Circulation



Circulation






Cardiac arrest

Critical care teams are often involved in the resuscitation of in-hospital cardiac arrests, and in the aftercare of successfully resuscitated patients.

Unexpected cardiac arrests in the ICU are relatively uncommon and they are often preceded by prolonged attempts to resuscitate or support failing organs. If CPR is required, follow BLS/ALS guidelines (image pp.100 and 101).


Causes

Cardiac arrests are often cardiogenic in origin, and are more common in patients with a history of ischaemic heart disease. Hypoxia, hypovolaemia/hypoperfusion, neurologic or metabolic causes are all common in critical care settings. Potentially reversible causes include:



  • Hypoxia.


  • Hypovolaemia.


  • Hypo/hyperkalaemia (and other metabolic disorders).


  • Hypothermia.


  • Hypoglycaemia.


  • Tension pneumothorax.


  • Tamponade, cardiac.


  • Toxins.


  • Thrombosis (coronary or pulmonary).


  • Severe acidaemia.


Presentation and assessment



  • Periods of physiological deterioration often precede within-hospital arrests.


  • 1/3 of in-hospital cardiac arrests present with pulseless electrical activity (PEA), 1/3 with asystole, and 1/3 with ventricular fibrillation/pulseless ventricular tachycardia (VF/VT).


  • Features requiring immediate assessment include:



    • Sudden loss of consciousness


    • Impalpable pulse, or loss of arterial pressure trace


    • Obvious apnoea, or terminal gasping


    • ECG trace of VT, VF, asystole, profound bradycardia or tachycardia


    • Sudden loss of end-tidal CO2 trace


Investigations

Investigations that may affect an ongoing cardiac arrest include:



  • U&Es (to identify hypo/hyperkalaemia):



    • The fastest way of measure this is often via a blood gas analyser using an arterial or venous sample


  • Finger-prick blood glucose (hyperglycaemia).


  • ABGs (to identify profound acidaemia).


  • Echocardiography (tamponade, hypovolaemia, right ventricular hypertension in PE, regional wall motion abnormality, aortic dissection).


Differential diagnoses



  • Equipment failure (ECG electrode failure or damped arterial trace).


  • Any cause of syncope or severe hypotension.




Immediate management



  • Adopt a SAFE approach (Shout for help, Approach with caution, Free from danger, Evaluate ABC); don gloves/PPE as appropriate.


  • Assess the patient: check for a response ‘shake and shout’:



    • If unresponsive call for help, position the patient on their back and open the airway (chin lift or jaw thrust)


    • Assess the breathing for up to 10 seconds (if ventilated confirm tube connections and tidal volume delivery)


    • At the same time manually confirm that the pulse is absent; do not rely on arterial pressure trace alone


  • If the patient has no signs of life, or is pulseless, or if there is any doubt, then commence CPR.


  • Ensure that the cardiac arrest team has been summoned (dial 2222).


  • ALS algorithms (Figs 4.1 and 4.2; image pp.100 and 101) should be followed; do not delay defibrillation if appropriate.


  • Obtain information about the patient as soon as possible from notes, staff or relatives as this may help identify underlying cause and will clarify the resuscitation status of the patient.



    • Where doubt exists as about the patient’s resuscitation status CPR should be commenced

Within the ICU/HDU



  • If a monitored cardiac VF/VT arrest is witnessed deliver 3 ‘stacked’ shocks, commencing CPR for 2 minutes immediately after the third.


  • Check the airway, and if in doubt about ETT or tracheostomy consider re-intubating or reverting to bag-and-mask ventilation.


  • If mechanically ventilated, turn the ventilator O2 to 100% and do not disconnect ventilator tubing during defibrillation:



    • Minimizing PEEP, if possible, may aid defibrillation


    • If CPR prevents the ventilator from working, switch to a self-inflating bag; this can also be left connected during defibrillation


  • Arterial pressure traces can be used to guide CPR; aim for a diastolic pressure >40 mmHg.


  • Drugs:



    • Whilst waiting for adrenaline bolus to be available consider increasing adrenaline/noradrenaline infusion rates


    • Central IV administration is usually the best route for drug delivery and is often available in ICU patients


  • Other treatments:



    • If hypovolaemia is suspected IV fluids may be rapidly infused


    • Thrombolysis (image p.94): where PE is strongly suspected consider giving a thrombolytic immediately


    • Needle thoracocentesis/pericardiocentesis: for tension pneumothorax or cardiac tamponade (image pp. 546, 530, 146, and 80)


    • Open-chest cardiac compression should be considered following cardiothoracic surgery or chest trauma


  • Echocardiography during the arrest may identify reversible causes.

