Shock is universally a topic that many nurses and nursing students find difficult to master. Maybe that’s because there are so many types of shock, a multitude of causes for shock and varying treatments depending on a complex array of factors. In this post we break down the basics of shock, differentiating between the four types of shock, how to recognize your patient is in shock and the general treatments for each type.

What is shock?

In short terms, shock is a syndrome of hypoperfusion and hypotension that leads to inadequate oxygen delivery to the tissues and impaired cellular metabolism that ultimately results in organ dysfunction/failure. So there’s a few things going on here.

  1. A state of hypoperfusion/hypotension (low blood pressure)
  2. Oxygen does not get to the tissues (causing global hypoxia)
  3. Cells don’t function property (they shift into anaerobic metabolism when they don’t get enough oxygen…remember the Kreb’s cycle? Here it is at work!). Anaerobic metabolism results in the production of lactate and ultimately leads to metabolic acidosis.
  4. Organs start to fail (let’s hope it doesn’t get to this point!)

The pump and the bucket

Huh? Are we talking about gardening all of a sudden? Nope…we’re talking about the general physiologic factors that come into play when your dealing with a patient in shock.

The pump: this is the heart. If you think of the heart as a pump, it makes learning about shock and the ways we treat it a little easier.

The bucket: Think of the body’s vasculature as a bucket…from heart to arteries to capillaries to veins and back to the heart…it’s all a closed system, kind of like a very weirdly shaped bucket. When the bucket is full, we have an adequate about of volume…when the bucket is low, we don’t have enough volume. Conversely, you could also have the wrong-sized bucket…maybe it’s too big for the amount of volume we currently have. This will all make sense as we get into each of the types of shock.

The four classifications of shock

There are four types of shock and your task is learning how to differentiate between each one. Here’s a quick little overview…then we’ll talk about each one in more detail further down. Ready?

Hypovolemic shock occurs when the body loses too much fluid through bleeding, vomiting (so much vomiting) diarrhea (so much diarrhea-ing), burns, polyuria and third spacing. You may see it referred to as either hemorrhagic or non-hemorrhagic, depending on what is causing the fluid losses. In hypovolemic shock, the bucket does not have enough fluid in it. The result is decreased venous return to the heart, which then leads to decreased cardiac output and hypoperfusion.

Distributive shock occurs when the bucket is too big, more or less. The main one here is septic shock, and other examples include anaphylaxis, spinal trauma and even endocrine disorders. The main issue here is decreased peripheral vascular resistance.

Cardiogenic shock occurs when the pump (heart) has failed. This can be due to a massive MI, a valve problem, arrhythmias or cardiomyopathy.

Obstructive shock occurs due to a mechanical barrier such as cardiac tamponade, a pulmonary embolism, tumors or a tension pneumothorax. Basically anything that obstructs the circulating volume of blood can be a precursor to hypoperfusion.

General assessments for shock

As you are evaluating your patient in shock, there are some clinical signs and symptoms you’ll assess regardless of which classification of shock you are dealing with. These are:

  • Heart rate (many things cause an elevated heart rate, so be careful!)
  • Respiratory rate and effort
  • Blood pressure (BIG ONE!)
  • Hemodynamics (if you’ve got fancy equipment!))
  • Mentation (muy importante!)
  • Urine output (an EXCELLENT indicator of end-organ perfusion)
  • Skin signs (often overlooked but one of the BEST things you an monitor!)

The stages of shock

Before we get into the nitty-gritty, let’s talk about the stages of shock. The really tough thing about shock is that there often aren’t SUPER NOTICEABLE signs in the early stages. To catch shock in an early stage, you’d usually need to have a high index of suspicion that your patient is at risk for going into shock.

Initial shock (Class I): During this phase of shock, the body is typically compensating for the hypoperfusion/hypotension so signs can be pretty easy to miss.

