It is estimated that nearly 325,000 people in the US die each year from a cardiac arrest. That means that cardiac arrest kills one person every two minutes. It is also estimated that nearly 200,000 cardiac arrests occur while the patient is being treated in the hospital – in-hospital cardiac arrest.

It has been demonstrated in experimental studies that female hormones, primarily estrogen and progesterone, exhibit a neuroprotective effect in animal models of global hypoxic-ischemic injury, stroke and traumatic brain injury.

So, does it mean that female patients, who naturally have higher levels of these hormones, do better after cardiac arrest?

A study by Topjian et al. attempts to answer this question. The authors of this study looked at the survival after an in-hospital cardiac arrest in two groups of patients. Female patients 15-44 years old were compared to the male patients of the same age. Females older than 56 years were compared to the males of the same age group.

The authors hypothesized that female patients of child bearing age will have a significantly higher levels of estrogen and progesterone compared to the male subjects of the similar age. This difference in hormone composition would dissipate after the menopause. Women older than 56 years would not have this advantage over older men. Women between 45 to 55 years were intentionally excluded from this study. The variability of hormonal composition in the perimenopausal period could potentially skew the results.

The findings of this study were quite revealing. After adjusting for confounding conditions, women of child bearing age (15 to 44 years) were more likely to survive to hospital discharge after a cardiac arrest than men in the same age group. Also, younger women had a more favorable neurological recovery compared to men.

In contrast, there was no difference in survival and recovery between men and women older than 56 years.

The authors concluded that administration of female sex hormones might improve the survival after a cardiac arrest. It is unclear if these hormones would have a similar effect in men. No clinical studies investigating the effect of female sex hormones after cardiac arrest have been published.

Interestingly, the improvement in survival exceeded that of any recently introduced advance in health care and treatment after cardiac arrest.

The treatment approach for the victims of cardiac arrest is unlikely to change based on the results of the single study. More evidence is needed before it can be introduced into the clinical practice. Yet, it does sound promising.

Therapeutic Hypothermia (TH) or intentional cooling of the human body was found to be beneficial after a person survives a cardiac arrest. Cardiac arrest, by definition, is a lack of adequate blood flow to the vital organs in the body due to a cessation of heart pumping function. The lack of blood and oxygen supply to the organs could lead to a severe and irreversible damage. Our brain is the most sensitive organ to a lack of oxygen supply. Just a few minutes of no blood flow to the brain could lead to anoxic encephalopathy or brain damage from the lack of oxygen.
 
Anoxic encephalopathy has a spectrum of manifestations. In it’s most severe form, the patient never regains consciousness and remains in a permanent vegetative state. The less severe forms of this condition may lead to disturbances with memory, cognition and emotions etc. It has been recognized that it is possible to “protect” the brain from the harmful effects of anoxia (lack of oxygen) by slowing down it’s metabolism.
 
One of the ways to do it is to cool the brain down. Cooling just the brain is technically difficult but not impossible. Recent research suggests that just the brain can be cooled off by using intranasal cooling (cooling through the patient’s nose). Cooling the whole body including the brain is more feasible. There are two main methods of cooling: external and internal. External cooling is achieved by applying ice packs, cooling blankets and special cooling pads to the surface of the body.
 
The internal cooling method is by using cold intravenous fluids and inserting special cooling catheters into the bloodstream to cool the patient’s blood directly. Using both methods at the same time is the most effective technique. Medical literature supports cooling after cardiac arrest to improve recovery and survival. Unfortunately, the adoption of this treatment modality in the clinical practice has been slow.
 
There are multiple barriers including complexity and labor intensity associated with the institution of therapeutic hypothermia. A recent paper published in the Journal of Trauma, suggest that hypothermia may also attenuate acute lung injury associated with hemorrhagic shock (shock due to bleeding).
 
By modulating the inflammatory response caused by severe bleeding, hypothermia decreased the incidence of lung injury in rats. This was an animal study and the real life clinical study needs to be conducted to confirm the results. Yet, it is becoming obvious that therapeutic hypothermia has it’s role in treating critically ill patients. The indications for using hypothermia will likely be expanded in the years to come. More effective and sophisticated cooling methods might also expand it’s use by providing more rapid and controlled cooling.

When I was in residency, my favorite Nephrologist told the story of his patient with chronic kidney disease who had "killed himself with V8 juice". The patient had been instructed a number of times regarding the potassium present in V8 but he liked it and did not want to stop drinking it and he eventually passed away with hyperkalemia.
I was reminded of this story recently when I was called to a code. There was an elderly male who was on our rehab floor who had the sudden loss of consciousness and pulselessness. CPR was started and the monitor showed persistent asystole. While the code was running, I was able to quickly scan through his chart and see that his creatinine had been rising and he had been on potassium supplementation three times a day and his potassium had been elevated that morning. I quickly have calcium, dextrose and insulin. He regained a rhythm and pulse and was transferred the ICU.
Hyperkalemia is known to cause cardiac conduction abnormalities. The usual progression is peaked T waves with shortening of the QT interval. This followed by progressive lengthening of the PR interval and QRS. The P wave eventually falls and the rhythm goes to asystole or ventricular fibrillation.
Whether is it V8 ingestion or iatrogenic potassium supplementation, we need to remember to be very careful with the potassium level in patients with renal disease.