In postoperative cardiac surgery patients follow the CALS algorithm (see image p.395).







Fig. 4.1 In-hospital resuscitation algorithm. UK Resuscitation Council guidelines 2010. Reproduced with the kind permission from the Resuscitation Council (UK).


Further management

Following the return of spontaneous circulation (ROSC):



  • ICU/HDU/CCU admission: it may be necessary to admit patients to a critical care setting for management of their underlying condition or post-arrest stabilization/treatments.



    • Any decision not to admit the patient following ROSC should be made by senior clinicians, where possible with the involvement of the patient’s relatives (and in light of the patient’s views, if known)


    • Transfer to a critical care environment is unlikely to be beneficial unless there is a period of cardiovascular stability







    Fig. 4.2 Adult advanced life support algorithm. UK Resuscitation Council guidelines 2010. Reproduced with the kind permission from the Resuscitation Council (UK).


  • Surgical intervention: on occasion urgent surgery is required following ROSC (e.g. following trauma or ruptured ectopic pregnancy); surgical advice must be sought, and a decision taken as to whether to transport to theatre or operate within the current environment.


  • Angiography: where there is evidence of an acute ischaemic event it may be necessary to perform urgent angiography/coronary intervention; obtain an urgent cardiological opinion.



  • Thrombolysis: this may be necessary if a massive/submassive PE is evident (or after a coronary occlusion where angiography is not possible).


  • General support:



    • Continued mechanical ventilation: where this is considered appropriate aim for a SaO2 >94% and a PaCO2 of 4.5-5 kPa


    • Sedation: if required use short-acting drugs (e.g. propofol) so that neurological status can be rapidly assessed after discontinuation


    • Circulatory support: inotropic support or fluid therapy may be required depending on the underlying disease or degree of cardiac stunning; if LVF is present consider specific treatments (image p.122)


    • Neurological support: employ measures to combat raised ICP (sedation, seizure, PaCO2 and glycaemic control; avoidance of hypoxia and hypotension; raising the bed-head to improve venous drainage)


    • Electrolytes: maintain blood glucose at 6-10 mmol/L; correct any hypomagnesaemia; maintain potassium at 3.5-4.5 mmol/L


    • Maintain haemoglobin of 8-10g/dL


    • Therapeutic hypothermia may be indicated (see Box 4.1)


    • Avoidance of pyrexia: if therapeutic hypothermia is not being employed, antipyretics, or surface cooling, may be necessary


  • Post cardiac arrest investigations should include: ABGs, FBC, U&Es, LFTs, blood glucose, cardiac enzymes, ECG, CXR.



    • Later investigations may also include echocardiography to assess cardiac damage and CT head to assess neurological damage


Pitfalls/difficult situations



  • ALS is unlikely to be successful in cases where maximal supportive therapy is already being provided.


  • In patients who are hypothermic, or undergoing general anaesthesia, prolonged CPR may still be successful.


  • After CVC insertion, chest trauma or chest surgery do not forget to exclude tension pneumothorax or tamponade.


  • Hypo/hyperkalaemia and hypo/hypermagnesaemia are relatively common in critical care environments.


  • Pregnancy (image p.429): use a wedge or tilt to decrease aortocaval compression where possible, urgently arrange for obstetric help (Caesarean section may facilitate resuscitation and save the fetus).


  • Hypothermia (image p.250): if first defibrillation is ineffective withhold further attempts until temperature is >30°C; actively re-warm.


  • Drowning or trauma (image pp. 404 and 414): consider the possibility of cervical spine trauma, and drug or alcohol intoxication.


  • Prognostication of neurological recovery after a cardiac arrest is difficult; absence of pupillary and corneal reflexes at 72 hours (or 72 hours after cooling) is associated with a poor outcome.




Box 4.1 Therapeutic hypothermia

Therapeutic hypothermia may improve the long-term neurological outcomes after cardiac arrest:



  • Indications include comatose patients (GCS <9) with ROSC after a VF/VT out-of-hospital arrest with short ‘down-times’.


  • It may also be beneficial for other types of arrest in other settings.

Relative contraindications include:



  • Hypothermic patients.


  • Cardiovascularly unstable patients (including inotrope-dependent shock, septic shock, major haemorrhage).


  • Pregnancy.


  • Coagulopathy.

Technique:



  • Rapid induction of cooling (e.g. an infusion of 20-30 ml/kg 0.9% saline or Hartmann’s).


