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Emergency care in cardiology (part 2)

Heart failure is a clinical syndrome characterised by:

 Typical symptoms: breathlessness, fatigue, ankle swelling.

 Typical signs: tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised jugular
venous pressure (JVP), peripheral oedema, hepatomegaly.
 Objective evidence of a structural or functional abnormality of the heart at rest:
cardiomegaly, third heart sound, cardiac murmurs, echocardiogram abnormalities, raised
natriuretic peptide concentration.

Heart failure should never be the only diagnosis, as it is a syndrome occurring as a result of other
diagnostic entities.

Classification

Acute and chronic

Heart failure has traditionally been described as acute or chronic, but this can be confusing and
should be used to describe time, rather than severity. New-onset (first presentation with acute or
slow onset), transient (recurrent or episodic) and chronic (persistent whether stable, worsening or
decompensated) heart failure may be a more useful classification.

Systolic and diastolic

Similarly, a distinction is frequently made between systolic and diastolic heart failure. This is
somewhat arbitrary and many patients with heart failure have evidence of both. Left ventricular
systolic dysfunction (LVSD) is usually defined as an LV ejection fraction <40% on
echocardiography. Some symptomatic patients have a normal ejection fraction and no obvious
cause for increased myocardial demand. This condition has been variously termed diastolic heart
failure, heart failure with preserved LV function, heart failure with a normal ejection fraction
(HFNEF) or heart failure with preserved systolic function (HFPSF).

High and low output

Certain medical conditions increase demands on cardiac output, causing a clinical picture of
heart failure and this is known as high-output cardiac failure. The primary abnormality is not the
heart and the heart failure is reversible with treatment. Low-output failure is where cardiac
output is inadequate to perfuse the body (ie ejection fraction <40%), or can only be adequate
with high filling pressures.

Epidemiology
 Prevalence of asymptomatic ventricular dysfunction is approximately 4%.
 1-2% of the adult population in developed countries has heart failure, with the prevalence
rising to 10% in patients 70 years of age or older.
 Community estimates of prevalence vary from 1.6 to 4.6 cases per 1,000 in men aged 45-
74 years and from 0.9 to 2.2 cases per 1,000 in women.
 In younger age groups, heart failure is more common in men because of the earlier onset
of ischaemic heart disease (IHD).
 Prevalence is increasing due to aging populations and improved survival after coronary
events and secondary prevention.
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A UK survey of heart failure management in general practice found an average prevalence of 8.3
per 1,000 population.

Aetiology

Coronary heart disease and hypertension are the most common causes of heart failure in the UK.

 Valve heart disease - approximately 10% of cases:

o Aortic stenosis can cause left ventricular hypertrophy (LVH) due to chronic
excessive afterload.
o Aortic or mitral regurgitation, atrial septal defect (ASD), ventricular septal defect
(VSD) and tricuspid incompetence cause excessive preload.
 Heart failure secondary to myocardial disease:
o Coronary heart disease ((MI) and ischaemia, arrhythmias, eg atrial fibrillation
(AF), heart block).
o Hypertension (increased vascular resistance, often with LVH but preserved
ejection fraction).
o Cardiomyopathies.
o Drugs, eg betablockers, calcium antagonists, anti-arrhythmics, cytotoxics.
o Toxins, eg alcohol, cocaine, mercury, cobalt, arsenic.
o Endocrine, eg diabetes, hypothyroidism, hyperthyroidism, Cushing's syndrome,
adrenal insufficiency, excessive growth hormone, phaeochromocytoma.
o Nutritional, eg deficiencies of thiamine, selenium, carnitine, and obesity,
cachexia.
o Infiltrative, eg sarcoidosis, amyloidosis, haemochromatosis, Löffler's
eosinophilia, connective tissue disease.
o Infective eg Chagas' disease, HIV.
 High-output failure - this occurs when cardiac output is normal or increased in the face of
much increased needs. It can occur with a normal heart, but even earlier if there is heart
disease. Causes include:
o Anaemia.
o Pregnancy.
o Hyperthyroidism.
o Paget's disease of bone.
o Arteriovenous malformations.
o Beriberi.

Presentation

In general, the heart fails as a whole, but sometimes a disproportionate burden falls on one
ventricle, and this influences the pattern of symptoms and signs. There is no symptom or sign
that is both sensitive and specific for chronic heart failure.

Symptoms

Patients do not necessarily have all, and some may be predominant at times. In addition, patients
may be depressed or complain of drug-related side-effects.

 Dyspnoea and fatigue (may limit exercise tolerance).

 Fluid retention (may cause pulmonary or peripheral oedema).
 Orthopnoea.
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 Paroxysmal nocturnal dyspnoea (PND).
 Nocturnal cough (± pink frothy sputum) or wheeze.
 Nocturia, cold peripheries, weight loss and muscle wasting.
 Right ventricular failure (RVF): peripheral oedema (up to thighs, sacrum, abdominal
wall), abdominal distension (ascites), nausea, anorexia, facial engorgement, pulsation in
the neck and face (tricuspid regurgitation), epistaxis.

Signs

The patient may look ill and exhausted, with tachypnoea, cool peripheries, peripheral ± central
cyanosis.

 There may be a tachycardia at rest, low systolic blood pressure (BP), a displaced apex
(LV dilatation) or RV heave (pulmonary hypertension), a narrow pulse pressure or
pulsus alternans (alternating large and small pulse pressures) and a raised JVP.
 There may be a gallop rhythm due to presence of S3 (see heart sounds) or murmurs of
mitral or aortic valve disease.
 Bilateral basal end-inspiratory crackles ± wheeze ('cardiac asthma').
 Pleural effusions.
 Tender hepatomegaly - pulsatile in tricuspid regurgitation, with ascites.
 Often extensive peripheral oedema.

The peak expiratory flow rate may be reduced but, if it is <150 litres/minute, suspect chronic
obstructive pulmonary disease (COPD) or asthma.

