Cardiovascular emergencies

Adult basic life support

Basic life support (BLS) is the backbone of effective resuscitation following a cardiorespiratory arrest. The aim is to maintain adequate ventilation and circulation until the underlying cause for the arrest can be reversed. 3–4 minutes without adequate perfusion (less if the patient is hypoxic) will lead to irreversible cerebral damage. The usual scenario is an unresponsive patient found by staff, who alert the cardiac arrest team. The initial assessment described below should have already been performed by the person finding the patient. The same person should have also started cardiopulmonary resuscitation (CPR). Occasionally you will be the first to discover the patient, and it is important to rapidly assess the patient and begin CPR. The various stages in basic life support are described here and summarized in Fig. 17.1.

Fig. 17.1 Adult basic life support. 2010 For further information see The Resuscitation Council (UK) website http://www.resus.org.uk/.

1. Assessment of the patient

2. Airway assessment

3. Assessment of circulation

Adult advanced life support

Fig. 17.2 Opening airways. Reproduced with permission from Ramrakha P, Moore K, Sam M (2010). Oxford Handbook of Acute Medicine, 3rd ed. Oxford: Oxford University Press.

Fig. 17.3 Insertion of nasopharyngeal airway. Reproduced with permission from Ramrakha P, Moore K, Sam M (2010). Oxford Handbook of Acute Medicine, 3rd ed. Oxford: Oxford University Press.

• Try to establish the events that precipitated the arrest from the history, staff, witnesses, and the hospital notes of the patient. Is there an obvious cause (myocardial infarction (MI), hypoxia, hypoglycaemia, stroke, drug overdose or interaction, electrolyte abnormality, etc.)? Record the duration of the arrest in the notes, with the interventions, drugs (and doses) in chronological order.

• Examine the patient to check both lung fields are being ventilated; check for ribs that may have broken during CPR. Listen for any cardiac murmurs. Check the neck veins. Examine the abdomen for an aneurysm or signs of peritonism. Insert a urinary catheter. Consider a nasogastric (NG) tube if the patient remains unconscious. Record the Glasgow Coma Score and perform a brief neurological assessment.

• Investigations: electrocardiogram (ECG) (looking for MI, ischaemia, tall T waves (K⁺)); arterial blood gases (ABG) (mixed metabolic and respiratory acidosis is common and usually responds to adequate oxygenation and ventilation once the circulation is restored; if severe, consider bicarbonate); chest X-ray (CXR; check position of ET tube, look for pneumothorax); urea and electrolytes (U&Es), and glucose.

• After early and successful resuscitation from a primary cardiac arrest, the patient may rapidly recover completely. The patient must be transferred to high-dependency unit (HDU) or coronary care unit (CCU) to monitor for 12–24 h. Commonly the patient is unconscious post-arrest and should be transferred to the intensive therapy unit (ITU) for mechanical ventilation and haemodynamic monitoring and support for ≥24 hours.

• Change any venous lines that were inserted at the time of arrest for central lines inserted with sterile technique. Insert an arterial line and consider a pulmonary artery (PA) catheter (Swan–Ganz) if requiring inotropes.

• Remember to talk to the relatives. Keep them informed of events and give a realistic (if bleak) picture of the arrest and possible outcomes.

• When appropriate, consider the possibility of organ donation and do not be frightened to discuss this with the relatives. Even if discussion with the relatives is delayed, remember corneas and heart valves may be used up to 24 hours after death.

Universal treatment algorithm

Fig. 17.4 The advanced life support 2010 universal algorithm for the management of cardiac arrest in adults. For further information see The Resuscitation Council (UK) website http://www.resus.org.uk/.

VF/VT

• VF/VT are the most common rhythms at the time of cardiac arrest.

• Success in treatment of VF/VT is dependent on the delivery of prompt defibrillation. With each minute, the chances of successful defibrillation decline by 7–10%.