  • Continued induction/maintenance using:



    • Peripheral cooling using exposure, tepid sponging and fans


    • Cooling blankets and mattresses


    • Cold IV fluid maintenance infusions


    • Use of intravascular cooling systems (i.e. CoolGardTM)


    • Trans-nasal evaporative cooling (e.g. RhinoChillTM)


    • Haemofiltration or cardiac bypass using cold fluids


  • Shivering may be controlled by deepening sedation and the use of neuromuscular blocking drugs (e.g. atracurium).


  • Monitor core body temperature, aiming for 32-34°C for 24-36 hours before rewarming at a rate of 0.25-0.5°C/hour.


  • Intravascular volume and electrolytes may require correction during cooling/rewarming.



Further reading

Choi HA, et al. Prevention of shivering during therapeutic temperature modulation: the Columbia anti-shivering protocol. Neurocrit Care 2011; 14(3): 389-94.

Nadkarni, VM, et al. First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults. JAMA 2006; 295(1): 50-7.

Resuscitation Council (UK). Advanced life support, 6th edn. London: Resuscitation Council (UK) (2011)

Intensive Care Society. Standards for the management of patients after cardiac arrest. London: Intensive Care Society, 2008.

Holzer M. Targeted temperature management for comatose survivors of cardiac arrest. N Engl J Med 2010; 363: 1256-64.



Hypotension and shock

Hypotension is defined as systolic BP <90 mmHg and/or MAP <60 mmHg.

Shock is defined as underperfusion of multiorgan systems. Clinical signs include tachycardia, hypotension, oliguria, and altered mental status.


Causes


Cardiogenic shock

(See causes listed on image p.122.)


Hypovolaemic shock: loss of intravascular volume



  • Haemorrhage (e.g. trauma, aortic dissection, postoperative bleeding).


  • GI loss of fluids (e.g. vomiting, diarrhoea, high-output stoma).


  • Renal loss of fluids (e.g. diabetes insipidus, excessive diuretics).


  • Fluid redistribution (e.g. burns, trauma, major surgery, sepsis, posture).


Distributive shock: venous dilation or obstruction



  • Overdose of sedatives or vasodilators.


  • Spinal/epidural anaesthesia or analgesia.


  • Autonomic neuropathy (e.g. spinal cord lesion/trauma, Guillain-Barré).


  • Anaphylaxis.


  • Major vein compression (e.g. tumour, pregnancy, ascites, extensive intra-abdominal surgery).


Obstructive shock: impairing ventricular filling



  • Cardiac tamponade (e.g. pericardial bleeding, pericardial effusion).


  • Constrictive pericarditis.


  • ↑intrathoracic pressure (e.g. tension pneumothorax, massive pleural effusion, mechanical ventilation).


  • PE.


Miscellaneous causes



  • Hepatic failure.


  • Thyrotoxicosis.


  • Myxoedema coma.


  • Adrenal insufficiency.


  • Poisoning (e.g. cyanide, carbon monoxide).


Presentation and assessment

Shock may be associated with a low cardiac output, or a compensatory high cardiac output; presentation depends on the 1° cause.

General presentation



  • Anxiety and sweating.


  • Tachypnoea, dyspnoea; Kussmaul’s breathing (if hypoperfusion causes reduced tissue perfusion and a metabolic acidosis).


  • Hypoxia, cyanosis.


  • Hypotension: systolic BP <90 mmHg (or >30mmHg below normal resting pressure); or MAP <60 mmHg.


  • Tachycardia (bradycardia may be a pre-terminal sign, or be associated with a arrhythmia).



    • Arrhythmias (e.g. AF, atrial flutter, VT, complete heart block)


  • Cardiac hypoperfusion: angina, or ECG evidence of ischaemia.



  • Renal hypoperfusion: oliguria/anuria, raised urea and creatinine.


  • Neurological hypoperfusion: confusion, syncope, ↓GCS.

In low-output shock expect:



  • Cold peripheries, poor peripheral perfusion and delayed capillary refill.


  • Thready pulse with reduced pulse pressure.


  • ↓cardiac output (cardiac index <2.2 L/minute/m2 with adequate preload).


  • ↑systemic vascular resistance.


  • In hypovolaemic shock JVP/CVP is ↓; there may be evidence of fluid or blood loss, or venous pooling.


  • In cardiogenic shock JVP/CVP may be ↑; S3 may be present:



    • Examination of the lungs may show evidence of pulmonary oedema


    • CXR and ECG are often abnormal with evidence of pulmonary oedema, enlarged heart, and/or arrhythmia

In high-output shock expect:



  • Bounding pulse with wide pulse pressure.


  • Strong apical cardiac impulse.


  • Normal or ↑ cardiac output.


  • ↓systemic vascular resistance.


  • Depending on the degree of skin perfusion peripheries may or may not be warm; capillary refill may be brisk or reduced.


