February 2, 2026

Shock is the “final common pathway to death.” This month’s message focuses on various topics related to this lethal condition. Today, we will focus on introductory concepts necessary for establishing a foundation to understand clinical manifestations of various shock types and treatment approaches. The four main classifications of shock are:  

1. Hypovolemic 

2. Distributive (the overall most common type of shock) 

3. Obstructive 

4. Cardiogenic  

To best understand shock, we must understand normal perfusion at the cellular level. Perfusion involves the transfer of oxygen (from the lungs) and glucose (eaten daily or broken down from glycogen stores in the liver during times of fasting or starvation) via the bloodstream to all our body cells. Cells take in oxygen and glucose and, through three complex processes (glycolysis, the Krebs Cycle, and the Electron Transport Chain), convert oxygen and glucose to carbon dioxide (CO2) and energy in the form of ATP. Energy is necessary for our cells to function (cellular reproduction, protein synthesis, immunity, repair damages, etc.). Without energy, cells die, and eventually the entire organism dies.  

Notice that CO2 is a byproduct of normal metabolism. Oxygen enters the cell, metabolism occurs, and CO2 is released from the cell and transported via the bloodstream to the lungs, where it is released during exhalation. It can be seen why and how CO2 production is an index of perfusion! No perfusion means no oxygen to the cells. No oxygen into the cells means no CO2 out of the cells! This is one reason why we measure and monitor CO2 levels in low perfusion states such as cardiac arrest. When return of spontaneous circulation (ROSC) occurs, CO2 levels rise—often even before the blood pressure rises (this is why we monitor CO2 capnography)! Metabolism under normal conditions is known as aerobic metabolism, meaning that oxygen is required. Aerobic metabolism is efficient and productive, yielding 36 molecules of ATP for every molecule of glucose burned. When oxygen is insufficient in quantity, the body switches to anaerobic metabolism, which only produces two molecules of ATP per molecule of glucose burned and produces lactic acid.  

Normal perfusion requires a functioning heart to pump blood into the cells. The heart must be able to contract effectively and therefore pump the blood with enough vigor; the heart rate must not be too fast or too slow. Heart valves must be intact to allow the one-way flow of blood into and out of the heart chambers. When the pump fails, this causes cardiogenic shock.  

Normal perfusion requires healthy blood vessels – the containers of the blood supply. Both arteries and veins are important in the normal perfusion cycle. Arteries carry blood from the heart to all cells, and veins return blood to the heart from the cells. Arteries are thick-walled vessels that can constrict, when necessary, as a compensatory mechanism to increase blood pressure to ensure perfusion during times of illness or trauma. Veins are essential to the perfusion process; if blood is not returned to the heart in adequate amounts, the heart cannot fill. If the heart cannot fill, the heart cannot expel or eject appropriate amounts of blood. Damaged veins remain dilated, therefore, causing blood to pool in the lower extremities. Damaged veins also become “leaky,” resulting in peripheral edema. Damaged or dysfunctional blood vessels (so-called container problem) are the mechanisms involved in distributive shock, which includes anaphylactic, septic, and neurogenic shock subcategories. Next week, we will discuss distributive shock, the most common type among the four main shock categories.  

Thanks for your time, 

Andrew P. Garlisi, MD, MPH, MBA, VAQSF

February 9, 2026

Of all the shock types, distributive shock is often the most misunderstood shock category and, in clinical practice among EMS providers and emergency physicians, the most often missed. Distributive shock is characterized by diffuse vasodilation and leaky vessels, causing abnormal distribution of blood cells and plasma. This results in reduced perfusion to cells and tissues, leading to a lack of ATP production and eventual organ damage. There are several subcategories of distributive shock, and they all share similar pathophysiology, albeit for different reasons.  

