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Flashcards in Cardiology - Heart failure Deck (56):

What is heart failure?

Heart failure is the inability of the heart to provide adequate blood flow and therefore oxygen delivery to peripheral tissues and organs. Underperfusion of organs leads to reduced exercise capacity, fatigue and shortness of breath. It can also lead to organ dysfunction (e.g. renal failure) in some patients.


What is the incidence and prognosis of heart failure?

Heart failure is prevalent in 1-3% of the general population, with approximately 10% amongst elderly patients.

Prognosis is poor with 25-50% of patients dying within 5 years of diagnosis.


List some of the causes of heart failure

Heart failure can be caused by factors originating within the heart ("intrinsic" causes) or those originating from outside the heart ("extrinsic").

Intrinsic diseases include:
- myocardial infarction
- coronary artery disease (most common cause)
- chronic hypertension
- valvular heart disease
- cardiomyopathy
- viral or bacterial cardiomyopathy
- myocarditis
- pericarditis
- arrhythmias
- congenital heart disease

Extrinsic diseases include:
- thyroid disease
- diabetes
- pregnancy
- septic shock


What is acute heart failure and how is it different from chronic heart failure?

Acute heart failure develops rapidly and can be immediately life threatening because the heart does not have time to undergo compensatory adaptations. Acute failure (hours/ days) may result from cardiopulmonary bypass surgery, acute infection, acute MI, valve dysfunction, severe arrhythmia. It is a term that is often used exclusively to mean new onset acute or decompensation of chronic heart failure characterised by pulmonary and/ or peripheral oedema with or without signs of peripheral hypoperfusion.

Chronic heart failure develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until very late. In chronic failure the heart undergoes compensatory adaptations (e.g. dilatation, hypertrophy). These adaptations are often deleterious in the long term and often lead to worsening condition.


What is the most common cause of heart failure?

Coronary artery disease (CAD). CAD reduces coronary blood flow and oxygen delivery to the myocardium. This leads to myocardial hypoxia and impaired function. Another common cause of heart failure is myocardial infarction, which is the final and often fatal culmination of CAD. Infarcted tissue does not contribute to the generation of mechanical activity so overall cardiac performance is diminished.


What is systolic dysfunction?

Overall, the changes in cardiac function associated with heart failure result in a decrease in cardiac output. This results from a decline in stroke volume that is due to systolic dysfunction, diastolic dysfunction or a combination of both.

Systolic dysfunction results from a loss of intrinsic inotropy (contractility) which can be caused by alterations in signal transduction mechanisms responsible for regulating excitation-contraction coupling.


How does systolic dysfunction affect the left ventricular end diastolic pressure volume loop?

Pressure volume loops are the best method for depicting the effects of loss of intrinsic inotropy on stroke volume and end diastolic volume. Loss of intrinsic inotropy decreases the slope of the LVEDPVR. This leads to an increase in end systolic volume. There is also an increase in end diastolic volume (compensatory increase in preload) but this is not as great as the increase in end systolic volume.

Thus, the net effect is decreased stroke volume (shown as a decrease in the width of the loop). Because stroke volume decreases and end diastolic volume increases, ejection fraction decreases. In fact systolic heart failure is often referred to as heart failure with reduced ejection fraction. Stroke work (area within the curve) is also reduced.


How does the force velocity relationship explain how changes in inotropy causes reduced stroke volume?

At any given preload and afterload, a loss of inotropy results in a decrease in the shortening velocity of cardiac fibres. Because there is only a finite time available for ejection, a reduced velocity of ejection results in less blood ejected per stroke. The residual volume within the ventricle is increased (the end systolic volume) because less blood is ejected.


In systolic ventricular dysfunction, why does preload rise as inotropy falls?

The reason for preload rising as inotropy falls acutely is that the increased end systolic volume is added to the normal venous return filling the ventricle. This leads to an increased end diastolic volume and pressure, which stretches the ventricle prior to contraction.


What is a consequence of raised end diastolic pressure in systolic dysfunction?

The rise in end diastolic pressure. If the left ventricle is involved, then left atrial and pulmonary venous pressures also rise. This can lead to pulmonary congestion and oedema. If the right ventricle is in systolic failure, the increase in end diastolic pressure will be reflected back into the right atrium and systemic venous vasculature. This can lead to peripheral oedema, distended neck veins and palpable liver.


How does the Frank-Starling mechanism compensate for reduced inotropy in systolic dysfunction?