  • Pyrexia and raised WCC where there is associated sepsis.

If the presentation does not fit a pattern, mixed shock should be considered (e.g. sepsis with myocardial dysfunction).


Investigations



  • ABGs (metabolic acidosis, hypoxia, compensatory hypocapnia).


  • FBC (anaemia with haemorrhage, raised WCC with infection).


  • Coagulation screen (deranged with haemorrhage or DIC).


  • U&Es (AKI), serum calcium, magnesium, phosphate.


  • Serum glucose (hypo/hyperglycaemia).


  • LFTs (deranged with ischaemia or liver failure).


  • Cardiac enzymes (if cardiac ischaemia suspected).


  • Blood, urine, sputum culture (if infection suspected).


  • 12-lead ECG (cardiac ischaemia, arrhythmias).


  • CXR (evidence of infection, cardiomegaly, pulmonary oedema).


  • Echocardiography (cardiac tamponade, hypovolaemia, RV hypertension in PE, regional wall motion abnormality, aortic dissection).


  • Cardiac output monitoring (pulmonary artery catheterization, TOD, or pulse contour analysis may assist in differentiating between low cardiac output or low SVR states).


  • US and/or CT scan of chest, abdomen, pelvis (if occult haemorrhage is suspected).


Differential diagnoses



  • Damped arterial pressure traces or poorly fitting BP cuffs can giving spurious readings, if in doubt re-check manually.


  • Mild ‘hypotension’ may be a normal finding in fit healthy individuals.




Immediate management



  • Give 100% O2.


  • The airway may be compromised due to impaired conscious level:



    • Intubate the trachea as appropriate


    • If this is impossible (i.e. in a remote location) the patient can be placed in the recovery position (depending on other injuries)


  • Ensure breathing/ventilation is adequate:



    • In severe shock ventilatory support (non-invasive or invasive) may be needed to optimize oxygenation, especially in fatigued patients


    • If pulmonary oedema is present treat appropriately (image p.86)


  • Assess hypotension: questions which need to be answered include:



    • Is this BP low for this patient? What is their normal BP? Is there evidence of, or potential for, impaired cerebral perfusion, cardiac ischaemia, oliguria?


  • Treat any identifiable underlying cause requiring immediate attention:



  • Take a focused clinical history, carefully examine the patient, and review notes/charts where possible; identify the likely cause.

Hypovolaemia or haemorrhage (image p.112):



  • Fluid resuscitate and treat underlying cause or proceed to surgery.


  • Ensure IV access (typically 2 large-bore cannulae).


  • Initial resuscitation is usually in the form of crystalloids/colloids or warmed blood in the case of haemorrhage, given rapidly until there are signs of adequate filling (restoration of MAP, neurological function, urine output; normalization of tachycardia).


  • In haemorrhage awaiting source control (e.g. ruptured AAA, penetrating trauma) limited resuscitation targets may be necessary: palpable radial pulse, systolic BP ≤80 mmHg (‘permissive hypotension’).


  • Inotropes/vasopressors can be used but may mask hypovolaemia.

Vasodilatation (image p.108): treat underlying cause and commence fluid resuscitation, with/without vasopressor therapy:



  • Response to fluid bolus may be predicted by ↑ cardiac output or CVP (if monitored) after straight leg raising (45° for 4 minutes).

Cardiogenic failure (image p.122):



  • Record 12-lead ECG and compare to previous ECGs, assessing for evidence of myocardial infarction/ischaemia (image p.126).


  • Aggressive fluid therapy is not recommended in cardiogenic shock, although up to 500 ml can be given initially.

Inotropes/vasoactive agents: noradrenaline or adrenaline may be indicated in septic shock. In the case of a mixed picture adrenaline or dopamine may be started until a clearer diagnosis is possible. Dobutamine has been used in cardiogenic shock, but may not improve outcome.



Further management



  • Admit patients with refractory hypotension (unresponsive to moderate fluid resuscitation) into a suitable critical care facility.


  • Continue respiratory support until cardiovascular stability is achieved.


  • Arterial and/or central venous cannulation are likely to be needed.


  • Monitoring may be needed to obtain information about:



    • Ventricular filling (e.g. CVP, echocardiography, pulmonary artery catheterization)


    • Cardiac output and SVR (e.g. echocardiography, oesophageal Doppler, pulse contour analysis, pulmonary artery catheterization)


  • Optimize preload using crystalloids, colloids (or blood if required).


  • Consider optimizing cardiac contractility using inotropes (e.g. adrenaline, dobutamine).


  • Optimize SVR using vasoconstrictors (noradrenaline) or vasodilators (glyceryl trinitrate).


