1. Description of the problem

What every clinician needs to know

There is no consensus on the absolute definition of a “low cardiac output state.” It is a syndrome evidenced by a low cardiac output or cardiac index (cardiac index <2.4L/min/m2) with evidence of organ dysfunction—for example, a high lactate or urine output <0.5 ml/kg/hour. There is a continuum from a low-cardiac-output state to cardiogenic shock.

The European Society of Cardiology (ESC) defines cardiogenic shock as “evidence of tissue hypoperfusion induced by cardiac dysfunction after correction of preload.” It is usually characterized by:

  • Systolic blood pressure of <90 mmHg (or a drop of >30 mmHg)

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  • Urine output of <0.5 ml/kg/hour

  • Heart rate >60 beats per minute

  • With or without evidence of congestion

The underlying cause of the myocardial dysfunction may be primarily cardiac or extracardiac. It may represent an acute deterioration in a patient with known chronic heart failure or it may be a transient and reversible episode with resolution of the acute trigger; it may, however, induce permanent damage leading to chronic heart failure.

Broadly, cardiac dysfunction can result from any cardiac structural disorder or functional disorder that disrupts cardiac filling or emptying.

Cardiac dysfunction results in a reduced cardiac output; the consequences of this are an imbalance between oxygen supply and demand in the tissues. The oxygen delivery by the heart to the tissues is not enough to keep up with cellular metabolic requirements. In essence, the tissues are starving for oxygen and nutrients.

In intensive care populations, other disease processes, such as sepsis, can further complicate the clinical picture.

The low-cardiac-output state can be thought of as the final common pathway of a multitude of diseases that affect the heart – it is a clinical syndrome. It is not enough to make the diagnosis of the low-cardiac-output state and it should NEVER be the final diagnosis – the underlying cause/trigger must be found and treated if possible.

It is a life-threatening condition that requires prompt recognition and treatment in order to preserve the oxygen supply to the myocardium and rest of the tissues while reducing the myocardial oxygen demand. If this does not occur a spiral of tissue hypoxia, increasing acidosis, worsening myocardial function and multiple organ dysfunction will lead to the patient’s death.

Clinical features of the condition
  • Fatigue, confusion, agitation and/or decreased level of consciousness

  • Cool peripheries, mottled peripheries and delayed capillary refill time

  • Hypotension

  • Tachycardia or bradycardia

  • Thready pulse

  • Raised jugular venous pressure

  • Breathlessness and hypoxaemia

  • Evidence of pulmonary and peripheral edema

  • Oliguria or anuria

  • Metabolic acidosis

Key management points

(Figure 1)

Figure 1.

Flowchart for Treating Low Cardiac Output

The main reason for hospitalization of patients with worsening or acute heart failure is related to symptoms of congestion. However, in some patients the dominant manifestations are of reduced cardiac output and tissue hypoperfusion with or without congestion. Immediate goals in the emergency treatment are:

  • Resuscitate the patient

  • Recognize the condition

  • Restore oxygenation

  • Improve organ perfusion and hemodynamics – optimize stroke volume and cardiac output

  • Improve symptoms

Subsequent goals of acute management are:

  • Optimal monitoring and support

  • Establishing the cause of reduced cardiac output; treat reversible causes.

2. Emergency Management

As with any acutely unwell patient, emergency management begins with assessment of ABC – airway, breathing and circulation.

Basic non-invasive monitoring should begin as soon as the patient arrives in the emergency department and/or as soon as the patient is identified, wherever in the hospital he or she may be:

  • Non-invasive blood pressure

  • Heart rate/ECG

  • Pulse oximetry

  • Respiratory rate

  • Temperature

  • Urine output

While none of these measurements will give you a direct measurement of cardiac output, together with clinical examination they provide useful information regarding peripheral perfusion.

If possible a focused history and a physical examination should be obtained, paying particular attention to:

  • Peripheral perfusion (including acid-base balance and lactate)

  • Auscultation of heart sounds and presence/absence of added sounds

  • Auscultation of lungs for pulmonary congestion

  • Jugular venous pressure as an indication of right heart filling pressures


The most likely reason that the airway would be compromised is a decreased level of consciousness secondary to decreased cerebral perfusion.

Oropharyngeal or nasopharyngeal airways may be useful airway adjuncts and may be all the support that is required; however, endotracheal intubation may be necessary if the patient is not protecting the airway despite these maneuvers.


Supplemental oxygen should be administered in as high a concentration as tolerated in order to maximize oxygen delivery to the tissues (care must be taken in patients with concomitant COPD with a hypoxemic drive to breathe). Aim for arterial oxygen saturations of greater than or equal to 95%.

If there is failure to achieve adequate oxygenation with high flow oxygen, continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation (NIPPV) should be used.

  • Start at a PEEP 5-7.5 cmH2O.

  • If using NIPPV start with an inspiratory pressure 12cmH2O and expiratory pressure (PEEP) of 5-7.5cmH2O.

Advantages of CPAP and NIPPV include:

  • Alveolar recruitment leading to improvement in gas exchange and therefore oxygenation

  • Reduction in work of breathing and hence respiratory muscle oxygen demand

  • Improves functional residual capacity

  • Increase in intrathoracic pressure leads to a reduction in left ventricular afterload and transmural filling pressures, resulting in improved cardiac output.

Patients who do not improve with these measures may go on to need intubation and ventilation. This will have the advantage of resting respiratory muscles and thereby decreasing oxygen requirements.

What needs to be borne in mind is that these patients may deteriorate precipitously from a cardiovascular point of view on administration of anesthetic agents due to loss of sympathetic drive. Intubation should be carried out in a controlled environment with experienced/senior colleagues in attendance, cardiovascular monitoring in place and drugs able to manipulate hemodynamics on hand (e.g., atropine, ephedrine and metaraminol).


