Cardiovascular support in intensive care
Intensive care exam revision for medical student finals, PLAB exams and MRCP PACES
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The most common reason a patient may require cardiovascular support on ICU is for the treatment of shock. The primary function of the cardiovascular system is to maintain perfusion of tissues and organs with oxygenated blood. If the cardiovascular system fails, blood pressure and cardiac output can drop leading to organ failure. Although it is important to treat the underlying cause of the shock (cardiovascular, septic, hypovolaemic or obstructive e.g. PE) patients may need cardiovascular monitoring and support on ICU while this is happening.
ICU offers the ability to monitor patients more invasively and intensively than on the wards. Not only are the nurse to patient ratios much less but ICU has the facility to implement invasive monitoring. Although a lot of clinical data can be gained from basic observations such as pulse, capillary refill time, blood pressure, respiratory rate, temperature, GCS and urine output, it is easier to assess clinical state and subtle responses to therapy with invasive monitoring in the critically ill patient.
Common types of invasive monitoring are central venous pressure monitoring and invasive arterial pressure monitoring. However, oesophageal doppler can be used to assess fluid status and specialist haemodynamic monitoring such as PICCO and LIDCO can also be used. In some cases pulmonary artery catheterisation is still used, but the use of this has decreased in frequency. Fluid filling and the use of inotropes and vasopressors can be far more accurately delivered with sophisticated invasive monitoring.
When invasive monitoring is used it is important that it is interpreted correctly. It is important to assess trends rather than absolute figures and to be aware of what outcome you are seeking from your therapy. It is also important not to lose sight of how helpful basic observations can also be e.g. urine output, pulse and blood pressure.
In order to treat shock the following principles should be followed:
- Treat the underlying cause
- Optimize circulating blood volume
- Optimize cardiac output
- Optimize blood pressure
- Optimize oxygen delivery
- Support any organ systems that may be failing
Invasive monitoring can help detect more accurately when therapy may need to be modified to target any of these areas.
Goal directed therapy uses the results from invasive and non-invasive monitoring to attempt to optimise the outcome in critically unwell patients. You can use goal directed therapy on the wards e.g. if the urine output is failing in a patient you can deliver fluid boluses with the goal of improving urine output to a normal volume (0.5ml/kg).
Goal directed therapy on ICU just uses more variables to guide treatment and if fluid filling is not achieving results there is the option to use drugs. The aim is to optimise the cardiovascular performance of individual patients with titration of fluids and drugs to achieve an optimal response for each patient.
- Is fluid status optimal? (Use arterial line, CVP and mixed venous saturations as a guide) If yes proceed to step 2) if no consider a fluid bolus and reassess. Optimise fluid status prior to proceeding.
- Is cardiac output optimal? If yes proceed to step 3) if no add in inotropic support and reassess. Optimise cardiac output prior to proceeding.
- Is blood pressure optimal? If yes continue to monitor and reassess and ensure oxygen delivery and tissue perfusion is adequate. If no add in a vasopressor.
These can be gained by obtaining a blood gas from a central line sample. A normal value is 55-75%. Mixed venous saturations are an indicator of oxygen delivery and consumption and will be substandard in an under-filled patient. Resuscitation guided by mixed venous saturations has been shown to improve outcome by reducing the severity of organ failure and duration of intensive care stay.
Inotropic drugs are used to optimise cardiac output. Examples are dobutamine, dopexamine, adrenaline and dopamine. Each drug has slightly different mechanisms of action but the aim of them all is to increase the heart rate +/- stroke volume. This is because Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR). Dobutamine and dopexamine increase heart rate and stroke volume but cause peripheral vasodilation, whereas adrenaline causes an increase in heart rate and stroke volume but causes vasoconstriction. When considering the use of an inotropic drug it is important to be aware of the mechanism of action so the effect of the drug can be effectively monitored. If the cardiac output is low but blood pressure well maintained, dobutamine or dopexamine may be logical choices whereas if cardiac output and blood pressure are both low adrenaline may be the inoptrope of choice. Dopamine has a variable action depending on its dosage and it is commonly used in Europe as a first choice inotrope.