Let’s examine the subcategories of distributive shock: 

1. Anaphylactic shock: This type of shock occurs as a result of exposure to an antigen (allergen) in an individual who is previously sensitized, resulting in a systemic allergic reaction with profound vasodilation and capillary leakage. Anaphylaxis is a Type I hypersensitivity reaction involving IgE antibodies, mast cells, and various chemicals, which are released as a result of IgE binding to the antigen (allergen). IgE, attached to the mast cells, binds the allergen, which triggers an outpouring of chemical mediators from the mast cells, such as histamine, leukotrienes, bradykinin, and prostaglandins. These chemicals cause systemic vasodilation and diffuse leakage of plasma from the capillaries. Hypotension (anaphylactic shock), hypovolemia, bronchoconstriction, laryngeal edema, vomiting, diarrhea, urticaria, and angioedema can result. Onset can be rapid after exposure and fatal. Treatment for anaphylactic shock can start with IM epinephrine 1 mg/mL concentration 0.3 to 0.5 mg IM, while an IV or IO line is being initiated. Once the IV is initiated, patients in anaphylactic shock can be treated with epinephrine 0.1 mg /mL concentration (which is 100 micrograms per mL). The dosage is 100 micrograms (or 1 mL) every minute until return of BP and strong radial pulse, maximum dose is 500 micrograms (5 mL) per protocol. Airway and ventilation should be secured and maintained. Normal saline fluid bolus will likely be necessary, as well as diphenhydramine 50 mg IV /IO/IM. Additionally, methylprednisolone 125 mg IV /IO/IM is recommended in our protocol.  

2. Neurogenic shock: A type of distributive shock that shares similar pathophysiological characteristics of other types of distributive shock—profound vasodilation due to loss of sympathetic nervous system stimulation is characteristic. This type of shock usually follows an injury to the spinal cord, which often is reversible. The sympathetic nervous system (sympathetic chain) lies longitudinally in close proximity to the vertebral column. Often, when there is trauma to the spinal cord above the T6 level, there is concomitant damage to the sympathetic nervous system, including impaired release of neurotransmitters epinephrine and norepinephrine. Loss of epinephrine and norepinephrine results in vasodilation and hypotension. Additionally, because epinephrine is deficient, there is a lack of Beta 1 adrenergic stimulation to the heart. Instead of a compensatory tachycardia, patients with neurogenic shock have relative bradycardia along with hypotension. Fluid bolus and vasopressors (epinephrine or norepinephrine IV) are the mainstays of treatment.  

3. Septic shock is the most missed of all shock types. Clinical presentations can be dramatic or relatively subtle. As in all distributive shock types, septic shock is characterized by vasodilation, which causes hypotension. Additionally, the pathophysiology of septic shock includes leaky blood vessels and disseminated intravascular clot formation. Most often, bacteria are the cause of septic shock. An infection can begin anywhere in the body (urinary tract, lungs, gut, skin, joints, etc.) and become disseminated. As a result, the body’s immune system releases large amounts of cells and inflammatory chemicals in an effort to combat the widespread infection. Unfortunately, and often, the immune response to overwhelming sepsis is exaggerated, and the inflammatory chemicals cause injury and can permanently damage body tissues and organs. Death often results from septic shock. Patients will have signs of infection, confusion, decreased urine output, hypotension, and elevated lactate levels. Fluids, vasopressors, and IV antibiotics given within one hour of sepsis identification provide the best chance for survival. Even with treatment, the mortality of septic shock is approximately 45%. I believe that one day soon, EMS providers will be able to obtain finger stick lactate levels, draw initial blood cultures in the squad, and provide first dose antibiotics for their patients in septic shock.

Thanks for your time, 

Andrew P. Garlisi, MD, MPH, MBA, VAQSF

February 16, 2016

To better understand shock, it is often helpful to use metaphors. For example, the heart can be thought of as the “pump” for the body. The blood vessels are the “containers” or pipes that carry the fluids and blood cells systemically. The “fluids” or fuel within the containers are the plasma and blood cells. If any one of these systems fails, shock occurs.  

When the “pump” (heart) fails, cardiogenic shock results. Cardiogenic shock can occur for many reasons, and providers often forget that conditions other than STEMI can cause the heart to become dysfunctional as a pump. The following are some of the more common etiologies of cardiogenic shock: 