  • Correct any electrolyte imbalance and severe metabolic acidosis (renal replacement therapy may become necessary).


  • If there is no response to volume replacement, consider the possibility of spinal shock (image p.409) or adrenal insufficiency (image p.236).


  • See Table 4.1 for drugs used to treat hypotension.



Interpretation of CVC variables


Central venous pressure (CVP)



  • There is no ‘normal’ or ‘average’ CVP number, the measurement is determined by venous return and right ventricular compliance.


  • CVP measurement should be regarded as a trend.


  • It is conventional to volume load an under-resuscitated patient to a target CVP of approximately:



    • 8-10 mmHg in non-ventilated patients


    • 12-16 mmHg in ventilated patients


  • But CVP monitoring is dynamic, i.e. patients should be volume-loaded until a rise in CVP (or cardiac output) is sustained:



    • Repeated fluid challenges are likely to be required in shocked patients with low intravascular volume with compensatory vasoconstriction (initial rises in CVP or cardiac output are often transient)


    • Vasodilatory challenges (e.g. general anaesthesia) will cause the CVP to fall


  • Complete heart block, AF, tricuspid stenosis, and tricuspid regurgitation will lead to difficulty in interpreting CVP readings.


Central venous O2 saturations (ScvO2)



  • ScvO2 may be measured on blood drawn from a CVC (mixed venous blood, image, must be drawn from a PAFC).


  • Low values (<65%) are associated with a worse outcome in trauma, severe sepsis, myocardial infarction, and cardiac failure.


  • ScvO2 is affected by O2 content, O2 consumption, and cardiac output.


  • ScvO2 may be ‘artificially’ high in the presence of a significant shunt.


  • It is conventional to resuscitate patients to a target ScvO2 of >70%.


  • Monitoring should be dynamic to ensure that any rise is sustained.




Causes of deranged systemic vascular resistance


↑systemic vascular resistance



  • Hypothermia.


  • Vasoconstriction, or vasoconstrictive drugs (e.g. noradrenaline).


  • Sympathetic stimulation.


↓systemic vascular resistance



  • Sepsis.


  • Hyperthermia.


  • Hyperthyroidism.


  • A-V shunts.


  • Liver failure.


  • Vasodilators.


  • Spinal/epidural block or spinal shock.



Flow rates of different gauge cannulae1



  • 14 G (orange) 250-360 ml/minute


  • 16 G (grey) 130-220 ml/minute


  • 18 G (green) 75-120 ml/minute


  • 20 G (pink) 40-80 ml/minute


  • 22 G (blue)


Pitfalls/difficult situations



  • A MAP of 65 mmHg in a young fit patient (e.g. due to an epidural) may cause no tissue hypoperfusion, whereas in patients with vascular disease it may lead to myocardial ischaemia (coronary blood occurs mainly in diastole), cerebral ischaemia, or acute pre-renal failure.


  • Overlapping aetiologies and mixed pictures occur (e.g. sepsis with myocardial failure).


  • ↑CVP and lack of response to inotropes in suspected cardiogenic shock could be due to cardiac tamponade, pulmonary hypertension/embolism, or right ventricular infarction; use of echocardiography, or a right heart catheter (or radiological examination for PE) may assist in making the diagnosis.




1At 10 kPa via 110-cm tubing (internal diameter 4mm); source: This information was published in Anaesthesia and Intensive Care A-Z: An Encyclopedia of Principles and Practice, Yentis S, Hirsch N, Smith G, fourth edition, copyright Elsevier 2009.


Further reading

Antonelli M, et al. Hemodynamic monitoring in shock and implications for management: international consensus conference. Intensive Care Med 2007; 33: 575-59.

Dellinger RP, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock. Crit Care Med 2008; 36: 296-327.

Jackson K, et al. The role of hypotensive resuscitation in the management of trauma. J Intensive Care Soc 2009; 10(2): 109-14.

Maizel J, et al. Diagnosis of central hypovolemia by using passive leg raising. Intensive Care Med 2007; 33: 1133-8.

Pinsky MR. Hemodynamic evaluation and monitoring in the ICU. Chest 2007; 132: 2020-9.

Rady MY. Bench-to-bedside review: Resuscitation in the emergency department. Crit Care 2005; 9: 170-6.









