Good Monday morning to all providers,

We have dedicated the month of October to shock. Shock is the medical provider’s mortal enemy. We focus this month on recognition, identification, and treatment. Each Monday morning will review the four categories of shock. Let’s start with recognizing our poorly perfused patient. The organ that is the most sensitive to poor perfusion is the brain. Altered mentation is one of the most critical and early signs of shock, and it can manifest as anxiousness, confusion, or outright unresponsiveness. Recognizing the source of altered mentation as shock allows the provider to provide early lifesaving care. It is why many of you enter the various sites of emergencies with an altered mental patient, and the first thing I see you do is checking for a pulse radially. The adult patient with a palpable radial pulse has a minimal systolic pressure of 80. If no radial pulse but a femoral pulse is present, then the minimal systolic adult pressure is 70. If there is no femoral, but there is a carotid, the minimal adult systolic pressure is 60.   Capillary refill is also a quick way of evaluating perfusion in the field and is an excellent rapid test. Of course, just looking and feeling the skin itself for diaphoresis, pallor, or rashes is a critical part of our shock evaluation.

Now that we have recognized shock as the patient’s immediate threat, the next move is to identify the cause of the shock. Identifying the cause of the shock is critical as it will guide your therapy.  

Our four categories of shock are:

1. Hypovolemic

2. Cardiogenic

3. Distributive 

4. Obstructive

Hypovolemic is a result of either volume loss from dehydration, emesis, diarrhea, or excessive urination. These are to volume losses and respond nicely to volume repletion. The other form of hypovolemic shock is hemorrhagic shock from frank blood loss. This can be from traumatic blood loss, now recognized as the number one cause of traumatic death. The other cause of hemorrhagic shock is from:

• emergent blood loss from GI bleeds

• ectopic pregnancies

• ruptured vascular emergencies

• hemorrhagic cystitis

Cardiogenic shock is “pump failure.” The cause of pump failure can be caused by the following:

• myocardial infarction

• arrhythmia

• heart failure

• viral cardiomyopathy

Distributive shock is a loss of normal vascular resistance. This can be caused by several significant emergencies including: 

• sepsis

• anaphylaxis

• neurogenic

• adrenal crisis

• or toxicologic causes

Obstructive shock is the last of our shock categories. Under this umbrella of shock are the following:

• massive pulmonary emboli

• tension pneumothorax

• pericardial tamponade

I hope you can take a minute and review the categories of shock as we dive deeper and discuss appropriate treatment each Monday. Thanks, and have a safe day out on the streets.

Sincerely,

Don Spaner MD

Cardiogenic Shock - October  13, 2022

Dear Providers,

Welcome back to another Monday morning message with today’s deep dive into cardiogenic shock. Recognizing that the shock patient is having a cardiac emergency helps you treat the patient, and just as important, it means getting the patient to the right place at the right time for the proper care. Since pump failure is the correlating event in cardiogenic shock, recognizing what is causing the pump failure is critical. Besides the signs of poor perfusion, expect the narrow pulse pressure of less than 20, as seen with obstructive and hypovolemic shock.

One of the more common causes of cardiogenic shock is in the setting of a STEMI. We need to see the akinetic areas of the heart affected by the lack of blood supply from the acute MI. The lack of blood flow means a lack of ability to produce ATP at the cellular level. The lack of ATP means there are no energy molecules to allow for the contraction of the myocardial cells. If 40% or more of the heart is not being perfused, the pump will fail, and the patient enters cardiogenic shock. Increasing the preload with a gentle fluid bolus is completely acceptable, and the 300-500cc may be enough to safely transport the patient to an emergent cardiac cath center. If the bolus continues to leave them in shock, the safest thing a provider can do is push dose epinephrine. Remember, this is only 10 micrograms at a time and may be the safest mode of stabilization while moving to an emergent cardiac cath center.

The next cause of cardiogenic shock is heart failure. Here the chronic weakness of the heart muscle fails. The usual clinical presentation of heart failure is volume overload, and not because the heart is beating stronger, but because the volume is building, the patient usually presents with hypertension. Nitrates and diuresis are the usual plans of care. However, once the pump can no longer keep up with the volume and the muscle has weakened to the point of hypotension, cardiogenic shock ensues. Adding volume will only make this weak pump weaker, but a very mild bolus of 300cc is acceptable. Adding more volume than this is detrimental. Again, the low dose push dose epi is the safest way to go until you arrive at the appropriate center.

