Perfusion and Shock: Cardiac Output, the Types of Shock, and Compensated vs Decompensated
What perfusion and cardiac output are, the four types of shock and how each looks in the field, and why compensated shock hides behind a normal blood pressure.
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Perfusion is the delivery of oxygenated blood to the body's tissues, and the removal of their waste, through the capillaries. Shock is inadequate perfusion: the cells are not getting enough oxygen to meet their needs, whatever the cause. Shock is not defined by a blood pressure. A patient can be in shock with a normal blood pressure, and recognizing them at that stage is much of the work of a field provider.
What perfusion means
In plain terms, perfusion is blood flowing through tissue. Adequate perfusion needs three things working together, often taught in EMS as the perfusion triangle: a pump (the heart), enough fluid (blood volume carrying oxygen on its hemoglobin), and the pipes (blood vessels with the right tone to hold pressure and direct flow). Each type of shock is a failure of one side of that triangle, or more than one.
When cells are under-perfused they switch from aerobic to anaerobic metabolism. That produces far less energy and makes lactic acid as a byproduct. Left uncorrected, cells stop working, then tissues, then organs. That is why shock is time-critical even while the patient still looks reasonably well.
Cardiac output: heart rate times stroke volume
Cardiac output is the volume of blood the heart pumps in one minute. It is the heart rate (beats per minute) multiplied by the stroke volume (the volume the left ventricle ejects with each beat). Standard physiology textbooks give a normal resting adult cardiac output of roughly 4 to 8 liters per minute, about 5 for a typical adult at rest, and it rises several-fold during hard exercise.
Cardiac output, and how a faster heart rate compensates (illustrative figures)
Given
- A resting adult with a heart rate of 70 beats per minute
- A stroke volume of 70 mL per beat (an illustrative textbook figure, not a measurement you take in the field)
- The same patient after blood loss: stroke volume down to 40 mL, heart rate up to 120
Steps
- Cardiac output = heart rate x stroke volume.
- At rest: 70 x 70 mL = 4,900 mL per minute, about 4.9 liters per minute.
- After blood loss: 120 x 40 mL = 4,800 mL per minute, about 4.8 liters per minute.
- The stroke volume fell by more than a third, yet the output barely changed, because the heart rate rose to make up the difference. That is compensation, and it is why a fast heart rate is an early sign of shock.
- There is a limit. At very fast rates the ventricle has less time to fill between beats, stroke volume falls further, and output drops.
About 4.9 liters per minute at rest and about 4.8 after blood loss: the rising heart rate held the output up while the stroke volume fell.
Training aid only. Verify every value against your local protocol and medical direction before acting on it.
What changes stroke volume
| Factor | What it means | What lowers stroke volume through it |
|---|---|---|
| Preload | How much the ventricle is stretched by the blood returning to it before it contracts. Within limits, more filling gives a stronger contraction (the Frank-Starling mechanism). | Too little returning blood: bleeding, dehydration, blood pooling in dilated vessels, a tension pneumothorax or cardiac tamponade blocking return, and positive-pressure ventilation. |
| Afterload | The resistance the ventricle pumps against, set mostly by the tone of the arteries. | A high afterload makes a weak ventricle work harder and can lower its output. Afterload falls in distributive shock as the vessels dilate. |
| Contractility | The strength of the squeeze, independent of how full the ventricle is. | A heart attack, cardiomyopathy, severe hypoxia or acidosis, and an overdose of a drug that depresses the heart, such as a beta blocker. |
Blood pressure is approximately cardiac output multiplied by systemic vascular resistance, the resistance of all the blood vessels together. That relationship explains a great deal of what you see in shock. When output falls, the body tightens its blood vessels to raise resistance, and the blood pressure can hold steady even while perfusion is failing.