Table 4.1 Drugs used to treat hypotension







































Drug

Dose

Comments


Adrenaline / Epinephrine

0.5-1 mg IM in anaphylaxis


0.5-1 mg IV/IO in cardiac arrest


0.05-3 µg/kg/minute IV infusion

β- and α-agonist: increases myocardial contractility, heart rate, and SVR


Agent of choice in anaphylaxis, cardiac arrest, and severe hypotension of undiagnosed cause Can cause increases in serum lactate


Noradrenaline/Norepinephrine

0.05-3 µg/kg/minute IV infusion

Predominantly α-agonist: (increases SVR); agent of choice in high-output and/or septic shock Should be used with caution in hypovolemic shock and cardiogenic shock


Dopamine

0.5-10 µg/kg/minute IV infusion

<5 µg/kg/minute, predominantly dopaminergic effects: increases renal/splanchnic perfusion 5-10 µg/kg/minute, mainly β and some α-agonism: increases heart rate, contractility and SVR Often used as first-line agent for moderate hypotension until the cause is established


Dobutamine

0.5-10 µg/kg/minute IV infusion

Predominantly β-agonistic: increases heart rate and myocardial contractility, and reduces systemic vascular resistance by dilating vascular supply to the muscles


Often used to treat cardiogenic shock


Can worsen hypotension if given in hypovolaemia


Metaraminol

Bolus 0.5 mg over 2-3 minutes

Used to increase systemic vascular resistance in high-output failure; boluses can be repeated until IV infusion of vasopressor is established


Phenylephrine

Bolus 0.1mg-0.5mg over 2-3 minutes

Same as metaraminol


Vasopressin

0.01-0.04 units/minutes IV infusion

Used to increase SVR in severe refractory septic shock


No evidence of superiority over noradrenaline


Terlipressin

1mg IV 8-hourly

Same as vasopressin




Anaphylaxis

Anaphylaxis is a severe, life-threatening, hypersensitivity reaction.


Causes



  • Insect bites (especially wasp and bee stings).


  • Foods and food additives (especially peanuts, fish, eggs).


  • Drugs and IV infusions, especially:



    • Antibiotics and vaccines


    • Colloids and blood products


    • IV contrast media


    • Pabrinex, parenteral vitamin K


    • Anaesthetic induction agents, neuromuscular blocking drugs


  • Latex allergy.


  • Idiopathic (no readily identifiable cause).


Presentation and assessment

Any combination of:



  • Cardiovascular collapse (75% of cases): cardiac arrest; or tachycardia, hypotension, and other signs of shock (image p.104).


  • Bronchospasm (40%): wheeze, cough, and/or accompanying desaturation, tachypnoea and dyspnoea.


  • Angioedema (12%): leading to laryngeal oedema and/or airway obstruction/stridor.


  • Cutaneous signs (72%): erythema, cutaneous rash, urticaria.


Investigations



  • Take blood samples for mast cell tryptase level:



    • As soon as possible after treatment of initial reaction, and


    • 1 hour after the reaction, and 6-24 hours after the reaction


  • ABGs (metabolic and/or respiratory acidosis).


  • FBC.


  • Clotting studies, fibrinogen (deranged with associated DIC).


  • U&Es, LFTs, magnesium.


  • CXR (to exclude differentials).

Tryptase samples should be stored at −20°C until it can be analysed. Concentrations peak at 1 hour, and concentrations of >20 ng/ml suggest anaphylaxis. A negative test does not exclude anaphylaxis. An immunologist may advise further tests after recovery.


Differential diagnoses



  • Airway/ETT obstruction, or endobronchial intubation.


  • Tension pneumothorax/haemothorax.


  • Air embolus/amniotic fluid embolus/fat embolus.


  • Severe bronchospasm/asthma.


  • Distributive shock (e.g. sepsis/neuraxial blockade/spinal cord injury).


  • Localized cutaneous reactions (e.g. type IV allergy: T cell mediated 6-48 hours after allergen exposure).


  • Hereditary angioneurotic oedema.


  • Thyroid crisis or carcinoid syndrome.




Immediate management



  • Stop trigger agents and call for help.


  • Give 100% O2.


  • Secure the airway and ensure breathing/ventilation is adequate; early endotracheal intubation may be required, especially in angio-oedema.


  • If already intubated exclude airway/breathing system obstruction.


  • Lie patient flat with legs elevated.


  • Give adrenaline (epinephrine): either IM or IV



    • IM dose 0.5-1 mg (0.5-1 ml of 1:1000) up to every 10 minutes


    • IV dose 50-100 mcg (0.5-1 ml of 1:10 000) over 1 minute, and repeat as necessary (only give if you are familiar with IV adrenaline usage)


    • Continuous ECG monitoring is advisable whilst giving adrenaline


  • Ensure IV access and commence rapid infusion of crystalloid.


  • Adrenaline infusions may be required.


  • If bronchospasm persists give: salbutamol 250 mcg slow IV or 2.5-5 mg via nebulizer; with/without magnesium sulphate 8 mmol IV (2g) and/or aminophylline 250 mg IV slowly (up to 5 mg/kg) if not already on theophylline.

