Heart failure

• The cardiac muscle is a specialized tissue

with unique properties like excitability,
contractility & automaticity
• The myocardium has two types of cells –
– The contracting cells participate in the
pumping action of the heart
– SA node, AV node & His-Purkinje system
comprise the conducting tissue of the
heart. Parts of the conducting tissue have
the characteristic property of
automaticity
• Automaticity is the ability of the cell to
generate electrical impulse spontaneously.
Normally the SA node acts as the pace
maker
• Excitability is the ability of the cell to
undergoe depolarization in response to a
stimulus
• Contractility is the ability of the
myocardium to contract adequately &
pump the blood out of the heart
 Cardiac action potential
• Phase 0:
– Rapid depolarization of the cell membrane
during which there is opening of the
voltage gated sodium channels & fast entry
of sodium ions into the cell through the
sodium channels
– The channels close in 1-2 milliseconds when
they enter as inactivated state
– This is followed by repolarization
 Cardiac action potential
• Phase 1:
– Is a short, initial, rapid repolarization due
to efflux of potassium ions & the
membrane potential returns towards 0 mv
• Phase 2:
– Is a prolonged plateau phase due to slow
entry of calcium ions into the cell through
the calcium channels
– Cardiac cell differs from other cells in
having this phase of action potential
 Cardiac action potential
• Phase 3:
– Is a second period of rapid repolarization with
potassium ions moving out of the cell through the
potassium channels (Ikr)
– Drugs that interfere with K+ channels prolong the
action potential by delaying this phase of
repolarization
• Phase 4:
– Is the resting phase during which potassium ions
return into the cell while sodium & calcium ions
move out of it
– The RMP is restored
– The sodium channels recover from inactivation
 Cardiac action potential

• During phases 1 & 2, the cell does not

depolarise in response to another
impulse, i.e. it is in absolute refractory
period. Effective Refractory Period
(ERP) – begins with the action potential &
includes the absolute refractory period
• During phase 3 & 4, the cell is in relative
refractory period & may depolarise in
response to a powerful impulse
 Congestive Cardiac Failure (CCF)
• Heart failure is the inability of the heart to
supply adequate blood flow & therefore
oxygen delivery to peripheral tissues & organs
• Heart failure may be defined as the state in
which the heart fails to maintain the adequate
cardiac output for the need of the body
despite an adequate venous filling pressure
• Under perfusion of organs leads to reduced
exercise capacity, fatigue, & shortness of
breath
• It can also lead to organ dysfunction (e.g.
renal failure) in some patients
 Pathophysiology of heart failure