The loss of inotropy causes a downward shift in the Frank-Starling curve. This results in a decrease in stroke volume and a compensatory rise in preload because of incomplete ventricular emptying which leads to an increase in left ventricular end diastolic volume and pressure (as end systolic volume is added to venous return). This rise in preload is compensatory as it activates the Frank-Starling mechanism to help maintain stroke volume despite a loss of inotropy.

If preload did not rise, then the decline in stroke volume would be even greater for a given loss of inotropy. In systolic failure there is also an increase in blood volume (caused by neurohormonal mechanisms) that contributes to left ventricular end diastolic filling. Ventricle remodelling occurs in chronic failure leading to dilation of the ventricle.


What changes in signal transduction mechanisms might cause systolic dysfunction?

There are multiple changes that can occur. For example, desensitisation of beta 1 adrenoceptors in the heart decreases inotropic responses to sympathetic stimulation. Uncoupling of the beta 1 adrenoceptor and the Gs GPCR reduces the ability to activate adenylate cyclase. If the ability to phosphorylate protein kinase A (via cAMP) to phosphorylate L type calcium channels is impaired, then calcium influx into the cell is reduced, leading to a smaller increase in Ca++ from the sarcoplasmic reticulum. This impairs excitation contraction coupling thereby decreasing inotropy.


What is excitation- contraction coupling and how can it be impaired in systolic heart failure?

Excitation contraction coupling is the process whereby action potentials trigger cardiac myocytes to contract. Ca++ influx during phase 2 of the action potential via L type calcium channels, triggers Ca++ release from the sarcoplasmic reticulum.

In systolic heart failure ECC, can be impaired at several sites. Firstly, there can be decreased influx of Ca++ through L type calcium channels (resulting to impaired signal transduction), which decreases subsequent Ca++ release by the SR. There can also be a decrease in TN-C affinity for calcium, so that for a given increase in calcium in the vicinity of the troponin complex has less of an activating effect on cardiac contraction.


Give some causes of systolic heart failure

Cardiomyopathy (dilated)

EF is usually <40%


What is diastolic dysfunction?

Ventricular function is highly dependent on preload as demonstrated by the Frank-Starling relationship. Therefore, if ventricular filling is impaired this will lead to a decrease in stroke volume. "Diastolic dysfunction" refers to changes in ventricular diastolic properties that have an adverse effect on ventricular filling and stroke volume. About 50% of patients with heart failure have diastolic failure (although systolic and diastolic heart failure normally co-exist) with or without normal ejection fraction.


How does diastolic dysfunction affect ventricular stroke volume, ventricular end-diastolic volume and pressure, and ejection fraction?

Ventricular filling (i.e. end diastolic volume and hence sarcomere length) depends on the venous return and compliance of the ventricle during diastole. A reduction in ventricular compliance, as occurs during hypertrophy, will result in decreased ventricular filling (end diastolic volume) and a greater end diastolic pressure. Stroke volume will therefore decrease. This is shown on the pressure-volume loop by an increase LVEDPV relationship.

Depending on the relative change in stroke volume, there may or may not be a decrease in ejection fraction. Heart failure caused by diastolic dysfunction is now called heart failure with preserved ejection fraction (HFpEF). Because stroke volume is decreased, there will also be a decrease in stroke work.


How does diastolic heart failure affect end diastolic pressure?

An important and deleterious consequence of diastolic dysfunction is the rise in end diastolic pressure. If the left ventricle is involved, then left atrial and pulmonary venous pressures will also rise. This can lead to pulmonary congestion and oedema. If the right heart is involved, then the increased right ventricular end diastolic pressure is reflected back on the right atrium and in turn into the peripheral venous system. This can cause peripheral oedema and ascites.


How does ventricular hypertrophy affect diastolic function?

Pathological hypertrophy occurs due to chronic pressure overload (e.g. afterload), caused by aortic stenosis or uncontrolled hypertension. In chronic pressure overload, the ventricular chamber radius may not change, however, the wall thickness increases dramatically as new sarcomeres are added in parallel to existing ones. This is called concentric hypertrophy, and means the ventricle is capable of generating greater force and pressure, while the increased wall thickness maintains wall stress.

This adaptation makes the ventricle less compliant (i.e. more stiff) which impairs ventricular filling and leads to diastolic dysfunction.


What is meant by the term "eccentric hypertrophy"? Under what circumstances does it occur?