  • Mildly tachycardic: the heart rate is speeding up to compensate for the drop in blood pressure and decreased oxygen delivery to the tissues. It very likely may not be enough to set off alarm bells in your head. Generally, any sustained increase of 10-20 BPM should be evaluated. It could be pain, could be anxiety, could be fever. There are many causes for elevated heart rate, so this one is VERY easy to miss.
  • Mildly tachypneic: also, VERY easy to miss. Your patient is breathing a little faster because oxygen delivery to the tissues is impaired, there’s a little metabolic acidosis going on thanks to altered cellular metabolism…and his body is compensating by upping the respiratory rate. What else causes the respiratory rate to increase? Yep…pain and anxiety.
  • Blood pressure is probably normal at this point: thanks to the body’s compensatory mechanisms, the patient’s blood pressure may be normal…but if you look closely you could possibly see a gentle downward trend (but the tough part is, it’s probably still in the “normal” range…see how tough this is?)
  • Urine output will be maintained at this point as the kidneys haven’t yet taken the full brunt of the shock state.
  • Extremities may be slightly cool in most cases (may be warm in distributive shock). If your patient’s hands/feet were warm when you checked pulses at 0730 but are now cool at 1030…you may want to investigate. This one is also easy to miss because many people generally have cold hands/feet…think of all those little old ladies who bundle up in blankets. Again, this is an easy one to miss…however it is also one of the FIRST signs to pick up on, if you are diligent! Get those gowns off and LOOK AT THE SKIN!
  • Anxiety could start coming into play. The patient may not be able to pinpoint the reason for his/her increased anxiety, but you may notice more restlessness than before. Not getting enough oxygen to the organs (brain!) can do that to a person. Of course, this one is also VERY easy to miss because, guess what? Being in the hospital is anxiety-producing all on its own. Oh boy…sounds like it’s going to be really tough to catch shock in the initial phase, huh?

The next stage is what we call compensatory shock (Class II). The body really kicks into high gear to compensate at this point, and this is the stage where you’re most likely to catch on that your patient is in trouble.

  • The decreased tissue perfusion triggers an endocrine response that tells the SNS it needs to join the party. What happens when the SNS is activated?
    • Increased heart rate: now your increase will most likely get noticed as it will be more significant than in the initial stage. This increase in heart rate helps keep cardiac output up.
    • Vasoconstriction: By squeezing down on the vessels, we can help keep blood pressure up (remember the garden hose analogy from this post?) This is a result of the renin-angiotensin system you learned about in A&P (hint: angiotensin II is a pretty potent vasoconstrictor!)
    • Increased respiratory rate: that mild tachypnea has progressed and now your patient is breathing in the high 20s-low 30s. No bueno. This is the body’s attempt to compensate for two things: lower oxygen levels and the metabolic acidosis caused by all that lactate production
    • Increased glucose via glucogenolysis: have you checked a blood sugar lately? An elevated blood sugar in a NON-diabetic patient is definitely cause for concern
    • Decreased urine output: endocrine system gets hip to the fact that we’re in trouble, so it puts out more ADH (antidiuretic hormone) which causes the kidneys to retain fluid in an effort to keep BP optimized. Recall that optimal urine output is 0.5mg/kg/hr. If your patient is putting out less than this, you gotta let somebody know. Another cause for decreased urine output is hypoperfusion of the kidneys, so this is definitely something you want to watch like a hawk.
    • Decreased bowel sounds: the body will shunt blood from the less vital organs in order to perfuse the brain and heart. If your patient’s gut isn’t making a lot of noise, this could be the reason.
    • Delayed capillary refill and cold extremities: here we are again with the poor skin perfusion, only at this stage it is likely to be more obvious.
    • May see diaphoresis at this point and the patient is often agitated and/or restless.

In progressive shock (Class III), you patient is in a very bad way. The compensatory mechanisms are starting to fail and hemostasis cannot be maintained. You will likely see:

  • Hypotension: if you are seeing hypotension, this is typically a late sign and you might be kicking yourself that you didn’t pick up on the earlier clues. Don’t beat yourself up…sometimes the patient transitions through the stages of shock very quickly.
  • Altered LOC: your patient has progressed from being restless or agitated to being really confused or lethargic.
  • Increased RR and WOB: as the global hypoxia continues, your patient will try to make up for it by breathing faster and harder. Many patients get intubated at this point as this level of respiratory effort is not sustainable.
  • Lactic acidosis: as those waste products build up, you’ll see an elevated lactate and an acidic pH.
  • Continued progression of all the other signs: tachycardia, decreased urine output, poor skin perfusion. At this stage the patient is looking at multiple organ dysfunction (MODS)

In the final stages of shock, called refractory shock (Class IV), it’s going to be very difficult to save the patient. It is called “refractory” because it is typically not responsive to treatments.