Vasopressors are vasoconstrictors. The commonly used agents are phenylephrine and noradrenaline. Both agents act on alpha-1 receptors and increase blood pressure by vasoconstriction. In appropriate doses the aim of vasopressors is to increase blood pressure and improve blood flow to vital organs. However if used in excessive doses they can cause reduced splanchnic blood flow, reduced renal blood flow, impaired peripheral perfusion and reduced cardiac output by increasing afterload. It is important that invasive monitoring and careful clinical judgement is used to titrate vasopressors to the lowest possible dose to achieve an appropriate response in the individual patient.
Inotropes and vasopressors should not be used until there has been adequate fluid filling, they should be given via central access and the intended goal of therapy should be clearly documented. Clinical judgement remains imperative despite invasive monitoring as the aim is to treat the patient not numbers. It may be acceptable to tolerate lower values of blood pressure if the patient is conscious and passing urine. Prior to the use of drugs to support the circulation it is also important to ensure that cardiac output and blood pressure have been optimised by treating any dysrhythmias, treating any mechanical causes of low blood pressure (e.g. massive PE) checking electrolytes and correcting severe acidosis (inotropic drugs do not work well at a PH < 7.2).
Hypotension is a much more common complaint on ICU but hypertension can also occur. This hypertension can either be due to physiological stresses from ICU treatment (e.g. ventilator weaning) or it may be the reason admission is required to ICU (e.g. malignant hypertension).
If hypertension is thought to be transient and as a result of ICU care it is important not to over treat this. Ensure the blood pressure reading is correct by checking the arterial line and performing non-invasive measurements. Ensure adequate analgesia and sedation, stop vasopressors and inotropes and reassess fluid status and consider diuretics if necessary.
If the patient is persistently hypertensive despite simple interventions or they have been admitted to ICU for the specific intent of treating hypertension then pharmacological therapy may be required. Malignant hypertension is when there is a sustained diastolic blood pressure over 110mmHg or a systolic blood pressure greater than 200mmHg. This is also associated with end organ damage e.g. myocardial ischaemia, renal failure and retinal signs. In this situation blood pressure needs to be lowered cautiously. Nifedipine can be used but this can drop blood pressure too quickly, hydralazine intravenously can be used as can GTN or labetalol infusions. It is important to involve the cardiology team or clinical pharmacology team in the management of these patients and ensure that they are closely monitored.
Disruptions to usual cardiac rhythm are common in ICU. Patients may have pre-existing arrhythmias that are exacerbated by critical illness or disturbances of physiology in the critically ill patient may precipitate an arrhythmia. It is important to treat bradycardia or tachycardia as per ALS guidelines and specialist cardiology input may be needed for pacing or cardioversion. However, it is also important to be alert to factors on ICU that may precipitate arrhythmias.
Tachycardias may be caused by pain and anxiety, increased catecholamines (either endogenous or from administered drugs), hypoxia, hypercarbia, electrolyte disturbance, hypovolaemia, pyrexia a cardiac event or endocrine abnormalities. It is imperative that any of these causes are identified and treated if present as this may treat the tachycardia and prevent further drug administration or cardioversion. However, if a patient is decompensated by a tachycardia ALS guidelines should be followed.
Bradycardia is a heart rate less than 60, often caused by 1st, 2nd and 3rd degree heart block. Bradycardia on ICU can also be caused by hypoxia, increased vagal tone secondary to suctioning, myocardial depressant drugs, brain injury or cervical spine injury. Drugs can be given to treat bradycardia e.g. atropine or glycopyrronium but these are usually short acting and if the patient is decompensated they may require external temporary pacing or cardiology input for a pacing wire +/- permanent pace maker.