inability to pump blood forwards to meet the metabolic need of the body or the ability to do so with an abnoramally high filling pressure

*forward failure or backford failure*

Ascites

Pharmological management of CHF

ACE inhibitor

eg Ramapril

 side effect cough

•Angiotensin Receptor Blocker

 e.g. Losartan

Effective if ACE-I intolerant

•Aldosterone antagonist

e.g. Spironolactone

side effect: hyperkalemia

Beta Blocker

(*not for asthma patient or need to have cardioselective beta blocker)

Calcium channel blocker

eg amlodipine

side effect flushing, headahce and ankle oedema

Nitrates

eg GTN

it is a syndrome, not a disease

• Systolic VS diastyolic heart disease
  
• Left ventricular or right ventricular failure
• left: lead to pulmonary congestion
• right: lead to systemic congestion
• isolated right: as in cor pulmonale as a consequence of lung disease
• right failure most often as a consequence of LV failure

Frank Starling Law: increase stroke voume when there is an increase in the end diastolic volume (venous return)

• Initial insult to the heart eg MI
• Myocardium loses its contractility and thus decrease stroke volume
• to compensate by using Frank Starling Law, there will be an increase in end diastolic volume
• however, if stroke volume cannot be compensated, there will be an increase in end sytolic volume because of the loss of intropy
• this will result in pulmonary or systemic congestion 

• The heart become stiff
• there is decrease of EDV and only pure diastolic failure, ESPVR and ejection fraction are preserved
• CO will decrease

• Patient with CHF have higher End systolic volume in the right heart
• This will reduce venous return, and thus increase the hydrostatic pressure in the capillary
• Also oncotic pressure is low in CHF patient becuase of dilution of albumin and liver dysfunction eg Nutmeg liver
• The excess interstitial fluid will manifest as oedema

• conorary heart disease
• hypertension
• valve disease
• infective eg viral myocarditis
• alcohol

• Frank starling mechanism
• neurohormonal activation
• Sympathetic: Tachycardia
• SNS, RAAS: vasoconstriction
• ADH, RAAS:salt and water retention
• Atrial natriuretic peptide
• Brain natriuretic peptide (found in ventricles)
• ANP and BNP: vasodilating, salt and water excreting and inhibit renin, and thus inhibit RAAS
• ventricular remodelling

• chronic stress to heart lead to alteration in size, shape, structure and function of the heart
• change is initially compensatory but become detrimental
• increased wall stress
• fibrosis
• apoptosis
• contractile dyssynchrony

• dyspnoea
• orthopnoea
• paroxysmal nocturnal dyspnoea
• fatigue

• resting tachycardia
• elevated jugular venuous pressure
• peripheral oedema
• increase RR
• lung crackles
• ascites

• ACE inhibitor
• eg ramipril
• vasodilator
• 1st line treatment
• s/e: cough
• Beta blocker
• eg bisoprolol
• start low, go slow
• reduce fibrosis, apoptosis and arrhymogenesis
• Angiotensin receptor blocker
• losartan
• aldosterone antagonist
• spironolactone
• hydralazine/nitrates
• inferior to ACEi and ARB
• consider in Afro-Carribbean patients because of low renin activity

Preload

contractility

afterload

• Sit up 
• reduce venous return and thus reduce work of breathing and heart
• 100% oxygen
• IV Furosemide
• IV nitrate
• IV diamorphine 
• anxiolytic
• ECG, X Ray, Blood gas

what is the relationship of stroke volume and end diastolic volume in

1) healthy person

2) increase in SNS

3) heart failure

How is the renin-angiotensin-aldosterone system (RAAS) activated in heart failure?

The failing heart causes a low blood pressure and reduced perfusion of the kidneys. Both of these can lead to activation of the RAAS

• when blood volume is low, sensed by juxtaglomerular cell and secrete renin
• renin will carry out the conversion of angiotensinogen to angiotensin I in the liver
• angiotensin I will convert to angiotensin II with the help of angiotensin converting enzyme found in the lung
• angiotensin II will cause vasoconstriction
• also angiotensin II will stimulate the secretion of aldosterone, which cause increase in sodium resorption and in turn water resorption and raise BP

     Explain briefly why the patient has the following symptoms and signs:-

c.    Ankle oedema

a) Failure of the right ventricle leads to congestion and raised pressures in the systemic veins. This may be seen as an elevation of the jugular venous pressure.

b) Failure of the left ventricle leads to congestion of the pulmonary veins. This causes venous engorgement and may lead to increased fluid in the interstitium. The engorged vessels and interstitium may in turn compress the surrounding airways and also reduce pulmonary compliance, thus increasing the work of breathing and making the patient breathless. This will be exacerbated by exercise when the demands on the heart and lungs are greater.

c) Increased venous hydrostatic pressure means there is a net movement of fluid out of the capillaries and into the interstitial tissues. This exceeds the lymphatic vessels ability to transport it away and results in an accumulation of fluid in the interstitial tissues (oedema).Oedema is most prominent and first seen in dependent parts of the body (usually the ankles in mobile patients, but may be the sacrum in bedbound patients) as the hydrostatic pressure in the capillaries in these regions are higher due to the effects of gravity.