Staging

The New York Heart Association's (NYHA) Classification of Heart Failure has provided a
clinically useful, functional classification, outlined below:

NYHA Heart Failure Severity Classification

 Class I: no symptoms on ordinary physical activity.
 Class II: slight limitation of physical activity by symptoms.
 Class III: less than ordinary activity leads to symptoms.
 Class IV: inability to carry out any activity without symptoms.

Pulmonary oedema occurs when fluid leaks from the pulmonary capillary network into the
lung interstitium and alveoli, and the filtration of fluid exceeds the ability of the lymphatics to
clear the fluid.

There are two main types of pulmonary oedema:

 Cardiogenic (or hydrostatic) pulmonary oedema caused by an elevated pulmonary

capillary pressure from left-sided heart failure.
 Non-cardiogenic pulmonary oedema:
o There is usually minimal elevation of pulmonary capillary pressure (except in
volume overload due to oliguric renal failure).
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o The oedema may be caused by altered alveolar-capillary membrane permeability -
eg, acute respiratory distress syndrome (ARDS), or lymphatic insufficiency - eg,
following lung transplant or lymphangitic carcinomatosis.
o Oedema is uncommon in diminished plasma oncotic pressure in
hypoalbuminaemic states such as severe liver disease, nephrotic syndrome and
protein-losing enteropathy.
o The mechanism for non-cardiogenic oedema is unknown in some conditions - eg,
narcotic overdose, high-altitude or neurogenic pulmonary oedema.

Aetiology
 Raised pulmonary capillary pressure:
o Heart:
 Ischaemic heart disease: acute myocardial infarction, acute coronary
syndromes.
 Mechanical complications of acute coronary syndrome (eg, rupture of
interventricular septum, mitral valve chordal rupture, right ventricular
infarction).
 Valvular – acute aortic regurgitation or mitral regurgitation, severe aortic
stenosis, endocarditis.
 Hypertensive crisis.
 Acute coronary embolism.
 Acute arrhythmia: rapid arrhythmia or severe bradycardia/conduction
disturbance.
 Acute myocarditis.
 Left atrial myxoma.
 Cardiac tamponade.
 Aortic dissection.
 Cardiomyopathy - eg, peripartum cardiomyopathy.
 Drugs: myocardial depression (eg, alcohol), fluid retention (eg, non-
steroidal anti-inflammatory drugs (NSAIDs)).
 Surgery and peri-operative problems.
o Renal:
 Acute kidney injury, chronic renal failure.
 Renal artery stenosis.
o Iatrogenic fluid overload.
o High-output heart failure - eg, septicaemia, thyrotoxic crisis, anaemia, shunts.
 Increased pulmonary capillary permeability:
o Acute respiratory distress syndrome (ARDS).
o High altitude.
o Inhaled or aspirated toxic substances.
o Radiation.
o Liver failure.
o Fat embolism or amniotic fluid embolism.
 Lymphatic obstruction - eg, mediastinal carcinomatosis, silicosis.
 Acute or chronic upper airway obstruction.
 Neurogenic (associated with changes in capillary hydrostatic pressure and changes in
pulmonary capillary permeability): develops within a few hours after a neurological
insult - eg, status epilepticus, head injury or cerebrovascular insult.
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Presentation

Acute pulmonary oedema is a very frightening experience for the patient and represents a
genuine medical emergency. This does not preclude a systematic assessment with a rapid,
focused history and examination.

 Signs:
o The patient is usually severely breathless, sweaty, nauseated and anxious.
o Initially they may have a dry or productive cough (sometimes with pink, frothy
sputum).
o Patients may also develop paroxysmal nocturnal dyspnoe or orthopnoea.
 History:
o Check for a past history of relevant conditions - eg, ischaemic heart disease,
valvular heart disease, diabetes.
o Review current medication.
o Ask about smoking and alcohol use.
 Signs:
o The patient is in respiratory distress, pale, sweaty, tachypnoeic and tachycardic.
o They may be cyanosed, have evidence of congested neck veins and a raised JVP.
o Basal/widespread rales or fine crackles are usually heard when listening to the
chest.
o Oxygen saturation is usually <90% on room air.
o Assess for a gallop rhythm (3rd heart sound) and murmurs suggestive of valve
stenosis or regurgitation.
o Hypotension - the triad of hypotension (systolic blood pressure <90 mm Hg),
oliguria, and low cardiac output is known as cardiogenic shock
o In hypertensive heart failure, a high blood pressure, tachycardia, and
vasoconstriction present with signs of pulmonary oedema without extensive
systemic congestion.
o Where pulmonary oedema occurs in association with right heart failure,
hepatomegaly and peripheral oedema are usual.

Investigations

These will not be available in the pre-hospital setting. For severe acute heart failure, treatment
should be started immediately and the condition stabilised before results of investigations are
available.

 Blood tests:
o Renal function, electrolytes, glucose, cardiac enzymes, clotting tests (INR).
o Arterial blood gases and pH.
o Brain natriuretic peptides - helpful in distinguishing acute pulmonary oedema
from other causes of dyspnoe
 ECG: look for evidence of arrhythmia, myocardial infarction or other cardiac disease -
eg, left ventricular hypertrophy.
 CXR: to exclude other causes of breathlessness and confirm pulmonary oedema.
 Echocardiogram: transthoracic echocardiography is usually adequate. Transoesophageal
echocardiography is not needed in routine diagnostic assessment unless transthoracic
echocardiography is inadequate (eg, because of obesity, chronic lung disease, ventilated
patients) and an alternative modality such as cardiac magnetic resonance (CMR) imaging
is not available
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 A urinary catheter enables accurate measurement of urinary output, which helps rapidly
to assess diuretic response and fluid balance.
 More invasive procedures are required for intensive support, including arterial and
central venous pressure lines and pulmonary artery catheters.

Management

oedema, each requires different management and has a different prognosis. This section is
mainly directed at the management of acute cardiogenic pulmonary oedema.

Management is otherwise supportive and directed at improving oxygenation, perfusion and

haemodynamics, and preventing further cardiac and/or renal damage.