1. STEMI: Acute myocardial injury (not infarction) is the proper description for “STEMI.” With STEMI, usually due to coronary obstruction, the compromised heart muscle becomes injured, but is still potentially salvageable. This is why we rush these patients into the cath lab for acute coronary intervention (balloon angioplasty and stent placement). If an infarction had occurred, the muscle would be dead, and there would be nothing to salvage. On an EKG, ST elevations represent an injury pattern, not an infarction. On an EKG, an infarction is characterized by significant Q waves – either broad beyond .04 seconds, or deep (> 25% the height of the succeeding R wave). STEMI is precipitated by rupture of an atherosclerotic plaque cap within the coronary artery, bleeding, and then fibrin clot formation via the Intrinsic arm of the Coagulation system. This clot formation further obstructs the coronary vessel, causing the injury noted on the EKG. Fibrin clot formation is the reason we provide aspirin, ticagrelor, or clopidogrel (antiplatelet agents) and heparin, the anticoagulant. Whether or not the patient can receive percutaneous coronary intervention (PCI) promptly will determine the outcome as far as myocardial damage is concerned. If the patient does not receive timely intervention, permanent myocardial damage will occur (infarction), and the involved heart muscle may become dysfunctional as a pump, depending on the degree of permanent damage.  
   

2. Valvular Heart Disease: Valvular heart disease is an often-forgotten etiology for cardiogenic shock. Heart valves are essential for normal cardiac function. These valves are designed to allow for “one-way flow” of blood between the heart chambers (the AV valves between the atria and ventricles) and one-way flow into the great vessels (Pulmonary Artery and Aorta). The tricuspid valve lies between the right atrium and right ventricle. The mitral valve lies between the left atrium and left ventricle. These valves are connected to the inner walls of the corresponding ventricular muscles (papillary muscles) via tendinous chords known as Chordae Tendineae. Acute STEMI can damage the ventricular papillary muscles and cause acute rupture of the chordae tendineae, resulting in cardiogenic shock. Heart valve diseases are more common and occur chronically, over time. Valves can degenerate from wear and tear over the years and become calcified and fibrotic. Rheumatic heart disease (following a bout of rheumatic fever) causes an immune-type damage to heart valves. Infective endocarditis (for example, due to IV drug abuse with contaminated needles) is also a major cause of valvular heart disease. 
   
   Regardless of the cause of the valvular disease, the valves can no longer function effectively. Valves that cannot open fully when they need to be open are called “stenotic.” For example, aortic stenosis is a heart valve condition where the aortic valve (due to damage or calcifications) can't open fully when it is supposed to. The result: when the left ventricle contracts during systole, the blood being ejected into the aorta will have a difficult time getting through that tight stenotic aortic valve, and the ventricle will not be able to eject the entire stroke volume. This places undue strain on the left ventricle, which, eventually, will fail over time. 
   

3. Arrhythmia: Various arrhythmias are obvious causes of cardiogenic shock. Slow arrhythmias such as Type 2 second degree heart block and complete heart block are commonly encountered and ultimately often require pacemaker intervention. Epinephrine or dopamine may be temporarily effective for a heart block. Fast arrhythmias such as wide-complex tachycardia (WCT) are challenging. WCT can be due to ventricular tachycardia, SVT with a bundle branch block, or Wolff-Parkinson White AVRT with antidromic conduction. Without prior knowledge of the patient’s baseline EKG, it is nearly impossible to determine the exact cause of WCT. The best rule is to consider and treat it as ventricular tachycardia until proven otherwise. Therefore, for cardiogenic shock unstable patients, synchronized cardioversion is the appropriate treatment.  
   

4. Congestive Heart Failure (CHF): CHF is not a diagnosis per se; it is more of a clinical syndrome rather than a single disease. It occurs when the heart is disabled and can no longer pump enough blood to meet bodily demands. There are many causes of CHF, which can be acute (acute cardiogenic pulmonary edema, aka flash pulmonary edema), or more subtle and chronic. Causes include ischemic heart disease, hypertension, valvular heart disease, cardiomyopathy, endocarditis/myocarditis, and arrhythmias. Patients can suffer from primarily right ventricular failure (leg edema, hepatojugular reflux, ascites, and JVD), left ventricular failure (shortness of breath, lung crackles, orthopnea, PND, hypoxia, and cyanosis), or both simultaneously. Finding and treating the underlying cause of CHF is essential, and treatment often involves oxygen, diuresis, arrhythmia management, and control of blood pressure. Surgery may become necessary if and when valvular dysfunction is the primary problem.