You should have basic monitoring in place by now.

Blood pressure is an “indicator” of organ perfusion but is an insensitive hemodynamic parameter. Mean arterial pressure (MAP) best approximates organ perfusion in non-cardiac tissues. A reduction in blood pressure due to reduced cardiac output will only be seen once compensatory mechanisms have been exhausted. There is no blood pressure that defines adequate organ perfusion, but for practical purposes a MAP of <65 mmHg is considered pathological. In patients who are normally hypertensive a MAP of >65 mmHg may be needed for organ perfusion.

A better way of assessing the circulation in low-cardiac-output states is to assess the adequacy of peripheral perfusion and oxygen delivery (see box 1) and to consider the equation below:

Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

– this is the volume of blood pumped to the circulation per minute.

Stroke volume is in turn dependent on preload, contractility and afterload, factors that are all interdependent.

Heart rate also affects these variables. Optimizing all of these factors will improve cardiac output.

Stabilizing and improving the circulation will depend partly on the cause of the low cardiac output and which of the above elements is compromised. For example, a patient post cardiac bypass for an aortic valve replacement may have a low cardiac output for several reasons:

  • Reduced preload (decreased intravascular volume post surgery)

  • Reduced myocardial contractility (post cardiac bypass)

  • Reduced heart rate (post surgery near AV node and hypothermia)

  • Increased afterload (increased systemic vascular resistance due to pain and/or vasoconstriction secondary to hypothermia)

All of these contributors to the cardiac output need to be addressed; in practice one may predominate more than the others.

The “circulation” variables that contribute to the cardiac output and that need to be considered and manipulated if required in low cardiac output states are:

  • Heart rhythm and rate

  • Preload

  • Afterload

  • Contractility

In the emergency situation it will be easier to assess some of these parameters than others — for example, heart rate and rhythm are relatively straightforward, whereas assessing and manipulating contractility takes more specialized monitoring and investigation and may not be available in the emergency department or ward but should be available on an intensive care unit.

1. Heart rate and rhythm

Cardiac output = Heart rate x Stroke volume

Increasing your heart rate will increase your cardiac output up to a point, and therefore a high heart rate may be appropriate in your patient who has a low cardiac output, as part of the body’s physiological response. A heart rate that is too fast or slow, however, will detrimentally affect the cardiac output.

Tachycardias lead to reduced time spent in diastole – this is the part of the cardiac cycle during which ventricular relaxation, filling and coronary blood flow occur. Above a heart rate of approximately 100 beats per minute, this leads to impaired coronary perfusion and oxygen delivery to the myocardium and potentially myocardial ischemia; impaired ventricular relaxation and filling and therefore a reduction in stroke volume and cardiac output. Sinus tachycardia in low cardiac output may be multifactorial:

  • Pain and/or anxiety

  • Restlessness/agitation

  • Respiratory distress and hypoxia

  • Physiological response to low cardiac output

If your patient is distressed, in pain, restless and dyspneic, morphine may be a useful drug. It relieves dyspnea and pain and may decrease agitation. It is also a mild venodilator (reducing afterload). Morphine administration may lead to a decrease in heart rate and increased cooperation, which may be especially useful if you are using CPAP or NIPPV.

  • Morphine bolus 2.5 mg IV can be given.

  • Antiemetics should always be given along with opiates.

  • Use CAUTION when giving opiates to those who: (a) are hypotensive; (b) have a reduced Glasgow Coma Scale score; (c) have high CO2 levels; and (d) have bradycardia.

A bradycardia may be the primary cause of low cardiac output. Hypothyroidism, hypothermia, drugs such as beta blockers and calcium channels blockers, inferior myocardial ischemia and conduction system dysfunction may all cause significant bradycardia.

If the heart rate is less than 40 bpm with evidence of hemodynamic compromise and/or impaired cardiac output, then efforts must be made to increase the heart rate:

  • Atropine 300-mcg boluses up to 1 mg

  • Glycopyrrolate 200-mcg boluses

  • Transcutaneous pacing (normally as a bridge to more definitive treatment only)

  • Transvenous pacing (requires an experienced operator)

  • Specific therapies are available for bradycardia secondary to excess digoxin, beta blockers, and calcium channel antagonists.

Dysrhythmias can lead can lead directly to low cardiac output or merely be a contributing factor. Patients who have ventricular tachycardia, supraventricular tachycardia or rapid atrial fibrillation with evidence of cardiovascular compromise (hypotension, myocardial ischemia or pulmonary edema/congestion, poor perfusion) should have urgent electrical cardioversion.

In patients whose rhythm is atrial fibrillation (or who have developed atrial fibrillation), the loss of the atrial kick as a contribution to left ventricular end-diastolic volume and hence stroke volume in certain populations (the elderly and those with preexisting cardiac failure) will significantly decrease cardiac output by up to 30%. They therefore may tolerate atrial fibrillation poorly and should also be considered for urgent cardioversion in order to optimize stroke volume.

2. Preload

End-diastolic ventricular volume acts as the preload for the ventricle. We know from Starling’s law of the heart that increasing ventricular filling and end-diastolic volume increases the amount of myocardial fiber stretch prior to each contraction and thereby increases the force of that contraction and as a result stroke volume.

Our aim in reduced-cardiac-output states is to increase cardiac output and stroke volume without fluid overloading the patient; therefore, we need to be able to optimize preload. The question we are asking here is, “Will the stroke volume and cardiac output increase with fluid loading?” This may involve given a bolus of fluid, which may seem counterintuitive in patients with evidence of low cardiac output and of congestion.

How do we assess preload?

To be able to optimize preload we need to know how to measure it first! Traditionally central venous pressure (CVP, measured using a central venous line) has been used as a surrogate of right atrial pressure and preload. However, more recently this has been called into question. CVP measurement as an indication of preload and ventricular function has been shown to be of limited use in clinical practice, especially in low-cardiac-output states.