Pre-hospital treatment

 Resuscitation - as necessary: sit the patient up; give oxygen (if available) by face mask:
100% if no pre-existing lung disease (but even in patients with chronic obstructive
pulmonary disease (COPD), give high oxygen flow initially but monitor with blood gases
to ensure hypercapnia is avoided). Aim for oxygen saturations ≥95% (>90% in those with
COPD).
 Judge clinical severity: some patients do not require hospital admission - eg, those with
mild and stable pulmonary oedema with a known cause that is treatable without
admission. However, most patients require urgent admission to hospital.
 Insert an intravenous cannula and give:
 Nitrates are first-line vasodilators where systolic blood pressure is >90 mm Hg and there
is no serious obstructive valvular disease. Give sublingual or buccal nitrate - eg, glyceryl
trinitrate (GTN) spray two puffs sublingual, or 1-3 mg buccal isosorbide dinitrate.
 Furosemide 20-40 mg intravenously (slowly) produces transient venodilation and
subsequent diuresis. This may need to be repeated based on response of clinical
symptoms - diuretic effectiveness is greatly reduced in the presence of hypotension and
when patients have been taking oral diuretics for a long time.
 Opiates: the use of opiates is controversial and opiates should not be given to patients
with acute decompensated heart failure (see 'Initial treatment', below). However,
analgesia and sedation may be appropriate where the patient is in pain or distressed.
Diamorphine 2.5-5 mg intravenously slowly (or morphine 5-10 mg intravenously slowly)
can be used to relieve anxiety, pain and distress.

Acute heart failure with pulmonary congestion/oedema without shock

Initial treatment:

 An intravenous loop diuretic is recommended to improve breathlessness and relieve

congestion. Symptoms, urine output, renal function and electrolytes should be monitored
regularly during use of the intravenous diuretic.
 High-flow oxygen is recommended in patients with a capillary oxygen saturation <90%
or PaO2 <60 mm Hg (8.0 kPa) to correct hypoxaemia. Oxygen should not be used
routinely in non-hypoxaemic patients, as it causes vasoconstriction and a reduction in
cardiac output.
 Thrombo-embolism prophylaxis (eg, with low molecular weight heparin (LMWH)) is
recommended in patients not already anticoagulated and with no contra-indication to
anticoagulation, to reduce the risk of deep venous thrombosis and pulmonary embolism.
 Opiates - eg, morphine:
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o May be useful in some patients with acute pulmonary oedema, as they reduce
anxiety and relieve distress associated with dyspnoea.
o However, opiates depress respiratory drive, potentially increasing the need for
invasive ventilation. Alertness and ventilatory effort should be monitored
frequently after administration.
o Some studies have suggested a strong association between the use of opiates and
increased mortality and morbidity (eg, intensive care unit admissions or
intubation rates) and opiates should not be used routinely in the treatment of acute
pulmonary oedema.
o Opiates should be avoided in acute decompensated heart failure.
 Vasodilators:
o An intravenous infusion of a nitrate should be considered in patients with
pulmonary congestion/oedema and a systolic blood pressure >110 mm Hg, who
do not have severe mitral or aortic stenosis, to reduce pulmonary capillary wedge
pressure and systemic vascular resistance.
o Nitrates may also relieve dyspnoea and congestion. Symptoms and blood pressure
should be monitored frequently during administration of intravenous nitrates.
 Inotropic agents:
o Are NOT recommended unless the patient is hypotensive (systolic blood pressure
<85 mm Hg), hypoperfused, or shocked because of safety concerns (atrial and
ventricular arrhythmias, myocardial ischaemia, and death).
o Inotropes cause sinus tachycardia and may induce myocardial ischaemia and
arrhythmias. There is concern that inotropes may increase mortality.
o Levosimendan (or a phosphodiesterase III inhibitor such as milrinone) may be
used to counteract the effect of a beta-blocker.
o Phosphodiesterase inhibitors (milrinone and enoximone) may be preferred to
dobutamine in patients on beta-blocker therapy or with inadequate response to
dobutamine. They are peripheral vasodilators and should only be used if systolic
blood pressure is adequate. They may increase mortality in those with coronary
artery disease.
o Levosimendan is a calcium sensitiser that appears effective in patients with
decompensated chronic heart failure already on beta-blockers.

Patients with hypotension, hypoperfusion or shock:

 Electrical cardioversion is recommended if an atrial or ventricular arrhythmia is thought

to be contributing to haemodynamic compromise.
 An intravenous infusion of an inotrope (eg, dobutamine) should be considered in patients
with hypotension (systolic blood pressure <85 mm Hg). The ECG should be monitored
continuously because inotropic agents can cause arrhythmias and myocardial ischaemia.
 Short-term mechanical circulatory support should be considered in patients remaining
severely hypoperfused despite inotropic therapy and with a potentially reversible cause
(eg, viral myocarditis) or a potentially surgically correctable cause (eg, acute
interventricular septal rupture).
 An intravenous infusion of levosimendan (or a phosphodiesterase inhibitor) may be
considered to reverse the effect of beta-blockade if beta-blockade is thought to be
contributing to hypoperfusion.
 A vasopressor (eg, dopamine or noradrenaline (norepinephrine)) may be considered in
patients who have cardiogenic shock, despite treatment with an inotrope. Intra-arterial
blood pressure measurement should be considered.
 Short-term mechanical circulatory support may be considered in patients deteriorating
rapidly before a full diagnostic and clinical evaluation can be made.
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Monitoring:

 Systolic blood pressure, heart rhythm and rate, saturation of peripheral oxygen (SpO2)
using a pulse oximeter, and urine output should be monitored on a regular and frequent
basis until the patient is stabilised.
 It is important to examine the patient repeatedly, including assessment for any new heart
murmurs - eg, a patient who has severe pulmonary oedema following a myocardial
infarction may go on to develop a ventricular septal defect or mitral regurgitation
(confirm with an echocardiogram).
 Renal function, electrolytes, serial ECGs and cardiac enzymes should also be closely
monitored.
 Intra-arterial line: insertion of an intra-arterial line should only be considered in patients
with persistent heart failure and a low systolic blood pressure despite treatment.
 Pulmonary artery catheterisation: right heart catheterisation does not have a general role
in the management of acute heart failure, but may help in the treatment of a minority of
selected patients with acute heart failure.