Calculate a mean arterial pressure from a blood pressure
The types of shock
Most EMS and medical texts group shock into four categories by which part of the circulation has failed. Some list septic, anaphylactic and neurogenic shock as separate types instead of grouping them as distributive, but the physiology is the same.
| Type | What has failed | Common causes | Field picture |
|---|---|---|---|
| Hypovolemic | Not enough volume in the circulation | Bleeding (trauma, gastrointestinal bleeding, a ruptured aortic aneurysm, an ectopic pregnancy) and fluid loss (vomiting, diarrhea, burns, DKA) | Pale, cool, clammy skin; fast, weak pulse; flat neck veins; a narrowing pulse pressure; thirst and anxiety |
| Cardiogenic | The pump | Heart attack, a heart rate that is too fast or too slow, cardiomyopathy, a failing valve | Cool, clammy skin; often shortness of breath and crackles as fluid backs up into the lungs; distended neck veins; chest pain or an abnormal rhythm |
| Obstructive | Blood flow is physically blocked | Tension pneumothorax, cardiac tamponade, a massive pulmonary embolism | Low blood pressure with distended neck veins, plus clues to the cause: absent breath sounds on one side and difficulty ventilating (tension), muffled heart sounds (tamponade), sudden breathlessness and low oxygen saturation (embolism) |
| Distributive | The vessels lose their tone and blood pools in the wrong places | Sepsis, anaphylaxis, spinal cord injury (neurogenic shock) | Varies by cause; often warm, flushed skin early, a low diastolic pressure and a wide pulse pressure |
Hypovolemic and hemorrhagic shock
Hemorrhagic shock, from bleeding, is the most common shock in trauma. External bleeding is obvious; internal bleeding is not. Blood can be lost into the chest, the abdomen, the pelvis and around broken long bones such as the femur, with little to see from the outside. Non-hemorrhagic hypovolemia comes from losing fluid rather than blood, and develops more slowly.
The ATLS (Advanced Trauma Life Support) course for physicians teaches four classes of hemorrhage by the share of blood volume lost. The classes are a teaching device that shows how compensation hides blood loss, not a scale to grade a real patient against. Real patients, especially older patients, athletes and anyone on a beta blocker, often do not follow them neatly.
| Class | Approximate blood volume lost | What tends to happen |
|---|---|---|
| I | Up to 15% | Little or no change in the vital signs |
| II | 15 to 30% | The heart rate rises, the pulse pressure narrows and the patient is anxious, but the systolic pressure is usually maintained |
| III | 31 to 40% | The systolic pressure falls, the heart rate is high and the mental status changes |
| IV | Over 40% | Marked hypotension, a very fast or absent peripheral pulse, and lethargy or unresponsiveness; immediately life-threatening |
Cardiogenic shock
Cardiogenic shock means the heart cannot pump enough blood even with enough volume in the system. The most common cause is a large heart attack. A rhythm that is too fast or too slow can also produce it, and correcting the rhythm may correct the shock. Because the failing ventricle cannot move what it already has, fluid can back up into the lungs; a patient in cardiogenic shock can be harmed by fluid that would help a bleeding patient, which is one reason fluid decisions belong to your protocol.
Obstructive shock
In obstructive shock the heart and the volume may both be fine, but something stops blood getting into or out of the heart: air under pressure in the chest (tension pneumothorax), fluid or blood in the sac around the heart (cardiac tamponade), or a clot blocking the pulmonary arteries (massive pulmonary embolism). The treatment is relieving the obstruction. Decompressing a tension pneumothorax is within paramedic scope in many systems under protocol; tamponade and a massive embolism need a hospital, fast.
Distributive shock: septic, anaphylactic and neurogenic
- Septic shock: an infection triggers a body-wide response that dilates vessels, makes them leak and depresses the heart. Look for fever or a low temperature, fast breathing, altered mental status and a source of infection. Early on the skin may be warm and flushed; later it becomes cool and mottled. Older patients may have no fever at all.
- Anaphylactic shock: a severe allergic reaction dilates the vessels and makes them leak, often with hives, swelling of the lips, tongue or throat, wheezing or stridor, and vomiting. Skin signs are absent in some patients. Epinephrine is the first-line treatment in every major anaphylaxis guideline; the dose and route are your protocol's. Give it as soon as anaphylaxis is recognized. Do not wait for low blood pressure or for skin signs.