Second-line therapies (when time allows):



  • Give chlorphenamine 10 mg IV slowly (ranitidine 50 mg IV may be given as well, but is of unknown benefit).


  • Give hydrocortisone 200 mg IV, then 100 mg IV 6-hourly.


Further management



  • If hypotension persists/relapses (5% of cases) start inotrope infusions.


  • Deflate the ETT cuff prior to extubation in order to ascertain a leak (to gauge the degree of airway oedema).


  • Refer the patient to an immunologist; include copies of the notes, drug chart, and a full description of the reaction chronology.


  • Serum IgE and skin-prick tests will be required.


  • Report anaphylactic reactions on a CSM ‘yellow card’.


  • If this was a ‘wrong blood’ reaction, send all products back to the lab and involve a haematologist.


Pitfalls/difficult situations



  • Monitor for a 2° deterioration or biphasic response.


  • Watch for the development of ARDS or DIC (may manifest hours later).


  • Myocardial infarction and arrhythmias can occur, especially if there is pre-existing ischaemic heart disease, or if hypoxia/acidosis is present.


  • Stridor may be mistaken for bronchospasm, and vice versa.


  • Do not forget that colloids and latex can cause anaphylaxis:



    • Latex anaphylaxis may present up to 30-60 minutes after an event due to delayed airborne exposure or mucous membrane contact.



Further reading

Association of Anaesthetists of Great Britain and Ireland. Suspected anaphylactic reactions associated with anaesthesia. Anaesthesia 2009; 64: 199-211.

NICE. Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode. London: NICE, 2011.



Haemorrhagic shock

Haemorrhagic shock occurs when loss of intravascular blood leads to hypotension and underperfusion of organs. Initially the body responds to hypovolaemia by peripheral vasoconstriction and tachycardia. Oliguria (urine <0.5 ml/kg/hour), and signs of organ failure (e.g. dyspnoea, myocardial failure, drowsiness) appear later.


Causes



  • Trauma.


  • GI bleeding.


  • Surgery or postoperative/post-procedure bleeding.


  • Bleeding in response to trivial trauma, associated with:



    • Coagulation factor abnormality (e.g. haemophilia)


    • Thrombocytopaenia


    • Splenomegaly


  • Other occult bleeding (thoracic, intra-abdominal or retroperitoneal; e.g. ruptured aortic aneurysm or ruptured ectopic pregnancy).


Presentation and assessment



  • There may be a bleeding site, or blood in postoperative drains.


  • Certain mechanisms of trauma can cause occult bleeding (image p.411).


  • Certain patients are more likely to have a coagulopathy (image p.302):



    • Patients receiving anticoagulant therapy


    • Patients with a history of congenital disease (may carry a card)


    • Patients being treated for haematological malignancy

In healthy individuals the physiological response to haemorrhage varies according to the volume of blood lost.

≤15% (0.75 L1) loss of total blood volume (TBV) results in:



  • Slight tachycardia and mild peripheral vasoconstriction (mildly ↑diastolic BP and narrowed pulse pressure).


  • Thirst may occur as accompanying symptom.

15-30% (0.75-1.5 L1) TBV loss:



  • Pulse rate increases to 100-120/minute (see image Pitfalls/difficult situations).


  • Vasoconstriction with clearly raised diastolic BP, narrowed pulse pressure and delayed capillary refill (>2 seconds).


  • Oliguria.


  • Patient may be anxious.

30-40% (1.5-2 L1) TBV loss:



  • Systolic hypotension develops; pulse becomes thready.


  • Dyspnoea develops.


  • Agitation ensues.

>40% (≥2 L1) TBV loss:



  • Severe hypotension.


  • Anuria.


  • Ashen complexion.


  • Drowsiness or unconsciousness.



Investigations

Blood crossmatch samples should be taken, other investigations include:



  • Diagnostic (to identify the bleeding source):



    • Plain radiographs (especially of pelvis and chest following trauma)


    • Abdominal US (may identify free blood, ruptured ectopic pregnancy, or aortic aneurysm)


    • CT scan, of pelvis, abdomen, or chest according to clinical indication


    • Diagnostic peritoneal lavage


    • Endoscopy (for suspected GI bleeding)


    • Angiography (may be diagnostic and/or potentially therapeutic)


    • Radio-labelled bleeding scan (may be considered if source unclear)


    • β-HCG, urine or blood (may aid in the diagnosis of ectopic pregnancy)


  • To monitor progress and identify the development of complications:



    • ABGs (metabolic acidosis)


    • FBC (anaemia, thrombocytopaenia); near-patient testing may be available, e.g. Haemacue®


    • Coagulation studies, including fibrinogen (↑ PT/APTT, ↓fibrinogen in DIC); near-patient testing may be available, e.g. ROTEM®


    • U&Es, LFTs, ECG (tachycardia, possible ischaemia)


Differential diagnoses

Any cause of shock must be considered, particularly:



  • Other causes of shock associated with trauma (e.g. tension pneumothorax, cardiac tamponade, cardiac contusion, spinal cord lesion).