Eccentric hypertrophy occurs when the ventricular chamber radius is increased, and the wall thickness is increased moderately. It occurs under conditions where volume and pressure load occur simultaneously. An example of this would be when systolic dysfunction and a volume overloaded state occur in a concentrically hypertrophied heart. This stimulates chamber dilatation which adds sarcomeres in series with one another.


What is afterload?

Afterload can be thought of as the "load" that the blood must eject blood against. In simple terms the afterload is closely related to aortic pressure. To appreciate the afterload on individual muscle fibres, afterload is often expressed as ventricular wall stress.


How is wall stress related to LaPlace's law?

Wall stress is proportional to (P x r)/ h (P, ventricular pressure; r, ventricular chamber radius; h, ventricular wall thickness). This relationship is similar to the law of LaPlace, which states that wall tension (T) is proportional to the pressure (P) times the radius (r) for thin walled spheres or cylinders. Therefore wall stress is wall tension divided by wall thickness. The exact equation depends on the cardiac chamber shape which changes during the cardiac cycle, therefore a single geometric relationship is assumed.


Why can ventricular hypertrophy be considered an adaptive mechanism for increased afterload?

The pressure that the ventricle generates during systole is very similar to the aortic pressure. At a given pressure, wall stress and therefore afterload are increased by an increase in ventricular chamber radius (dilation). A hypertrophied ventricle, which has a thickened wall, has less wall stress and afterload. Hypertrophy can therefore be thought of as a mechanism that permits more muscle fibres to share in the wall tension that is determined at a given pressure and radius.

Afterload is increased by aortic stenosis, systemic vascular resistance, and ventricular dilatation. When afterload increases there is an increase in end systolic volume and a decrease in stroke volume.


What role might altered sarcoplasmic reticulum function play in diastolic dysfunction?

In some forms of diastolic heart failure, there is an impairment of the SR-ATP dependent calcium pump. This defect would retard the rate of uptake of Ca++ by the SR and reduce the rate of relaxation, leading to diastolic dysfunction.


How does combined systolic and diastolic dysfunction alter stroke volume, end-systolic and end-diastolic volumes, end-diastolic pressure, and ejection fraction?

It is not uncommon in heart failure to have both systolic and diastolic dysfunction. Therefore, the slope of the left ventricular end systolic pressure volume relationship (LVESPVR) is decreased and the slope of the passive filling curve (reciprocal of compliance) is increased.

When this occurs, there is a dramatic reduction in stroke volume because end systolic volume is increased and end diastolic volume is decreased. Both ejection fraction and stroke work are decreased.

This combination of systolic and diastolic dysfunction, coupled with compensatory volume expansion can lead to very high end diastolic pressures that can cause pulmonary congestion and oedema as well as systemic oedema and ascites.


What humoral and autonomic changes occur in heart failure and how do these changes help to compensate for impaired cardiac function?

Neurohumeral responses occur during heart failure. These include:
- activation of sympathetic nerves
- renin-angiotensin-aldosterone system
- ADH release
- ANP release

The net effect of these neurohumeral responses is to produce:
- atrerial vasoconstriction (to help maintain ABP)
- venous constriction (to increase venous pressure)
- increased blood volume (to help increase cardiac filling).

These responses can be viewed as compensatory mechanisms for the reduced cardiac output state in heart failure, but they can also aggravate heart failure by increasing ventricular afterload (which further decreases stroke volume) and increasing preload to the point where pulmonary or systemic congestion occur.


How does activation of sympathetic nerves serve as a compensatory mechanism in heart failure?

Low cardiac output states activate the sympathetic nervous system. They cause (i) cardiac stimulation, (ii) peripheral vasoconstriction and (iii) promote renin activation.

Sympathetic activation of the heart causes an increase in heart rate and inotropy via noradrenaline acting at beta 1 adrenoceptors. The increase inotropy may not be sufficient to restore normal inotropy in ventricles having systolic dysfunction. Inotropic responses may also be blunted because of down regulation of beta adrenoceptors. Sympathetic over activation can cause ventricular hypertrophy and enhanced arrhythmogenesis that can be deleterious.

Peripheral vasoconstriction is mostly mediated by activation of post junctional alpha 1 adrenoceptors. Arterial vasoconstriction increases total peripheral resistance which raises arterial pressure. However, this contributes to increased afterload on the heart which can further depress systolic function. Contraction of venous vessels enhances venous return and preload which helps maintain cardiac output by the Frank-Starlin mechanism.