- Neurogenic shock: an injury to the spinal cord, typically in the neck or upper back at about the sixth thoracic level or above, cuts the sympathetic nerves that keep the vessels toned and the heart rate up. The result is low blood pressure with a normal or slow heart rate, and warm, dry skin below the injury. It is not the same as spinal shock, which is the temporary loss of reflexes and function below a cord injury.
The Sepsis-3 definitions of 2016 introduced qSOFA, a quick bedside score that flags an adult with suspected infection who is at higher risk of a poor outcome: one point each for a respiratory rate of 22 or more, altered mentation and a systolic pressure of 100 mmHg or less, with 2 or more counting as higher risk. It is not a diagnosis. A score below 2 does not rule sepsis out, and qSOFA is not validated in children. The Surviving Sepsis Campaign's 2021 guideline recommends against using it alone as a screening tool for sepsis. Your protocol's sepsis criteria are the ones your service screens with.
Score qSOFA for an adult with suspected infection
Compensated vs decompensated shock
When perfusion starts to fall the body fights back. The sympathetic nervous system speeds the heart, strengthens its contraction and tightens the blood vessels in the skin, gut and kidneys to send what blood there is to the heart and brain. Breathing speeds up. Hormones tell the kidneys to hold on to fluid. Most of what you see in early shock is this compensation, not the shock itself.
| Stage | What is happening | What you see |
|---|---|---|
| Compensated | Perfusion is falling, but the body's responses are holding the blood pressure up | Anxiety or restlessness, a fast heart rate, fast breathing, pale, cool, clammy skin, delayed capillary refill, a narrowing pulse pressure, thirst, and a normal systolic pressure |
| Decompensated (progressive) | The compensation is failing and the blood pressure falls | A falling systolic pressure, worsening mental status from confusion to unresponsiveness, weak or absent peripheral pulses, mottled or bluish skin, little or no urine |
| Irreversible | Cells and organs are damaged beyond recovery, even if circulation is restored | Cannot be identified with confidence in the field, which is why shock is treated early and aggressively |
Why blood pressure falls late
Blood pressure depends on both the output of the heart and the resistance of the vessels. In compensated shock, the vessels clamp down and the heart beats faster, so the pressure stays normal while the tissues are already short of blood. By the time the systolic pressure falls, compensation is failing, and in the ATLS teaching a patient has typically lost around a third of their blood volume by then.
- Children compensate strongly and for a long time, then deteriorate abruptly. Low blood pressure in a child is a late, ominous sign.
- Older adults have less reserve and may decompensate sooner, and their usual blood pressure may be high, so a normal-looking reading can be low for them.
- Beta blockers, other rate-controlling drugs and pacemakers can stop the heart rate rising, removing one of the earliest signs.
- In pregnancy the circulating volume increases, so a pregnant patient can lose a large amount of blood before the vital signs change, and the fetus may be under-perfused first.
- Fit, young adults compensate well and may look deceptively stable.
Recognizing shock in the field
- Mental status: the brain is sensitive to falling perfusion. Anxiety, restlessness and confusion are early signs; drowsiness and unresponsiveness are late ones.
- Skin: color, temperature and moisture. Pale, cool and clammy skin is typical of hypovolemic, cardiogenic and obstructive shock; warm, flushed skin is common early in distributive shock. Mottling is a late sign. In darker skin, look at the inside of the lips, the gums, the nail beds and the inner eyelids for pallor.
- Capillary refill: the commonly taught upper limit is about 2 seconds. It is most useful in children; cold surroundings and older age make it unreliable in adults.
- Heart rate: a fast heart rate is one of the earliest signs of compensation. A slow heart rate in a shocked patient is a late, dangerous sign, especially in a child, unless it is explained by neurogenic shock, medication or a pacemaker.
- Respiratory rate: fast breathing appears early, as the body responds to acid and low oxygen delivery.
- Blood pressure and pulse pressure: the pulse pressure is the systolic minus the diastolic. A narrowing pulse pressure, as the diastolic rises with vasoconstriction, is an early sign in hypovolemic, cardiogenic and obstructive shock. A low diastolic pressure and wide pulse pressure suggest distributive shock. The trend over several readings tells you more than any one reading.
