angeloreo.blogg.se - Pulseless electrical activity

This new classification system of PEA has 3 potential benefits compared to the traditional ACLS 5 H’s and 5 T’s

Hyperkalemia or Sodium Channel Blocker Toxicity –> Sodium bicarbonate.

Hyperkalemia –> Intravenous calcium chloride or gluconate.

Hyperkalemia and/or sodium channel blocker toxicity. This typically suggests a metabolic or toxic ingestion problem.

Pulmonary Embolism –> Thrombolytic therapy.

Mechanical Hyperinflation –> Adjust ventilator.

Tension Pneumothorax –> Needle decompression.

Step 1: Determine if the PEA is narrow (QRS duration Pericardiocentesis.

What is the new diagnostic classification of PEA? *Hypoglycemia and trauma have been removed from the most recent ACLS guidelines. A New Simplified and Structured Method in the Evaluation and Management of Pulseless Electrical Activity What are the traditionally taught H’s and T’s of PEA? In 2014 a review article was published that was developed by several departments from the Carolinas Medical Center in Charlotte, NC that tried to simplify the diagnostic approach to PEA. This is traditionally done with recalling the 5 to 6 H’s and T’s, but during cardiopulmonary resuscitation it is difficult to recall all 13 causes of PEA by trying to recall this list. Both the European and American ACLS guidelines stress the importance of quickly finding and addressing the cause of PEA. Chest compressions were started advanced cardiac life support was initiated, and the patient was intubated.Patients with pulseless electrical activity (PEA) account for almost 1/3 of cardiac arrest and even more troublesome is that the survival rate is significantly worse than patients with shockable rhythms.

The morning that was planned for elective placement of hemodialysis catheter, she experienced ventricular tachycardia followed by pulseless electrical activity (PEA) arrest. She experienced accompanying symptoms of nausea and vomiting plans were made for initiation of hemodialysis to treat uremia. Diuretics were held, but renal function worsened to a BUN of 116 mg/dL and creatine of 4.65 mg/dL over 1 week. While maintaining negative fluid balance with oral furosemide, she experienced an acute kidney injury that was attributed to prerenal azotemia from over-diuresis.

Repeat echocardiogram demonstrated chronic diastolic dysfunction, RV failure, pulmonary hypertension (right ventricular systolic pressure, 78.7 mm Hg), and no pericardial effusion. With diuresis, her hemodynamics improved as did her renal function, and she was transferred to the hospital ward. Her ICU course was complicated by new onset atrial fibrillation for which she was started on apixaban 5 mg bid and rate control. She was admitted to the ICU and found to have new right ventricular (RV) failure for which she underwent aggressive diuresis, transiently requiring inotropic support. Laboratory results were remarkable for BUN 56 mg/dL, creatinine 2.41 mg/dL (from baseline creatinine 1.8 mg/dL,) and pro-brain natriuretic peptide >15,000 pg/mL chest radiography revealed bilateral pleural effusions. She had rales at both lung bases and significant pitting edema in the lower extremities. On examination, she was mentating well but was in mild distress. Her BP was 70/40 mm Hg oxygen saturation was 84% on room air respiratory rate was 30 breaths per minute, and heart rate was 73 beats per minute. A 73-year-old woman with a history of heart failure with preserved ejection fraction, severe pulmonary hypertension (World Health Organization class 2), and chronic kidney disease stage 3 presented to the ED after 2 days of weakness and shortness of breath.