Indeed, CVP measurements do not predict pulmonary edema development in left ventricular failure. Absolute values of CVP are not useful and do not tell us whether a patient will respond to a fluid bolus, in terms of increasing his or her stroke volume and cardiac output. Monitoring CVP response to fluid boluses may be more useful and an increased and sustained rise in CVP may suggest that the patient is preload-optimized and should not have more fluid.

More sophisticated and advanced ways of assessing preload are available; the most established of these is the pulmonary artery catheter (PAC). PACs measure the pulmonary artery occlusion pressure (PAOP), which in turn provides you with an estimate of pulmonary venous pressure and left ventricular pressure. It does not, however, correlate with left ventricular end-diastolic volume. An added benefit is that they can also provide you with a measure of cardiac output, stroke volume, and mixed venous blood oxygen saturations.

PAOP has not, however, been demonstrated to be a good indicator of preload or preload responsiveness but is a good measure of back pressure and hydrostatic forces producing pulmonary edema. There is not a value of PAOP that has been shown to provide you with a maximal stroke volume. More usefully, some studies have shown that patients with a PAOP >18 mmHg do not benefit in terms of stroke volume from a fluid challenge in an attempt to optimize preload, and patients with PAOP <8 mmHg all showed an increase in stroke volume in response to a fluid challenge to optimize preload.

In more recent years devices that measure volume (as opposed to pressure) have been developed. Intrathoracic blood volume has been demonstrated to be a reliable preload index. Systolic blood pressure variation, pulse pressure variation and stroke volume variation using thermodilution and pulse contour analysis have also been shown to be good preload indices and predictors (in terms of stroke volume and cardiac output) of fluid responsiveness.

Patients have been demonstrated to exhibit greater cyclical changes in these parameters when the ventricle is operating on the steep part of the Starling curve, therefore providing an indication of preload status and likely response to a fluid challenge. A stroke volume variation of 10-15% in mechanically ventilated patients is thought to represent preload responsiveness.

PiCCO, which measures intrathoracic blood volume, also has the advantage of measuring extravascular lung water, which is a reflection of the degree of pulmonary edema in your patient. There are many other commercially available devices, including LiDCOplus, Vigileo, FloTrac; like the PAC they are able to provide continuous cardiac output monitoring.

Esophageal Doppler can also be used in ventilated patients to measure flow in the descending aorta and thereby estimate stroke distance and volume, cardiac output and flow time. Stroke volume variation can also be calculated. Transthoracic echocardiography uses the Doppler principle to calculate stroke volume and cardiac output and so can also be used to assess preload responsiveness.

In practice in the emergency department you may not have access to any of the devices that measure these parameters. You may have to assess whether you need to optimize preload clinically, and this can be very difficult, especially in patients with a low-cardiac-output state. Aspects of the clinical examination to pay particular attention to include:

  • Presence of thirst

  • Peripheral temperature

  • Capillary refill time

  • Blood pressure

  • Urine output

  • Lactate

  • Acid-base balance

In the intensive care unit you should be able to perform a fluid challenge to assess for preload responsiveness using one of the above-mentioned technologies. This is done by rapidly infusing 250 ml fluid (crystalloid or colloid) rapidly over 5 minutes. If there is a significant increase in stroke volume (>10%) or a reduction in stroke volume variation (<10%), then you should continue to give fluid boluses to optimize the preload until your patient is no longer fluid-responsive.

If you are concerned that your patient is congested and has pulmonary edema such that you do not want to give him or her any “excess” fluid that may be detrimental, you can do a passive leg raise – lifting the patient’s legs to 45 degrees. This empties a “fluid challenge” from the venous capacitance vessels into the circulating blood volume. If you achieve a favorable response you can then go on to give a “real” fluid challenge. If there is no response, then by lowering the legs you “reverse” your fluid challenge!

Don’t forget: “normal” individuals will be fluid-responsive! Your patient only needs to be preload-optimized if he or she has evidence of impaired peripheral perfusion!

3. Afterload

Afterload is the sum of all forces opposing ventricular emptying and reflects the resistance against which the ventricle is ejecting. Increases in the afterload cause an increase in work for the myocardium.

Afterload can be estimated as “systemic vascular resistance” and is calculated (ie, it is not measured) by cardiac output monitoring devices using the equation:
Systemic vascular resistance (SVR) = (MAP – CVP)/CO.

Normal values SVR 100-1500 dyne s/cm3. SVRI = 1970-2390 dyne s/cm5/m2

There is no evidence that titrating therapy to it is valuable.

A high afterload can be the cause of a low-cardiac-output state (eg, systemic hypertensive crisis or aortic stenosis). These patients can present with very high blood pressure or normal or low blood pressure, evidence of poor peripheral perfusion, and pulmonary edema. They need their afterload reduced.

This can be achieved by using a vasodilator in patients who have a systolic blood pressure of greater than or equal to 110 mmHg. Vasodilators are not recommended in those with a systolic BP less than 90 mmHg and a MAP less than 65 mmHg to avoid hypotension and further compromising organ perfusion. In those with low blood pressure inotropes may be the first line of treatment (see below).

A. Nitroglycerine infusion

  • Start 10-20 mcg/min and increase up to 200 mcg/min

  • Predominantly venodilator effect

  • Decreases systolic blood pressure

  • Decreases left- and right-sided filling pressures

  • Decreases systemic vascular resistance

  • Relieves pulmonary congestion

  • Does not increase myocardial oxygen demand or reduce stroke volume

B. Sodium nitroprusside infusion

  • 0.3 mcg/kg/min up to 5 mcg/kg/min

  • Balanced vasodilator

  • Combined preload and afterload reduction

  • Otherwise as above

C. Furosemide

  • Should only be used in patients who are fluid overloaded!

