Core Measures For Ami After Cardiac Arrest

A 68 year old male presented to the emergency department at 0800 hours via ambulance after experiencing chest discomfort and intermittent palpitations since 0500 hours. Prior to presentation, the patient stated he

The patient is a 72-year-old female who arrived to the emergency department in cardiac arrest. Emergency medical services reports the patient was last seen eating breakfast at her nursing home and was found an hour later face down and unresponsive. After it was determined the patient was in asystole, an intravenous catheter was started and two rounds of Epinephrine was administered. Upon arrival to the emergency department the patient had pulseless electrical activity with sinus tachycardia on the monitor. Airway management was in process with a bag valve mask on 100% oxygen and chest compressions in progress. After intubation and stabilization the

S.D. was admitted to the telemetry unit and an IV amiodarone drip was started. The purpose of the drug was to convert her atrial fibrillation to normal sinus rhythm. Although her heart rate has decreased to 108 beats/minute, she remains in atrial fibrillation 24 hours later. A cardiologist was consulted and electrical cardioversion is

African American male that is seen today for followup post hospital discharge. He is a 48-year-old gentleman with complicated cardiac history as well as neurological history including congestive heart failure. History of strokes 01/2017, possible sick sinus syndrome. He has an implanted pacemaker that was placed in 06/2017, as well as hypertension. He was taken to the Central Hospital on 09/01 with presentation of chest pain, noted to be around his pacemaker site. He identified being in seizure and suddenly felt chest pain with shortness of breath, and was offered nitro, he developed headaches and dyspnea post nitro treatment, of note is that the EKG that was obtained during that process, did not identify any pacemaker spike despite having a

Another Consultation Report dated 12/06/2016, indicated that the claimant presented with exacerbation of COPD, acute bronchitis, and pseudomonas aeruginosa. The CT scan of the chest revealed bilateral lower lobe atelectatic changes, fibrosis, and a small 1 cm left lower lobe nodular density. A pulmonary consultation was recommended. His blood pressure was 142/79 mmHg. The physical examination revealed bilateral decreased breath sounds and scattered wheezes. His glucose was 189. DuoNeb, IV Solu-Medrol, and IV antibiotics were prescribed.

Her drug screen showed positive benzodiazepines and blood alcohol was negative. Troponins were negative. Also, her initial work up showed acute kidney injury with a creatinine of 1.84, and potassium of 5.8. Her chest x-ray showed small amount of infiltrate in the right lower lobe. The CT scan of the head did not show any acute changes. The abdominal CT scan showed constipation and 6 mm opacity in her bladder. She had an electroencephalogram (EEG) which revealed diffuse generalized nonspecific encephalopathy. In addition, there was slowing of the left hemisphere consistent with left intracerebral lesion. The assessment diagnoses were acute respiratory failure (ABG of 87.287, pCO2 of 45.2, pO2 of 380 and biacarbonate of 20 on vent settings), altered mental status, attempted suicide, infectious process, medication use, hyperglycemic nonketotic, and less likely cerebrovascular accident given that her CT scan of the head was normal. She was admitted to the Intensive Care Unit under the care of Dr. Modupe Kehinde. She was intubated for airway protection and remained intubated until 5/23/2016 (7 days). She was on ventilator and was given nutritional support

States that it started 3 days back and uses oxygen at home. States that he is a former smoker and laying on his back feels better. Also says he has a list of medication, more than 20. Pt has a history of COPD, CHF, DM,morbid obesity, HTN, HLM, hypothyroid, and sleep apnea. Has no accessory muscle use. CC is shortness of breath. Assessment is that there is no deformities or trauma of the head or neck area. Chest shows no signs of deformities or trauma. The abdominal area is tender and warm to the touch. Pelvis and back was not assessed. The upper and lower extremities show signs of low circulation and swelling. PMS=4. I helped with placing the BP cuff on the left arm and attaching it to the monitor. First vitals were recorded. O2 was given by the Nurse and then Albuterol by nebulizer. After 30 minutes, I assisted the Nurse and other hospital workers in moving the PT to a bigger bed. Second set of vitals were recorded. After becoming stable the Pt was moved up to the floor.

