Atropine Resistant BRADYCARDIA

Atropine Resistant BRADYCARDIA

Symptomatic sinus bradycardia is routinely treated in the emergency department with atropine and pacing. The current cases illustrate the importance of considering hyperkalamia, particularly in the presence of atropine-resistant symptomatic bradycardia. 

The administration of calcium in such cases acts to stabilise the myocardium and resolve the bradycardia. Blood gas analysis provides a rapid estimate of serum potassium concentrations, facilitating timely treatment. 

The classic ECG signs of hyperkalamia include :

Serum potassium > 5.5 mEq/L is associated with repolarization abnormalities:

• Peaked T waves (usually the earliest sign of hyperkalaemia

Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:

• P wave widens and flattens 
• PR segment lengthens 
• P waves eventually disappear 

Serum potassium > 7.0 mEq/L is associated with conduction abnormalities and bradycardia:

• Prolonged QRS interval with bizarre QRS morphology 
• High-grade AV block with slow junctional and ventricular escape rhythms 
• Any kind of conduction block (bundle branch blocks, fascicular blocks) 
• Sinus bradycardia or slow AF 
• Development of a sine wave appearance (a pre-terminal rhythm)

Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:

• Asystole 
• Ventricular fibrillation 
• PEA with bizarre, wide complex rhythm 

Case Presentation : 

46-year-old male was brought to Emergency Room with H/O two episodes of giddiness, one at 12 noon and another at 3:00 PM while he was shopping.He had significant hypertension for the last 4 years-On irregular medications. He also had knee joint pain for the past 1 year, which is aggravated for the past 2 weeks for which he was taking Non-steroidal anti inflammatory drug (T.Aceclofenac).

O/E :

He was conscious and well oriented for time, place and person.

IV access done,O2 and monitor attached.

Vitals-SPO2-99% with 2L O2 by face mask,BP-100/60mm of Hg,RR-20/min,HR-38/min,GRBS-113mg/dl,Temp-98.6deg f.

No pallor, icterus, cyanosis, lymphadenopathy, edema Normal Heart sounds.No added sounds or murmurs. Respiratory System-Normal vesicular breath sound heard on either side

A-Airway Maintained

B-Breathing Normal

C-Circulation Pulse was regular at the rate of 40/min

ECG : 

Rate 33,absent P waves, severe bradycardia with irregular narrow QRS escapes and tall T waves in V2, V3, and V4.

Intravenous Atropine 0.5mg was given-No effect on the heart rate. A second dose of atropine was repeated. But no response. 

As the ECG suggests hyperkalemia, anti hyperkalemia measures were initiated from ED

Calcium Gluconate 10%, 10ml over 10 min. 

25% dextrose(100ml)with 8 u insulin infusion 

Nebulisation with Asthaline 

Soda bicarbanate 50ml IV 

Emergency serum electrolytes were sent along with CBC, ESR, Renal Function Test and Urine R/E.

Normal Saline 500ml was started at the rate of 100ml /hr.

Transcutaneous pacing was arranged.

Lab results-Serum K+-8.3,Na+137,Creatinine 2.4.

Other lab results were normal . Patient was shifted to ICU and nephrology consultation was done.

Working diagnosis : Acute renal failure with Hyperkalemia? Analgesic induced

Discussion : 

Many other ECG abnormalities have, however, been attributed to hyperkalaemia. These include both tachycardia and bradycardia and also idioventricular rhythm, heart block and a pseudo-infarction pattern with massive ST segment elevation.

Life-threatening hyperkalamia causing profound bradycardia can appear to resemble complete heart block ; however, there is an absence of P waves. This phenomenon is not described in the emergency medicine literature, however, and appears to be poorly recognised as a cause of symptomatic bradycardia. The effects of calcium occur within 1– 3 minutes but last for only 30–60 minutes and definitive treatment is needed to lower serum potassium levels. When arrhythmias are present, a wealth of anecdotal and animal data suggest that intravenous calcium is effective in treating arrhythmia.