1)    Why does the ankle oedema seem to get better overnight?

At night, when the lower limbs are raised the effect of gravity is reduced, the hydrostatic pressure falls and there is a redistribution of some of the tissue fluid back into the circulation, thus reducing the ankle oedema.

1)    Explain the mechanism by which she became breathless when lying flat?

Lying flat increases venous return as blood from the lower limbs and abdomen can more easily return to the heart as the effect of gravity is removed. The increase in venous return to a failing left ventricle causes a rise in pulmonary venous pressures, which leads to pulmonary venous engorgement, (potentially interstitial oedema), compression of the airways and a fall in pulmonary compliance thus leading to the breathlessness.

1)    Why is ramipril helpful in patients with heart failure?

By preventing the formation of angiotensin II it reduces vasoconstriction (in both veins and arterioles). This reduces preload and afterload and thus reduces the work of the failing heart. In addition it reduces the formation of aldosterone and thus reduces sodium and water reabsorption and therefore circulating volume.

ACE inhibitors often cause a slight deterioration in renal function (probably due to their effects on preventing efferent arteriole constriction by angiotensin II). In most patients this is only minor and temporary, however in some patients it can be substantial and progressive, hence the importance of monitoring, especially when these drugs are started or there has been a change in dose    

What class of drugs does bisoprolol belong to?

and why it is used in heart failure

Beta adrenergic receptor antagonist (beta blocker)

They attenuate the negative aspects of cardiac remodelling, fibrosis, apoptosis and arrhythmias that are partially attributed to the constant activation of the sympathetic nervous system in heart failure

1)    Explain the mechanism by which the patient on ACEi has developed a dry cough.

Angiotensin converting enzyme (ACE) is also responsible for the breakdown of bradykinin. It is thought that the accumulation of bradykinin in certain patients causes the dry cough.

1)    Explain why losartan is a good alternative choice of drug for ACEi

Losartan is an angiotensin II receptor blocker (ARB) – it therefore has similar effects to ACE inhibitors but as ACE is no longer blocked, then bradykinin can be broken down (and therefore can’t accumulate to cause a cough). However, you do lose the vasodilatory effects of bradykinin which may be beneficial in heart failure.

You are asked to see a 56 year old man who is an inpatient on the ward following a recent non ST-elevation myocardial infarction (NSTEMI). He is extremely short of breath and sat upright on the bed using his accessory muscles of respiration. He is coughing up pink frothy sputum.

He is pale, anxious, sweaty and cold to touch. His pulse rate is 124/min regular; respiratory rate is 32/min and his blood pressure is 180/72. His oxygen saturation on air is 82%. Auscultation of his lungs reveals widespread coarse crackles bilaterally, which are loudest at the bases.

He is treated initially with morphine, oxygen, furosemide, and a nitrate infusion is set up.

1)    Why is this patient so breathless?

He has developed pulmonary oedema due to acute left ventricular failure (LVF). The LVF has led to a sudden rise in the pressure within the pulmonary veins and capillaries sufficient to cause oedema to develop within both the interstitium and the alveoli.

1)    What is causing the widespread crackles patient with CHF? Why are these noises loudest at the bases?

The reopening of partially occluded oedematous airways and movement of air through these oedematous airways is causing the crackles.

The oedema will be worse at the bases due to the greater hydrostatic pressure in these pulmonary vessels due to the effect of gravity in an upright patient.

1)    Why is patient coughing up pink frothy sputum in pulmonary oedema?

The rise in pulmonary venous pressure may well be sufficient to rupture some vessels causing small bleeds into the airways. This gives a pink tinge to the sputum which is formed by the pulmonary oedema.

1)    Explain how the compliance of their lungs with acute exacebation of CHF changed from normal?

The lungs are oedematous and contain much more fluid than usual and thus will be stiffer and harder to ventilate i.e. their compliance will be significantly reduced.

1)    Why is his oxygen saturation reading low?

There will be a ventilation perfusion mismatch in his lungs, as alveoli that were previously well ventilated are now oedematous, impairing gas exchange. The V/Q ratio is likely to low and there will be a shunt of deoxygenated blood passing through the lungs which fails to be oxygenated or only partially by these oedematous alveoli.

MAP = Cardiac output x systemic vascular resistance

Despite a fall in cardiac output, blood pressure can still be maintained and even raised if there is significant vasoconstriction and therefore an increase in systemic vascular resistance

1)    How will the nitrate infusion help this patient?

1)    What is the mechanism of action of the nitrate infusion?

Nitrates are a source of nitric oxide (NO). This binds to and activates guanylate cyclase in vascular smooth muscle cells. This enzyme converts GTP to cyclic GMP (cGMP), which in turn activates protein kinase G (PKG) whose downstream effects lead to smooth muscle relaxation.

1)    Explain why bisoprolol should NOT be given to this patient at the moment?

Although beta blockers are indicated for use in patients with chronic stable heart failure, they are contraindicated in acute heart failure, as their negative inotropic effect will exacerbate the situation.