  • Patients with low cardiac output are often intravascularly fluid deplete and diuresis is not the treatment they need.

  • However, some patients, especially those with underlying chronic heart failure, may have inappropriate sodium and water retention, leading to “fluid overload” and symptoms of congestion.

4. Contractility

Contractility is the force generated by the myocardium independent of preload or afterload; if you like, it’s the strength and efficiency of contraction.

If you have optimized the heart rate and rhythm, preload and afterload and you still have evidence of poor perfusion and/or congestion, then you are left with contractility as the remaining factor that contributes to cardiac output.

Echocardiography remains the investigation that is required to directly assess contractility; it has the added advantage of also being able to measure cardiac output and preload responsiveness in addition to being able to diagnose some of the causes of a low-cardiac-output state (such as aortic stenosis, cardiac tamponade or myocardial ischemia).

In practice, if you still have evidence of reduced oxygen delivery, then ideally at this stage, if you are not already doing so, you should be using a hemodynamic monitoring device (such as those mentioned previously) that is able to give you a figure for stroke volume, cardiac output and cardiac index (CI), which is the cardiac output corrected for body surface area.

Normal values: Cardiac output 5-7 L/min

Cardiac index: 2.2–4.0 L/min/m2

Stroke Volume: 70 ml (average 70-kg man)

Having said that, there is no real “normal” cardiac output (CO). Cardiac output varies with demand: it either meets that demand or is unable to do so and you will get evidence of poor peripheral perfusion and tissue hypoxia. If this is the case, you need to continue to optimize oxygen delivery by aiming for a hemoglobin of greater than or equal to 10 g/dl and ensuring optimal oxygen saturations (SaO2).

Systemic O2 delivery = Hb x SaO2 x CO

Myocardial contractility is adversely affected by:

  • Hyperkalemia

  • Hypomagnesemia

  • Hypocalcemia

  • Severe acidosis

  • Hypoxia

  • Hypoglycemia

These things need to be corrected as far as is possible. Although it may not be possible, especially for severe metabolic acidosis, as the poor cardiac output and resulting poor oxygen delivery may be the direct cause of the acidosis.

Consideration now needs to be given to an inotrope if you still have signs of poor peripheral perfusion despite optimizing all the previously mentioned variables. Inotropes are drugs that increase the cardiac contractility. They should be given to patients with low blood pressure +/- a low cardiac index in the presence of signs of hypoperfusion or congestion.

In practice the inotrope that is most commonly used is dobutamine. Caution must be used in patients who are already tachycardic or in atrial fibrillation as dobutamine increases AV node conduction and may precipitate fast ventricular rhythms. Also, it causes venodilation, which may result in hypotension (secondary to reduction in preload) requiring the use of a vasopressor such as noradrenaline if a fluid challenge does not improve blood pressure and there is ongoing evidence of tissue hypoperfusion despite an improvement in cardiac output.

Dobutamine increases myocardial oxygen demand and is far from the ideal inotrope, especially in patients with acute cardiac ischemia or post cardiac surgery. There is some evidence to suggest that Levosimendan, which does not increase myocardial oxygen demand, is a better drug under these circumstances.

Given the side effect profile of these drugs and the current equipoise in the literature regarding their effect on long-term outcomes, they should be weaned as quickly as able once stability has been achieved.
Inotrope doses can be increased in response to several parameters:

  • Cardiac output/cardiac index

  • Indicators of peripheral perfusion – lactate, SvO2

Vasopressors should never be first-line therapy in low-cardiac-output states as they increase systemic vascular resistance and further impair cardiac output. Patients for whom sepsis is the cause of the reduced cardiac output are likely to require vasopressors and inotrope therapy.

Patients who require vasoactive drugs should have invasive arterial lines placed for continuous blood pressure monitoring.

There are devices that are used in low-cardiac-output states when the above methods have not been successful in restoring cardiac output and oxygen delivery.

1. Intra-aortic balloon pump

Most commonly used in patients with ischemic heart disease either pre or post percutaneous intervention or post cardiac surgery. It consists of a balloon, which is inserted into the aorta (via the femoral artery). It inflates during diastole and deflates in systole. It works by increasing the diastolic blood pressure and therefore coronary perfusion (hence its main role is in coronary artery disease) and reducing afterload, thereby increasing cardiac output.

2. Ventricular assist device (VAD)

VADs are not commonly used. They can be left- or right-sided systems and can only be implanted in specialist centers. They are mechanical devices that partially or completely take over the work of the heart. They are most commonly used as a bridge to transplantation in patients who have a good quality of life. They have also been used as a bridge to recovery in, for example, acute myocarditis. They have been used as “destination therapy” in heart failure.

Special circumstances

Some causes of low-output states can be reversed with specific therapies; therefore, these diagnoses should be sought out early during initial assessment and resuscitation to enable you to treat them urgently and ideally reverse the low-cardiac-output state:

  • Acute myocardial infarction

  • Cardiac tamponade

  • Tension pneumothorax

  • Pulmonary embolism

  • Acute valve failure

Acute myocardial infarction

If a patient has chest pain associated with ST-segment elevation on an ECG, coronary reperfusion should take place as quickly as possible. Primary percutaneous coronary intervention is the gold standard therapy. If this is unavailable at your institution the patient can be thrombolysed. Re-establishing coronary blood flow in this clinical scenario is the most important consideration. If you are able to achieve this, myocardial function should subsequently improve, although this may not be immediate.

Patients who have evidence of a non-ST-segment-elevation myocardial infarction should be treated with antiplatelet therapy. They may require coronary angiography subsequently.