• Precordial thump: if arrest is witnessed or monitored, a sharp blow with a closed fist on the patient’s sternum may convert VF/VT back to a perfusing rhythm. It is particularly effective if delivered within 30 s after cardiac arrest.

• Shock cycles are generally in groups of three. Initially 200 J, 200 J, and 360 J, with subsequent cycles at 360 J.

• After each shock (or sequence), the carotid pulse should be palpated only if the waveform changes to one usually capable of providing a cardiac output.

• The shock cycle is repeated every minute if VF/VT persists.

• Myocardial and cerebral viability must be maintained after each shock cycle, with chest compressions and ventilation.

• In between cycles of defibrillation, reversible factors must be identified and corrected, the patient intubated (if possible) and venous access obtained.

• Adrenaline should be given every 3 minutes (1 mg IV and 2–3 mg via endotracheal route).

Non-VF/VT rhythms

• The outcome from these rhythms is generally worse than VF/VT unless a reversible cause can be identified and treated promptly.

• Chest compressions and ventilation should be undertaken for three minutes with each loop of the algorithm (1 min if directly after a shock).

• With each cycle, attempts must be made to intubate the patient, gain IV access and give adrenaline.

Asystole

• Atropine 3 mg IV should be given to block all vagal output.

• In the presence of P waves on the ECG strip/monitor, pacing (external or transvenous) must be considered.

PEA

• Identification of the underlying cause and its correction are both vital for successful resuscitation. Resuscitation must be continued while reversible causes are being sought.

Primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction (see p. 268)

• Primary percutaneous coronary intervention (PCI) is the current gold standard reperfusion strategy for treatment of ST-segment elevation MI (STEMI).

• Primary PCI requires significant coordination between the emergency services, community hospitals, and invasive centres. It must only be performed if: (1) a primary PCI programme is available; (2) the patient presents to an invasive centre and can undergo catheterization without delay.

Indication for primary PCI

• All patients with chest pain and ST-segment elevation or new left bundle branch block (LBBB) fulfil primary PCI criteria (compare with indications for thrombolysis).

• This will include a group of patients where ST-segment elevation may not fulfil thrombolysis criteria.

• In general, patients in whom thrombolysis is contraindicated should be managed by primary PCI. Cases where there is significant risk of bleeding must be managed individually.

Acute MI: thrombolysis protocol

See Fig. 17.5.

Fig. 17.5 Acute MI: thrombolysis protocol. BP = blood pressure; CVA = cerebrovascular accident; INR = international normalized ratio.

Acute myocardial infarction

ST elevation myocardial infarction (STEMI)	p. 256
STEMI: diagnosis	p. 258
STEMI: general measures	p. 262
STEMI: reperfusion therapy (thrombolysis)	p. 264
STEMI: reperfusion by primary PCI	p. 268
Rescue PCI	p. 269
STEMI: additional measures	p. 270
Right ventricular (RV) infarction	p. 272
STEMI: predischarge risk stratification	p. 274
STEMI: complications	p. 276
Ventricular septal defect post-MI	p. 278
Acute mitral regurgitation post-MI	p. 280
Pseudoaneurysm and free-wall rupture	p. 281
Cocaine-induced MI	p. 282
Ventricular tachyarrhythmias post-MI	p. 284
Atrial tachyarrhythmia post-MI	p. 284
Bradyarrhythmias and indications for pacing	p. 285
Bradyarrhythmias post-MI	p. 285
Hypotension and shock post-MI	p. 286
Non-ST elevation myocardial infarction (NSTEMI)/unstable angina (UA)	p. 290

Treatment options in tachyarrhythmias

Ventricular tachycardia: drugs

See Table 17.1.