After stabilisation:

 Angiotensin-converting enzyme (ACE) inhibitor/angiotensin-II receptor antagonist

(AIIRA): in patients with reduced EF not already receiving an ACE inhibitor (or AIIRA),
this treatment should be started as soon as possible, blood pressure and renal function
permitting.
 Beta-blocker: in patients with reduced EF not already receiving a beta-blocker, this
treatment should be started as soon as possible after stabilisation, blood pressure and
heart rate permitting.
 Mineralocorticoid (aldosterone) receptor antagonist (MRA): in patients with reduced EF
not already receiving an MRA, this treatment should be started as soon as possible, renal
function and potassium permitting. As the dose of MRA used to treat heart failure (HF)
has a minimal effect on blood pressure, even relatively hypotensive patients may be
started on this therapy during admission.
 Digoxin: in patients with reduced EF, digoxin may be used to control the ventricular rate
in atrial fibrillation, especially if it has not been possible to up-titrate the dose of beta-
blocker. Digoxin may also provide symptom benefit and reduce the risk of hospital
admission for heart failure in patients with severe systolic heart failure.
 It is common to restrict sodium intake to <2 g/day and fluid intake to <1.5-2.0 L/day,
especially during the initial management of an acute episode of heart failure associated
with volume overload, although there is no firm evidence to support this practice.

Non-invasive ventilation:

 Continuous positive airway pressure (CPAP) and non-invasive positive pressure

ventilation (NIPPV) relieve dyspnoea and improve certain physiological measures (eg,
oxygen saturation) in patients with acute pulmonary oedema.
 Non-invasive ventilation should be considered in dyspnoeic patients with pulmonary
oedema and a respiratory rate >20 breaths/minute to improve breathlessness and reduce
hypercapnia and acidosis.
 Non-invasive ventilation can reduce blood pressure and should not generally be used in
patients with a systolic blood pressure of <85 mm Hg (and blood pressure should be
monitored regularly when this treatment is used).
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 A recent large RCT showed that neither type of non-invasive ventilation reduced
mortality or the rate of endotracheal intubation when compared with standard therapy,
including nitrates and opiates.

Endotracheal intubation and invasive ventilation:

 The primary indication for endotracheal intubation and invasive ventilation is respiratory
failure leading to hypoxaemia, hypercapnia, and acidosis.
 Physical exhaustion, diminished consciousness, and inability to maintain or protect the
airway are other reasons to consider intubation and ventilation.

Mechanical circulatory support:

 The conventional indications for an intra-aortic balloon pump (IABP) are to support the
circulation before surgical correction of specific acute mechanical problems, during
severe acute myocarditis and in selected patients with acute myocardial ischaemia or
infarction before, during, and after percutaneous or surgical revascularisation.
 There is no good evidence that an IABP is of benefit in other causes of cardiogenic
shock.
 More recently, balloon pumps (and other types of short-term, temporary circulatory
support) have been used to bridge patients until implantation of a ventricular assist device
or heart transplantation.
 Ventricular assist devices and other forms of mechanical circulatory support (MCS) may
be used as a 'bridge to decision' or longer term in selected patients.

Ultrafiltration:

 Venovenous isolated ultrafiltration is sometimes used to remove fluid in patients with

heart failure, although it is usually reserved for those unresponsive or resistant to
diuretics.

Other treatments:

 Arrhythmias: See separate article on Atrial Fibrillation. Pacing is recommended in

patients haemodynamically compromised by severe bradycardia or heart block.
 Renal dysfunction may limit the use of ACE inhibitors and AIIRAs; progressive acute
kidney injury and volume overload may require renal replacement therapy.
 Surgical options include coronary revascularization, correction of anatomical lesions,
valve replacement or reconstruction, mechanical assist devices for temporary circulatory
support and heart transplantation.

Pulmonary embolism (PE) is a medical emergency. It may present with very few clinical signs
and/or symptoms, making it easy to miss, and a high index of suspicion is warranted.

PE results from obstruction within the pulmonary arterial tree. The emboli can be caused by:

 Thrombosis - accounts for the majority of cases and has usually arisen from a distant vein
and travelled to the lungs via the venous system.
 Fat - following long bone fracture or orthopaedic surgery.
 Amniotic fluid
 Air - following neck vein cannulation or bronchial trauma.
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The rest of this article deals with thrombotic PE.

Epidemiology

The incidence of venous thromboembolism (VTE) varies from 1-1.5 per 1,000 person-years.

Risk factors

Clots form when one or more of the following factors are present: increased blood coagulability,
reduced mobility or blood vessel abnormalities. These correspond to some of the risk factors for
VTE (see below). A number of patients may not have any risk factors, making the diagnosis
difficult.

Risk factors for venous thromboembolism

Major risk factors: relative risk of 5-20 Minor risk factors: relative risk of 2-4
Surgery: Cardiovascular:
 Major abdominal/pelvic surgery  Congenital heart disease.
or hip/knee replacement  Congestive cardiac failure.
(risk lower if prophylaxis used).  Hypertension.
 Postoperative intensive care.  Paralytic stroke.

Obstetrics: Oestrogens:
 Late pregnancy.  Pregnancy (but see major risk factors for
 Puerperium. late pregnancy and puerperium).
 Caesarean section.  Combined oral contraceptive.
 Hormone replacement therapy.
Lower limb problems:
 Fracture. Haematological:
 Varicose veins - previous  Thrombotic disorders (a detailed list is
varicose vein surgery; available)
superficial thrombophlebitis; varicose Consider this in cases of PE aged <40
veins per se are not a risk factor. years, recurrent VTE or a positive family
history.
Malignancy:  Myeloproliferative disorders.
 Abdominal/pelvic.
 Advanced/metastatic. Renal:
 Nephrotic syndrome.
Reduced mobility:  Chronic dialysis.
 Hospitalisation.  Paroxysmal nocturnal haemoglobinuria.
 Institutional care.
Miscellaneous:
Previous proven VTE:  Chronic obstructive pulmonary disease
 Intravenous (IV) drug use (COPD).
(could be major or  Neurological disability.
minor risk factor:  Occult malignancy.
no data on relative risk).  Long-distance sedentary travel.
 Obesity.
Other:  Other chronic diseases: inflammatory
 Major trauma. bowel disease, Behçet's disease.
 Spinal cord injury.
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Risk factors for venous thromboembolism
 Central venous lines.

