Shock: Clinical practice



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Shock: Clinical practice


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USMLE® Step 1 style questions USMLE

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A 34-year-old man comes to the emergency department by ambulance from a motor vehicle accident. He was riding in the bed of a pickup truck and was ejected at a high speed. He has not received any intravenous fluids. Physical examination shows an unresponsive man with an absence of deep tendon reflexes and flaccid quadriplegia. Additionally, he has dry, flushed, and warm skin with fecal incontinence and priapism. A cervical spine MRI is obtained and is shown below. A Swan-Ganz catheter is inserted to assess hemodynamic variables. Which of the following findings is most likely to confirm the diagnosis?


Content Reviewers:

Rishi Desai, MD, MPH

Shock is most commonly due to hypotension, which is a systolic blood pressure less than 90 mm Hg, or a mean arterial pressure less than 65 mm Hg, that leads to inadequate tissue perfusion and injury to various organ systems, like the brain, heart, kidneys, and liver.

If left untreated, shock can cause irreversible multi-organ failure and death.

Shock can be thought of with the following equation. The mean arterial pressure is equal to the cardiac output times the systemic vascular resistance.

The cardiac output is equal to the heart rate times the stroke volume, and the stroke volume is dependent on the preload and the contractility.

So, the causes of shock can be either due to a decline in the cardiac output or the systemic vascular resistance. When one parameter declines, normally the other increases to try to compensate.

A decrease in the cardiac output can be due to a decreased preload, decreased contractility or a heart rate that’s too fast or too slow.

Decreased preload can be due to extracellular fluid volume depletion, such as from diarrhea, excessive diuresis, dehydration, or hemorrhage. These are all causes of hypovolemic shock.

Preload can also decrease if there is something obstructing the entry of blood into or out of a cardiac chamber, and this is called obstructive shock.

For example, tension pneumothorax and pericardial tamponade can compress the inferior vena cava, obstructing blood flow to the right ventricle, decreasing the cardiac output.

A massive pulmonary embolism can obstruct blood from circulating through the pulmonary vessels and getting to the left ventricle.

Cardiogenic shock is when the decline in cardiac output is secondary to a decrease in contractility, such as in congestive heart failure, myocardial infarction, myocardial contusion, or due to dysrhythmias.

Okay, on the other hand of the equation, we have things that decrease the systemic vascular resistance, or in other words result in peripheral vasodilation. These include anaphylactic, septic, and neurogenic shock, as well as certain disease states like acute adrenal insufficiency.

Okay, the approach to an individual with suspected shock starts with the ABCs; airway, breathing and circulation. The goal here is to detect life-threatening emergencies and address them immediately.

The airway is evaluated for patency, and the easiest way to do this is to ask the individual to speak to you.

A clear, coherent voice usually means that they can protect their own airway.

If the individual is not breathing, or is unconscious with a Glasgow Coma Scale, or GCS less than 8, then endotracheal intubation and mechanical ventilation is performed.

Also, signs like lip and tongue swelling or inspiratory stridor suggest anaphylactic shock.

As for breathing, ventilation and oxygenation are assessed.

For example, hypoxemia, decreased air entry, hyperresonance on percussion, and tracheal deviation to the opposite side may be seen in a tension pneumothorax. In such a case, immediate needle decompression is performed by inserting a needle in the 2nd intercostal space on the affected side, which alleviates the compression of the inferior vena cava.

Alright, as for the circulation, IV access should be obtained by inserting two large-bore peripheral intravenous lines.

If it’s difficult to obtain intravenous access, such as in someone with hypovolemic shock, then an intraosseous line should be inserted.

Central venous access such as an internal jugular, subclavian or femoral vein lines should be obtained if blood products or prolonged infusions of vasopressors are to be given.

However, resuscitation should not be delayed simply because central venous access is not available.

A small bolus of IV crystalloid fluid may be given initially as a “fluid challenge”, which assesses the person’s response to fluids.

Parameters like the mean arterial blood pressure or the urine output may be used to assess responsiveness.

For example, hypovolemic and septic shock usually respond well to fluids, whereas cardiogenic and obstructive shock do not.

Alright, now the vital signs offer more clues. Fever or hypothermia can occur in septic shock, although they’re not always present.

Shock caused by decreased cardiac output usually leads to a narrow pulse pressure, like a pressure of 70 over 60 for example.

On the other hand, shock caused by a decreased systemic vascular resistance usually manifests as a wide pulse pressure, like a pressure of 100 over 30.

It’s also important to know a person’s baseline blood pressure. For example, a blood pressure of 110 over 80 is actually low for someone with uncontrolled hypertension who has a baseline of 180 over 120.

A recently studied parameter is the shock index, which is the heart rate divided by the systolic blood pressure.

A shock index greater than 0.8 usually indicates shock, and the higher the number, the worse the shock, but a normal shock index value doesn’t exclude shock.

Now tachycardia and tachypnea are classic compensatory responses to shock, however, if someone is on a medication like a beta blocker, this may blunt the tachycardia.

Also, neurogenic shock, a complete heart block, or an overdose on beta blockers or calcium channel blockers can all cause bradycardia.

On physical exam, cold extremities usually signify shock caused by a decreased cardiac output, because the body attempts to redirect blood flow away from the skin to more vital organs like the brain and heart.