Table 17.1 Dosages of selected antiarrhythmics for the acute treatment of VT

Drug	Dosage
Magnesium sulphate	Loading dose 8 mmol (2g) IV over 2–15 min (repeat once if necessary) Maintenance dose 60 mmol/48 mL saline at 2–3 mL/h
Lidocaine	Loading dose 100 mg IV over 2 min (repeat once if necessary) Maintenance dose 4 mg/min for 30 min 2 mg/min for 2 h 1–2 mg/min for 12–24 h
Procainamide	Loading dose 100 mg IV over 2 min Repeat every 5 min to max 1 g Maintenance dose 2–4 mg/min IV infusion 250 mg q6h PO
Amiodarone	Loading dose 300 mg IV over 60 min via central line followed by 900 mg IV over 23 h or 200 mg PO tds x 1 week then 200 mg PO bd x 1 week Maintenance dose 200–400 mg od IV or PO
Disopyramide	Loading dose 50 mg IV over 5 min repeated every 5 min up to maximum 150 mg IV 200 mg PO Maintenance dose 2–5 mg/min IV infusion 100–200 mg q6h PO
Flecainide	Loading dose 2 mg/kg IV over 10 min (max 150 mg) Maintenance dose 1.5 mg/kg IV over 1 hour then 100–250 mcg/kg/h IV for 24 h or 100–200 mg PO bd

Supraventricular tachyarrhythmias

See Table 17.2.

Table 17.2 Dosages of selected antiarrhythmics for SVT

Drug	Dosage
Digoxin	Loading dose: IV 0.75–1 mg in 50 mL saline over 1–2 h PO 0.5 mg q12h for 2 doses then 0.25 mg q12h for 2 days Maintenance dose: 0.0625–0.25 mg daily (IV or PO)
Propranolol	IV 1 mg over 1 min, repeated every 2 min up to maximum 10 mg PO 10–40 mg 3–4 times a day
Atenolol	IV 5–10 mg by slow injection PO 25–100 mg daily
Sotalol	IV 20–60 mg by slow injection PO 80–160 mg bd
Verapamil	IV 5 mg over 2 min; repeated every 5 min up to maximum 20 mg PO 40–120 mg tds
Procainamide	IV 100 mg over 2 min; repeated every 5 min up to maximum 1 g PO 250 mg q6h
Amiodarone	Loading dose: IV 300 mg over 60 min via central line followed by 900 mg IV over 23 h or PO 200 mg tds x 1 week then 200 mg PO bd x 1 week Maintenance dose: 200–400 mg od IV or PO
Disopyramide	IV 50 mg over 5 min; repeated every 5 min up to maximum 150 mg IV 100–200 mg q6h PO
Flecainide	2 mg/kg IV over 10 min (max 150 mg) or 100–200 mg PO bd

Acute pulmonary oedema: assessment

Presentation

• Acute breathlessness, cough, frothy blood-stained (pink) sputum

• Collapse, cardiac arrest, or shock

• Associated features may reflect underlying cause:

• chest pain or palpitations—? ischaemic heart disease (IHD)/MI, arrhythmia

• preceding history of dyspnoea on exertion—? IHD, poor left ventricular (LV) function

• oliguria, haematuria—? acute renal failure

• seizures, signs of intracranial bleed.

Causes

A diagnosis of pulmonary ooedema or ‘heart failure’ is not adequate. An underlying cause must be sought in order to direct treatment appropriately. Causes may be divided into:

• increased pulmonary capillary pressure (hydrostatic)

• increased pulmonary capillary permeability

• decreased intravascular oncotic pressure.

Often there is a combination of factors involved (e.g. pneumonia, hypoxia, cardiac ischaemia); see Drugs for hypertensive emergencies, p. 760.

The main differential diagnosis is acute (infective) exacerbation of chronic obstructive pulmonary disease (COPD) (previous history, quiet breath sounds ± wheeze, fewer crackles). It may be difficult to differentiate the two clinically.

Principles of management

1. Stabilize the patient—relieve distress and begin definitive treatment.

2. Look for an underlying cause.

3. Address haemodynamic and respiratory issues.

4. Optimize and introduce long-term therapy.

Initial rapid assessment

• If the patient is very unwell (e.g. unable to speak, hypoxic, systolic BP <100 mmHg), introduce stabilizing measures and begin treatment immediately before detailed examination and investigations (see Pulmonary oedema: management, p. 728).