Presentation

The symptoms and signs of PE are not specific. Severe cases of PE can lead to collapse or
sudden death. Some PEs are rapidly fatal. In the majority of the fatal cases the PE is not
clinically diagnosed prior to death.

Symptoms include:

 Dyspnoea.
 Pleuritic chest pain, retrosternal chest pain.
 Cough and haemoptysis.
 Any chest symptoms in a patient with symptoms suggesting a deep vein thrombosis
(DVT).
 In severe cases, right heart failure causes dizziness or syncope.

Signs include:

 Tachypnoea, tachycardia.
 Hypoxia, which may cause anxiety, restlessness, agitation and impaired consciousness.
 Pyrexia.
 Elevated jugular venous pressure.
 Gallop heart rhythm, a widely split second heart sound, tricuspid regurgitant murmur.
 Pleural rub.
 Systemic hypotension and cardiogenic shock.

Investigations

General investigations

 Baseline investigations - as for any ill patient: oxygen saturation, FBC, biochemistry,
baseline clotting screen. Troponin and brain natriuretic peptide levels may also be
elevated.
 ECG - may be normal, or show any of these changes: sinus tachycardia, atrial
fibrillation, nonspecific ST or T-wave abnormalities, right ventricular strain pattern V1-3,
right axis deviation, right bundle branch block (RBBB), or deep S-waves in I with Q
waves in III and inverted T waves in III ('S1,Q3,T3' pattern). A large PE can show ECG
features of acute cardiac ischaemia (eg, ST depression).
 CXR - mainly useful to exclude other chest disease, and is needed for interpreting V/Q
scans. It is usually normal, but may show: decreased vascular markings, atelectasis or a
small pleural effusion. An occasional late sign may be an homogeneous wedge-shaped
area of pulmonary infarction in the lung periphery (Hampton's hump) with its base
contiguous to a visceral pleural surface and its rounded convex apex directed toward the
hilum.
 Arterial blood gases - may show reduced PaO2, reduced PaCO2 due to hyperventilation
or acidosis.
 Echocardiography - may show thrombus in proximal pulmonary arteries and, if normal,
can exclude haemodynamically important PE. It cannot exclude smaller PEs. It may
show signs of right ventricular strain or right ventricular hypokinesis.
 Cardiac troponins - can be indicative of right heart strain.
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 D-dimers - fibrin D-dimer is a degradation product of cross-linked fibrin. The
concentration increases in patients with acute VTE and provides a very sensitive test to
exclude acute DVT or PE. D-dimer tests have less specificity and are less useful in some
groups of patients - eg, those with high clinical probability; those admitted to hospital for
another reason, in whom the suspicion of PE is raised during their hospital stay;
individuals older than 65 years; pregnant women.

Specific investigations for VTE

The choice and order of investigations will depend on the clinical likelihood of PE, how ill the
patient is and availability of the test. The 'gold standard' test is conventional pulmonary
angiography, but this is invasive and usually unavailable urgently. Investigation strategies are
detailed as part of the initial management and pregnancy sections below. An explanation of the
scope of each test helps in understanding these strategies:

 Leg ultrasound: in patients with co-existing clinical DVT, lower limb ultrasound as the
initial imaging test is often sufficient to confirm VTE - and hence to start anticoagulation.
However, a singe normal leg ultrasound cannot exclude DVT.
 Isotope lung scanning (V/Q scan): although there have been controversies about the
accuracy of isotope scans, they are reliable enough to exclude or confirm PE, if
performed according to UK protocols. However, if the result is 'indeterminate', further
imaging is needed. V/Q scanning is unlikely to be available out-of-hours. Also the results
will be reported as low, moderate or high probability.
 CTPA has become the method of choice for imaging the pulmonary vasculature in
patients with suspected PE.

It is important to appreciate that, although there are risk scores and various D-dimer assays
available, clinical suspicion of VTE may still need to be followed up when these results are
negative. In this situation it is best to discuss the case further with respiratory physicians and
radiologists.

Management

Initial resuscitation

 Oxygen 100%.
 Obtain IV access, monitor closely, start baseline investigations.
 Give analgesia if necessary (eg, morphine).
 Assess circulation: suspect massive PE if systolic BP is <90 mm Hg or there is a fall of
40 mm Hg, for 15 minutes, not due to other causes.

Anticoagulation therapy

 Offer a choice of low molecular weight heparin (LMWH) or fondaparinux to patients

with confirmed PE, with the following exceptions:
o For patients with severe renal impairment or established chronic kidney disease
(estimated glomerular filtration rate (eGFR) <30 ml/min/1.73 m2) offer
unfractionated heparin (UFH) with dose adjustments based on the activated
partial thromboplastin time (aPTT) or LMWH with dose adjustments based on an
anti-Xa assay.
o For patients with an increased risk of bleeding, consider UFH.
 13
o For patients with PE and haemodynamic instability, offer UFH and consider
thrombolytic therapy.
 Start the LMWH, fondaparinux or UFH as soon as possible and continue it for at least
five days or until the international normalised ratio (INR) is 2 or above for at least 24
hours, whichever is longer.
 Offer LMWH to patients with active cancer and confirmed PE, and continue the LMWH
for six months. At six months, assess the risks and benefits of continuing anticoagulation.
 Offer a vitamin K antagonist (VKA) to patients with confirmed PE within 24 hours of
diagnosis and continue the VKA for three months. At three months, assess the risks and
benefits of continuing VKA treatment.
 Offer a VKA beyond three months to patients with an unprovoked PE, taking into
account the patient's risk of VTE recurrence and whether they are at increased risk of
bleeding.
 Rivaroxaban:
o Rivaroxaban is recommended by NICE as an option for treating PE and
preventing recurrent DVT and PE in adults.
o The duration of treatment recommended depends on bleeding risk and other
clinical criteria.
o Short-term treatment (at least three months) is recommended for people with
transient risk factors such as recent surgery and trauma. Longer treatment is
recommended for people with permanent risk factors, or idiopathic (unprovoked)
DVT or PE.

