Low Cardiac output

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.

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

Airway

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.

Breathing

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).

Circulation

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