• If the patient is stable and/or if there is doubt as to the diagnosis, give oxygen and diuretic, but await the outcome of clinical examination and CXR before deciding on definitive treatment.

Urgent investigations for all patients

• ECG	• Sinus tachycardia most common
	• ? any cardiac arrhythmia (atrial fibrillarion (AF), SVT, VT)
	• ? evidence of acute ST change (STEMI, NSTEMI, unstable angina (UA))
	• ? evidence of underlying heart disease (left ventricular hypertrophy (LVH), p mitrale)
• CXR	• To confirm the diagnosis, looking for interstitial shadowing, enlarged hila, prominent upper lobe vessels, pleural effusion, and Kerley B lines. Cardiomegaly may or may not be present. Also exclude pneumothorax, pulmonary embolus (oligaemic lung fields), and consolidation
• ABG	• Typically ↓PaO2. PaCO2 levels may be ↓ (hyperventilation) or depending on the severity of pulmonary oedema. Pulse oximetry may be inaccurate if peripherally shut down
• U&Es	• ? pre-existing renal impairment. Regular K+ measurements (once on IV diuretics)
• Full blood count (FBC)	• ? anaemia or leucocytosis, indicating the precipitant
• Echocardiography (ECHO)	• As soon as practical to assess LV function, valve abnormalities, ventricular septal defect (VSD), or pericardial effusion

P_aCO₂ = partial pressure of carbon dioxide in the arterial blood; P_aO₂ = partial pressure of oxygen in the arterial blood.

---

Investigations for patients with pulmonary oedema

All patients should have:

• FBC, U&Es, C-reactive protein (CRP)

• serial biochemical markers of myocardial injury (creatine kinase (CK), CK-MB, troponins)

• liver function tests (LFTs), albumin, total protein

• ECG

• CXR

• ECHO (± transoesophageal echocardiography (TOE))

• arterial blood gases.

Where appropriate, consider:

• septic screen (sputum, urine, blood cultures)

• Holter monitor (?arrhythmias)

• coronary angiography (?IHD)

• right and left heart catheter (if ECHO is unable to provide adequate information on pressures, shunts, valve disease)

• endomyocardial biopsy (myocarditis, infiltration)

• multigated acquisition (MUGA) scan

• cardiopulmonary exercise test with an assessment of peak oxygen consumption.

---

Pulmonary oedema: causes

Look for an underlying cause for pulmonary oedema.

Note: the critical LA pressure for hydrostatic ooedema = serum albumin (g/L) x 0.57.

Pulmonary oedema: management

Stabilize the patient

• Patients with acute pulmonary oedema should initially be continuously monitored and managed where full resuscitation facilities are available.

• Sit the patient up in bed.

• Give 60–100% oxygen by face mask (unless contraindicated, COPD).

• If the patient is severely distressed, summon the ‘on-call’ anaesthetist and inform ITU. If dyspnoea cannot be significantly improved by acute measures (below) the patient may require continuous positive airways pressure (CPAP) or mechanical ventilation.

• Treat any haemodynamically unstable arrhythmia (urgent synchronized DC shock may be required (see DC cardioversion, p. 818).

• Give:

• diamorphine 2.5–5 mg IV (caution abnormal ABGs)

• metoclopramide 10 mg IV

• furosemide 40–120 mg slow IV injection.

• Secure venous access and send blood for urgent U&Es, FBC, and cardiac enzymes (including troponin).

• Unless thrombolysis is indicated, take ABG.

• If the systolic blood pressure is ≥90 mmHg and the patient does not have aortic stenosis:

• give sublingual glyceryl trinitrate (GTN) spray (2 puffs)

• start IV GTN infusion 1–10 mg/h, increase the infusion rate every 15–20 minutes, titrating against blood pressure (aiming to keep systolic BP ∼100 mmHg).

• If the systolic blood pressure is <90 mmHg, treat patient as cardiogenic shock (see NSTEMI/UA: invasive versus non-invasive strategies, p. 301).