Cardiac tamponade

Cardiac tamponade can be difficult to diagnose clinically. Clinical signs include hypotension, tachycardia +/- pulsus paradoxus, raised JVP, and quiet heart sounds, but these are very nonspecific. You need a high index of clinical suspicion to make the diagnosis. Although cardiac tamponade is a clinical diagnosis, the diagnosis should be supported by echocardiographic findings.

Any pericardial effusion causing hemodynamic compromise or a low cardiac state should be drained as a matter of urgency. This can be done percutaneously or surgically.

Tension pneumothorax

A tension pneumothorax should be able to be diagnosed clinically as a cause of low-cardiac-output state caused by an obstruction to filling and emptying of the ventricle.

Clinical features include hypotension, tachycardia, dyspnea, clammy skin, trachea deviated away from side of pneumothorax, lack of breath sounds and hyperresonance on the affected side.

It should be treated by inserting a large (>18G) cannula into the second intercostal space in the midclavicular line on the affected side and letting the air out. A chest drain should then be inserted.

Pulmonary embolism

Pulmonary emboli also cause a low-cardiac-output state by obstruction to emptying. In this instance, right ventricular emptying (ie, the right ventricular afterload) becomes very high and due to ventricular interdependence the left ventricular stroke volume and cardiac output decreases in tandem.

Patients classically present with dyspnea and pleuritic chest pain. They can also have symptoms and signs associated with low cardiac output. ECG may reveal a sinus tachycardia or S
1Q3T3 or the patient may be in atrial fibrillation. Echocardiography may demonstrate acute right ventricular strain.

Patients who exhibit signs of cardiovascular compromise should be thrombolysed to break up the clot. There are reports in the literature of patients undergoing thrombectomy or embolectomy to relieve cardiac compromise.

Acute valve failure (eg, mitral regurgitation)

Once acute valve failure in the context of a low-cardiac-output state has been diagnosed, urgent referral to the cardiothoracic surgeons for consideration of surgery needs to occur.

See Table I. Laboratory tests assessing adequacy of peripheral perfusion

Table I.
    • When CO is impaired there is a decrease in peripheral perfusion and an imbalance between oxygen delivery and the metabolic requirement of the cells.
    • The cells switch to anaerobic metabolism. Pyruvate and lactic acid are produced as byproducts. This is detectable as a high lactate on blood gas measurement causing an acidosis or acidemia.
§ Lactate > 2mmol/L
§ Base deficit > -4 mmol/L correlates with inadequate tissue oxygenation and increased morbidity.
· Impaired oxygen delivery also leads to
•Low mixed venous oxygen saturation (SvO2) and central venous oxygen saturation (ScvO2)
• Normal SvO2 70-75%
• SvO2 measurement is a way of assessing the overall balance between oxygen transport and consumption.
• An SvO2 <65% indicates increased oxygen extraction by the cells, which is suggestive of impaired tissue perfusion or an increase in metabolic rate.
· SvO2 will be influenced by all factors involved in oxygen delivery:
• Cardiac output
• Hemoglobin
• Partial pressure of oxygen arterial blood
• Oxygen saturations

See Table II. Signs of low perfusion vs congestion

Table II.
Symptoms and signs of low perfusion Symptoms and signs of congestion
Fatigue Fatigue
Confusion Tachycardia
Agitation Raised jugular venous pressure
Decreased level of consciousness Breathlessness and hypoxemia
Cool peripheries, mottled peripheries Pulmonary edema
Delayed capillary refill time Peripheral edema
Thready pulse Hepatic congestion
Metabolic acidosis
Raised lactate
SvO2 <65%

See Table III. Inotropes

Table III.
Dobutamine Inodilator
Stimulates beta 1 and 2 adrenergic receptors
Upregulation adenyl cyclase
Increases intracellular calcium concentration
Positively inotropic
Positively chronotropic
Vasodilator – resulting afterload reduction
Increased heart rate
Increased myocardial oxygen demand
Patients receiving beta blockers may be relatively immune to its effect and require high doses.
5-20 mcg/kg/min
No loading dose required.
Hemodynamic actions are dose related.
Dopexamine Inodilator
Stimulates beta 1 and 2 adrenergic receptors
Upregulation adenyl cyclase
Increases intracellular calcium concentration
Positively inotropic and chronotropic
Vasodilator – afterload reduction
Increased heart rate
Increased myocardial oxygen demand
0.25-2 mcg/kg/min
Dopamine Dominant effect dependent on dose
<2 mcg/kg/min – acts on dopamine receptors – vasodilation
2-5 mcg/kg/min – beta 1 adrenergic receptors – inotropic
5-15 mcg/kg/min – beta 1 adrenergic receptors – inotropic and alpha 1adrenergic receptors – vasoconstriction
Increased afterload at higher doses
Some evidence of worse outcomes compared to other ‘inotropes’
No loading dose required
Milrinone Inodilator
Type III Phosphodiesterase inhibitor
Increases intracellular cyclic adenosine monophosphate and as a result calcium
Positively inotropic
Arterial and venous dilatation – decreased SVR, PVR and PAOP
No increase in myocardial oxygen demand
Accumulates in renal failure
150-750 ng/kg/min
Loading dose 50 mcg/kg – given slowly over 10 minutes – in practice omitted due to hypotension
Levosimendan Inodilator
Calcium sensitizer
Binds to calcium saturated troponin C in cardiac myocytes – prolonging the conformational change and increasing contractile force
Stimulates ATP sensitive potassium channels
Positively inotropic
Reduces SVR and PVR and PAOP
Improves coronary perfusion
No increase in myocardial oxygen demand
Active metabolite with long half-life
Hypotension 0.05-0.2 mcg/kg/min
Loading dose 3-12 mcg/kg/min over 10 minutes – in practice omitted due to hypotension
Adrenaline Inoconstrictor
Acts on alpha and beta adrenergic receptors
Positively inotropic and chronotropic
Potent vasoconstrictor
Increased myocardial oxygen demand
Vasoconstriction – increased afterload
0.01-1 mcg/kg/min

3. Diagnosis

How do I establish a specific diagnosis?