  • Hypovolaemic shock 2° to fluid losses other than blood:



    • Profound dehydration (e.g. DKA, vomiting, diarrhoea, diuresis)


    • Massive ‘third-space’ losses (e.g. profound ileus, sepsis, major burn)


  • Cardiogenic shock; left or right ventricular failure (e.g. myocardial infarction, aortic stenosis, hypertrophic cardiomyopathy, PE).


  • Distributive shock (e.g. sepsis, anaphylaxis, neuraxial blockade).



Immediate management



  • Give 100% O2 initially, then titrate SpO2 to 94-98%.


  • In cases of trauma ensure cervical spine protection.


  • Secure the airway and ensure breathing/ventilation is adequate; endotracheal intubation may be required.


  • Assess the degree of blood loss and control haemorrhage if possible:



    • Compression/elevation of external bleeding sites, or use of a tourniquet in life-threatening haemorrhage from a limb


    • The patient may require immediate life-saving surgery (e.g. ectopic pregnancy, ruptured spleen)


    • Stabilize fractures


    • Consider endoscopic or interventional radiological procedures


    • Reverse the effects of any anticoagulants if they are present (e.g. using vitamin K IV, or prothrombin complex IV)


    • Administering tranexamic acid IV 1 g and vitamin K IV 10 mg may promote haemostasis in major haemorrhage



  • Commence circulatory support in shocked patients:



    • Head-down tilt (Trendelenburg) may be required


    • Insert large-bore (14 G) IV cannulae into both antecubital fossa


    • In difficult cases the use of femoral veins, external jugular veins may be required; or an IV cutdown at the ankle or antecubital fossa (image p. 540) or insert IO access


    • Take a sample for blood crossmatching when inserting cannulae


    • Start restoring intravascular volume (image p.116)


    • Commence blood transfusion1 alongside crystalloids/colloids as soon as possible if bleeding is >30%TBV, >1.5 L, or Hb <8 g/dl with ongoing haemorrhage


    • O-negative or type-specific blood may be required in severe haemorrhage whilst waiting for crossmatched blood


  • In haemorrhage awaiting source control (e.g. ruptured AAA, penetrating trauma) limited resuscitation targets may be necessary: palpable radial pulse, systolic BP ≤80 mmHg (‘permissive hypotension’).


  • Use inotropes/vasopressors with caution (they may mask under-resuscitation).


  • Where there is massive blood loss (≥6 units of blood or ≥30% TBV lost) involve haematologists for guidance on appropriate blood and component therapy; common protocols include the following:



    • FFP (12 ml/kg; or approximately 2 bags) if PT or APTT >1.5 × normal, or if more than 4-6 units of stored blood is transfused


    • Platelets (0.5-1 units/10 kg body weight; or 1-2 adult doses) if the count is <50 × 109/L


    • Cryoprecipitate (1 pack/10 kg body weight) if fibrinogen <0.8 g/L


    • Repeat coagulation studies every 2 hours, or after every 4-6 units of packed red cells


  • Consider using recombinant factor VIIa.


  • Cell-salvage may be available in some settings.


Further management



  • Many centres now have ‘major haemorrhage packs’ consisting of various quantities of packed red cells, fresh frozen plasma, cryoprecipitate, and platelets for use in the event of massive transfusion requirements.


  • Look for and treat complications of massive blood transfusion (e.g. hypothermia, hypocalcaemia, hyperkalaemia, coagulation factor depletion, thrombocytopaenia, metabolic acidosis).


  • Some or all of the following monitoring is likely to be needed:



    • CVC to assess intravascular fluid status


    • Urinary catheterization to allow urine output measurements


    • Arterial line insertion for invasive BP measurements


    • CO monitoring to assess cardiac contractility and vascular resistance


  • Inotropic support may be required, but this should be discontinued as soon as volume replacement and the control of bleeding allows; adrenaline or noradrenaline are the initial agents of choice.




Major haemorrhage protocol

Once severe haemorrhagic shock has been identified contact consultant-in-charge, switchboard, haematologist/blood bank; provide the following information:

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Jun 13, 2016 | Posted by in CRITICAL CARE | Comments Off on Circulation

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