• Insert a urinary catheter to monitor urine output.

• Repeat ABG and K⁺ if the clinical condition deteriorates/fails to improve, or after 2 h if there is improvement and the original sample was abnormal.

• Monitor pulse, BP, respiratory rate, O₂ saturation with a pulse oximeter (if an accurate reading can be obtained), and urine output.

If the patient responds arrange appropriate investigations as listed on Acute pulmonary oedema: assessment, p. 724 to help with further management. However, if there is further deterioration, specific measures should be taken to address problems.

Further management

The subsequent management of the patient is aimed at ensuring adequate ventilation/gas exchange and haemodynamic stability and correcting any reversible precipitins of acute pulmonary oedema.

• Assess the patient’s respiratory function:

• does the patient require respiratory support?

• Assess the patient’s haemodynamic status (see Cardiogenic shock, p. 288):

• is the patient in shock (?(see Cardiogenic shock, p. 288).

• Look for an underlying cause (see Pulmonary oedema: causes, p. 726).

• Conditions that require specific treatment:

• acute aortic and mitral regurgitation

• diastolic LV dysfunction

• fluid overload

• renal failure

• severe anaemia

• hypoproteinaemia.

If the patient remains unstable and/or deteriorates, assess their respiratory function.

Assessment of respiratory function

• Wheeze may be caused by interstitial pulmonary oedema. If there is a history of asthma, give nebulized salbutamol (2.5–5 mg), nebulized ipratropium bromide (500 mcg), and hydrocortisone (200 mg) IV. Consider commencing aminophylline infusion. This will relieve bronchospasm, as well as ‘off-load’ by systemic vasodilatation. However, it may worsen tachycardia, and can be arrhythmogenic and lower K⁺ (supplement to ensure K⁺ 4–5 mmol/L).

• Indications for further respiratory support include:

• patient exhaustion or continuing severe breathlessness

• persistent P_aO₂<8 kPa

• rising P_aCO₂

• persistent or worsening acidosis (pH < 7.2).

• CPAP: this may be tried for co-operative patients, who can protect their airway, and have adequate respiratory muscle strength and who are not hypotensive. The positive pressure reduces venous return to the heart and may compromise BP.

• Endotracheal intubation and mechanical ventilation may be required, and some positive end-expiratory pressure (PEEP) should be used.

• Discuss the patient with the on-call anaesthetist or ITU team early.

Assess the patient’s haemodynamic status

It is important to distinguish between cardiogenic and non-cardiogenic pulmonary oedema, as further treatment is different between the two groups. This may be difficult clinically. A PA (Swan–Ganz) catheter must be inserted if the patient’s condition will allow.

• Non-cardiogenic pulmonary oedema occurs when the hydrostatic pressure within the capillary system exceeds the plasma oncotic pressure. In patients with hypoalbuminaemia this will occur at a pulmonary capillary wedge pressure (PCWP)<15 mmHg. The critical PCWP may be estimated by serum albumin (g/L) x 0.57. Thus, a patient with a serum albumin of 15 g/L will develop hydrostatic pulmonary oedema at a LA pressure of 8 mmHg; a serum albumin of 30 g/L will require an LA pressure of >17 mmHg, and so on …

• Cardiogenic pulmonary oedema is often associated with significant systemic hypotension or low-output states. Contributing factors include conditions where there is ‘mechanical’ impairment to forward flow (e.g. valvular heart disease (especially if acute), VSD), or severe myocardial disease (large MI, ongoing ischaemia, acute myocarditis, cardiomyopathy).

• The gradient between PA diastolic pressure (PAD) and PCWP (PAD – PCWP) is generally <5 mmHg in cardiogenic and >5 mmHg in non-cardiogenic pulmonary oedema (e.g. ARDS).

• The pulse and BP are most commonly elevated due to circulating catecholamines and overactivity of the renin–angiotensin system (RAS). Examination reveals sweating, cool ‘shut-down’ peripheries, high pulse volume (assess carotid or femoral pulses).