How does activation of the renin-angiotensin-aldosterone system serve as a compensatory mechanism in heart failure?

Enhanced sympathetic outflow to the kidneys causes an increase in renin release (mediated by beta 2 adrenoceptors). Plasma renin activity is therefore often elevated in heart failure. Increased renin causes formation of angiotensin II and aldosterone. These cause Na+ and water retention which increases blood volume. ATII also has direct vasoconstrictor effect on blood vessels by binding to AT1 receptors. This helps to maintain arterial pressure.

Renal artery hypotension (caused by low cardiac output and therefore low perfusion pressure) and decreased sodium delivery to the macula densa also contribute to renin release in heart failure.


How do natriuretic peptides counter-regulate the renin-angiotensin-system?

Natriuretic peptides are hormones synthesised by the heart, brain or other organs. Atrial natriuretic peptide (ANP) is a 28 amino acid peptide that is synthesised, stored and released by atrial myocytes in response to atrial distension, ATII stimulation, endothelin and sympathetic stimulation (beta adrenoceptor mediated). Therefore, high levels of ANP are found during hypervolaemic states, such as heart failure.

Natriuretic peptides have 2 main mechanisms of action: (i) vasodilator effects and (ii) renal effects that lead to natriuresis and diuresis.

NPs cause venodilation (increased venous compliance) which decreases central venous pressure, which reduces cardiac output by reducing ventricular preload. NPs also dilate arteries, which decreases systemic vascular resistance.

NPs affect the kidneys by increasing glomerular filtration rate and filtration fraction, which produces natriuresis (increased sodium excretion) and diuresis (increased water excretion). These renal effects are potassium sparing. NPs also decrease renin release which decreases circulating levels of angiotensin II and aldosterone. They are therefore counter regulatory to the RAA system.


List some causes of diastolic failure

Restrictive cardiomyopathy
Constrictive pericarditis


What are the symptoms of left sided heart failure?

Poor exercise tolerance
Nocturnal cough (+/- pink, frothy sputum)
Cold peripheries
Weight loss
Muscle wasting


What causes right ventricular failure?

LVF (due to pulmonary hypertension)
Pulmonary stenosis
Lung disease (cor pulmonale)


List some symptoms of right heart failure

Peripheral oedema
Facial engorgement
Pulsation in neck and face (tricuspid regurgitation)
Palpable liver


What is meant by low output heart failure?

In this form of heart failure, cardiac output is low and fails to increase normally with exertion. It is caused by either pump failure, excessive preload or chronic excessive afterload.

Causes of pump failure = systolic and/or diastolic HF, decreased HR (beta blockers, heart block, post MI), negative inotropic drugs.

Excessive pre load = mitral regurgitation or fluid overload (e.g. NSAID causing fluid retention). Fluid overload may cause LVF in a normal heart if renal excretion is impaired, or big volumes are involved. More common if here is simultaneous compromise of cardiac function, and in the elderly.

Chronic excessive afterload = aortic stenosis, hypertension


What is high output heart failure?

This is rare. Here, output is normal or increased in the face of increased needs. Failure occurs when cardiac output fails to meet these needs. It will occur with a normal heart, but even earlier if there is heart disease.

Paget's disease
Wet beri-beri


What criteria is used to diagnose heart failure?

To diagnose HF there should be symptoms of HF and objective evidence of cardiac dysfunction (at rest). Diagnosis can be made using Framingham criteria. This requires the simultaneous presence of at least 2 major criteria or 1 major and 2 minor.

Major: PND, crepitations, S3 gallop, neck vein distension, hepatojugular reflux, cardiomegaly on X ray

Minor: ankle oedema (bilateral), dyspnoea, tachycardia, hepatomegaly, pleural effusion (transudative)

Other signs: exhaustion, cool peripheries, cyanosis, decreased BP, narrow pulse pressure, pulsus alternans, displaced apex (LV dilatation), RV heave (pulmonary hypertension) murmurs of mitral or aortic valve disease


How should cases of suspected HF be investigated?

According to NICE, if ECG and B type natriuretic peptides are normal, heart failure is unlikely and an alternative diagnosis should be considered, if either is abnormal then echocardiography is required.

1) Bloods - FBC, U&E, BNP

2) Imaging
CXR - ABCDE features
Echo is the key investigation - can confirm cause, and indicate level of LV dysfunction (ejection fraction)

3) ECG - may indicate cause (look for evidence of ischaemia, MI or ventricular hypertrophy). It is rare to get completely normal ECG in heart failure


What are the chest x ray features of heart failure?