This is very important. As mentioned above, diagnosing a low-cardiac-output state is not enough – the cause of the low cardiac output has to be established. In some circumstances (eg, pulmonary embolism or myocardial infarction causing a low cardiac output), treating the underlying cause is the most important consideration, so it is imperative to be able to make the diagnosis.

These patients are often very unwell and unstable. Clinical assessment, diagnosis, resuscitation and treatment often occur concurrently in the acute setting.

Firstly the low-cardiac-output state needs to be recognized. Once this has occurred, then the cause of the low cardiac output needs to be established and managed.

See Table IV. Etiology of low cardiac states by pathophysiological category

Table IV.
Coronary artery disease
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Restrictive cardiomyopathy
Postpartum cardiomyopathy
Decompensation of chronic heart failure
Post cardiac surgery
Toxins Alcohol
Drugs (e.g., beta blockers)
Cytotoxic agents
Nutritional Obesity
Thiamine deficiency
Infiltrative Sarcoidosis
End-stage renal failure
HIV infection
Chagas disease
Pericardial effusion and cardiac tamponade
Tension pneumothorax
Pulmonary embolism
Valvular disease Aortic stenosis
Aortic regurgitation
Mitral regurgitation
Mitral stenosis
Volume overload
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Major surgery
High airway pressure in ventilated patients
Severe brain injury

As described above, the first consideration should be – airway, breathing and circulation.

As with any acutely unwell patient, the diagnostic approach begins with history and examination, followed by immediate or basic investigations, followed by more specialized investigations.


The patient may be too unwell to provide a history. However, if you can establish one you should. Relatives and friends are a valuable source of information if you cannot get any from the patient. A full “standard” history should be taken, with particular emphasis on establishing the following points.

  • Symptoms


    Duration and pattern

    Presence of orthopnea or paroxysmal nocturnal dyspnea

    Presence of frothy pink sputum

    Swelling of ankles

    Chest pain

    Ischemic or pleuritic in nature

    Exacerbating or relieving factors




  • Previous history

    Chronic heart failure

    Ischemic heart disease

    Valvular disease and/or dysfunction

    Congenital heart disease

    Previous cardiac surgery

    Renal impairment

    Any other medical history

  • Risk factors




    Smoking/Alcohol excess

    Family history

  • Drug History

  • Intercurrent illness precipitating acute or chronic heart failure (e.g., infection)


Again, a full examination should be undertaken, with particular emphasis being paid to the following points:

  • Hemodynamic parameters and vital signs

    Blood pressure – adequate perfusion pressure

    Heart rate and rhythm

    Gallop rhythm or third heart sound

    Oxygen saturations

    Respiratory rate

  • Indicators of peripheral perfusion

    Consciousness level

    Peripheral skin temperature

    Central temperature

    Capillary refill time

    Urine output

  • Indicators of congestion

    Raised JVP

    Peripheral edema



    Pleural effusions

    Pulmonary edema

  • Indicators of underlying etiology

    Cardiovascular examination

    Heart sounds and murmurs

  • Evidence of valvular dysfunction

    Pericardial rub

  • Evidence of pericardial effusion +/- cardiac tamponade

Electrocardiogram (ECG)

An ECG should be performed in every patient as early as possible in assessment. It may demonstrate a variety of abnormalities and is unlikely to be normal if heart failure is present. It may provide evidence of the underlying cause of the cardiac dysfunction.

  • Bradycardia

  • AV block

  • Sinus tachycardia

  • Atrial tachyarrhythmias

  • Ventricular tachyarrhythmias

  • Ischemia

  • Left ventricular hypertrophy

  • Low-voltage complexes

Chest X-ray (CXR)

A CXR should be performed in all these patients. Important features include:

  • Heart size

    It is difficult to assess on an AP film, but a clearly enlarged heart may be obvious.

    May suggest cardiomegaly or left ventricular hypertrophy

  • Pulmonary venous congestion

    Indicates elevated left ventricular filling pressure

  • Interstitial edema

    Indicates elevated left ventricular filling pressure (although may have other causes)

  • Pleural effusions

    Can indicate elevated left ventricular filling pressures (more likely if bilateral)

    Can also be caused by many other pathologies

    Parapneumonic effusion


    Pulmonary embolism


    Post cardiac surgery

    Low oncotic pressure

  • Kerley B lines

    Increased lymphatic pressure

  • Consolidation

    Infection or malignancy – alternative causes of symptoms and signs

  • Pneumothorax

    Alternative cause for symptoms or signs – especially if a tension pneumothorax

Basic laboratory tests

Basic blood tests should be performed in all patients; these should include:

  • Full blood count

    Ideally Hb > 10g/dL to optimize oxygen delivery to the tissues

    Chronic anemia is common in chronic heart failure.

    An markedly raised white cell count may raise the suspicion of an alternative diagnosis.

  • Serum electrolytes

    Normal potassium, magnesium and calcium levels are necessary for optimal cardiac function.

  • Urea and creatinine

    Renal function is frequently impaired in chronic heart failure.

    Low cardiac output leads to poor peripheral perfusion; this will result in reduced renal perfusion and deterioration in renal function unless forward flow and perfusion is improved.

  • Glucose

    Hypoglycemia will impair cardiac function.

    Untreated hyperglycemia has also been shown to lead to poorer outcomes in critically ill patients.

  • Liver function tests

    May be deranged if right ventricular impairment and hepatic congestion are present

    Albumin may be low if malnourished.

  • Coagulation screen

    Required in all patients who are taking anticoagulants

    Raised INR may be secondary to liver congestion.