Management

The general approach involves combination of diuretics, vasodilators ± inotropes. Patients may be divided into two groups:

• patients in shock (with systolic BP<100 mmHg)—see Pulmonary oedema: management, p. 728

• haemodynamically stable patients with systolic BP >100 mmHg— (see Pulmonary oedema, p. 726–733.

Patients with systolic BP<100 mmHg

• The patient is in incipient (or overt) shock. The most common aetiology is cardiogenic shock but remember non-cardiogenic causes (e.g. ARDS, septic shock).

• Optimal monitoring and access: central line ± PA catheter (Swan–Ganz), urinary catheter, arterial line (monitoring BP and ABG). Internal jugular lines are preferable, as the risk of pneumothorax is lower.

• Ensure the patient is not underfilled, using PCWP as a guide (<10 mmHg) (mistaken diagnosis e.g. septic shock from bilateral pneumonia).

• Is there a mechanical cause that may require emergency surgery?

• Arrange an urgent ECHO to rule out:

— VSD and acute mitral regurgitation (MR) in all patients with recent MI with/without new murmur (see Ventricular septal defect post-MI, p. 278; Acute mitral regurgitation post-MI, p. 280)

— prosthetic heart valve dysfunction (e.g. dehiscence, infection) or pre-existing native aortic or mitral disease that may require surgery.

• Discuss the patient early on with cardiologist/cardiac surgeon.

The choice of inotropic agent depends on the clinical condition of the patient and, to some extent, the underlying diagnosis:

• Systolic BP 80–100 mmHg and cool peripheries: start dobutamine infusion at 5 mcg/kg/min, increasing by 2.5 mcg/kg/min every 10–15 minutes to a maximum of 20 µg/kg/min until BP>100 mmHg. This may be combined with dopamine (2.5–5 mcg/kg/min). However, tachycardia and/or hypotension secondary to peripheral vasodilation my limit its effectiveness. Phosphodiesterase inhibitors (enoximone or milrinone) should be considered where dobutamine fails.

• Systolic BP <80 mmHg: give a slow IV bolus of adrenaline (2–5 mL of 1 in 10 000 solution Minijet^®) and repeat if necessary.

• Dopamine at doses of >2.5 µg/kg/min has a pressor action in addition to direct and indirect inotropic effects and may be used at higher doses (10–20 mcg/kg/min) if the blood pressure remains low. However, it tends to raise the pulmonary capillary filling pressure further and should be combined with vasodilators (e.g. nitroprusside or hydralazine) once the blood pressure is restored (see below). Beware of arrhythmias at these doses.

• Adrenaline infusion may be preferred to high-dose dopamine as an alternative inotrope. Once the blood pressure is restored (>100 mmHg), vasodilators such as nitroprusside/hydralazine or GTN infusion should be added to counteract the pressor effects. Adrenaline can be combined with dobutamine and/or a phosphodiesterase inhibitor, especially in the context of a poor ventricle.

• Intra-aortic balloon counter pulsation should also be used with/without inotropes in the context of a potentially reversible cause for the pulmonary oedema and shock (e.g. ongoing myocardial ischaemia, VSD, acute MR).

• Further doses of diuretic may be given.

Patients with systolic BP ≥100 mmHg

• Further doses of diuretic may be given (furosemide 40–80 mg IV q3–4h or as a continuous infusion (20–80 mg/h)).

• Continue the GTN infusion, increasing the infusion rate every 15–20 min up to 10 mg/h, titrating against blood pressure (aiming to keep systolic BP ∼100 mmHg).

• Angiotensin-converting enzyme inhibitors (ACE-Is) can be used if BP is adequate and there are no other known contraindications (e.g. RAS, renal failure). Arteriolar vasodilators (nitroprusside or hydralazine) may also be added in or used instead of GTN (± ACE-I) in patients with adequate BP. Arterial pressure should be monitored continuously via an arterial line to prevent inadvertent hypotension.