Thanks for your time, 

Andrew P. Garlisi, MD, MPH, MBA, VAQSF

February 23, 2026

Obstructive shock is where the heart, although normal, is unable to pump blood due to physical obstruction, leading to reduced tissue perfusion and hypotension. Mechanical barriers exist that prevent the heart from functioning properly. Causes of obstructive shock include: 

1. Massive Pulmonary Embolism (PE) - Pulmonary emboli come in different varieties. They can be small, single, multiple, or massive. They can occur chronically and acutely. Most pulmonary emboli originate in the deep leg veins or pelvic veins. Risk factors for PE should be familiar to the high-performance paramedic: pregnancy, birth control pills, prolonged immobilization, cancer, history of prior deep vein thrombosis (DVT), post-surgery, and some inherited blood disorders such as Factor V Leiden and Protein C/S deficiency. Massive PE or saddle pulmonary emboli are immediately life-threatening and likely to cause obstructive shock. Saddle pulmonary emboli are large clots that lodge in the bifurcation of the main pulmonary artery, the right and left main trunks. It is known to cause hemodynamic collapse. With total obstruction of the pulmonary artery, the right ventricle cannot pump blood into the lungs. The right ventricular strain results from the increase in pulmonary vascular resistance. The right ventricle acutely dilates and fails, which causes a marked decrease in blood introduced into the left ventricle –in other words, there is reduced left ventricular preload. A decrease in left ventricular preload reduces cardiac output and causes shock. Symptoms include sudden dyspnea, pleuritic chest pain, syncope, tachycardia, and hypotension. Jugular vein distention (JVD) will be noted due to right ventricular failure. Patients are often cyanotic. Diagnosis in the emergency department can be made via CT pulmonary angiography, and echocardiography reveals right ventricular dilation and reduced wall motion. Treatment for massive PE can include thrombolysis, and in some cases, surgical or catheter-directed embolectomy, if thrombolysis is ineffective.  

2. Tension Pneumothorax (TP) - A condition where air enters the pleural space between the lung and the chest wall, causing compression of the lungs, heart, and great vessels. The air within the pleural space causes tremendous pressure within the chest cavity, and the heart is no longer able to adequately fill or eject adequate stroke volume. Penetrating trauma is one mechanism for TP. TP can also occur due to overzealous mechanical ventilation. It is also possible for TP to result from spontaneous rupture of a bleb in patients with asthma chronic obstructive pulmonary disease. Patients with TP present with dyspnea, pleuritic chest pain, tachypnea, unilateral loss of breath sounds, and hypotension. JVD is present, and cyanosis and tracheal deviation may occur as a late sign. Treatment should be performed as soon as a clinical diagnosis is made (do not wait for chest X-ray confirmation!). Needle decompression with a 14-gauge needle (for the adult patient) in the second ICS, mid-clavicular line must be performed immediately. The second rib can be found by locating the angle of Louis, which is approximately one inch below the suprasternal notch. As an alternative site, needle decompression may be performed in the 4th ICS anterior or mid-axillary line. In the emergency department, a chest tube will be placed to ensure adequate continued evacuation of the pleural space air and or blood.  

3. Cardiac Tamponade (CT) - This life-threatening condition results from excess blood or fluid that accumulates within the pericardial space, thereby impeding ventricular filling and reducing cardiac output. Most cases of CT are secondary to penetrating trauma. Other causes include blunt trauma, aortic dissection, malignancy, pericarditis, tuberculosis, and uremia. The rate of fluid accumulation within the pericardial space often determines when hemodynamic compromise occurs. As little as 200 mL of blood accumulation acutely (as with penetrating trauma) can cause CT, whereas slow accumulation of fluid or blood (as can occur with cancer metastasis to the pericardium) can result in 2 liters of pericardial fluid before CT results. The high-performance medic can recognize the presence of CT by utilizing knowledge of the pathogenesis of the condition as well as signs and symptoms. Patients will complain of shortness of breath, chest discomfort or pain, and will exhibit Beck’s triad of hypotension, JVD, and muffled heart sounds. EKG may reveal low voltage QRS or electrical alternans, alternating QRS amplitudes. Along with the usual ABC’s stabilization attempts, treatment includes surgical drainage of the blood or fluid. Needle aspiration could be performed initially, followed by a surgical pericardial window procedure (where a small section of the pericardium is removed and a drainage tube is placed). 

Thanks for your time, 

Andrew P. Garlisi, MD, MPH, MBA, VAQSF