On the other hand, in shock caused by a decreased systemic vascular resistance, the extremities are usually warm due to peripheral vasodilation.

Increased jugular venous distension suggests obstructive shock, whereas a flat jugular vein signifies hypovolemic shock.

Other common findings include signs of decreased end-organ perfusion, such as oliguria, which is defined as a urine output less than 0.5 CCs per kilogram per hour.

Other signs are an altered mental status, which indicates decreased brain perfusion, and a prolonged capillary refill time, which indicates decreased skin perfusion.

Generalized hives and wheals, flushing and angioedema suggest anaphylactic shock.

Okay, now during the resuscitation, the rapid ultrasound for shock and hypotension, or the RUSH exam can be very helpful. The sequence of the exam can be remembered with the mnemonic “HI MAP”.

So “H” is for heart, and here we’re mainly looking for a pericardial tamponade, which is immediately treated by doing a pericardiocentesis. It’s also possible to look at the way the heart is beating which may be abnormal in someone with cardiogenic shock.

In addition, a significantly enlarged right side of the heart may be due to right heart strain from a pulmonary embolism.

Okay, “I” is for the inferior vena cava, which provides an idea about the volume status and the central venous pressure, or CVP, which reflects the amount of blood returning to the right heart.

A dilated IVC means that the CVP is high, which points towards obstructive or cardiogenic shock.

A flat and collapsed IVC tells us that the CVP is low, which points towards hypovolemic or distributive shock.

“M” is for Morrison’s pouch, or the hepatorenal recess, which is where fluid or blood can collect in the setting of trauma. We also look for free fluid in the splenorenal recess and in the pelvis - any signs of trauma might mean needing to go directly to surgery for exploration.

The “A” is for the aorta, where we measure the aortic diameter looking for any signs of an aortic aneurysm. It’s crucial that we look at the entire aorta, beginning from the xiphoid process all the way down the abdomen until you see the aorta bifurcate into the common iliacs, which is usually just under the umbilicus.

Finally, there’s “P”, which is a reminder to look for a pneumothorax.

Alright, now lab work depends on your clinical suspicion. A CBC may reveal a high hematocrit in non-hemorrhagic hypovolemic shock, due to hemoconcentration.

Hemorrhagic shock may initially show a normal hematocrit, because a person loses red blood cells and a proportional amount of plasma with it. But later, only after they’re resuscitated with fluid, does the anemia appears.

An elevated eosinophil count can occur in anaphylaxis or adrenal insufficiency.

Leukocytosis may indicate septic shock, but it could just be a response to the stress of any type of shock.

On the other hand, leukopenia or presence of immature neutrophils called band cells are more specific for sepsis.

Thrombocytopenia, as well as coagulation studies such as a prolonged prothrombin time may clue towards coagulopathy as a cause of hemorrhagic shock.

Lactate levels may reflect poor tissue perfusion, and elevated levels are correlated with increased mortality, especially in septic shock.

Lactate levels are quite helpful in identifying shock, especially in individuals who have a normal blood pressure, and serial lactate levels can be used to assess response to therapy.

While high lactate levels are abnormal, low lactate levels should not reassure you if there are other concerning signs of shock.

In shock, there’s also usually a high anion-gap metabolic acidosis.

Elevated blood urea nitrogen and creatinine levels can indicate that there’s a pre-renal acute kidney injury secondary to hypovolemia.

An ECG may show ischemic changes, electrical alternans which is alternating amplitudes of the QRS complex, a sign of pericardial effusion, or even signs of right ventricular strain in pulmonary embolism like the S1Q3T3 pattern.

If a myocardial infarction is suspected, then troponin levels may be obtained, and if congestive heart failure is suspected, then a chest x-ray and brain-natriuretic peptide, or BNP levels can be checked.

If septic shock is suspected, then blood cultures, urinalysis, and a chest x-ray should be checked to look for a source.

When suspecting anaphylactic shock, serum tryptase levels, a marker released from mast cells should be obtained.

Management depends on the cause of shock. So let’s start with hypovolemic shock, which may be non-hemorrhagic or hemorrhagic.

Non-hemorrhagic hypovolemic shock may result from gastrointestinal losses like vomiting or diarrhea, renal losses such as excessive diuresis in diabetic ketoacidosis or diabetes insipidus, excessive sweating like in hyperthermia or hyperthyroidism, or third-spacing.

Third spacing includes anything that causes intravascular fluid to shift into the interstitial or intracellular space - like burns, intestinal obstruction, or acute pancreatitis.

In addition to the manifestations of shock, other clues include signs of dehydration such as dry mucous membranes and decreased skin turgor.

Treatment includes replacing the lost fluids, usually with IV crystalloids like normal saline, correcting any electrolyte abnormalities, and addressing the underlying cause.

Hemorrhagic shock usually results from trauma, and can be obvious such as bleeding from the scalp or a long-bone fracture, or it could be occult such as intraperitoneal or retroperitoneal bleeding. It can also be non-traumatic, such as gastrointestinal or genitourinary bleeding, or a ruptured ectopic pregnancy.

Importantly, a ruptured abdominal aortic aneurysm should be suspected in an elderly individual presenting with back or flank pain, syncope and hypotension.

Management includes applying direct pressure to the bleeding if possible, and providing blood products.