BP Sympathetic tone

 Renal blood flow

 CO Compensatory  CO

CCF Heart  After

Renin release
 Aldosterone
load

Na+ and water  Preload

Angiotensin I
retention Vasoconstriction

Angiotensin II
 In heart failure –
 Decreased force of contraction
 Decreased cardiac output
 Increased after load
 Increased preload
 Aim of treatment of heart failure –
 Correction or amelioration of underlying disease
 Control of precipitating factor
 Reduction of demand on heart by restriction of
physical work
 To improve the myocardial contractility
 In peripheral edema, pulmonary edema – to
reduce edema or congestion
 To reduce cardiac preload and after load
 Drugs in heart failure
 Positive inotropic that improve cardiac contractility in
CHF -
 Cardiac glycoside e.g. Digitalis.
 Phosphodiesterase inhibitor e.g. Amrinone.
 Sympathomimetic drugs - β1 agonist e.g. Dopamine,
Dobutamine, Dopexamine
 Newer agents – Istaroxime, Levosimendan
 Diuretics to decrease Na+ and H2O retention –
frusemide, chlorthiazide, spironolactone.
 Vasodilators – decrease preload and afterload –
 ACEI – captopril, lisinopril, enalapril.
 Arterial vasodilator – hydralazine
 Venodilator – GTN, isosorbide dinitrate
 Arterial and venous dilator – prazosin, nitropruside
 β blockers – carvedilol, metoprolol
 Cardiac glycoside or cardenolides
• These are the agents which have cardiotonic
property or action. Cardiotonic drugs increase
myocardial contractility and output in a
hypodynamic heart without a corresponding
increase in O2 consumption.
Source Glycosides
Digitalis purpurea (leaf) Digitoxin
Gitoxin
Gitalin
Digitalis Lanata Digitoxin
Digoxin
Gitoxin
Strophanthus Gratus (seed) Strophanthin G (Ouabain)
Source Glycosides
Strophanthus Kombe (seed) Strophanthin K
Urginia maritima (bulb) Proscillaridine A
Thebetia neriifolia (nut) Thebetin
Convalleria majalis Convallotoxin
Bufo vulgeris (animal source) Bufo toxin
Semisynthetic drugs Acetyl digoxin
Digoxigenin
 Clinically used –
 Digoxin (most commonly used)
 Digitoxin
 Ouabain.
• Chemistry of cardiac glycosides –
• All of the glycosides - of which digoxin is
the prototype – combine a steroid nucleus
linked to an unsaturated 5 membered
lactone ring at the 17 position and a series
of sugars at carbon 3 of the nucleus.
Because they lack an easily ionizable group,
their solubility is not pH dependent.
• P/K –
• It has both lipophilic (steroid nucleus) and
hydrophilic (lactone ring, hydroxyl group, sugar)
groups. The balance of these two has an important
effect on pharmacokinetics.
• Steroid nucleus with lactone ring is essential for
myocardial action. A sugar molecule present which
is important for pharmacokinetic property.
• Fairly well absorbed after oral administration.
• 10% individual harbor a kind of enteric bacteria
which inactivates the digoxin. So, in that case
large dose is required.
• Digitoxin – also well absorbed but is not degraded
by such bacteria.
• β methyl digoxin – semisynthetic derivative of digoxin
is also well absorbed and after absorption it is
converted into digoxin.
• Once absorbed into the body fluid, glycosides are
widely distributed throughout the body including
CNS.
• The concentration of digoxin is 10 to 50 times more
in the tissue fluid of heart, liver and kidney than the
plasma.
• Digoxin is not extensively metabolized and is
excreted as unchanged (2/3) state through kidney.
• Digitoxin is metabolized by the liver and excreted
into the intestine via bile.
• The active metabolites (like digoxin) and unchanged
agents then can be reabsorbed into the body fluid
establishing an enterohepatic circulation (long t ½).
• Therapeutic index – narrow (1.5 - 3).
 M/A – (A) Mechanical effect - Digitalis increase the
force of contraction which is independent of
innervation by direct action. They bind with Na +-K+
ATPase, a membrane associated enzyme present in the
myocardial fiber and causes inhibition of that enzyme
and inturn causes increase concentration of Na + inside
the cell cytoplasm. There is a normal mechanism of Na +-
Ca++ exchanger system present in the myocardial fiber
by which Ca++ is effluxed which depends upon the
external Na+ concentration. By the inhibition of Na +-
K+ATPase as because the Na+ concentration increase
within the myocardial fiber, this exchanger mechanism
is inactivated and which inturn causes increase
concentration of Ca++. Further more it influences Ca++
entry through voltage gated calcium channel.
• Once the Ca++ enter into the cell cytoplasm causes the
release of Ca++ from sarcoplasmic reticulum. This
increased free Ca++ react with actin-troponin-
tropomyosin complex and causes contraction.
 Digoxin
(-) membrane bound Na+ K+ ATPase
(-) of Na+ pump
Increase [Na+] intracellular concentration
(-) of Na+/Ca++ exchange
Increase [Ca++] intracellular concentration
