A 24 years old lady with a history of HbH thallasemia with post splenectomy 8 years ago on frequent blood transfusion presented to ED with a history of shortness of breath. This patient frequently defaulted treatment and had been non compliant to medication. A month prior, she was admitted into medical ward for decompensated cardiac failure due to cardiomyopathy as a result of iron deposition.

She was seen gasping and was able to speak in few words at best. What was noticeable was her leg swelling was worsening and was tender on palpation. Her jugular venous pulse was strong and reaching her earlobe. She was put on high flow mask and a baseline ECG was recorded as below.

Do you recognize any particular pattern in this 12-lead ECG?

Answer:
The 12-leads ECG showed a variant of the SI QIII TIII of pulmonary embolism.  Noted that there is right axis deviation with a prominent S wave in lead I (hence SI), and T wave in lead III. (TIII). There is no Q wave though in lead III (QIII). Another distinctive pattern seen was T wave inversion of V1 - V3 as well as P pulmonale (tall tented P waves) seen esp in lead II.

The patient had been having DVT from prolonged immobilization and US Doppler revealed significant DVT over the right lower limb. CT Pulmonary Angiography confirmed the diagnosis with multiple scattered areas of embolization in the lungs. The patient was started on unfractionated heparin infusion and overlapped with warfarin. Her condition improved after 1 week of admission. She was discharged with warfarin, however, knowing that her prognosis is guarded in view of her condition and prolonged non-conpliance to medical therapy.

A week after discharge, the patient was readmitted into ED red zone with another spell of shortness of breath. It was another episode of pulmonary embolism with pulmonary hypertension with biventricular failure and the patient was intubated and admitted into CCU but did not make it through after 2 days there. The parents were counselled of the prognosis and they did not wish for active resuscitation in view of her deteriorating condition thereafter.

A 68 years old lady presented to the ED with productive cough for the past 3 days. She was brought today in view of her complains of generalized lethargy and weakness. Prior to further investigations, a baseline ECG was done. She was initially sent for green zone fast track, but was subsequently uptriage to yellow. What are your findings?

Answer:
This is a rare pattern of atrial bigeminy. While most are familiar with the easy-to-spot ventricular bigeminy with a wide QRS complex, this can be rather confusing as one may thought of Mobitz type II or 2:1 block. However, a closer look will reveal a few things:
1) The QRS complex exhibits grouped beating, being regularly irregular
2) There are presence of P waves prior to each QRS complexes
3) All P wave have an associated QRS complexes
4) The 2nd P wave have slightly different morphology than the 1st P wave, suggestive of 1st P wave originated from the sinus focus whilst the 2nd P (premature atrial contraction) may originate from another focus.

Atrial bigeminy, as a manifestation of premature atrial contraction, is a harmless rhythm in the proper clinical context. Most people with atrial bigeminy do not have organic heart disease, albeit the fact that it is more common in people with heart disease than those without. There are certain factors linked to the occurence of atrial bigeminy, such as caffein intake, emotional stress, smoking, alcohol use and fatigue. One things is of concern is that patioent with atrial bigeminy may not have the 2nd QRS wave transmitted into a pulse, which had caused this patient to have a pulse rate of 50-60 despite a heart rate of 100-110.

In this patient, no identifiable cause was found despite the alert and uptriage to Red Zone initially. Repeated ECG 1 hour later showed resolution to sinus rhythm and her pulse rate returned to 80-90 beats per minute. Nevertheless, the patient was admitted for community acquired pneumonia with a high CURB-65 score.

A 53 years old Malay gentleman with no known medical illness came to ED complaining of worsening epigastric pain for the past 3 days.He had earlier seek treatment from a GP 2 days ago and was treated as gastritis. He was discharged with syrup MMT and oral ranitidine. He claimed that the symptoms improved after taking the medication, albeit not completely.

However, today, the pain worsened and became rather severe, hence the reason he made a trip down to the ED. He was given syrup MMT and ranitidine and a baseline ECG was done. Routine blood investigations was done and it was noted that cardiac enzymes were normal as well.

2 hours later, the patient was noted to be sweating. He looked lethargic and pale. He still complained of epigastric pain. A repeat ECG was done in view of the patient's discomfort.

Normal 12-lead ECG 

Posterior lead ECG

Inferior ECG

What would be your intepretation? Is there any bedside test to confirm your diagnosis? Any further blood investigations that can be taken?

Answer:

The 12-lead ECG showed significant ST - elevation over the inferior leads II, III, aVF whilst the lead V1-V3 showed ST depression. In a case of inferior MI, it is prudent to do a right sided ECG and posterior lead ECG The reason being is that inferior segment of the heart is supplied by the right coronary artery, which also supplies the right and posterior aspect of the heart. An occlusion at the right coronary artery that affects the inferior aspect may affect the other 2 as well. Of coursem other signs may include bradycardia and subsequent hypotension, as a result of sinuatrial node involvement, which is also supplied by the right coronary artery.

The right sided ECG showed no ischemic changes over the right aspect of the heart, but a quick look at the posterior leads showed significant ST-elevation as well.

Hence, this is an acute inferoposterior myocardial infarct. A bedside ECHO can be done and for this patient, there is hypokinesia over the inferoposterior region, correlating with the ECG findings. Cardiac triple test (bedside rapid test) was done for this patient. Myoglobin and CKMB was positive whilst TnI was negative, suggestive of recent onset basis. (Kindly refer to Malaysian CPG for acute coronary syndrome to have a quick review of the peak and through of the cardiac enzymes).

The patient was started on streptokinase fibrinolytic therapy in view of no PCI in the center. 1.5mU Streptokinase was given in 100cc normal saline over 1 hour (there are 2 other recommended regime). The streptokinase was witheld once midway as patient developed hypotension (side effects of streptokinase therapy) and restarted slowly once BP picked up after 1 pint of NS was given. Repeated ECG showed good resolution of the ST elevation and the patient was sent to CCU for close monitoring and management.

The latest CPG on tuberculosis is out. Among all, this is one of the most comprehensive CPG, covering almost all aspects of the management of TB.

• Management of Tuberculosis 3rd Edition- 2012
  Download Links: Box.net | Mediafire

For a view of the whole collection of Malaysia CPG's available in Medical PBL (Trust me, we do have quite a collection), kindly do refer to: ==> HERE

With the recent updates from MOH, the CPG guidelines for atrial fibrillation and stable angina pectoris is out. Here is the link to download the respective files. We hope that these CPG's will be put into good use to aid all medical practitioners in managing the conditions mentioned.

• Management of Atrial Fibrillation  - 2012
  Download Links: Box.net | Mediafire 

• Management of Stable Angina Pectoris  - 2012
  Download Links: Box.net | Mediafire 
  

Source:
1 )National Heart Association of Malaysia
2) Academy of Medicine of Malaysia

For a view of the whole collection of Malaysia CPG's available in Medical PBL (Trust me, we do have quite a collection), kindly do refer to: ==> HERE