the dying heart…

The Dying Heart…

Amal Mattu, MD, FAAEM, FACEP Professor and Vice Chair

Department of Emergency Medicine University of Maryland School of Medicine

Baltimore, Maryland

Pulseless Electrical

Activity

Amal Mattu, MD, FAAEM, FACEP Professor and Vice Chair

Department of Emergency Medicine University of Maryland School of Medicine

Baltimore, Maryland

Case

• 55 yo M brought by EMS for cardiac arrest

Case


– Visiting Baltimore for convention

– Was with colleagues and told them that he wasn’t feeling well

Case


– Visiting Baltimore for convention

– Was with colleagues and told them that he wasn’t feeling well

– Slumped over at the breakfast table and fell to the floor

Case


– Friends called 911 immediately, + CPR

– EMS arrived (BLS) after 5-10 min

Case


– Friends called 911 immediately, + CPR

– EMS arrived (BLS) after 5-10 min

•No pulse or spont. respirations

•Compressions, bagging

Case

Courtesy Dr. Eric Lung

Case


– Patient arrives with same rhythm…what do you do?

Questions

• What is PEA??

Questions

• What is PEA??

– Pulseless electrical activity

– Formerly referred to as EMD

•“Electromechanical dissociation”

PEA

• PEA is defined by a rhythm that should normally produce a pulse

– Not VF, VT, torsades, rapid afib, etc.

– Not extreme bradycardia

– Not brady-asystole (agonal)

• These other rhythms have different protocols for treatment

PEA

• Pulseless electrical activity

– Increasing proportion of SCA rhythms over the past several decades

PEA

• Pulseless electrical activity

– Increasing proportion of SCA rhythms over the past several decades

•35-40% of in-hospital cardiac arrests

•22-30% of OOHCA

•Reduction in % of VF possibly due to increased use of beta-blockers?

Cardiac Arrest “Types”

• Electrical mechanisms associated with SCA are generally divided into tachyarrhythmic and non-tachyarrhythmic categories

• Non-tachyarrhythmic categories

– PEA

– Asystole

– Extreme bradycardia, agonal

Cardiac Arrest “Types”

ACLS and PEA

• What does ACLS recommend for PEA?

ACLS and PEA


– Vasopressors EPI, VP

– IVF?

– Atropine if rhythm is slow

– Compressions?

ACLS and PEA


– Would you do compressions on this patient in PEA? Would it hurt??

ACLS and PEA


– Dx: pericardial tamponade

– Compressions might be harmful

ACLS and PEA


– Vasopressors EPI, VP

– IVF?

– Atropine if rhythm is slow

– Compressions?

– Then quickly determine and treat the underlying cause

ACLS and PEA

• The H’s and T’s

• H’s • T’s

ACLS and PEA

• H’s

– Hypovolemia

– Hypoxia

– Hydrogen ion (acidosis)

– HyperK

– HypoK

– Hypothermia

– Hypoglycemia

• T’s

ACLS and PEA

• H’s

– Hypovolemia

– Hypoxia

– Hydrogen ion (acidosis)

– HyperK

– HypoK

– Hypothermia

– Hypoglycemia

• T’s

– Toxins

– Tamponade

– Tension PTX

– Thrombosis (MI)

– Thrombosis (PE)

– Trauma (hemorrhage)

ACLS and PEA

ACLS and PEA

• Is there an easier method?

Littman, et al. approach to PEA

• What is the likelihood of the Hs and Ts causing PEA?

– Which are the truly common causes?

• Is there a simple, rational approach to workup and treatment?


• Use the ECG and U/S


• Step 1: use the ECG


• Is the QRS narrow or wide?


• Narrow QRS RV inflow or outflow

problem (“pseudo-PEA”)

– Tamponade

– Tension PTX

– Mechanical hyperinflation

– Massive PE

– Severe hypovolemia or hemorrhage


• Narrow QRS Note that chest

compressions can be harmful here!!