A - alveolar oedema (peri hilar bats wings shadowing)
B - kerley B lines (interstitial oedema)
C - cardiomegaly
D - dilated prominent upper lobe vessels (upper lobe diversion)
E - pleural effusion


What general measures should be adopted to treat heart failure?

These include:
- effective patient education
- maintain nutritional status
- smoking cessation
- avoidance of excessive salt or alcohol intake
- regular moderate exercise
- vaccinations for influenza and pneumococcus

Treatment of the underlying cause (e.g. coronary artery disease, valvular disease, hypertension etc) prevents progression


What is the rationale for putting patients with heart failure on diuretics?

These reduce the plasma volume, thereby reducing preload and improving pulmonary and systemic venous congestion. In some patients with severe chronic heart failure, IV loop diuretics or combination therapy with a loop and thiazide diuretic may be required. Aldosterone receptor antagonists such as spironalactone are potassium sparing diuretics that improve long term outcome in patients with severe heart failure and those with heart failure following MI.


Why should patients with heart failure be started on ACEi?

ACEi's (e.g. enalapril, lisinopril) are first line in mild heart failure. Venous dilatation reduces the filling pressure (preload) and arteriolar dilatation lowers the afterload. The reduction in vascular tone decreases the work and oxygen demand of the failing heart. Cardiac output increases and because renovascular resistance falls, there is an increase in renal blood flow. This latter effect, together with reduced aldosterone, increases Na and water excretion, contracting the blood volume and reducing venous return to the heart. They improve effort tolerance and mortality in moderate to severe heart failure and following MI. They may cause hypotension in hypovolaemic and elderly patients, so should be started with caution.

ARBs produce haemodynamic and mortality benefits similar to those on ACEi. They are a useful alternative for patients intolerant of ACEi.


What vasodilators are used in heart failure?

These may be useful in the treatment of chronic heart failure when ACEi or ARBs are contraindicated. Venodilators (e.g. nitrates) and arterial dilators (e.g. hydralazine) may be used, but may cause hypotension.


Why are beta blockers used in heart failure?

These help to counteract the adverse effects of enhanced sympathetic stimulation in chronic heart failure and reduce the risk of arrhythmias and sudden death. They must be introduced slowly to avoid precipitating acute-on-chronic heart failure. But when used appropriately, they have been shown to improve ejection fraction, improve symptoms and reduce mortality.

Carvedilol, bisoprolol and metoprolol given with an ACEi inhibitor and diuretic have been shown to reduce mortality.


What is ivabradine?

This acts on the SAN to reduce heart rate. It reduces mortality and admissions in moderate to severe LV dysfunction, and is useful if beta blockers are contraindicated.


Is digoxin useful in heart failure?

Digoxin can be used for rate control in patients in AF with heart failure. It may reduce episodes of hospitalisation in patients with severe heart failure but has no effect on long term survival.

Amiodarone is also useful for controlling arrhythmias in patients with poor LV function, as it has little negative inotropic effect.


Why is CRT used in heart failure?

Cardiac resynchronisation therapy restores the normal contraction pattern of the left ventricle, which may be dysynchronous in patients with impaired LV function and left bundle branch block.


Why are implantable cardiac defibrillators used?

These reduce the risk of sudden death in selected patients with chronic heart failure, particularly those with a history of ventricular arrhythmia.


What group of patients can cardiac revascularisation be used on?

Bypass grafting or percutaneous coronary intervention may improve function in areas of "hibernating" myocardium with inadequate blood supply, and can be used to treat carefully selected patients with heart failure and coronary artery disease.


When is cardiac transplantation considered for patients with heart failure?

Transplantation is an established and successful form of transplant for patients with intractable heart failure. Coronary artery disease and dilated cardiomyopathy are the most common indications. The use of transplantation is limited by the availability of donor hearts, and so is generally reserved for young patients with severe symptoms. Serious complications include rejection, infection (due to immunosuppressive therapy) and accelerated atherosclerosis.

Ventricular assist devices have been employed as a bridge to transplantation, and more recently as potential long term therapy. There is currently a high rate of complications (e.g. haemorrhage, systemic embolism, infection).


What are the mechanical effects of digoxin?