Increase [Ca++] pumped into the S.R.
Increase excitation contraction coupling
Increase force of contraction
 Positive inotropic effects
Increase the force of contraction of
heart – the stroke volume increases &
thereby the cardiac output
These effects are dose dependent
The systole is shortened & the diastole is
prolonged which allows more rest to the
heart & better filling of coronaries
The ventricles are more completely
emptied because of more forceful
contaractions
The inotropic effects are more
pronounced on the failing heart
 (B) Electrical effect - Negative chronotropic effect i.e.
decrease H.R. Digitalis also acts through sympathetic
and parasympathetic nervous system throughout the
therapeutic and toxic dose range. At the therapeutic
range of dosing the parasympathetic effect is more.
This therapeutic dose range effect is due to
 Increased vagal tone reflexly by sensitization of
baroreceptors, as well as by stimulation of vagal
centre
 Decreased sympathetic overactivity due to improved
circulation
 Direct decreasing action on S.A. nodal discharge
 Slows A.V. nodal conduction directly
 Slowing of Action Potential within atria and
ventricular muscle.
 These effects leads to normalization of tachycardia in
H.F. (in normal person no effect)
 (C) electrophysiological effects:
The effects vary with dose & in different parts
of the heart
These effects are as a result both direct &
autonomic effects of digitalis
The action potential duration is reduced which
may be due to increased potassium conductance
following increased intracellular calcium
Digitalis shortens the refractory period of the
purkinje fibers, the atria & the ventricular
muscles
The automaticity of the ventricles & the Purkinje
cells are enhanced but more pronounced effect
is on AV conduction. Cardiac glycosides depress
AV conduction & increase the AV nodal
refractory period
 (C) electrophysiological effects:
 Increase myocardial automaticity at high (toxic)
concentration. Glycoside  (-) Na+K+ATPase 
increase intracellular Na+  Increase rate of
depolarization  rapid onset of successive action
potential  increase automaticity  arrhythmia.So,
slight increase in dose of digitalis will cause
arrhythmia. At toxic dose – sympathetic effect is
more.
 Digitalis also produces the characteristic ECG
changes like T wave inversion, changes in P wave,
increased PR interval, (in AV node) shortened QT
interval & ST segment depression
 (D) Extracardiac actions:
 Kidney: diuresis occurs which relieves edema in CCF
patients
 CNS: High doses stimulate CTZ resulting in nausea &
vomiting
 Digoxin induced increased force of contraction
has some characteristics –
 Sympathomimetic drug increase force of
contraction with increase O2 consumption. But
digoxin increase force of contraction without
increase O2 consumption. This increase force of
contraction is a direct action.
 How digitalis improves in H.F.?
 Digoxin  increase C.O. complete ventricular
emptying  decrease residual volume 
decrease heart size  Starling Law can
operate again on heart  heart can contract.
 Effect of administration of electrolyte on
effect of digoxin – K+, Ca++, Mg++  toxicity.
 Drug interactions
• Diuretics: causes hypokalemia which
increases the risk of digitalis arrhythmia;
potassium should be given prophylactically
• Quinidine: reduces binding of digoxin to
tissue proteins as well as its renal & biliary
clearance by inhibiting efflux transporter P-
glycoprotein  plasma concentration of
digoxin is doubled  toxicity can occur.
Verapamil, diltiazem, captopril, propafenone
& amiodarone also increase the plasma
concentration of digoxin to variable extents
 Drug interactions
 K+ and digitalis, interact in two ways.
 First – they inhibit each other’s binding to
Na+/K+ ATPase; therefore, hyperkalemia
reduces the enzyme inhibiting action of
cardiac glycosides, whereas hypokalemia
facilitates these actions.
 Second – abnormal cardiac automaticity is
inhibited by hyperkalemia.
 Ca++ facilitates the toxic actions of cardiac
glycosides by accelerating the overloading of
intracellular Ca++ stores that appears to be
responsible for digitalis-induced abnormal
automaticity. Hypercalcemia therefore
 Drug interactions
 increases the risk of digitalis induced arrhythmia.
 Decreased Mg++ concentration enhances toxicities of
cardiac glycosides.
 Adrenergic drugs: can induce arrhythmia in
digitalized patients; both increase ectopic
autimaticity
 Digoxin absorption may be reduced by
metoclopramide, sucralfate, antacids, neomycin,
sulfasalazine. Absorption of digoxin is increased by
atropine drugs, including tricyclic antidepressants
 Propranolol, verapamil, diltiazem & disopyramide: may
additively depress A-V conduction & oppose positive
inotropic action