– Tamponade

– Tension PTX


– Massive PE



• Next, look at the bedside ultrasound if Dx unclear, usually hyperdynamic

– Tamponade

– Tension PTX


– Massive PE



• Next, look at the bedside ultrasound if Dx unclear, usually hyperdynamic


• Treat the cause or give VOLUME

– Tamponade

– Tension PTX


– Massive PE



• What if the QRS is wide?


• Wide QRS metabolic, tox, or severe

LV problem (“true PEA”)

12-Lead 1Name:

Patient ID:

Incident ID:

Device:

Device Configuration:

Software Revision:

LP15 MEDIC 22 LP1541440753

2DJ55RO402B9OR

3306808-005

LIFENET® Report Renderer (5.2.1.134) Page: 1 of 1

Name:

ID:

Age: 50

12-Lead 1

3/4/2014

PR 0.098s

QT/QTc:

P-QRS-T Axes:

030414175431

Patient ID:

Incident ID:

Sex: F

17:57:16

HR 60bpm

QRS 0.138s

0.392s/0.392s

-32768° -32768° -32768°

• Abnormal ECG **Unconfirmed**

• Accelerated idioventricular rhythm

• Lead(s ) uns uitable for analys is : II aVR aVF V1 V2

• Pos s ible inferior infarct - age undetermined

• Marked precordial ST depres s ion, CONSIDER ACUTE INFARCT

• Anterolateral ST-T abnormality may be due to myocardial infarct or CVAI

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

x1.0 .05-150Hz 25mm/sec

Physio-Control, Inc. Comments:

MEDIC 22 BCFD 3306808-005 LP1541440753

ST measurements are measured at the J point and are expressed in mm.

I

-1.15

II

-327.68

III

-6.04

aVR

-327.68

aVL

2.44

aVF

-327.68

V1

-327.68

V2

-327.68

V3

2.54

V4

-3.35

V5

-9.68

V6

-8.84

To ensure printer accuracy, confirm that the calibration markers are 10mm high and the grid squares are 5mm wide.


• Wide QRS metabolic, tox, or severe

LV problem (“true PEA”)

– Severe hyperK+

– Sodium channel blocker toxicity

– Severe metabolic acidosis

– Massive MI with pump failure


• Next, look at the bedside ultrasound if Dx unclear, usually hypokinetic

– Severe hyperK+



– Massive MI with pump failure


• Give empiric NaHCO3, Ca++, consider cath or lytics if MI suspected by Hx

– Severe hyperK+



– Massive MI with pump failure (usually die)


• What’s missing?



– Hypoxia

– HypoK+

– Hypoglycemia

– Hypothermia



– Hypoxia no evidence

– HypoK+ no evidence

– Hypoglycemia no evidence

– Hypothermia use a thermometer!



– Other toxins, e.g. BBs and CCBs

•Typically present with hypotension, sinus brady or sinus arrest, AV blocks

•If PEA occurs, typically narrow QRS and slow and dx almost always established by then

Littmann /Bustin /Haley

Med Princ Pract 2014;23:1–6DOI: 10.1159/000354195

2

plify the evaluation of patients who present with cardiac arrest due to PEA [9, 10] . There were also attempts to use the electrocardiogram (ECG) and bedside echocardio-gram to guide the diagnosis and management of PEA [10–16] . Over the last few years we have developed a teaching tool that simplifies the diagnostic approach by differentiating narrow- and wide-complex rhythms on initial telemetry (QRS duration <0.12 and 0.12 s, respec-tively), and by eliminating those diagnoses which rarely if ever cause PEA. Our algorithm does not apply in the specific trauma setting. This algorithm has not been sys-tematically tested but is supported by scientific and clini-cal principles and by a thorough review of the literature.

The New PEA Algorithm: Diagnostic Aspects

The multiple Hs and Ts that are frequently quoted as possible causes of PEA are listed in figure 1 . It seems ob-vious that recollection of these can be near impossible in the acute setting. Our simplified algorithm that focuses on differentiation between narrow or wide QRS complex-es is shown in figure 2 . This should be an easy distinction that can be discerned by simply looking at the telemetry monitor during resuscitation. The general assumption is that narrow-complex PEA is generally due to a mechani-cal problem frequently caused by right ventricular inflow

or outflow obstruction, whereas wide-complex PEA is typically due to a metabolic problem or ischemia and left ventricular failure. Wide-complex PEA may also indicate agonal rhythm.