Digoxin is a cardiac glycoside. It increases the force of cardiac contraction in the failing heart. This benefit has been doubted in patients with chronic heart failure who are in normal sinus rhythm, but recent trials have shown that digoxin can reduce symptoms of heart failure in patients who are already receiving diuretics and ACEi. Digoxin is particularly indicated in patients with heart failure caused by AF.


What is the mechanism of action of digoxin?

Digoxin inhibits membrane Na+/K+ ATPase which is responsible for Na+/K+ exchange across the muscle cell membrane. This increases intracellular Na+ and produces a secondary increase in intracellular Ca++ that increases the force of myocardial contraction. The increase in intracellular Ca++ occurs because the decreased Na+ gradient across the membrane reduces the extrusion of Ca++ by the Na+/ Ca++ exchanger (antiporter) that occurs during diastole.

Digoxin and K+ compete for the receptor (Na+/K+ ATPase) on the outside of the muscle cell membrane, so the effects of digoxin may be dangerously increased in hypokalaemia, produced for example with diuretics.


What are the electrical effects of digoxin?

These are due to a complicated mixture of direct and indirect actions.

Direct effects:
In atrial and ventricular cells, the action potential and refractory period are shortened, because the increased intracellular Ca++ stimulates potassium channels. Toxic concentrations cause depolarisation (resulting from Na+ pump inhibition) and oscillatory depolarising afterpotentials appear after normal action potentials (caused by increased intracellular Ca++). If these delayed afterpotentials reach threshold, action potentials are generated causing "ectopic beats". With increasing toxicity, the ectopic beat itself elicits further beats causing a self sustaining arrhythmia (VT), which may progress to VF.

Indirect effects:
Digoxin increases central vagal tone and facilitates muscarinic transmission in the heart. This (i) slows the heart rate down, (ii) slows atrioventricular conductance, and (iii) prolongs the refractory period of the AVN. Use of this is made in the treatment of AF, but at toxic levels heart block occurs.


Does digoxin affect other organs?

Digoxin affects ALL excitable tissues, its cardioselectivity resulting from greater dependence of myocardial function on the rate of sodium extrusion. The most common extracardiac action is on the gut, and digoxin may cause anorexia, nausea, vomiting, or diarrhoea. These effects are partly brought about by action on smooth muscle cells and are partly the result of central vagal and CTZ stimulation. Less common effects include confusion and psychosis.


How is digoxin toxicity treated?

Digoxin toxicity is quite common, because arrhythmias can occur at concentrations only two or three times that of optimal therapeutic concentration. According to severity, treatment may require withdrawal of the drug, potassium supplements, antiarrhythmic drugs (phenytoin or lidocaine) or in very severe intoxication, digoxin specific antibody fragments (Fab).


What is the mechanism of action of sympathomimetic agents used to treat heart failure?

Sympathomimetic agents activate cardiac beta receptors and stimulate adenylyl cyclase (via Gs GPCR). The rise in cAMP activates cAMP dependent protein kinase, which leads to phosphorylation of the L type Ca++ channels and an increase in the probability of their opening time. This increases the influx of Ca++ and hence the force of myocardial contraction. In contrast to digoxin, which has a neutral effect on survival, other positive inotropes have been found to increase mortality. For this reason, non glycoside inotropes are used only for the short term treatment of refractory patients or those awaiting transplantation.


When are sympathomimetic agents used?

Dobutamine is given by slow intravenous infusion in acute severe heart failure. It stimulates beta 1 adrenoceptors in the heart and increases contractility with little effect on rate. In addition, its action on beta 2 adrenoceptors causes vasodilation.

Dopamine given by intravenous infusion in low doses to healthy volunteers increases renal perfusion by stimulating dopamine receptors in the renal vasculature. This finding has long encouraged the use of low dose dopamine to treat cardiogenic shock, where deterioration of renal function is common.


Outline the management of severe pulmonary oedema

- Sit the patient upright in order to reduce pulmonary congestion
- High concentration oxygen (60%)
- CPAP 5-10 mmHg by mask
- Continuous monitoring of cardiac rhythm, BP and oxygen sats
- Nitrates (e.g. IV GTN 10-200 micrograms/min or buccal GTN 2-5 mg) titrated upwards every 10 mins, until clinical improvement or systolic BP falls <110 mmHg
- Loop diuretic (e.g. furosemide 500-100 mg IV)

- IV opiates - with caution, can cause respiratory depression

If above methods are ineffective:
- Inotropic agents (particularly in hypotensive patients)
- Insertion of an intra-aortic balloon pump (for cardiogenic pulmonary oedema, and shock)

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