presentasi

1. Cardiac failure
By Dr. Osman Bukhari

2. Cardiac failure :
Occurs when the heart is unable to
maintain sufficient cardiac output to
.meet the demands of the body
.Incidence increases with age .Many pts. are admitted repeatedly Despite improvement in management
mortality is still high
…….Pathophysiology
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3. :Manifestations of cardiac failure
: Left cardiac failure - 1
Symptoms include: fatigue, exertional
dyspnoea, orthopnoea & paroxysmal
. nocturnal dyspnoea
Signs include: Cardiomegaly with
displaced & often sustained apical
impulse, triple & gallop rhythm, basal
lung crackles, pulsus alternans,
.functional MR & pulmonary edema
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4. Cardiomegaly

5. LVF & pulmonary oedema

6. :-Causes
.HT- 1
.Ischemic heart disease- 2
.Ao stenosis & regurgitation- 3
.Mitral regurgitation- 4
.Cardiomyopathy- 5
Myocarditis.
.arrhythmias
High output states (anemia , A-V
fistula, thyrotoxicosis, PDA, pagets
disease of bone, beri-beri & gram
.(negative septicemia
7- - 6
-8

7. :Right cardiac failure - 2
Symptoms include:
- fatigue, anorexia and nausea related
to distension and fluid accumulation
.in areas drained by systemic veins
Rt hypochondrial pain swelling of of the LLs -
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8. Signs: include:
- increased JVP
tender smooth hepatomegaly
dependent pitting edema
ascites & pleural transudates
tachycardia.
LPH, TR, Rt. S3
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9. Pitting oedema of the LL

10. Causes
Lt heart failure- 1
( Chronic lung disease (core pulmonale- 2
Pulm embolism- 3
Pulm HT- 4
.Tricuspid valve dis- 5
Pulm valve dis- 6
Lt to Rt shunts ( ASD , VSD(
8- isolated Rt. Vent. Cardiomyopathy
-7

11. .IHD- 9
Constrictive pericarditis & cardiac
. tamponade
.High output states- 11
- 10
.CCF: Combines both Lt & Rt HF- 3

12. Acute heart failure
.Extensive acute MI- 1
.Rupture of IVS producing VSD- 2
Papillary or chordal rupture in
-3
endocarditis producing MR
4Sudden Ao valve rupture in
endocarditis
5Acute pulmonary embolism & cardiac
.tamponade
In all these conditions the heart size is
. relatively normal

13. High output states are associated with
tachycardia, gallop rhythm & patients
.are often warm with distended veins

14. Factors precipitating HF in controlled
. patients
. Increased salt intake- 1
.Uncontrolled HT- 2
.Anaemia & pregnancy- 3
.Fluid overload- 4
.MI- 5
.Arrhythmias specially AF- 6
.Pulm. Embolism- 7

15. Infections sp. chest infections causing - 8
hyperdynamic circulation.
9.Thyrotoxicosis
.Drug non compliance- 10
Renal failure secondary to diuretic
- 11
induced volium depletion or due to
. intrinsic renal disease

16. Investigations in HF
This is to confirm HF & to establish the
.underlying cause
CXR: Shows cardiac size & evidence of - 1
pulmonary congestion (upper lobe
venous diversion; bat win appearance
(in pulm oedema
ECG: Shows arrhythmias, ischemia , - 2
.
chamber hypertrophy etc
Echo: (2- dimentional & doppler echo( - 3
show valves, chambers size, ejection
.
fraction, intracardiac thrombi

17. CXR with right apical fibrosis

18. Electrocardiogram

19. Echocardiography

20. .CBC, LFT & blood urea & electrolytes- 4
Cardiac enzymes in acute MI- 5
.Cardiac catherization- 6
Ambulatory ECG monitoring in
-7
. suspected arrhythmias
. Stress ECG- 8

21. Coronary angiography

22. Treatment of HF
Preventive measures in HF include:
- Cessation of smoking
Control of DM
Effective treatment of HT
TR of hypercholesterolemia
.pharmacological TR following MI