The four most common mechanical causes of PEA ar-rest include cardiac tamponade, tension pneumothorax, mechanical hyperinflation and pulmonary embolism ( fig. 2 ). The clinical scenario can usually help navigate between these causes. Jugular venous distension and muffled heart sounds suggest tamponade. Rib fracture, severe emphysema, positive pressure ventilation and hy-perexpanded chest indicate pneumothorax, mechanical hyperinflation or auto-PEEP [17, 18] . Cancer history and deep venous thrombosis suggest pulmonary embolism. In all of these cases cardiac ultrasound usually shows pre-served or even hyperdynamic left ventricular function in-dicative of pseudo-PEA ( fig. 2 ) [10–14] . A collapsed right ventricle suggests inflow obstruction from tamponade, pneumothorax or hyperinflation. A dilated right ventri-cle, on the other hand, indicates possible pulmonary em-bolism. Thoracic ultrasonography may also help in direct pleural assessment and in the diagnosis of pneumotho-rax.

Wide-complex PEA usually suggests a metabolic prob-lem such as severe hyperkalemia with or without meta-bolic acidosis, or sodium channel blocker toxicity ( fig. 2 ) [19, 20] . Again, the clinical scenario is usually helpful: in

FREQUENTLY LISTED

CAUSES OF PEA (Hs & Ts)

• Hypovolemia

• Hypoxia

• Hydrogen ion

– acidosis

• Hyperkalemia

• Hypokalemia

• Hypothermia

• (Hypoglycemia)

• Toxins

• Tamponade

• Tension PTX

• Thrombosis

– coronary

• Thrombosis

– pulmonary

• (Trauma)

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Fig. 1. Causes of PEA listed by European and American guidelines. Hypoglycemia and trauma have been removed from the most re-cent ACLS guidelines [6, 7] . PTX = Pneumothorax.

PEA – EVALUATION

• Cardiac tamponade

• Tension PTX

• Mechanical hyperinflation

• Pulmonary embolism

• Severe hyperkalemia

• Sodium-channel blocker toxicity

QRS NARROWMECHANICAL (RV) PROBLEM

QRS WIDEMETABOLIC (LV) PROBLEM

ACUTE MI Myocardial rupture

ACUTE MI Pump failure

AGONAL RHYTHM

BEDSIDE US: LV HYPERDYNAMIC

PSEUDO-PEA

LV HYPOKINETIC OR AKINETIC

TRUE PEA

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Fig. 2. New classification of PEA based on its initial electrocardio-graphic manifestation. LV = Left ventricular; PTX = pneumotho-rax; US = ultrasound; RV = right ventricular.

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Summary

Severe hypovolemia or hemorrhage

A Simplified Teaching Tool for PEA Med Princ Pract 2014;23:1–6DOI: 10.1159/000354195

3

patients with critical illness, sepsis, shock or renal failure, the diagnosis of wide-complex PEA is usually hyperkale-mia. Identification of an arteriovenous fistula or dialysis catheter also suggests hyperkalemia. In patients who were ‘found down’ or who present following ingestion or sui-cide attempt, the cause of wide-complex PEA is almost always sodium channel blocker toxicity [21] . In wide-complex PEA, a metabolic or ischemic cause is supported by the echocardiographic observation of left ventricular hypokinesis or standstill ( fig. 2 ). Other possible causes of wide-complex PEA include a mechanical etiology with preexisting aberrancy or pulmonary embolism – a me-chanical cause that can be associated with complete right bundle branch block. In these cases too, bedside ultra-sound can quickly point to a mechanical cause.