Provide patients who are having anticoagulation treatment with an anticoagulant information
booklet and an anticoagulant alert card and advise them to carry the anticoagulant alert card at all
times.

Other treatments

 Consider pharmacological systemic thrombolytic therapy for patients with PE and

haemodynamic instability. Do not offer pharmacological systemic thrombolytic therapy
to patients with PE and haemodynamic stability.
 Offer temporary inferior vena caval filters to patients with PE who cannot have
anticoagulation treatment, and remove the inferior vena caval filter when the patient
becomes eligible for anticoagulation treatment.
 Consider inferior vena caval filters for patients with recurrent PE despite adequate
anticoagulation treatment only after considering alternative treatments such as increasing
target INR to 3-4 for long-term high-intensity oral anticoagulant therapy, or switching
treatment to LMWH.
 Ensure that a strategy exists for removing the inferior vena caval filter at the earliest
possible opportunity.

Surgical embolectomy has been performed for high-risk PE, and also for selected patients with
intermediate- or high-risk PE, particularly if thrombolysis is contra-indicated or has failed.
Surgical embolectomy has also been successfully performed in patients with right heart thrombi
straddling the interatrial septum through a patent foramen ovale.
 14
Supraventricular tachycardia (SVT) is generally used to refer to atrioventricular nodal
re-entry tachycardia (AVNRT), atrioventricular re-entry tachycardia (AVRT), and atrial
tachycardia.

SVT is usually paroxysmal and episodes may occur regularly or very infrequently (sometimes
years apart). Episodes may only last for a few minutes or may last for up to several months.

SVT is caused by:

 Abnormalities of impulse conduction (re-entrant tachycardias).

 Disorders of impulse initiation (automatic tachycardias) causing a narrow complex
tachycardia.

Re-entrant tachycardias

These are the most common type:

 Atrioventricular nodal re-entrant tachycardia (AVNRT):

o Due to the presence of two functionally and anatomically distinct conducting
pathways in the atrioventricular node. One of these is fast-conducting, the other
slow-conducting.
o During an episode of SVT one of these acts as the antegrade limb of a re-entrant
circuit, while the other acts as the retrograde limb. AVNRT is the most common
form of SVT.
 Atrioventricular re-entrant tachycardia (AVRT):
o Due to the presence of accessory pathways that connect the atria and ventricles,
but that lie outside the atrioventricular node.
o Accessory pathways may be capable of antegrade or retrograde conduction, or
both.
o Wolff-Parkinson-White syndrome is the most well-known type of AVRT.

Automatic tachycardias
 Focal junctional tachycardia:
o Due to abnormally rapid discharges from the junctional region.
o This type of SVT originates from the atrioventricular node, or bundle of His.
o This type is also known as automatic or paroxysmal junctional tachycardia.
 Focal atrial tachycardia:
o Due to regular atrial activation from atrial areas with centrifugal spread.
o Neither the sinus nor the atrioventricular node plays a role in the initiation or
continuation of this type of SVT.

Presentation
 PSVT may be associated with minimal symptoms or present with syncope.
 Symptoms vary with the ventricular rate and duration of the SVT. Symptoms are more
likely in those with underlying heart disease, and include:
o Palpitations and dizziness, which are the most common symptoms reported.
o Other symptoms, including fatigue, light-headedness, chest discomfort, dyspnoea,
polyuria and syncope (uncommon).
 Examination may be normal if seen after the attack, with normal cardiac function and no
underlying heart abnormality.
 15
 During an attack, tachycardia may be the only finding if the patient is otherwise healthy
and there is no cardiac dysfunction. During an episode of SVT the pulse rate is 140-250
beats per minute (bpm).
 Resulting heart failure may cause tachypnoea, hypotension, raised JVP, third heart sound
and basal lung crepitations.

Management
 Possible precipitating factors - eg digoxin, caffeine, alcohol, nicotine intake, recreational
drugs or hyperthyroidism - should be addressed.
 An ECG should be performed as soon as possible.
 The choice of long-term therapy depends on the exact nature of the tachyarrhythmia and
the frequency and duration of episodes and risks associated with the arrhythmia (eg, heart
failure, sudden death).
 The most effective and rapid means of terminating any haemodynamically unstable
tachycardia is direct current (DC) cardioversion.
 In haemodynamically stable regular narrow QRS-complex tachycardia, vagal
manoeuvres - eg, Valsalva, carotid massage, facial immersion in cold water. Carotid
massage is usually reserved for young patients. Due to the risk of stroke from emboli,
auscultate for bruits before attempting this manoeuvre. Do not perform carotid massage
on both sides simultaneously.
 If vagal manoeuvres fail, intravenous adenosine or verapamil can be used:
o Intravenous adenosine is the treatment of choice except for people with severe
asthma. Adenosine has a rapid onset and short half-life. It blocks conduction
through the atrioventricular node. Adenosine has a high incidence of minor but
unpleasant side-effects (eg, nausea, chest tightness, shortness of breath and
headache).
o Intravenous verapamil, although effective, is rarely used now. It has a more
prolonged action than adenosine on blocking atrioventricular node conduction,
and there is a risk of prolonged depression of ventricular function and
hypotension, especially if the person is taking a beta-blocker. It still has a place if
adenosine is contra-indicated (eg, in somebody with severe asthma).
 Sinus tachycardia:
o Beta-blocker or non-dihydropyridine calcium-channel blocker - eg, diltiazem,
verapamil.
o Exclude any secondary cause - eg, hyperthyroidism, phaeochromocytoma.
 Sinus node re-entry tachycardia:
o Beta-blockers are first-line and diltiazem or verapamil are also effective.
o Radiofrequency catheter ablation is generally successful.
 Focal atrial tachycardia:
o Calcium-channel blockers or beta-blockers are considered first-line.
o Flecainide, sotalol or amiodarone may also be effective.
 Multifocal atrial tachycardia:
o Therapy is mainly directed at chronic pulmonary disease (usually associated) and
electrolyte disturbances, which may be the underlying cause. Digoxin toxicity is
also an uncommon cause.
o Long-term therapy is otherwise with calcium-channel blockers.
o Beta-blockers are usually contra-indicated because of pulmonary disease and
there is no role for DC cardioversion or ablation.
 Long-term preventative treatment:
o Not required in all people.
o The frequency and severity of the episodes of SVT need to be balanced against
the risks of long-term therapy.
 16
o The choice of maintenance therapy depends on the underlying type of SVT.
 Radiofrequency catheter ablation:
o Is associated with a high success rate and low complication rate for people with
SVT.
o Radiofrequency catheter ablation is indicated in the following situations:
 As first-line therapy as a curative option.
 If the SVT is refractory to antiarrhythmic drug therapy.
 If the person is intolerant of antiarrhythmic drug therapy.
 If antiarrhythmic drug therapy is contra-indicated.