Have you ever declared a patient dead after a prolonged resuscitation, just for the patient to “come back” the moment you stop CPR? It happened to me once when I was a resident.

An elderly patient with severe emphysema was admitted for a COPD exacerbation. He was getting progressively less responsive after he was taken to a medical floor. The patient was likely retaining CO2 leading to a carbon dioxide narcosis.

Eventually, his heart stopped. The code blue was called. CPR was initiated. The breathing tube was placed. The patient was bag-ventilated by a respiratory therapist. The patient was being resuscitated according to ACLS protocol. Pulseless electrical activity (electrical rhythm on a monitor with an absence of heart beat or pulse) was noted on a monitor. Twenty to twenty five minutes into the code – there is still no pulse.

The patient was pronounced dead. CPR was discontinued and bag-ventilation was stopped. A few seconds later – the patient still had a rhythm. What is even more shocking, he had a thready pulse. Resuscitation resumed and he was transferred to ICU.

So, what happened?
Reviewing this case later, we came up with the conclusion that the excessive bagging during the code caused air-trapping in the patient’s lungs leading to a significant Auto-PEEP(PEEP- positive end expiratory pressure, or residual pressure in the lungs after an expiration) and increased intrathoracic pressure (pressure inside your chest). This significantly diminished venous return to the patient’s heart and precluded him from regaining a pulse. Once he was disconnected from the bag, the pressures in his lungs equilibrated allowing for his heart to fill with blood.

In the rush of the moment, nobody noticed that he was being overzealously bagged by the respiratory therapist. Patients with emphysema require a prolonged expiratory time and tend to trap air if not allowed to exhale completely. Excessive bagging can cause air-trapping and Auto-PEEP.

Since then, I often ask to slow down bag-ventilation during a cardiac arrest to allow the patient to exhale by the elastic recoil of the chest.

The patient above did not do well and the family decided to withdraw care.

Reviewing recent medical literature, I came across an interesting study from Europe. The investigators in several European cities were using an intranasal cooling device to cool the patients having cardiac arrest. I am myself very interested in cooling cardiac arrest patients. There is a body of evidence that the patients have better neurological outcomes when therapeutic hypothermia (cooling to 32 – 33 degrees Celsius) is utilized. I have been using an intravascular cooling system in my ICU. When cooling is being initiated in ICU, there is always a delay in time. The sooner this treatment is started the better our chances on preserving the neurological function. Ideally, the cooling should be initiated immediately at the scene. Using cooling packs and cold saline is somewhat cumbersome and might interfere with the resuscitation. A company from San Diego came up with an intranasal cooling device called RhinoChill to provide cooling immediately after the cardiac arrest. It sprays a rapidly evaporating chemical onto nasal mucous membrane, thus, cooling it down. It does make sense physiologically. The inner surface of the nose is reach in vascular supply and it’s proximity to the brain makes it an ‘ideal’ place for cooling. The data is promising so far. If it goes mainstream, we might see it next to the cardiac defibrillators at the airports (just kidding).

Some things just don’t make any sense. It’s like in the “Red fish, blue fish” book be Dr Seuss: “did you ever fly a kite in bed?...did you ever walk with ten cats on your head?... Think about it. Does it make any sense? No, it doesn’t. What about doing CPR on your patient for two hours straight? Does that make any sense? At that time it seemed like it did. Even though, critical care medicine is inherently chaotic, we don’t like any surprises.
You often know who is “supposed” to die and who is not. A thirty one year old previously healthy man just was not supposed to die. You can’t let it happen.

Just a few days ago he was fine. Later he developed some flu-like symptoms and now he is in ICU with severe pneumonia, full-blown Acute Respiratory Distress Syndrome and multiple organ failure. You’ve tried everything there is to try: maximum ventilatory support, Nitric Oxide and even prone positioning (turning the patient on his abdomen) – nothing is working. Transfer to the outside facility for ECMO (extra-corporeal membrane oxygenation) is simply unrealistic – the patient is not going to survive the transport. And now he is coding (developing cardiac arrest). This is one of those what I call a “Rolling Code”. The patient loses his pulse for five to ten minutes. CPR and ACLS (advanced cardiac life support) is initiated. He regains spontaneous circulation just to lose it a few minutes later. Every time you feel his pulse, you “reset the clock” and start all over again. Remember, you just can’t let him die, so you do it again and again and again.

The family was summoned into the room to witness the code. His parents are sitting quietly in the corner staring into space. Twenty, thirty minutes into the code the silence in the room is almost wicked. Nobody talks. All you can hear is the sound of chest compressions and bag-ventilation. If you believe in afterlife, every time the patient “dies” the soul is leaving his body.

You hold the chest compressions after another round of Epinephrine and Atropine – “yeah, we got the pulse”. Every possible medication is running into his vein to keep him alive. The periods between arrests become shorter and shorter. You check his pupils – fixed and dilated. The patient likely sustained a severe brain damage from the lack of oxygen supply. Now, it’s time to talk to the family again and stop. You have done everything you could and beyond, way beyond. Sometimes, it’s not up to us to decide who is not “supposed” to die.