Patients with acute myocardial infarction (MI) can also present with PEA. Patients who undergo prehospital resuscitation for MI and PEA typically have a dismal prognosis, despite aggressive management including thrombolytics [22, 23] . In hospitalized patients with acute MI, PEA is usually a relatively late manifestation. Here too, the ECG is crucial in distinguishing a mechanical cause such as myocardial rupture from pump failure [24, 25] . The former is usually associated with narrow QRS complexes, whereas the latter is associated with widened QRS complexes ( fig. 2 ). Immediate recognition of possi-ble myocardial rupture can be life-saving as with emer-gent surgical intervention some patients may survive for decades [25] . Wide-complex PEA associated with acute MI or with other agonal rhythms, on the other hand, has dismal prognosis with no effective treatments.

An important question is whether this simplified al-gorithm covers all important causes of PEA? We believe that it does. A recent thorough review of the PEA litera-ture by Desbiens [9] and our independent review did not find any evidence that hypoxemia, hypokalemia or hypo-glycemia presents primarily with PEA. Hypothermia is not listed in our new algorithm, but there the clinical picture is usually quite obvious. Of ‘toxins’, the initial presentation of β-blocker, calcium channel blocker and digitalis toxicity is almost always hypotension, sinus bra-dycardia, sinus arrest or atrioventricular block [26, 27] . Some of these do progress to PEA but by that time the diagnosis is usually well established [28–30] . Standard treatments are available for these conditions [26, 31] . Of the other possible ‘Ts’, we have excluded trauma, as have the newest guidelines [6, 7] , because traumatic arrests have unique management strategies separate from cur-rent ACLS guidelines [32] , and signs are usually apparent on exam.

The New PEA Algorithm: Therapeutic

Considerations

How this simplified and structured approach to PEA can guide initial treatment is shown in figures 3 and 4 . For patients with narrow-complex PEA from a suspect-ed mechanical etiology, aggressive intravenous fluid ad-ministration should be initiated as these causes are po-tentially fluid responsive. After that, based on the most likely clinical scenario or results of bedside ultrasonog-

PEA – MANAGEMENT


• Tension PTX

• Mechanical

hyperinflation


QRS NARROW

MECHANICAL (RV) PROBLEM

WIDE OPEN

FLUIDS, PLUS:

PERICARDIOCENTESIS

NEEDLE DECOMPRESSION

VENTILATOR

MANAGEMENT

THROMBOLYSIS!

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Fig. 3. Treatment recommendations for narrow-complex PEA. PTX = Pneumothorax: RV = right ventricular.

QRS WIDE

METABOLIC (LV) PROBLEM

PHARMACOLOGIC

MANAGEMENT

IV CALCIUM

CHLORIDE

IV SODIUM

BICARBONATE

BOLUSES

• Severe

hyperkalemia

• Sodium-channel

blocker toxicity

PEA – MANAGEMENT

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Fig. 4. Treatment recommendations for wide-complex PEA. IV = Intravenous; LV = left ventricular.

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Summary


3





Considerations


PEA – MANAGEMENT


• Tension PTX

• Mechanical

hyperinflation


QRS NARROW


WIDE OPEN

FLUIDS, PLUS:

PERICARDIOCENTESIS


VENTILATOR

MANAGEMENT

THROMBOLYSIS

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QRS WIDE


PHARMACOLOGIC

MANAGEMENT

IV CALCIUM

CHLORIDE

IV SODIUM

BICARBONATE

BOLUSES

• Severe

hyperkalemia

• Sodium-channel

blocker toxicity

PEA – MANAGEMENT

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Summary

Note that chest compressions could be harmful here


3





Considerations


PEA – MANAGEMENT


• Tension PTX

• Mechanical

hyperinflation


QRS NARROW


WIDE OPEN

FLUIDS, PLUS:

PERICARDIOCENTESIS


VENTILATOR

MANAGEMENT

THROMBOLYSIS

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QRS WIDE


PHARMACOLOGIC

MANAGEMENT

IV CALCIUM

CHLORIDE

IV SODIUM

BICARBONATE

BOLUSES

• Severe

hyperkalemia

• Sodium-channel

blocker toxicity

PEA – MANAGEMENT

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Summary

Thanks! Questions: [email protected]

Thanks! PDF of slides: lectures.umem.org/Mattu

the dying heart…

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