The next class of cardiogenic shock is arrhythmic in origin, which can be due to rapid unstable rhythms that need immediate intervention. Recognizing that the production of energy throughout the cells is dependent on Glucose + Oxygen = ATP+CO2+H2O. Just a reminder that the waste product of CO2 is a great way to measure perfusion. If you are dealing with a rapid rhythm such as rapid atrial fibrillation or rapid atrial flutter and wondering, do I need to take the risk of emergency synchronized cardioversion, look for shock. If the patient is hypotensive, has low CO2,  or has altered mental, you must intervene; the patient will not make it to the emergency department. That is the same for any unstable event like ventricular tachycardia requiring synchronized cardioversion or severe bradycardia events like complete heart block in shock that need emergency transcutaneous pacing. The care for these causes of cardiogenic shock is to stabilize the rhythm, which in an unstable situation usually requires a form of electricity.

Lastly, in the cardiogenic shock category is the very serious cause for heart failure involving inflammatory illnesses of the heart muscle. They are commonly viral and referred to as viral myocarditis, and other origins, like bacterial and fungal myocarditis, have also caused this. These patients can go into heart failure and cardiogenic shock requiring appropriate fluids and push dose epi, but more serious cases find themselves in tertiary care centers on ECMO.

Cardiogenic shock can have many sources and our paramedic providers are well-trained to make decisions in the following:

• listening to the heart for loud murmurs

• taking a good history

• 12 lead evaluation

• utilizing fluids judiciously

• push dose epinephrine or synchronized cardioversion

Recognize the cardiogenic source, identify the cause, and treat appropriately as you get them to the right place at the right time for the proper care. Stay safe in the field, and thanks for taking the time to review. Hope to see you back here next week.

Sincerely,

Don Spaner MD

Obstructive Shock - October 17, 2022

Dear Providers,

Thanks for taking a minute for another dive into our month of shock. Today’s review is about obstructive shock. Here again, patients in shock with an obstructive cause will have the ability to maintain vascular resistance, so they will present in shock with a narrow pulse pressure. The three main causes of obstructive shock are: 

1. tension pneumothorax

2. pericardial tamponade

3. massive pulmonary emboli

Suspecting the appropriate cause of the obstruction can save a life with rapid intervention. Remember, the blood can’t move forward. This is very unusual in that you have a sudden shock patient with no cardiac cause, and yet you see JVD. This is not a volume issue; it’s an obstruction issue.

The obstructive shock that EMS makes the biggest difference in tension pneumothorax, which should only be suspected in traumatic chest wall injuries. The spontaneous pneumothorax patient never has a large enough one-way valve injury to cause tension on the large vessels of the superior and inferior vena cava. However, large traumatic injuries that lack air movement in shock deserve a needle decompression. This may be a life-saving procedure in the field. It doesn’t fix the pneumothorax, but it will take the pressure off the cava system, This way, preload can return to the heart. If the needle is successful, the radial pulse will return. If the patient drops their pressure again (needle them again), right next to the previous 14g long needle in the appropriate location as trained. A young Army medic saved his platoon sergeant’s life with five needles placed until they got to our CSH.  

The second cause of obstructive shock is pericardial tamponade. Remember Beck’s Triad, muffled heart sounds, hypotension, and JVD. This is an acute event. Pericardial effusions that build over an extended period, as in renal failure patients, seldom go into cardiac tamponade. However, aortic dissections i.e. as well as trauma to the heart, can bleed into the pericardium. These sudden events, in which the pericardium can’t acutely stretch and adjust to an acute bleed, will cause the tamponade. The bolus of fluid in the field is acceptable, but they need an emergent cardiac intervention. Even if the emergency physician does a pericardiocentesis, the blood will reaccumulate, therefore, you must take these patients where cardiothoracic surgery can care for them immediately. These are usually at higher-level trauma centers, and take them to the highest appropriate trauma center available.

Lastly, massive pulmonary emboli are becoming more common with the advent of Covid. We have sadly seen these in very young patients. The use of emergency bedside ultrasounds has helped the emergency physician improve our ability to make the diagnosis rapidly in the setting of large saddle emboli, where we can see the strain of the right ventricle. Patients at risk for massive pulmonary emboli is extensive and are the same patients at risk for DVTs, including:

• post-surgical patients

• hypercoagulable patients

• immobilized extremity injuries

• vascular injuries

• sepsis

• Covid patients

If you have an at-risk patient who is short of breath, hypoxic, and hypotensive, think obstructive shock secondary to massive PE. We usually heparinize the non-shock patients, and those in shock receive lytic therapy, or they go directly to interventional labs for emergent thrombectomies. There is very little the field medic can do in this case but high flow oxygen, EKGs, and transport to a thrombectomy-capable center. These require vascular surgeons and a biplanar vascular lab.