23. TR of chronic HF aims at:
- Relieving symptoms,
Retarding disease progression,
Correction of the cause ,
-TR of aggravating factors,
Compliance with drug therapy.
, Improving survival
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24. :General TR- 1
Physical activity: ranges from bed rest
in severe HF to low level exercise in
compensated HF . Avoid strenuous
.exercise
Dietary modifications: WT reduction,
salt restriction, alcohol abstinence &
fluid restriction in severe HF
.and dilutional hyponatraemia
.Education -
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25. (Drug TR Of HF( Pharmacotherapy- 2
Diuretics Vasodilators Digoxin AntiarrhythicsAnticoagulants Inotropic drugs BBStatins -

26. (Drug TR Of HF( Pharmacotherapy- 2
:Diuretics- 1
Act by promoting renal excretion of salt
and water reducing preload & rapidly
improves dyspnoea & systemic
congestion. They also cause arteriolar
. vasodilatation reducing after load
Loop diuretics: e.g. frusemide (lasix(
have a rapid onset of action & short
duration of action.They cause
(hypokalaemia ( add slow-K

27. b-Thiazide diuretics: e.g.
hydrochlorothiazide and Chlorthalidone
have mild diuretic effect, but act
synergistically when combined with
loop diuretics. Not effective in renal
impairment.
Metolazone is a powerful thiazide & is
combined with loop diuretics in severe
. and resistant HF
Loop & thiazide diuretics have no proven *
survival benefit. They give symptomatic
relieve

28. c- Potassium sparing diuretics:
Care with ACE-I & avoided in renal
impairment .
Spironolactone reduces mortality in
doses of up to 25 mg when added to
conventional therapy in moderate to
severe HF. Risk of hyperkalaemia is
..high with doses of > 50 mg
Ameloride & triamterene are weak but
useful when combined with loop
..diuretics

29. :Vasodilater therapy- 2
a- ACE-Is
reduce after load & pre load
- reduce circulating levels of
catecholamines,
reduce BP
reduce cardiac dilatation & CCF after
extensive MI
improve exercise tolerance & survival
.
in pts. with severe HF

30. ACE-I should be carefully introduced in
pts. on high doses diuretics & in the
presence of hyponatraemia.
.Care with K- sparing diuretics
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31. b- ARBs have similar effects to ACE-I but
.
do not affect bradykinin metabolism
c- Alpha blockers (prazocin( & direct
smooth muscle relaxants (hydralazine(
are not very effective in HF.
CCBs reduce after load but have no
prognostic benefit in HF. Diltiazem and
.verapamil are CI in HF
d- Nitrates (glyceride trinitrates and
isosorbide mononitrates( reduce
preload and reduce pulm edema.Only

32. combination with hydralazine have
. proven prognostic value
BB used in pts. with chronic stable
HF (e.g. metoprolol, bisoprolol,
atenolol and carvedilol(, improve
symptoms, exercise tolerance, LV
function and mortality in pts. with HF.
.Initial doses should be low
:Inotropic drugs- 4
Digoxin
- Sympathomimetic-
-3

33. Digoxin :
cardiac glycoside, It blocks AV node
and increases myocardial contractility. used in severe HF with conventional
therapy, AF, atrial flutter & SVT.
90% is excreted unchanged in urine
and accumulation can occur in renal
failure. Digitoxin is used In renal
failure.
Usual dose is 0.125-0.25 mg/d. with
dose of 1mg in emergency

34. :Dose is reduced in
elderly
renal failure
hyperthyroidism
4- quinine therapy
electrolyte disturbance e.g.
Hypokal & hypo Mg.
.Ca is dangerous in digitalized pts
2-- 1
-3
-5
IV