 Succinylcholine: can induce arrhythmia in digitalized
patients
 Indication – CHF with atrial fibrillation
Supraventricular arrhythmia – atrial
fibrillation, atrial flutter
 Precaution & Contraindications:
– Ventricular tachycardia – there may be
precipitation of ventricular fibrillation and death
may occur
– Hypokalemia – enhances digitalis toxicity
– Elderly, renal or severe hepatic disease: patients
are more susceptible to digoxin toxicity
– Myocardial ischemia – severe arrhythmias are
more likely
– Thyrotoxicosis – patients are more prone to
develop digitalis arrhythmias
– Myxoedema – these patients eliminate digoxin
more slowly; cumulative toxicity can occur
– Partial A-V block – may be converted to
complete A-V block by digoxin
– Acute myocarditis – Diphtheria, acute
rheumatic carditis, toxic carditis –
inotropic response to digitalis is poor,
more prone to arrhythmias
– Wolff-Parkinson-White syndrome –
digitalis is contraindicated because it
decreases the ERP of bypass tract in 1/3
patients. In them rapid atrial impulses may
be transmitted to ventricles  ventricular
fibrillation may occur. Digitalis can
increase the chance of reentry by slowing
conduction in the normal A-V bundle &
accelerating it in the aberrant pathway
 Adverse effect –
 Cardiac toxicity –
 Rhythm disturbances are due to
hyperkalemia: as Na+/K+ ATPase is inhibited
 prevent intracellular accumulation of K+
 Increased myocardial automaticity 
arrhythmia. If excess dose  slowing of AV
conduction  Heart block.
 Mild case – sinus bradycardia, 1st degree H
block
 Moderate case – pulsus bigemini, 2nd degree
heart block
 Severe cases – ventricular ectopic,
ventricular tachycardia & fibrillation. Atrial
tachycardia with H block. AV dissociation
even complete heart block
 Adverse effect –
 GIT – anorexia, nausea, vomiting and
diarrhoea.
 CNS – vagal and CTZ stimulation. Less
often, disorientation and hallucination
(especially in elderly) and visual
disturbances are noted.
 Long term use – gynecomastia in male
(rare).
 Visual effects – xanthopsia (yellow color
vision), photophobia, blurring
• Treatment of cardiac toxicity:
– Stop digitalis
– Oral or parenteral K+ supplements are
given (but K+ is contraindicated in
presence of hyperkalemia or AV block)
depending on the severity. Mild cases
respond to oral potassium chloride (5gm
daily in divided doses). When parenteral K +
is required, it should be given slowly as a
drip with constant ECG monitoring
– Ventricular arrhythmias are treated with
IV phenytoin/lignocaine
• Treatment of cardiac toxicity:
– Bradycardia, heart block is treated with
atropine & supraventricular arrhythmias
with propranolol
– In severe toxicity temporary cardiac
pacemaker should be inserted
– Antidigoxin immunotherapy (Digibind
obtained from sheep) is now available.
Antidigoxin antibodies bind cardiac
glycosides & reverse their effects. These
antibodies are life saving in severe toxicity
due to cardiac glycosides
 Phosphodiesterase inhibitors (PDIs)
• Amrinone (inamrinone), Milrinone,
Vesnarone.
• M/A –
– Heart  PDIs  (-) PDE3  cAMP 
prolong influx of Ca++ during action
potential  contractility.
– Vessel  cAMP in arterial and venous
smooth muscle  marked vasodilatation.
•  CO   stroke volume.
•  PR  vasodilatation   pulmonary
capillary wedge pressure.
 Phosphodiesterase inhibitors (PDIs)
• But because of the adverse effects &
increased mortality seen with the use of
these drugs, they are generally not
preferred
• Sildenafil
– Inhibits PDE 5 which is abundant in the
lungs
– Found to be useful in patients with
pulmonary hypertension & CHF
– Improves cardiac function, haemodynamics
of the heart & overcomes ventricular
hypertrophy & enhances exercise capacity
• Indication –
– For short term therapy in patient with CCF
who are refractory to the treatment with
digoxin and diuretics (only for acute HF or
for an excerbation of Chronic HF).
• Adverse effects –
– GIT – nausea and vomiting.
– Automaticity  arrhythmia.
– Vesnarone – agranulocytosis.
– Amrinone – thrombocytopenia.
– Milrinone has short t½ & fewer side
effects
 β1 agonist
• M/A – (+) β1  (+) adenyl cyclase  cAMP  [Ca++] influx
 actin myosin coupling  force of contraction  CO.
• Dopamine –Low dose (0.5-2 mcg/kg/min): activate
Dopamine receptors
• Intermediate dose(2-10): activate Beta receptors
• High dose(>10): activate Alpha receptor
• So, it is a drug of choice.
Very short t½ (2 – 3 minutes) due to metabolism by COMT.
So, we have to give in IV infusion.
1 – 5 μgm/kg/min  good β effect.
> 5 μgm/kg/min  α1 effect   PR.
dose  arrhythmia develop.
• Dobutamine – relatively selective for β 1
receptor. So used in acute CHF for short
term use. Has less tendency to cause
arrhythmia.
• Dopexamine –
– is an agonist at D1, D2 & β2 adrenergic
receptors because of which it has