Obstructive shock is a challenging diagnosis in the field. However, a good history and thoughtful review of the information can frequently bring you to the appropriate conclusion. Traumatic chest injuries with a lack of air exchange and shock deserve a needle decompression as trained. Pericardial tamponades deserve recognition and transport to the appropriate surgical trauma center. Massive PE patients get high-flow oxygen, EKGs, and transport to a vascular facility. Thanks again for taking the time to review. Hope to see you back here next week.  

Sincerely,

Don Spaner, MD

Hypovolemic Shock - October 27, 2022

Dear Providers,

The deep dive category for this Monday is hypovolemic shock. Patients experiencing this fall under two categories: hemorrhagic shock or hypovolemic shock. 

Either category presents volume loss as the main problem, and we won’t see any JVD as the tank is nearly empty, and there is no obstruction. Pressors never play a role in hypovolemic shock because they are maximally vasoconstricted in response to an empty tank. So, you will see hypotension with a narrow pulse pressure. They need to stop the volume loss and refill the tank with the appropriate solution.

The first category of hypovolemic shock is hemorrhagic shock. Decades ago, the initial trauma courses and the American Heart Association, taught ABCDE as the appropriate sequence of critical cardiac and trauma care. The data from the military, after initial numbers from Operation Enduring Freedom, recognized hemorrhagic loss as the most common cause of death on the battlefield, as well as the most preventable cause of death. Medics and front-line soldiers received tourniquet training and stopped the bleeding procedures to spare blood loss until definitive care could be obtained.

The focus turned to BACDE, and blood loss became a top priority in military and civilian operations. We also learned unfortunate lessons from Vietnam and even Desert Storm, in which casualties did far worse with massive amounts of crystalloid infusions. Events like abdominal compartment syndrome were now being explained by aggressive crystalloid fluid replacement in hemorrhagic shock. Terms like permissive hypotension started to be used for penetrating hemorrhagic shock patients. We recognized that platelets, clotting factors, and oxygen-carrying red blood cells were being massively diluted. Clots that were formed were losing their integrity secondary to over- aggressive blood pressure treatment with crystalloids.  

Research from the battlefield also showed that blood products needed to be replaced. Trauma teams were no longer just focusing on red blood cell transfusions, rather clothing factors through plasma and platelet transfusions with red blood cells, fixing the ratio to 1:1:1 became the new military standard of care. 

I was exposed to whole blood transfusions for the traumatically injured casualty in Afghanistan, 2003, Iraq, 2008 and 2011. Here the prescreened soldier was actively donating whole blood, and this warm nectar of life would go directly into the casualty as the surgical team fought hard to control the bleeding. Remember, the hemorrhagic shock patient needs to lose 30-40% of their blood before you even see hypotension. A traumatic hemorrhagic shock patient needs TXA as well, and we are changing this to 2Gm over ten minutes in your 100-cc bag which will require 100 drops from a macro drop set per minute to properly administer the TXA.

The non-trauma patient in hemorrhagic shock needs a similar emergent transfusion and surgical care. The losses from non-traumatic blood loss can be just as rapid and severe as traumatic blood loss. Think about the 55-year-old hypertensive patient with acute left flank pain. We have a large differential diagnosis, but he has a pale, prolonged cap refill, altered mental status, and is now hypotensive in shock with compensating rapid breathing and has a palpable pulsatile mass. The differential quickly narrows to a ruptured AAA. The prehospital provider must go immediately to the vascular center for emergent surgical care and massive blood product transfusion. The same applies to the hemorrhagic shock patient from a ruptured ectopic pregnancy or massive GI bleed. TXA can be considered using medical control for these concealed hemorrhagic shock blood losses.

The other category of hypovolemic shock is volume loss. These are commonly seen with dehydration, emesis, or severe diarrhea and seen in severe burns. Certain diseases also are well known for volume loss. DKA and pancreatitis are two excellent examples of diseases known for wasting volumes. Sepsis is another disease that requires appropriate volume replacement, this will be further discussed next week. The critical point is that these patients will also present in shock with narrow pulse pressures requiring fluid replacement and constant reevaluation.

The hypovolemic shock patient is critically ill. Identifying the source as either blood loss or volume loss helps to direct and care appropriately for these patients. The protocol discusses appropriate volume replacements for adult and pediatric hypovolemic shock patients. Thanks for checking in again for a Monday Morning Medical message. Hope to see you next week for another installment of our shock series. Distributive shock is up next. We’re saving the best for last. Stay safe in the field, and thanks again.

Sincerely,

Don Spaner, MD