  • Decreased LOC (possibly obtunded)
  • Urine output very very very low (usually > 5ml/hr)
  • Respiratory rate is going to be pretty high…usually above 35. The patient cannot sustain this for long, so if he’s not intubated you might want to call the doc.
  • Skin signs are VERY poor at this point…most likely to see mottling at this stage.
  • Blood pressure low despite fluids and vasoactive medications
  • Low O2 sats despite oxygen; patient may be on max ventilator settings at this point

General treatment for shock

The treatment for all shock states is generally the same with a few differences relative to the shock classification. The idea is to stabilize the patient as much as you can with broad-based treatment and then target your therapies based on what is specifically happening with the patient.

  • Optimize oxygen delivery
    • Provide oxygen! Many patients will need to be intubated, but if you catch shock early, you may be able to give O2 via a mask or even a high-flow nasal cannula. The sicker they are, the more likely they’ll get themselves an ET tube.
    • Restore volume! Give fluids and/or PRBCs to fill up that bucket.
    • Medications (will depend on type of shock the patient is experiencing).
  • Reduce oxygen consumption
    • Decrease WOB (intubate or give oxygen!)
    • Treat pain, treat anxiety
    • Keep patient normothermic (shivering increases oxygen demands as does fever)
    • Decrease oxygen demands with mechanical ventilation, sedation, or even neuromuscular blocking agents like Nimbex or Vecuronium.

Signs and treatment of hypovolemic shock

As you recall, hypovolemic shock means the bucket does not have enough fluid in it. This can be due to hemorrhage or non-hemorrhagic causes. Common signs associated with hypovolemic shock include:

  • Decreased cardiac output (normal is 4-8L/min)
  • Increased SVR (normal is 900-1300)
  • Decreased CVP (normal is 2-6 mmHg)
  • Cool skin, delayed cap refill
  • Low BP, low urine output
  • Tachycardia

Treatments for hypovolemic shock:

  • To improve oxygen delivery in hypovolemic shock, you’ll fill up the bucket! If it’s due to blood loss, give blood…if it’s due to fluid loss (vomiting, burns, diarrhea, polyuria), then you’ll give fluid!
  • Identify and treat the source of the loss. If your patient is bleeding, they need intervention STAT! If they’re vomiting uncontrollably, try to fix it (Zofran, Reglan, Phenergen are all common medications). If it’s due to polyuria, are they in diabetes insipidus? You get the idea.
  • Ensure your patient has two large-bore IVs at all time…may need a central line as well.
  • Monitor your patient for improvements in HR, BP and urine output. You’ll typically see the heart rate improve first, then the blood pressure, then urine output last.

Signs and treatment of distributive shock

In distributive shock, the causes are so varied that your targeted treatment is going to be pretty different depending on what’s causing it. The signs will also vary as well, but let’s just talk about a few of the most common ones (anaphylactic, septic and neurogenic).

Anaphylactic shock occurs with massive allergic reactions. Large amounts of vasoactive substances are released from mast cells causing systemic vasodilation and increased capillary permeability. The result is a sudden and global drop in blood pressure. The most acute problem your patient has is the respiratory  compromise that accompanies the reaction.

Signs of anaphylactic shock

  • In addition to hypotension and tachycardia…
  • Wheezes, hives, uticaria, itching, cutaneous flushing
  • Tightness in chest, throat swelling/fullness

Additional treatment for anaphylactic shock

  • Maintain the airway (get that ETT in there!)
  • Epinephrine epinephrine epinephrine
  • Fluids to support blood pressure
  • Histamine blockers (Pepcid, Tagamet, Benadryl)
  • Bronchodilators
  • Steroids to reduce airway inflammation

Septic shock occurs in cases of severe infection that trigger a complex series of events leading to massive vasodilation and increased capillary permeability. The result is hypotension and global tissue hypoxia.

Signs of septic shock

  • Elevated temperature above 38 (note that the elderly, young children and immunocompromised may show low temps below 36)
  • Tachycardia (sepsis screening triggers at HR > 90) and tachypnea
  • Elevated WBC or very low WBC
  • Decreased CVP and SVR
  • Hypotension despite fluid resuscitation

Additional treatment for septic shock

  • When a patient screens positive for sepsis they’re going to get fluids. We classify them as in “septic shock” when their hypotension persists despite getting all these fluids (30ml/kg)
  • Vasopressors (levophed is first, then vasopressin, then epinephrine and phenylephrine) to increase SVR and, ultimately, blood pressure.
  • Antibiotics (control the source of the infection…this is KEY!!!)