On arrival to UKMC the patient received a Glasgow Coma Score of 3, which is an indication that intubation is needed. Bipap therapy was attempted but failed, due to respiratory failure. This was confirmed by arterial blood gases. After being assessed by the team at UKMC, the patient was intubated for respiratory failure, as well as shock of an unclear etiology. Rapid sequence intubation drugs, Etomidate and Succinylcholine where administered prior to intubation. A 7.5 endotracheal tube was used

On the early morning of August 17, 2002, James C., a patient in one of the wards under the supervision of Ellen Hughes Finnerty, RN, went into respiratory depression. Between 3:00 and 4:00 a.m., Ann Mugi, the patient’s primary nurse, sought the assistance of a respiratory therapist, Hiran Obeyesekere, to help her care for the patient. As Obeyesekere suctioned the patient airway, Mugi called the service of the patient’s primary care physician, Dr. Jackson, to report the changes in the patient’s respiratory status, e.g., respiratory rate of 40 breaths per minute and low urine output.

A.W., a 52-year-old woman disabled from severe emphysema, was walking at a mall when she suddenly grabbed her right side and gasped, “Oh, something just popped.” A.W. whispered to her walking companion, “I can’t get any air.” Her companion yelled for someone to call 911 and helped her to the nearest bench. By the time the rescue unit arrived, A.W. was stuporous and in severe respiratory distress. She was intubated, an IV of lactated Ringer’s (LR) to KVO (keep vein open) was started, and she was transported to the nearest emergency department (ED).

The incident happened on Nov 21st, 2017. The patient has sleep apnea and a health history of chronic bronchitis (no episode in recent 2 years). Her respiration rate was 16 and all lung fields were clear upon auscultation. After I took the patient’s vital signs, I noticed that her oxygen saturation was low (83%). Then, I notified the nurse and asked the patient to do take some deep breath. After that, we put her on 2L of oxygen and her oxygen saturation went up to above 90s. However, the patient had a bladder control problem (was incontinent), so I took the oxygen off because she went to the toilet for around 4-5 times in an hour. However, I forgot to monitor her O2 saturation right away. Instead, I checked her oxygen saturation after she finished her dinner, and it dropped to 86%. The instructor showed me how deep breathing exercise can help the patient increase her oxygen level quickly. I notified the nurse and we put the patient on 2L of oxygen, but again I forgot to check her oxygen saturation right away. Instead, I checked her oxygen around 7pm later.

The case I will discuss comes from the Journal of General Internal Medicine and is as follows: the patient is an 80-year-old woman who suffers from nonresectable lung cancer and has been diagnosed with lobar pneumonia. Other conditions present are: hypertension, diabetes, chronic renal insufficiency and severe degenerative joint disease. While improvement was seen with initial treatment, the patient suffered worsening hypoxemia, level of consciousness obtunded, and developed acute renal failure. Thus, the only means to prevent death was intubation with

A: Janie is a 60 year old Female with PMH of A-Fib, COPD, Hypothyroidism, HTN, Lung Cancer and recently diagnosed Pulmonary Embolism. Janie presents to ER for evaluation on SOB, cough with greenish sputum, sore thoart, hoarseness and generalized weakness. Janie lives at home with her husband, use to smoke ½ pack per week, but quit many years ago, denies alcohol or drugs. Family history is non-contributory. Allergies: NKDA. Differential diagnosis includes worsening Lung Ca, PE, COPD and CHF. Janie uses home O2 at 4 L/NC. V/S: T=98.7, HR=89, R=16, B/P=132/56, O2 sats=100% on 4L/NC, Pain=6/10. Labs: WBC=7.6, H&H=8.5/27, Na=141, Troponin=0.08/0.06, BNP=495, INR=4.2, UA=3+ protein, 1+ blood and 6-10 RBC. CXR: Impression:1). COPD with nonspecific coarsening of the basilar interstitium. 2). Mild cardiomegaly with borderline cardiac compensation. 3). Right

Patient is a 45 yo male; 5’7”, 221 lbs who entered the emergency room at 6:30 am on 9/7/14 with severe chest pain (onset at 6:00 am) radiating to his arm, L arm numbness and nausea and vomiting. Past medical history reported by wife includes peptic ulcer, tobacco use (1-2ppd for 27 years), elevated blood pressure (controlled by lopressor). Wife did not know of any family history but reports patient’s father is deceased, died at 42 in his sleep. Mother alive and with high blood pressure.

After reading this scenario about this patient, there are a few things that I wonder about and things that could have potentially contributed to this patient’s death. First, I do not understand why they did not place an Ewald tube down this patient and perform some sort of gastric lavage with activated charcoal (Gastric, 2017). They did all the work to stabilize the patient, but did not remove the remainder of the product, causing the acidosis. Basically, I feel that the patient came in with metabolic acidosis because of the aspirin, was stabilized, but then developed metabolic acidosis again. Which could have lead to a whole new list of complications to develop.