Toxicity…

AMISULPRIDE TOXICITY.

Amisulpride – What is it ?

a benzamide neuroleptic (atypical antipsychotic) with high affinity for the dopamine (specifically D2-2) receptor. 

    • used for acute & chronic schizophrenia (both negative & positive symptoms)
    • unlike other neuroleptics, it has minimal affinity for 5HT, alpha, H1 or cholinergic receptors.

Dose-based Risk Assessment.

      • < 8g = mild-moderate sedation, mild anticholinergic features.
        • QT prolongation & torsades are reported (in as little as 4.6g ingestion)
      • 8-15g = Increasing sedation & depressed level of consciousness.
        • Cardiotoxicity includes hypotension, QRS & QT prolongation, bundle-branch blocks & torsades.
      • > 15g = Significant risk of delayed coma & cardiotoxicity…

Signs & Symptoms.

      • Mild-Moderate: Mydriasis, lethargy, drowsiness and sedation, bradycardia, agitation, hyperthermia and extrapyramidal symptoms.
      • Severe toxicity: Seizures, coma, hypotension, and QTc prolongation. Torsades & VT are reported in intentional overdose.

Management…

Management.

  • Resuscitation area / full cardiorespiratory monitoring.
      • Patients may require intubation / mechanical ventilation
      • Minimum of 16 hours telemetry mandated for ingestion >4g
  • Decontamination (oral activated charcoal) is recommended for > 4 grams in previous 4 hours.
      • No antidote.
      • Enhanced elimination not useful
  • Control of QT / risk of Torsades
      • Magnesium (2g IV over 1-2 minutes, repeat x1 –> infusion of 0.5-1.0g / hour)
      • Chemical or electrical atrial overdrive pacing.
  • Correct electrolyte abnormalities (specifically hypomagnesaemia, hypokalaemia & hypocalcaemia)

Disposition.

As a rule; all ingestions > 4 grams should be monitored for at least 16 hours and until all ECG intervals are normal….

  • Asymptomatic adults with inadvertent/minor exposure may be monitored at home.
  • Significant/deliberate amisulpride overdose are observed for at least 16 hours after ingestion.
    • Continuous cardiac monitoring and serial ECGs.
    • If no dysrhythmias or QT prolongation at 16hrs –> discharged after psychiatric evaluation.
  • Dysrhythmias or QT prolongation on ECG –> intensive care setting for continuous cardiac monitoring and treatment.

As for our patient…

ECG:  Sinus rhythm @ 83bpm. Normal axis. PR ~200ms. QRS ~120ms. QTc ~560ms !!!

His management (after discussion with our Toxicology gurus) included;

  • Intubation
  • NG tube w/ activated charcoal administration
      • Two further doses of charcoal
  • MgS04 (20mmol x2)
  • Isoprenaline infusion with target HR >100 bpm
      • Dropped QT down to ~500msec

He survived his first night in the ICU….

References
  1. Murray L, Daly F, Little M & Cadogan M. Toxicology Handbook. 2nd Edition. Elsevier 2011.
  2. Isbister GK et al. Amisulpride deliberate self-poisoning causing severe cardiac toxicity including QT prolongation and torsades de pointes. Med J Aust 2006; 184 (7): 354-356.
  3. Isbister GK, Balit CR, Macleod D, Duffull SB. Amisulpride overdose is frequently associated with QT prolongation and torsades de pointes. J Clin Psychopharmacol. 2010 Aug;30(4):391-5.
  4. http://lifeinthefastlane.com/book/toxicology/amisulpride/
  5. Micromedex 2.0 (Toxicology Summary) “SULPIRIDE AND RELATED AGENTS”
  6. http://lifeinthefastlane.com/ecg-library/basics/qt_interval/

Filed Under: ECG, Toxicology Tagged With: Amisulpride, ECG, QT interval, toxicology

generally unwell (part 2)…

October 8, 2012 By Christopher Partyka Leave a Comment

For those joining the story for the first time, you can catch up here….

My interpretation of the ECG;

Sinus rhythm with 1st degree HB, an ‘odd’ axis. Wide complex QRS (~140-160ms) with symmetrical tall T-waves.
? Hyperkalaemia. Needs urgent bloods….

The nurse returns…

No one can place an IV or take bloods from her. So off you go, USS in tow to the bedside.

IV placed; bloods taken; urgent VBG to the iStat…..


[Read more…]

Filed Under: ECG, Uncategorized Tagged With: ECG, hydronephrosis, hyperkalaemia, obstructive uropathy

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