Neurogenic shock occurs in patients with spinal cord injury and is due to a loss of sympathetic innervation. It’s more likely to present in patients with an injury at C3-C5 level. In

Signs of neurogenic shock

  • Massive vasodilation and decreased venous return leading to decreased SVR, CVP, CO and PAWP
  • Decreased HR (recall that the PNS is now driving the train!)
  • Pooling of blood in vessels
  • Warm, flushed skin
  • Hypotension with wide pulse pressure

Additional treatment for neurogenic shock

  • Obviously, if this is a new spinal cord injury you’ll work with your team to stabilize the spine. Your patient will be on a backboard and be wearing a c-spine collar. Hopefully you’re at a trauma center. Spine stabilization is key to getting the SNS working again.
  • IV fluids to help restore preload
  • Vasopressors to support the blood pressure
  • Treat bradycardia as needed

Signs and treatment of cardiogenic shock

Cardiogenic shock is a pump problem! The heart has failed and is no longer able to pump adequately. The signs will be specific to whatever is causing the pump to fail, but one of the most common is left-sided heart failure. And since right-sided heart failure is a common cause of left-sided heart failure we’ll talk about both here:

  • Left-sided heart failure (thinks about where blood is coming from BEFORE it gets to the left-side and this will help you remember the pathophysiology…it’s the lungs, so this where the fluid backs up!)
    • Pulmonary congestion
    • Dyspnea
    • Coarse lung sounds
    • Distant heart sounds
    • Elevated PAWP
    • Low cardiac output
  • Right-sided heart failure (before blood gets to the right side, it’s in the systemic vasculature so this is where it backs up)
    • Systemic venous congestion and peripheral edema
    • Elevated CVP
    • Jugular venous distention (JVD)
    • Normal or low PAWP

Treatment for cardiogenic shock

  • Reduce myocardial oxygen demand while improving oxygen supply
  • Give fluids (unless pt is fluid overloaded)
  • Inotropes to improve cardiac output
    • Dobutamine or dopamine
    • Milrinone to also decrease afterload (has vasodilatory effects)
  • Possibly give diuretics to remove excess fluid
  • Vasopressors to increase BP via vasoconstriction
  • Very sick patients may need an IABP
  • In the cases of myocardial infarction, patient needs revascularization

Signs and treatment of obstructive shock

Whenever there is a THING obstructive blood flow in the great vessels or the heart itself, we consider this obstructive shock. This “thing” can be fluid around the heart (cardiac tamponade), a tension pneumothorax that’s putting pressure on the heart and great vessels, or a blood clot in the lungs (pulmonary embolism). The signs/symptoms can vary based on the cause of the obstruction:

  • Signs of pulmonary embolism
    • SOB, increased WOB, tachypnea, dropping O2 sats
    • Feeling of impending doom
    • Chest pain
    • Cough with or without hemoptysis
    • Pulsus paradoxus (SBP increases on expiration, drops on inspiration by 10mmHg or more)
  • Signs of tension pneumothorax
    • Drop in BP due to decreased venous return
    • Increased SOB and WOB; drop in O2 sats
    • Displaced trachea if it’s really bad
    • Decreased or absent lung sounds on the side of the pneumothorax
  • Signs of cardiac tamponade
    • Beck’s triad: elevated CVP, decreased BP, muffled heart tones
    • PEA (pulseless electrical activity)…obviously this is a very bad sign!
    • Pulsus paradoxus

Treatment for obstructive shock

The goal with obstructive shock is to remove the thing causing the obstruction…easy enough, right?

  • Tension pneumothorax gets a needle decompression and/or chest tube
  • Cardiac tamponade needs a pericardiocentesis
  • Pulmonary embolism needs heparin, thrombolytic therapy and/or an IVC filter

Miscellaneous nursing interventions for a patient in shock

In addition to recognizing and treating each various type of shock, there are a few other general things you’ll want to do for a patient heading down this road:

  • Foley catheter so you can monitor urine output very closely
  • Anticipate a fair amount of lab studies…CBC, coags, chemistry, cardiac enzymes, ABG, lactate and blood cultures
  • Make sure the patient is on a cardiac monitor (and get a 12-lead while you’re at it)
  • Anticipate the MD placing a central line, pulmonary artery catheter and/or an arterial line
  • Set up hemodynamic monitoring lines (CVP, ABP, etc)

Most of all, don’t be afraid to voice your concerns for your patient. Even small changes can indicate a worsening shock state, so keep on top of your thorough assessments and advocate fiercely for your patient. You’ll do great!


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The basics of shock for nurses