Definition

Ventricular tachycardia (VT) is a broad complex tachycardia originating from a ventricular

ectopic focus. It is defined as three or more ventricular extrasystoles in succession at a rate of
more than 120 beats per minute (bpm). Accelerated idioventricular rhythm refers to ventricular
rhythms with rates of 60-100 bpm:

 The rate is usually greater than 120 bpm with broad QRS complexes.
 VT may be monomorphic (typically regular rhythm originating from a single focus with
identical or similar QRS complexes) or polymorphic (may be irregular rhythm, with beat
to beat variation in QRS complexes).
 Monomorphic VT is the most common form of sustained VT.
 Non-sustained VT is defined as a run of tachycardia of less than 30 seconds' duration; a
longer duration is described as sustained VT.
 Sustained VT is associated with:
o Late phase of myocardial infarction (frequently with left ventricular aneurysm).
o Cardiomyopathy (including hypertrophic and alcoholic).
o Right ventricular dysplasia.
o Myocarditis.
o Drugs - eg, class 1 anti-arrhythmics (flecainide, and disopyramide).

Types of ventricular tachycardias

Fascicular tachycardia

 Uncommon and not usually associated with underlying structural heart disease.
 It originates from the left bundle branch.
 It produces QRS complexes of relatively short duration (0.11-0.14 seconds) and so is
commonly misdiagnosed as a supraventricular tachycardia (SVT).
 The QRS complexes have a right bundle branch block pattern.

Right ventricular outflow tract tachycardia

 Originates from the right ventricular outflow tract.

 The ECG typically shows right axis deviation, with a left bundle branch block pattern.
 The tachycardia may be provoked by catecholamine release, sudden changes in heart
rate, and exercise.
 It usually responds to drugs such as alpha-blockers or calcium antagonists.

Torsades de pointes tachycardia

 17
.

Polymorphic ventricular tachycardia

 Has the same ECG characteristics as torsades de pointes but in sinus rhythm the QT
interval is normal.
 The ECG trace is also similar to that of atrial fibrillation (AF) with pre-excitation.
 It is much less common than torsades de pointes.
 If sustained, it often leads to cardiogenic shock.
 It can occur in acute myocardial infarction and may deteriorate into ventricular
fibrillation (VF).

Epidemiology
 VT is a fairly frequently observed dysrhythmia but actual incidence is difficult to
quantify because of the overlap with VF. Shockable rhythms (pulseless VT and VF) are
seen in about half of witnessed cardiac arrests in public locations where a defibrillator
has been available. Coronary disease is the usual cause, which is common throughout
most of the developed world.
 VT incidence rates peak in the middle decades of life, following structural heart disease.

Risk factors

 VT is often a symptom of coronary heart disease or structural heart disease.

 VT can be triggered by electrolyte deficiencies - eg, hypokalaemia, hypocalcaemia,
hypomagnesaemia.
 Use of sympathomimetic agents (eg, caffeine or cocaine) may stimulate VT in vulnerable
hearts.

Presentation
 Most patients present with symptoms of either ischaemic heart disease or haemodynamic
compromise resulting from poor perfusion.
 Symptoms may include chest pain, palpitations, dyspnoea, dizziness, syncope and other
symptoms of heart failure.
 Signs reflect the degree of haemodynamic instability, including respiratory distress, basal
fine lung crepitations, raised JVP, hypotension, anxiety, agitation, lethargy, coma.

nvestigations
 ECG:
o Complexes of atypical morphology are often difficult to interpret. Such
tachycardias could be paroxysmal supraventricular tachycardia (PSVT) with
aberrant conduction. If the patient is unstable, or differentiation between VT and
SVT is uncertain, treat rhythm as VT. Some therapies for PSVT (eg, verapamil)
can be lethal when employed in VT.
o No absolute ECG criteria exist for establishing the presence of VT. However,
several factors suggest VT, including the following:
 Rate greater than 100 bpm (usually 150-200).
 Wide QRS complexes (>120 ms).
 Presence of AV dissociation.
 Fusion beats.
 18

o Retrograde ventriculoatrial conduction may occur, which can generate an ECG

complex similar to PSVT with aberrant conduction.
 Electrolytes, including serum calcium, magnesium, and phosphate levels. Ionised calcium
levels are preferred over total serum calcium. Hypokalaemia, hypomagnesaemia, and
hypocalcaemia may predispose patients either to conventional VT or torsades de pointes.
 Levels of therapeutic drugs - eg, digoxin.
 Evaluate for myocardial ischaemia: serum troponin I levels, or other cardiac markers.
 CXR: if there is a possibility of congestive heart failure or other cardiopulmonary
pathology as contributing factors.