vasodilator properties – reduces peripheral
vascular resistance & improves renal blood
flow. Thus cardiac work load reduces due
to reduced afterload
– It also has mild inotropic properties by β1
receptor stimulation
• Newer agents:
– Levosimendan:
• In addition to PDE inhibition levosimendan
sensitizes the troponin system to calcium &
thereby has positive inotropic effects
• It also has vasodilator properties including
coronary vasodilatation & has been approved
for use in heart failure in some countries
• It is not an arrhythmogenic drug
• It may be used in acute decompensated
heart failure as an alternative to dopexamine
• Used IV in a loading dose of 6-24 μg/kg
followed by 0.05-0.2 μg/kg/minute
– Istaroxime:
• Is undergoing clinical trials for use in
heart failure
• It acts as an inotropic agent in two ways
–Inhibits Na+ K+ ATPase like digoxin
–Also facilitates the sequestration of
calcium in the sarcoplasmic retibulum
• It may have some advantages over digoxin
like being less arrhythmogenic
– Other drugs like Nesiritide (a recombinant
natreuretic peptide), vasopresin receptor
antagonists like Conivaptan & Tovaptan are
under clinical trials
 Diuretics
• Thiazide, frusemide.
• Beneficial effect both in acute and CHF.
• Role of diuretics in HF –
• Act on renal tubule  prevent reabsorption
of Na+ and H2O   Na+ and H2O excretion
 plasma volume   venous return  
preload.
•  Na+ and H2O excretion  relieve of edema.
•  Systemic and pulmonary venous congestion
 So also there will be small  in afterload.
• However, they have some disadvantages:
– Long term diuretic therapy may cause
hypokalemia, & also activate renin angiotensin
system leading to deleterious effects on the
cardiovascular system
– Diuretics do not stop the progression of the
heart failure & only suppress the symptoms
– Hence the current recommendation in mild
heart failure is diuretics for short periods as &
when required
• IV frusemide along with an ACEIs is particularly
useful in acute heart failure
• Long term frusemide therapy may be needed in
more severe disease
• Spironolactone & eplerenone, the K+ sparing
diuretics are aldosterone antagonists
– The role of aldosterone in the
pathophysiology of cardiac failure is now
clearly established
• Na+ & water retention
• Expansion of ECF volume  increased
preload
• Fibroblast proliferation & fibrotic
change in myocardium  worsening
systolic dysfunction & pathological
remodeling
 • Hypokalemia & hypomagnesemia 
increased risk of ventricular
arrhythmias & sudden cardiac death
• Enhancement of cardiotoxic &
remodeling effect of sympathetic
overactivity
– Spironolactone though a weak diuretic can
benefit the patients with heart failure
because it antagonises the above effects
of aldosterone
 Vasodilators
• Arteriolar dilators (hydralazine) relax
arterial smooth muscles, thus reducing
peripheral vascular resistance & thereby
afterload  the work on heart is reduced
• Venodilators (nitrates)  reduce the venous
return to the heart (decrease preload) thus
reducing the stretching of the ventricular
walls & myocardial oxygen requirements
• Both areteriolar & venular dilators (ACEIs,
sodium nitropruside, prazosin) – reduce both
preload & afterload
• Hydralazine:
– being an arterioalar dilator improves renal
function as it causes good renal
vasodilatation
– It may be given in combination with a
nitrate in patients who have some
contraindication for ACEIs/ARBs. The
combination improves long term survival
though less than with ACEIs
• Organic nitrates:
– Nitroglycerine & isosorbide dinitrate are
good vasodilators with a rapid & short
action
 – They can be used for short periods to
decrease the ventricular filling pressure in
acute heart failure
– Can be used IV in acute CCF
– may be given in combination with
hydralazine
• ACE Inhibitors:
– Reduction of afterload:
• Angiotensin II (Ang-II) is a powerful
vasoconstrictor present in high
concentrations in plasma
– ACEIs prevent the conversion of
angiotensin I to angiotensin II & thereby
reduce the afterload
– Reduction of preload:
• Aldosterone causes salt & water
retention & increases plasma volume
• ACEIs prevent the formation of
aldosterone (by reducing Ang-II) &
thereby reduce the preload
• They also prevent bradykinin
degradation & increase bradykinin levels
which also causes vasodilatation
 – Reversing compensatory changes:
• Angiotensin II formed locally in the
myocardium is responsible for various
undesirable compensatory changes like
ventricular hypertrophy & ventricular
remodeling seen in CCF. ACEIs reverse
these changes
• Sodium nitropruside:
– Powerful vasodilator
– Since it dilates both areterioles & venules,
it reduces both ventricular filling pressure
& peripheral arterial resistance
 – It is given IV