Long-term management

• Unless a contraindication exists, start an ACE-I, increasing the dose to as near the recommended maximal dose as possible. In the context of LV impairment, ACE-Is have significant prognostic benefit.

• If ACE-Is are contraindicated or not tolerated, consider the use of hydralazine and long-acting oral nitrate in combination.

• If the patient is already on high doses of diuretics and ACE-Is, consider the addition spironolactone (25–50 mg) (NB: monitor renal function and serum potassium).

• In the context of stable patients (no clinical features of failure) and poor LV function, β–blockers have significant mortality and some symptomatic benefit (NB: start with a very small dose and increase gradually every 2 weeks with regular monitoring). Bisoprolol, carvedilol, and metoprolol can all be used.

• Ensure all arrhythmias are treated.

• Digoxin can be used for symptomatic improvement.

• Consider multisite pacing (biventricular) in the context of severe LV dysfunction, broad QRS complex ± MR on ECHO.

• Patients in AF, or with poor LV function should be considered for long-term anticoagulation.

• Patients <60 years with severe irreversible LV dysfunction and debilitating symptoms must be considered for cardiac transplantation.

Pulmonary oedema: specific conditions

Diastolic LV dysfunction

• This typically occurs in elderly hypertensive patients with LV hypertrophy, where there is impaired relaxation of the ventricle in diastole. There is marked hypertension, pulmonary oedema, and normal, or only mild, systolic LV impairment.

• With tachycardia, diastolic filling time shortens. As the ventricle is ‘stiff’ in diastole, LA pressure is increased and pulmonary oedema occurs (exacerbated by AF, as filling by atrial systole is lost).

• Treatment involves control of hypertension with IV nitrates (and/or nitroprusside), calcium-channel blockers (verapamil or nifedipine) and even certain β-blockers (e.g. carvedilol, bisoprolol).

Fluid overload

• Standard measures are usually effective.

• In extreme circumstances, venesection may be necessary.

• Check the patient is not anaemic (haemoglobin (Hb)≥10 g/dL). Remove 500 mL blood via a cannula in a large vein and repeat if necessary.

• If anaemic (e.g. renal failure) and acutely unwell, consider dialysis.

Known (or unknown) renal failure

• Unless the patient is permanently anuric, large doses of IV furosemide may be required (up to 1 g given at 4 mg/min) in addition to standard treatment.

• If this fails, or the patient is known to be anuric, dialysis will be required.

• In patients not known to have renal failure, an underlying cause should be sought.

Anaemia

• Cardiac failure may be worsened or precipitated by the presence of significant anaemia. Symptoms may be improved in the long term by correcting this anaemia.

• Generally, transfusion is unnecessary with Hb>9 g/dL unless there is a risk of an acute bleed. Treatment of pulmonary oedema will result in haemoconcentration and a ‘rise’ in the Hb.

• If the anaemia is thought to be exacerbating pulmonary oedema, ensure that an adequate diuresis is obtained prior to transfusion. Give slow transfusion (3–4 h per unit) of packed cells, with IV furosemide 20–40 mg before each unit.

Hypoproteinaemia

• The critical left atrial (LA) pressure at which hydrostatic pulmonary oedema occurs is influenced by the serum albumin and approximates to serum albumin concentration (g/L) x 0.57.

• Treatment involves diuretics, cautious albumin replacement, spironolactone (if there is secondary hyperaldosteronism), and treatment of the underlying cause for hypoproteinaemia.

Acute aortic regurgitation

Presentation

• Sudden, severe aortic regurgitation (AR) presents as cardiogenic shock and acute pulmonary oedema.

• The haemodynamic changes are markedly different from those seen in chronic AR. The previous normal-sized LV results in a smaller effective forward flow and higher LVEDP for the same degree of AR.

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Valvular Heart Disease
2. Practical Procedures
3. Eponymous syndromes
4. Practical procedures

Stay updated, free articles. Join our Telegram channel

Join