ECG in Critical Care Unit

DR.RAKESH YADAVPROF OF CARDIOLOGY

AIIMS

• ECG changes and arrhytmia in CCU are common

•Practically all critically ill pts ( specially with P/H of CAD

will have some form of arrhy and ECG changes

during the coarse of hospitalization

•Majority are benign but fatal arrhythmias can occur

in unpredictable manner

Ventricular

VPBs

NSVT

AIVR

Sustained VT

Monomorphic

Polymorphic

VF

TYPES

Atrial

Sinus Tachycardia

APC

AVNRT/AVRT

EAT

AF/Aflutter

BradyarrhySinus BradycardiaAV BlockAsystole

Management of Arrhythmia

Prophylaxis

Acute Precipitating

factors

Proper Recognition

Electrolyte imbalance

Acid-base balance disturbances,

Hypoxemia,

Anemia,

Drugs ( Digitalis intoxication ,

QT , beta agonists)

Pericarditis,

Pulmonary emboli,

Pneumonia or other infections.

Approach to management……….

• Type of arrhythmia

• Time of Onset

• Hemodynamic effect

• Prognostic importance

• Unstable

• Treat first, diagnose later

• Patient stable

– 12 ECG Analysis

Arrhythmias occurring in patients require

aggressive treatment when they

– Impair hemodynamics

– Compromise myocardial viability by

augmenting myocardial oxygen

requirements

– Predispose to malignant ventricular

arrhythmias

Ventricular Arrhythmias

• Premature beats >90%

• NSVT Upto 40%

• VT/VF Upto 5%

All these, in early hours of ACS, are associated with good long term prognosis.

Ventricular premature beats

– Common

– It was believed that frequent VPB (>5/min), VPBs with

multiform configuration, early coupling (the “R-on-T”phenomenon), and repetitive patterns in the form of

couples or salvos presaged VT/VF

– Prediction of VT/ VF development is not reliable even with

high grade VPBs

Do not treat them with antiarrhythmics

1. Conservative course

2. No prophylactic drug

3. If associated with augmented sympathetic tone

(sinus tachycardia, BP rise), add B-blocker

4. Correction of PP

Accelerated Idioventricular rhythm

Accelerated Idioventricular rhythm

– Usually seen in setting of AMI

– Ventricular rate of 60-125/min

– Incidence of 20%

– Possibly due to abnormal

automaticity of Purkinje fibers

– Usually noted during 48 hours

– Prediction of reperfusion is poor

– No prognostic implication

– No treatment

NSVT

• NSVT very common specially in setting of ACS / ED

• No increased mortality risk, either during hospitalization or over the first year

• NSVT after 48 hours – may be Long term high risk

• No treatment required, treat ppt factors

VT & VF

• VT or VF not uncommon

• In AMI

– Primary

• Occurring within 48 hours in a stable patient

– Secondary

• Occurring after 48 hours

• Occurring after a previous episode

• Occurring within 48 hours in a patient with Killip class 2 or more

Management of sustain VT & VF

Tt of acute

episodePrevention

Primary Secondary•Unstable Hemody

•Stable Hemody

Cardio version DrugsExternal

ICD

Acute management of VT

• Cardioversion

– DC

–Thump

• Drugs

– I/V Lidocaine

– I/V Amiodarone

– I/V Mg+

Tt of precipitating causes

•Electrolyte imbalance

•Hypoxia

•Hypotension

•Ischemia

•Pacing if brady

•Anxiety

•Drugs

Supraventricular arrhythmias..

Sinus tachycardia

– Common • causes are anxiety, persistent pain, LVF, fever, pericarditis,

hypovolemia, pulmonary embolism, administration of drugs such as atropine, epinephrine, or dopamine; & atrial infarction.

– It is an undesirable rhythm in patients with ACS • Intensifying myocardial ischemia

• persistent heart failure and under these circumstances is a poor prognostic sign associated with an excess mortality.

An underlying cause should be sought

Appropriate treatment instituted

(e.g., analgesics for pain, diuretics for heart failure,

oxygen, beta blockers and nitroglycerin for ischemia,

and aspirin for fever or pericarditis.

• Atrial premature beats

– No specific treatment

• PSVT

– Requires immediate treatment

– Carotid sinus massage, adenosine

– I/V B blockers, CCB

– Hemodynamic unstable DC

cardioversion

• 56 year admitted in Medical ICU

• Next day develop some chest pain

• ECG done

•A short PR interval (<0.12 second)

•Widening of QRS & Delta Wave

•Secondary changes in T wave

• Atrial flutter/ fibrillation

– Flutter rare; but AF common in 10%-20%

of the cases

Usually Transient

• Frequent in older individuals with H/T or MR

• Hemodynamic collapse:

DC 200J (50J for Flutter)

Amiodarone if not responding to DC

• No hemodynamic compromise, ongoing ischemia control HR:

B-blocker

Diltiazem

Digoxin

DC synchronized 200J

• Anticoagulant

AF/Flutter: Management

Bradyarrhythmias

1. Sinus bradycardia

2. AV conduction block

3. Asystole

Sinus Bradycardia

• Common early response with no prognostic significane

• Frequent within 1 hr of inferior MI and with reperfusion

(BJ Reflex)

Treat only if HR, 40-50/mt with hypotension with atropine

0.5mg IV 10-20 mts , max 2mg.