– Has a rapid (30-60 sec) & short action (3minutes).
Hence it is useful in acute severe heart failure
• Prazosin:
– α1 antagonist, powerful vasodilator
– Can be used in acute heart failure for
longer periods than nitrates
• Calcium channel blockers:
– These are not routinely used in heart
failure
– Amlodipine or felodipine may be tried in
patients in whom other vasodilators are
contraindicated
 β blockers
Most patients with chronic HF respond favorably to
certain β blockers in spite of the fact that these drugs
can precipitate acute decompensation of cardiac function.
Trial of β blockers are based on the hypothesis that
excessive tachycardia and adverse effects of high
catecholamine levels on the heart contribute to the
downward course of HF patients.
Suggested mechanism of beneficial action include –
attenuation of the adverse effects of high concentration
of catecholamines (including apoptosis), up-regulation of β
receptors, decreased HR, and reduced remodelling
through inhibition of mitogenic activity of catecholamines.
They can improve symptoms, reduce the frequency of
hospitalization and reduce mortality in chronic HF.
 Chronic heart failure
• General measures –
• Effective education of patients – explanation
of nature of disease, treatment and self-
help strategies.
• Diet – good general nutrition and weight
reduction for the obese, avoidance of high-
salt foods and added salt, especially for
patients with severe CCF.
• Moderate or eliminate alcohol consumption.
• Stop smoking.
• Regular moderate aerobic exercise within
limit of symptoms.
 Chronic heart failure
• In patients with coronary artery disease,
secondary preventive measures such as low-
dose aspirin and lipid-lowering therapy are
required.
• Moderate or eliminate alcohol consumption.
• Stop smoking.
• Regular moderate aerobic exercise within
limit of symptoms.
• In patients with coronary artery disease,
secondary preventive measures such as low-
dose aspirin and lipid-lowering therapy are
required.
• Drug therapy – cardiac function can be
improved by increasing contractility,
optimizing preload or decreasing afterload.
• Drugs that reduce preload are most
appropriate in patients with high end-
diastolic filling pressures and evidence of
pulmonary or systemic venous congestion
(backward failure); drugs that reduce
afterload or increase myocardial
contractility are more useful in patients
with signs and symptoms of a low cardiac
output (forward failure).
• Diuretics – 1st line treatment.
• Vasodilators – venodilators (nitrate) reduce
preload, and arterial dilators (hydralazine)
reduce afterload. T^heir use is limited by
pharmacological tolerance and hypotension.
• ACEI, ARBs
• β blockers
• Digoxin – 1st line therapy in pt. é HF& Atrial
Fibrillation.
 Steps in the treatment of Chronic HF –
 Reduce workload of the heart
 Limit activity, put on bed rest
 Reduce weight
 Control HTN
 Restrict sodium intake
 Restrict water (rarely required)
 Give diuretics
 Give ACEI or ARBs
 Give digitalis if systolic dysfunction
with 3rd heart sound or atrial
fibrillation is present
 Give β blockers to patients with
stable class II-IV heart failure
 Give vasodilators
 Cardiac resynchronization if wide
QRS interval is present in normal
sinus rhythm
 Acute heart failure
 This needs urgent hospital treatment:
 Sit the patient up in order to reduce
pulmonary congestion.
 Give O2 (high-flow, high concentration). Non-
invasive positive pressure ventilation by a
tight-fitting face mask results in a more rapid
improvement in the patients clinical state.
 Administer nitrates (I.V. GTN 10-200µ gm/min
or buccal GTN 2-5 mg) titrated upwards every
10 minutes, until clinical improvement occurs
or systolic BP falls to < 110 mm Hg.
 Administer a loop diuretic (IV furosemide)
 Strict bed rest with continuous monitoring of
cardiac rhythm, BP and pulse oximetry.
 I.V. opiates may be cautiously used when the
patients are in extremis. They reduce anxiety
(perception of shortness of breath), and
reduce cardiac preload (reduce venous tone)
and afterload (decrease peripheral resistance)
but run the risk of respiratory depression and
exacerbation of hypoxia and hypercapnia.
 If these measures prove ineffective,
inotropic agents may be required to augment
cardiac output, particularly in hypotensive
patients.
Clinical pharmacology of drugs used in CHF
• Spironolactone, eplerenone are the only drugs
found to reduce mortality as well as morbidity
in CCF
• β-blockers should be started only when the
patient is in compensated heart failure.
Carvedilol is now the preferred β-blocker in
CCF
• ACEIs have better efficacy than ARBs due to
raised bradykinin levels. An ARB is however an
alternative
• Salt, water & physical activity restriction are
important lifestyle modifications in CCF