    Should be measured in all critically ill patients

  • Thyroid function

    Hyperthyroidism may cause “high-output cardiac failure.”

    Hypo- or hyperthyroidism may cause intrinsic myocardial dysfunction.

Other blood tests

  • Natriuretic peptides

    BNP or NT-proBNP

    High levels indicate increased ventricular wall stress.

    Abrupt changes in left ventricle filling pressures may not be reflected in peptide level due to their long half-life.

    Other causes of elevated natriuretic peptides include:

    Renal impairment

    Left ventricular hypertrophy

    Myocardial ischemia




    Liver cirrhosis

    Probably more useful test when diagnosing heart failure in an outpatient setting

  • Cardiac troponins

    Troponin I or T

    Marker of myocyte necrosis

    Should be measured if there is any evidence of myocardial ischemia

    May be mildly raised in acute or severe heart failure and myocarditis, sepsis and renal failure


This is a pivotal investigation. Not only can it confirm or refute the clinical diagnosis of a low cardiac output or heart failure, but you can also optimize preload by measuring stroke volume and stroke volume variation using the Doppler principle. Furthermore, the etiology of reduced or low cardiac output will often be diagnosed by echocardiography.

Transthoracic echocardiography should be performed as soon as is possible after the clinical diagnosis of low cardiac output. In addition to quantifying the degree of cardiac impairment by measuring systolic and diastolic function, a wealth of information can be obtained about cardiac anatomy, valves and valvular dysfunction, myocardial and pericardial disease and regional wall motion abnormalities suggesting ischemia.

Systolic function is assessed by measuring left ventricular ejection fraction (LVEF); >45-50% is considered normal. This is not synonymous with contractility. Diastolic function is measured by looking at diastolic mitral inflow patterns, pulmonary vein flow and tissue Doppler at the mitral annulus. CO and SV are obtained using the Doppler principle, measuring the velocity time integral in the aortic outflow tract. Pulmonary artery pressure can also be estimated if there is a jet of tricuspid regurgitation present, by measuring the regurgitant jet velocity. High pulmonary artery pressure in the presence of a dilated right ventricle with septal flattening or the septum bowing into the left ventricle suggests an acutely raised right ventricle pressure and should raise the possibility of a pulmonary embolus as the cause of low cardiac output.

Coronary angiography

If the patient has chest pain and evidence of an ST-elevation myocardial infarction (STEMI) on ECG, primary percutaneous coronary intervention should occur as soon as possible if your institution has the facilities available – it is the gold standard treatment for revascularization in a STEMI.

Coronary angiography should also be considered post cardiac arrest that is thought to be ischemic in origin, especially if there is evidence of heart failure. It may also be considered in patients who have recovered from a low-cardiac-output state when the cause has not been elucidated.


The causes of a low cardiac output are many and varied and include systemic pathology such as an inflammatory processes or sepsis in addition to primary cardiac pathology such as post cardiac surgical states and valve dysfunction. Despite the primary insults being so varied, the ultimate pathophysiological pathway is the same.

The low-cardiac-output state may be transient and reversible with treatment of the underlying insult, an acute worsening of a chronic state or an acute problem that progresses into a chronic condition.

A low cardiac output state is said to occur when there is an imbalance between metabolic cellular requirements and oxygen delivery (i.e., any impairment in oxygen delivery secondary to cardiac dysfunction).

We know that the primary function of the heart is to pump oxygenated blood to the tissues in order to provide them with sufficient oxygen and nutrients to fulfill their metabolic needs. When we are healthy the heart achieves this with ease. At times of increased oxygen demand by the tissues (e.g., during exercise, pain, fever, ‘illness’) the cardiac output increases to meet the increased oxygen demand.

Oxygen delivery to the tissues depends upon cardiac output and the arterial oxygen content:

DO2 (Oxygen delivery) = CO x Arterial oxygen content

Arterial oxygen content = (Hemoglobin x SaO2 x1.34)

When the CO is reduced, the oxygen delivery to the tissues will decrease as a direct result. In the same way, if the hemoglobin and/or oxygen saturations are reduced, the oxygen delivery to the tissues will be impaired. Under these circumstances oxygen extraction will be increased at a cellular level. Arterial oxygen content needs to be maximized when there is a decrease in CO.

Despite these measures the oxygen delivery may fail to meet the cellular oxygen demand. At this point the cells switch from using oxygen as an energy substrate to anaerobic glycolysis, which produces lactate as a byproduct. Therefore, lactate levels are a marker of effectiveness of oxygen delivery, oxygen extraction by the tissues and tissue oxygenation. As tissue perfusion decreases, increasing renal and hepatic dysfunction (secondary to hypoperfusion) will result in further increases in lactate due to an inability to effectively excrete it.

In certain situations, such as sepsis and post cardiac arrest syndromes (both of which may be the primary cause of a low cardiac output), oxygen delivery may be maintained but tissue extraction is impaired at the cellular level, which compounds tissue hypoxia.

Increasing acidosis secondary to poor peripheral perfusion and inadequate oxygen delivery further impairs myocardial function/contractility, leading to a downward spiral of worsening cardiac output, peripheral perfusion, vasoconstriction and metabolic acidosis.

Any decrease in cardiac output after an ‘acute critical event’ will lead to a decrease in perfusion as described above. Many other processes are involved in the vicious cycle that ultimately leads to worsening heart failure, multiple organ dysfunction and death.

A reduction in cardiac output will lead to a compensatory increase in heart rate as described above. This increases the myocardial oxygen demand. The greater the tachycardia, the less time spent in diastole; therefore ventricular filling, preload, stroke volume and cardiac output are reduced in addition to a reduction in coronary artery blood flow, which will compound any ischemia and further impair myocardial contractility.