Bradycardia

AV Block:

1. Io heart block

2. IIo Heart block – type I

- type II

3. IIIo heart block

IIo Heart block – type I

Type II second degree AV Block

There are intermittent blocked P waves

In the conducted beats, PR intervals remain

constant

Complete AV Block

Independent P waves and QRS complexes

Ventricular rate slower than the atrial rate

Ventricular activation is maintained either by

a junctional (narrow QRS usually) or a

ventricular (wide QRS) focus

43 years admitted in CCU for fall

No previous H/O of any illness

Examination – normal

ECG -F/H of SCD

• Epsilon wave (most specific finding, seen in 30% of patients)

• T wave inversions in V1-3 (85% of patients)

• Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)

• Localised QRS widening of 110ms in V1-3

• Paroxysmal episodes of ventricular tachycardia with a LBBB

morphology

12 year admitted in CCU for fever

60

years

• 60 yrs

asympto

matic

INTRODUCTION

The Brugada syndrome is

characterized by abnormal findings

on the surface ECG in conjunction

with an increased risk of ventricular

tachyarrhythmias and SCD.

Typically, the ECG findings consist

of a pseudo-right bundle branch

block and persistent ST segment

elevation in leads V1 to V3 ,

unrelated to ischemia, electrolyte

disturbances or obvious structural

heart disease.

Hyperkalemia• ECG changes

– The earliest EKG

• correlate is T wave tenting,

– classically described as symmetrically narrow or

peaked, though the deflection is often wide and of

large amplitude (II, III, and V2 to V4)

– The QT interval is shortened at this

stage

– In addition, the inverted T waves associated with

LVH can pseudonormalize

– These T wave changes is often seen when potassium

levels exceed 5.5 mEq/L.

Hyperkalemia

• Further increase,

• P wave Abnormality

– Flattening

– PR interval prolongation

– sometimes second- or third-degree AV block

– These changes generally occur when potassium levels exceed 6.5

mEq/L .

– As the serum potassium level increases further, there is

eventual loss of the P wave,

Hyperkalemia

When serum level rise to levels above two times

normal,

• SA and AV blocks, often with escape beats.

• Other blocks including IVCD, BBB, and fascicular blocks have

been reported.

• Interestingly, bypass tracts are more sensitive to delayed

conduction from potassium elevation

• Moderate to severe hyperkalemia occasionally induces ST

elevations in the right precordial leads (V1 and V2) and simulates

an ischemic current-of-injury pattern.

Hyperkalemia• With extremely high serum potassium levels,

– a markedly prolonged and wide QRS complex can fuse with the T

wave, producing a slurred, “sine-wave” appearance on the EKG .

–

– This finding is a pre-terminal event unless treatment is initiated

immediately. The fatal event is either asystole, or ventricular

fibrillation.

• Peaked T waves (tenting)

• Flattened P waves

• Prolonged PR interval (first-degree heart block)

• Widened QRS complex

• Deepened S waves and merging of S and T waves

• Idioventricular rhythm

• Sine-wave formation

• VF and cardiac arrest

Hypokalemia

• The earliest EKG change associated with

hypokalemia is a decrease in the T wave

amplitude.

• As potassium levels decline further,

– ST segment depression and actual T wave

inversions can be seen.

– The PR interval can be prolonged and there can

be an increase in the amplitude of the P wave.

Hypokalemia

With even lower serum potassium levels,

– Development of U waves.

– The U wave is described as a positive deflection after the T-wave that is often best seen in the mid-precordial leads, such as V2 and V3.

– These changes have been reported in almost 80% of

patients with potassium levels < 2.7 mEq/L

– With extreme hypokalemia, giant U waves may often

mask the smaller preceding T waves or after P waves

• T-wave flattening

• ST-segment changes

• Arrhythmias (especially if the patient is taking

digoxin)

• Pulseless electrical activity (PEA) or asystole

Hypercalcemia.

• Concentration above the normal range of

– 8.5 to 10.5 mEq/L (or an elevation in ionized calcium above 4.2 to 4.8 mg/dL

• Hypercalcemia is the cardinal feature of hyperparathyroidism. It is typically chronic, mild and well tolerated.

ECG changes of hypercalcemia include

• Shortened QT interval (usually when Ca2+ is >13 mg/dL)

• Prolonged PR and QRS intervals

• Increased QRS voltage

• T-wave flattening and widening

• Notching of QRS

• AV block: progresses to complete heart block, then to cardiac arrest when serum calcium is >15 to 20 mg/dL

Changes of hypocalcemia include

• QT-interval prolongation

• Terminal T-wave inversion

• Heart blocks

• Ventricular fibrillation

• Hypocalcemia can exacerbate digitalis toxicity.

A long-QT interval made of a long ST-segment

with a delayed onset of the T wave.

32 years lady admitted in CCU with fever

50 years lady H/o syncope admitted in

CCUfound to have 70% lesion in mid LAD

Brought to near by hospital

….Life is not fair, you must have to do the best you can in the situation you are in

Stephen Howking