Associated diseases
 Arrhythmia may occur with or without either myocardial ischaemia or infarction.
 Accelerated idioventricular rhythm (sometimes termed slow ventricular tachycardia):
o Presents with a rate of 60-100 bpm.
o Typically occurs with underlying heart disease (ischaemic or structural).
o It is transient, and only rarely is associated with haemodynamic compromise or
collapse.
o Treatment is usually not required unless there is haemodynamic impairment.

Management

Address the ABCs of resuscitation and provide basic life support and advanced life support as
necessary, urgent transfer to hospital, venous access, oxygen and ECG rhythm strip monitoring.

Pulseless VT

Is treated as for VF in line with the advanced life support algorithm

Unstable VT (reduced cardiac output)

 VF or pulseless VT is treated by unsynchronised defibrillation; whereas other VTs can be

treated with synchronised cardioversion.
 Most patients respond to low levels of energy (eg, starting at 50 J biphasic or 100 J
monophasic).
 Synchronised defibrillation in unstable VT may cause R-on-T deterioration to VF.
 Defibrillation is followed by airway management if required, supplemental oxygen,
vascular access, and anti-arrhythmic therapy.
 Advanced cardiac life support: amiodarone is often used for haemodynamically unstable
VT. Replenishment of magnesium and/or other electrolytes may be a valuable adjunct to
anti-arrhythmic therapies.

Stable VT

 Stable VT patients do not experience symptoms of haemodynamic decompensation.

 19
 Unlike other dysrhythmias, VT tends to deteriorate into unstable states and more
malignant dysrhythmias.
 Therefore, stable VT should be treated with lidocaine or timely cardioversion if lidocaine
is ineffective.
 The evidence on percutaneous (non-thoracoscopic) epicardial catheter radiofrequency
ablation for VT is limited but has shown that the procedure is effective in carefully
selected patients and raises no major safety issues.

Refractory VT

 After the initial dose of amiodarone 300 mg IV, it may be followed by an infusion of 900
mg over 24 hours.

Implantable cardioverter defibrillators (ICDs)

National Institute for Health and Care Excellence (NICE) guidance recommends that
ICDs should be considered for patients in the following categories:

 Sustained VT causing syncope.

 Sustained VT with ejection fraction less than 35%.
 Previous cardiac arrest due to VT or VF.
 Myocardial infarction complicated by non-sustained VT, or inducible VT on
electrophysiological testing, or an ejection fraction less than 35%

Synonyms: Adams-Stokes, Morgagni, Morgagni-Adams-Stokes and Spens'

syndrome

A classic Stokes-Adams attack is a collapse without warning, associated with loss of

consciousness for a few seconds. Typically, complete (third-degree) heart block is seen on the
ECG during an attack (but other ECG abnormalities such as tachy-brady syndrome have been
reported).

Cardiologists, and other doctors specialising in syncope, do not use the term 'Stokes-Adams
attack' as often these days. The development of investigation techniques and improvements in
the understanding of the physiology of the cardiovascular system have meant that there has been
a move away from clinical diagnoses to a more rigid diagnostic classification.

Epidemiology
 The condition is usually associated with ischaemic heart disease and so tends to occur in
the elderly.
 Stokes-Adams attacks have been reported in much younger age groups, including those
with congenital heart block.
 There may be a familial tendency to Stokes-Adams attacks. This was first recognised by
William Osler in 1903, within his own family.

Aetiology

With congenital heart block, it has been described as being precipitated by bradycardia or
tachycardia.

 Heart block may result from:

 20
o Myocardial infarction.
o Fibrosis (usually associated with ischaemia).
o Atrioventricular (AV) nodal disease.
o Structural or valvular heart disease.
o Myocarditis.
o Electrolyte disturbance.
o Drugs.
o Rheumatic diseases including ankylosing spondylitis, Reiter's syndrome,
rheumatoid arthritis, scleroderma.
o Infiltrative processes including amyloidosis, sarcoidosis, tumours,
 Stokes-Adams attacks have been described as due to:
o Chronic or paroxysmal AV block in 50-60% of patients.
o Sino-atrial (SA) block in 30-40% of patients.
o Paroxysmal supraventricular tachycardia or atrial fibrillation in up to 5% of
patients.

Presentation
 There is collapse, usually without warning.
 Loss of consciousness is usually between about 10 and 30 seconds.
 Pallor, followed by flushing on recovery, can be reported.
 Some seizure-like activity sometimes occurs if the attack is prolonged.
 If anyone manages to check the pulse during an episode, it will be slow, usually less than
40 beats per minute.
 Recovery is fairly rapid, although the patient may be confused for a while afterwards.
 Typically, complete (third-degree) heart block is seen on the ECG during an attack but
other ECG abnormalities such as tachy-brady syndrome have been reported. Attacks can
happen a number of times in one day.
 They are not posture-related.

Management
 Reversible causes such as drug toxicity should be addressed.
 Underlying heart disease should be managed appropriately.
 A cardiac pacemaker may be required.

Anti-arrhythmic drugs can be classified clinically into:

 Those that act on supraventricular arrhythmias - eg, adenosine, verapamil, cardiac

glycosides and beta-blockers.
 Those that act on both supraventricular and ventricular arrhythmias - eg,
amiodarone, beta-blockers, disopyramide, flecainide, and propafenone.
 Those that act on ventricular arrhythmias - eg, lidocaine and moracizine.

Anti-arrhythmic drugs can also be classified according to their effects on the electrical behaviour
of myocardial cells during activity but this classification is of less clinical use. The Vaughan
Williams classification is based on the movement of ions (sodium, potassium, calcium) into heart
cells:

 Class I: membrane-stabilising (Ia) procainamide, disopyramide, (Ib) lidocaine, (Ic)

flecainide.
 21
 Class II: reduce adrenergic input - beta-blockers.
 Class III: potassium blockers - eg, amiodarone, sotalol.
 Class IV: calcium influx blockers - eg, verapamil (but not dihydropyridines).