- Pulses: a weak, thready or absent radial pulse with a present central pulse suggests poor perfusion. The old rule of thumb that ties a palpable pulse at each site to a particular systolic pressure is not reliable and should not replace a measured pressure.
- Monitoring: the pulse oximeter may give a poor or no reading when peripheral perfusion is poor. A falling EtCO2 with unchanged breathing can reflect a falling cardiac output.
Shock index
The shock index is the heart rate divided by the systolic blood pressure. It reflects the point where the heart rate has risen and the pressure is starting to give, sometimes before either number looks alarming on its own. Emergency department studies by Rady and colleagues in the 1990s are the usual source for a normal adult range of about 0.5 to 0.7 and for an index above 0.9 being associated with critical illness; some trauma studies use 1.0. It is a ratio, not a diagnosis. A normal index does not rule out shock. Beta blockers and pacemakers hold the index down with the heart rate, the adult range does not apply to children, and the adult range does not apply in pregnancy, where the index runs higher.
Calculate the shock index from a heart rate and a systolic pressure
Field priorities
The principles below are taught in every EMS curriculum. How each one is carried out, and every fluid volume, blood pressure target and medication, is set by your protocol and your medical direction.
- Stop life-threatening external bleeding first: firm direct pressure, a tourniquet for life-threatening bleeding from a limb, and wound packing for a junctional wound where you are trained. Many trauma approaches put massive bleeding ahead of the airway for this reason.
- Airway, breathing and oxygenation: keep the airway open, give oxygen to a patient who is hypoxic or critically ill, and assist ventilation if breathing is inadequate. Do not over-ventilate: positive-pressure breaths lower the return of blood to the heart.
- Position: lay the patient supine unless the airway or breathing needs another position, such as the recovery position for a patient at risk of aspiration with no suspected spinal injury. Tipping the patient head-down (Trendelenburg) is not recommended. A patient struggling to breathe, such as one in cardiogenic shock with fluid on the lungs, may need to sit up. In late pregnancy, manually displace the uterus to the left or tilt the patient to the left so the uterus does not compress the vena cava.
- Keep the patient warm: cover them, warm the ambulance and limit exposure. Hypothermia worsens bleeding, and with acidosis and impaired clotting it forms what trauma teaching calls the lethal triad.
- Treat a cause you can treat: a tension pneumothorax, anaphylaxis or an unstable rhythm can each be addressed in the field under protocol, including epinephrine for anaphylaxis without delay.
- Vascular access and fluids as your protocol directs. Many trauma protocols limit fluid before bleeding is controlled and accept a lower-than-normal pressure (permissive hypotension), some systems carry blood, a patient in cardiogenic shock may be harmed by fluid, and a patient with a head injury is commonly an exception to accepting a low pressure. Every figure in those decisions is your protocol's.
- Transport without delay. Do procedures en route where you can, tell the receiving facility early, and let your protocol decide the destination.
- Reassess often: mental status, skin, heart rate, blood pressure and pulse pressure, and the trend between them.
The short version
- Perfusion is blood flow delivering oxygen to the tissues. Shock is perfusion too poor to meet the cells' needs, and it is not defined by blood pressure.
- Cardiac output is heart rate times stroke volume, roughly 4 to 8 liters per minute in a resting adult. Stroke volume depends on preload, afterload and contractility.
- The four types of shock: hypovolemic (volume), cardiogenic (pump), obstructive (blockage) and distributive (vessel tone: septic, anaphylactic, neurogenic).
- Compensated shock keeps the blood pressure normal with a fast heart rate and tight vessels. Decompensated shock is when the pressure falls, and that is late.
- Look at mental status, skin, capillary refill, heart rate, pulse pressure and the shock index, and trend them.
- Stop the bleeding, support the airway and oxygenation, lay the patient supine unless the airway or breathing needs another position, keep them warm and transport. Fluids, pressure targets and drugs are your protocol's.