35. SE of Digoxin include:
HA, fatigue, muscle weakness, abd.
.Pain, N, V, Wt. loss & gynaecomastia
Digoxin toxicity include:
anorexia, N, V, coloured vision with
halo around objects (xanopsia(,
arrhythmias & fits.
- TR
of digoxin toxicity:
By
stopping the drug, restoration of
ser.
K and management of
arrhythmias. Digoxin abs. in life
.threatening toxicity

36. Adr., dobutamine, dopexopamine & dopamine
are IV adrenergic agonist. They increase CO &
improve perfusion but increase myocardial O2
requirements & aggravate cardiac ischemia.
Volume depletion should be corrected before
their use. Main use in pts. with acute LVF,
following cardiac surgery & in pts. with end
.stage HF as a bridge to transplantation
Dobutamine is a B2 agonist increasing
cardiac contraction & has vasodil. effect
by alpha blocker effect. Dose 2.5-10
.mcg/kg/minute

37. Dopexamine is B2 agonist with additional
action on peripheral dopamine receptors
.improving renal perfusion
Dopamine in low dose (2-4 mcg/kg/min.)
improves renal perfusion. In dose of 410 mcg/kg/min. increases HR & cardiac
contractility. Higher doses increase BP at
. the expense of tissue perfusion
Noradr. Raise BP by peripheral
.vasoconstriction

38. Anticoagulants to prevent
thromboembolism in pts. with AF ,
endocardial thrombus & PH of
.thromboembolism
-5
:Antiarrhythmic agents- 6
Drugs
- DC shock
Implantable cardiovertor - defibrillator
)ICD
(
Statins- 7
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BB, ACE-I, statins & spironolactone may
.reduce sudden death in pts. with MI and HF

39. Non-pharmacological Tr. of HF:
.1- Revascularization
.Pacemaker or ICD- 2
Valvular surgery & correction of other
. causes of HF
.Cardiac transplantation- 4
.Ultra-filtration- 5
.Intra-aortic balloon pump- 6
-3

40. Pace maker

41. In summary:
1-
All pts. with clinical HF should
receive diuretics & ACE-I.
2Patients with AF should be
.digitalized
Pts. in SR improve with addition of - 3
. Digoxin or BB
Pts. with asymptomatic LV
-4
dysfunction benefit from
prophylactic ACE- I therapy or ARB

42. Pts. with ischemic HF & intolerant to - 5
ACE-I or in whom it is CI may
benefit from nitrate/ hydralazine
. therapy
.Spironolactone should be added- 6

43. Pulmonary edema
.Life-threatening emergency .Usually preceded by PND Interstitial edema usually occurs with
. capillary pressure of 20 mmHg
Alveolar edema occurs with pressure of
. 25-30 mmHg
Causes are those of LVF, MS & increased pulmonary capillary
).permeability
(Adult RDS
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44. Pulmonary oedema

45. :Clinical features include
Extreme SOB
.Wheezing
.Anxiety & sweating .Cough with frothy blood tinged sputum
Tachypnea, cyanosis, tachycardia and
. gallop rhythm
.Crackles & wheeze in z chest .Low arterial PO2 CXR shows diffuse haziness & bat wing
.
appearance
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46. :Treatment Include
Admission in CCU.
- .Cardiac bed
Continuous flow high O2 conc and in .severe cases pt. is ventilated
). IV morphine 10-15 mg( + antemetic Avoided if SBP < 90
IV loop diuretic which produces
immediate vasodilt. In addition to
. more delayed diuresis
Venodilt. & arterial vasodilators to
. decrease pre-load & after load

47. Aminophylline 5 mg/kg IV ( 250-500)
slowly to avoid the risk of precipitating
ventricular arrhythmias. It is
bronchodilator., vasodilt. & increases
cardiac contractility. Usually used when
.bronchospasm is present
.Monitor rhythm, O2 saturation Venesection & mechanical methods of
reducing venous return are ineffective
. and rarely used
Treat precipitating factors (arrhythmias, .) chest infection, etc

48. Correct the underlying cause of
increased pulmonary capillary
permeability (toxins, hypoxia,
.). infections, DIC, etc
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