Delayed Recovery of Spontaneous Circulation Following CPR
An 89-year-old Caucasian woman, body mass index (BMI) 17.2, with a known medical history of hypertension, rate controlled atrial fibrillation, hypothyroidism, aortic insufficiency, lymphedema and hypoxia secondary to partial lung resection on home medications of warfarin, levothyroxine, metoprolol, montelukast, furosamide, ipratropium bromide, and fluticasone presented to North Shore-LIJ Plainview's emergency department at 2:30 p.m. after a witnessed fall not associated with head trauma or loss of consciousness. Her vital signs on presentation were blood pressure of 144/81mmHg; pulse of 119 beats per minute; respiratory rate of 18 breaths per minute; temperature of 98 degrees Fahrenheit, and oxygen saturation of 85 percent on room air. Our patient's baseline oxygen saturation was unknown and she denied being on home oxygen therapy. On physical examination our patient was not wheezing on presentation but revealed shortness of breath on room air with diffusely scattered rhonchi. An ipratropium-albuterol nebulizer was administered over 10 minutes, and our patient was then put on oxygen supplementation.
On examination, our patient was alert and oriented to person, place and time but experienced a decreased range of motion of the upper extremities. The left lower extremity was shortened and externally rotated with at the hip joint. Arterial blood gas on room air showed a pH of 7.28 (reference range 7.38 to 7.42), partial carbon dioxide (CO2) (PCO2) of 44mmHg (reference range 35 to 45mmHg), calculated bicarbonate (HCO3) of 19mmHg (reference range of 22 to 29mmHg) partial oxygen (O2) (PO2) of 58mmHg (reference range of 80 to 100mmHg) and calculated base excess of −5.8 (reference range of −2.0 to 2.0). These results implied hypoxia with mixed metabolic and respiratory acidosis. Laboratory test results revealed a nearly therapeutic international normalized ratio (INR) of 1.93 with a basic metabolic profile including serum potassium within normal limits (4.1mEq/L). Our patient's glucose level on arrival was 158mg/dL. An electrocardiogram (ECG) revealed atrial fibrillation at 113 beats/minute along with right bundle branch and left anterior fascicular block. We were unable to obtain a previous ECG for comparison. Her lactate level was not obtained at this time. Relevant imaging studies included a pelvic X-ray revealing a left subcapital femoral neck fracture (Figure 1), X-ray of the left wrist, which demonstrated a non-displaced fracture of the distal radius (Figure 2), and a portable chest X-ray showing partial right lung resection and bilateral haziness with questionable consolidation. Our patient's respiratory status was stabilized on 100 percent fraction of inspired oxygen (FiO2), non-rebreather mask, and our patient was placed in a volar wrist splint to await transfer to a monitored in-patient bed.
(Enlarge Image)
Figure 1.
X-ray of the left hip and femur: a left subcapital femoral neck fracture (black arrow) can be seen.
(Enlarge Image)
Figure 2.
X-ray of the left wrist: a non-displaced fracture of the left distal radius (black arrow) can be seen.
At 3:30 a.m., our patient suddenly became bradycardic and progressed to asystole. She was found to be pale and pulseless. Cardiopulmonary resuscitation (CPR) was immediately begun following an Advanced Cardiac Life Support (ACLS) protocol. Initial respiratory support with a bag mask was attained and our patient's trachea was secured with intubation at 3:32 a.m. As per the ACLS protocol, 1mg of intravenous epinephrine was given, followed by 40mg of intravenous vasopressin given at 3:36 a.m. Our patient received her second dose of 1mg epinephrine at 3:40 a.m. Finally at 3:46 a.m., our patient received one ampule of sodium bicarbonate. Our patient remained unresponsive to continued resuscitation efforts so CPR was abandoned at 3:48 a.m. Right femoral venous access had been attempted during the resuscitative effort, and cardiac monitors were unwittingly left on our patient during cleaning and removal. At 3:51, before the complete removal of the femoral venous catheter, a single ventricular contraction was noticed on the monitor. This single contraction progressed to a couplet, then a triplet and finally into a normal sinus rhythm with a palpable pulse at 3:53 a.m. Her initial blood pressure was measured at 80/50mmHg and our patient was started on a norepinephrine drip at 10μg/min through the femoral venous access. A right femoral arterial line was also established for continuous blood pressure monitoring. Her blood pressure stabilized at a mean arterial pressure of 70 and our patient was transferred to our Intensive Care Unit (ICU) at 4:30 a.m. In the ICU, a hypothermia protocol was initiated and vasopressors were titrated to maintain systolic blood pressure greater than 90mmHg. Unfortunately at 10:55 a.m. our patient went into ventricular tachycardia and, despite resuscitative efforts, our patient was pronounced dead at 11:03 a.m.