Reduced cardiac output in turn leads to a reduction in renal perfusion. The reduction in renal perfusion results in activation of the renin-angiotensin-aldosterone system (RAAS) via renal beta-adrenergic stimulation. This ultimately acts to retain sodium and hence water by increasing sodium reabsorption. Angiotensin II promotes constriction of arterioles within the renal and systemic circulation in addition to promoting sodium reabsorption and is a potent stimulator of aldosterone production. Aldosterone also stimulates sodium and water retention. The overall result is an inappropriate expansion of intravascular and extravascular volumes in addition to inappropriate vasoconstriction, which increases afterload and may further worsen cardiac output. In the longer term RAAS promotes remodeling and fibrosis in heart, kidneys and other organs.

  • A decrease in arterial pressure is detected by arterial baroreceptors when cardiac output is low. This leads to sympathetic stimulation and an increase in systemic vascular resistance (via vasoconstriction) in order to maintain arterial pressure. However, this also results in an increased afterload, putting the failing ventricle under even more strain.

  • The myocardium may be ‘stunned’ after a period of prolonged ischemia such as after a cardiac arrest. The myocardial dysfunction may persist after coronary blood flow has been restored and may persist for some time.

If you are unable to reverse the insult that lead to the low-cardiac-output syndrome, then your patient will be unable to respond to your treatment. This emphasizes how important it is to identify the underlying cause of the low-cardiac-output state.


The prevalence of the ‘low cardiac output state’ is difficult to define. What we do know is that the overall prevalence of heart failure is increasing; this is in part due to the aging population and increased survival after acute myocardial infarction and improved primary and secondary prevention. The number of people living with heart failure in the community is increasing and this is associated with an increase in admissions of people with acute exacerbations of chronic heart failure. The ESC state that ‘heart failure’ is the cause of 5% of hospital admissions across their member states and 2% of national health expenditure.

The low cardiac output state may be under-reported, as the underlying cause may be listed as a diagnosis in preference (i.e., in sepsis, aortic stenosis or myocardial infarction).

Special considerations for nursing and allied health professionals.


What's the evidence?

Description of the problem

Masse, L, Antonacci, B. “Low cardiac output syndrome: identification and management”. Critical Care Nursing Clinics of North America. vol. 17. 2005. pp. 375-383. Overview of low cardiac output (primarily in children) but underlying principles the same. Excellent description of principles.

Priori, SG, Garcia, MAA. “Executive summary of the guidelines on the diagnosis and treatment of acute heart failure. The task force on acute heart failure of the European Society of Cardiology”. European Heart Journal. vol. 26. 2005. pp. 384-416.

Dickstein, K, Cohen-Solal, A. “ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008”. European Heart Journal. vol. 29. 2008. pp. 2388-2442. European Society of Cardiology – explanation of issues and management (above 2)

Emergency management

Gray, A, Goodacre, S. “Noninvasive Ventilation in Acute Cardiogenic Pulmonary Edema”. NEJM. vol. 359. 2008. pp. 142-151. Trial of NIV in cardiogenic pulmonary edema compared with conventional therapy.

Cecconi, M. “Hemodynamic monitoring in acute heart failure”. Heart Failure Review. vol. 12. 2007. pp. 105-111. Overview of hemodynamic monitoring used when assessing cardiac output.

Binanay, C, Califf, RM. “Evaluation study of congestive heart failure and pulmonary artery catheter effectiveness: the ESCAPE trial”. JAMA. vol. 294. 2005. pp. 1625-1635.

Pinsky, MR. “Clinical significance of pulmonary artery occlusion pressure”. Intensive Care Medicine. vol. 29. 2003. pp. 175-178. Evidence for use of PAC in heart failure (above 2 )

Linton, RA, Linton, NW. “Is clinical assessment of the circulation reliable in post-operative cardiac surgical patients?”. Journal Cardiothoracic Vascular Anesthesia. vol. 16. 2002. pp. 4-7. Reliability of clinical assessment in assessing cardiac output – one example

Perel, A. “Intrathoracic blood volume and global end diastolic volume should be included among indexes used in intensive care for assessment of fluid responsiveness in spontaneously breathing patients”. Critical Care Medicine. vol. 34. 2006. pp. 2266-2267.

Cavallaro, F, Sandroni, C. “Functional haemodynamic monitoring and dynamic indices of fluid responsiveness”. Minerva Anaestesiology. vol. 74. 2008. pp. 123-135.

Sakka, SG, Ruhl, CC. “Assessment of cardiac preload and extravascular lung water by single transpulmonary thermodilution”. Intensive Care Medicine. vol. 26. 2000. pp. 180-187. Assessing preload with other cardiac monitoring devices (above 3)

Price, S, Nicol. “Echocardiography in the critically ill: current and potential roles”. Intensive care medicine. vol. 32. 2006. pp. 48-59. Role of echocardiography in these patients

Shin, DD, Brandimarte, F. “Review of current and investigational pharmacologic agents for acute heart failure syndromes”. American Journal of Cardiology. vol. 99. 2007. pp. 4A-23A. Emergency treatment – drugs including inotropes. Overview.


Dickstein, K, Cohen-Solal, A. “ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008”. European Heart Journal. vol. 29. 2008. pp. 2388-2442. European guidelines for diagnosis and treatment of heart failure.

Alwi, I. “Cardiogenic shock in acute coronary syndrome”. Acta Med Indones-Indones J Intern Med. vol. 36. 2004. pp. 48-53. Low cardiac output states after cardiac ischemia.

Masse, L, Antonacci, B. “Low cardiac output syndrome: identification and management”. Critical Care Nursing Clinics of North America. vol. 17. 2005. pp. 375-383. Low cardiac output overview in children – as above


Andrew, D. Bersten, Neil, Soni. Oh’s Intensive Care Manual.

Guyton and Hall Textbook of Medical Physiology.