Case Presentation
An 89-year-old Caucasian woman, body mass index (BMI) 17.2, with a known medical history of hypertension, rate controlled atrial fibrillation, hypothyroidism, aortic insufficiency, lymphedema and hypoxia secondary to partial lung resection on home medications of warfarin, levothyroxine, metoprolol, montelukast, furosamide, ipratropium bromide, and fluticasone presented to North Shore-LIJ Plainview's emergency department at 2:30 p.m. after a witnessed fall not associated with head trauma or loss of consciousness. Her vital signs on presentation were blood pressure of 144/81mmHg; pulse of 119 beats per minute; respiratory rate of 18 breaths per minute; temperature of 98 degrees Fahrenheit, and oxygen saturation of 85 percent on room air. Our patient's baseline oxygen saturation was unknown and she denied being on home oxygen therapy. On physical examination our patient was not wheezing on presentation but revealed shortness of breath on room air with diffusely scattered rhonchi. An ipratropium-albuterol nebulizer was administered over 10 minutes, and our patient was then put on oxygen supplementation.
On examination, our patient was alert and oriented to person, place and time but experienced a decreased range of motion of the upper extremities. The left lower extremity was shortened and externally rotated with at the hip joint. Arterial blood gas on room air showed a pH of 7.28 (reference range 7.38 to 7.42), partial carbon dioxide (CO2) (PCO2) of 44mmHg (reference range 35 to 45mmHg), calculated bicarbonate (HCO3) of 19mmHg (reference range of 22 to 29mmHg) partial oxygen (O2) (PO2) of 58mmHg (reference range of 80 to 100mmHg) and calculated base excess of −5.8 (reference range of −2.0 to 2.0). These results implied hypoxia with mixed metabolic and respiratory acidosis. Laboratory test results revealed a nearly therapeutic international normalized ratio (INR) of 1.93 with a basic metabolic profile including serum potassium within normal limits (4.1mEq/L). Our patient's glucose level on arrival was 158mg/dL. An electrocardiogram (ECG) revealed atrial fibrillation at 113 beats/minute along with right bundle branch and left anterior fascicular block. We were unable to obtain a previous ECG for comparison. Her lactate level was not obtained at this time. Relevant imaging studies included a pelvic X-ray revealing a left subcapital femoral neck fracture (Figure 1), X-ray of the left wrist, which demonstrated a non-displaced fracture of the distal radius (Figure 2), and a portable chest X-ray showing partial right lung resection and bilateral haziness with questionable consolidation. Our patient's respiratory status was stabilized on 100 percent fraction of inspired oxygen (FiO2), non-rebreather mask, and our patient was placed in a volar wrist splint to await transfer to a monitored in-patient bed.
(Enlarge Image)
Figure 1.
X-ray of the left hip and femur: a left subcapital femoral neck fracture (black arrow) can be seen.
(Enlarge Image)
Figure 2.
X-ray of the left wrist: a non-displaced fracture of the left distal radius (black arrow) can be seen.
At 3:30 a.m., our patient suddenly became bradycardic and progressed to asystole. She was found to be pale and pulseless. Cardiopulmonary resuscitation (CPR) was immediately begun following an Advanced Cardiac Life Support (ACLS) protocol. Initial respiratory support with a bag mask was attained and our patient's trachea was secured with intubation at 3:32 a.m. As per the ACLS protocol, 1mg of intravenous epinephrine was given, followed by 40mg of intravenous vasopressin given at 3:36 a.m. Our patient received her second dose of 1mg epinephrine at 3:40 a.m. Finally at 3:46 a.m., our patient received one ampule of sodium bicarbonate. Our patient remained unresponsive to continued resuscitation efforts so CPR was abandoned at 3:48 a.m. Right femoral venous access had been attempted during the resuscitative effort, and cardiac monitors were unwittingly left on our patient during cleaning and removal. At 3:51, before the complete removal of the femoral venous catheter, a single ventricular contraction was noticed on the monitor. This single contraction progressed to a couplet, then a triplet and finally into a normal sinus rhythm with a palpable pulse at 3:53 a.m. Her initial blood pressure was measured at 80/50mmHg and our patient was started on a norepinephrine drip at 10μg/min through the femoral venous access. A right femoral arterial line was also established for continuous blood pressure monitoring. Her blood pressure stabilized at a mean arterial pressure of 70 and our patient was transferred to our Intensive Care Unit (ICU) at 4:30 a.m. In the ICU, a hypothermia protocol was initiated and vasopressors were titrated to maintain systolic blood pressure greater than 90mmHg. Unfortunately at 10:55 a.m. our patient went into ventricular tachycardia and, despite resuscitative efforts, our patient was pronounced dead at 11:03 a.m.
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