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Nanokha Dan
Namutyaba Najiba
Ssenoga Dickson
Namutebi Sarah
Tutor:
Dr. Kwarisiima
Levi
objectives
 To define HF
 To classify HF
 To discuss clinical presentation and complications of HF
 To discuss examination and investigations
 To discuss management of HF
DEFN
 Heart failure is defined as the pathophysiologic state in
which impaired cardiac function is unable to maintain an
adequate circulation for the metabolic needs of the tissues
of the body.
 It may be acute or chronic.
 The term congestive heart failure(CHF) is used for the
chronic form of heart failure in which the patient has
evidence of congestion of peripheral circulation and of
lungs.
 CHF is the end-result of various forms of serious heart
diseases.
CAUSES OF HEART FAILURE
 Intrinsic pump failure. (weakening of heart muscle) due to
Ischemic heart disease, myocarditis, metabolic disorders,
fibrillations, flutter)
 Increased workload which increases myocardial demand. May be
pressure load (systemic/pulmonary arterial HTN, valvular stenosis,
lung diseases) or volume load(valvular insufficiency, severe
aenemia, thyrotoxicosis, arteriovenous shunts, hypoxia in lung
disease)
 Impaired filling of cardiac chambers (cardiac tamponade,
constrictive pericarditis)
CAUSES
 Systolic dysfunction (EF<40%). –ischemia, HTN, drugs(anthracyclines,
cyclophosphamide)
 Diastolic dysfunction – massive Left ventricular hypertrophy, myocardial
fibrosis, amyloid deposition, constrictive pericarditis and restrictive
cardiomyopathy. – common in elderly women and diabetics
 Valve dysfunction – endocarditis (viral, bacterial rheumatic heart disease,
calcifications)
 Fluid or pressure overload in a normal heart
 Increased demand e.g. hyperthyroidism and anaemia
Types of heart failure
 Acute or chronic
 Right sided or left sided
 Forward or backward
 HF with reduced EF and HF with reserved EF, MID range
Acute vs chronic heart failure
Acute Chronic
 Sudden and rapid onset
 No oedema but has hypotension
 Can occur in large MI, valvular
rupture, cardiac tamponade, massive
pulmonary embolism, acute viral
myocarditis, acute bacterial toxaemia
 Slow dev’t
 Has oedema
 Develops compensatory mechanisms
like tachycardia, cardiac dilation,
hypertrophy to maintain CO
 May be due to myocardial ischemia
from atherosclerotic coronary artery
disease; multivalvular heart disease,
systemic HTN; chronic lung disease.
Left Vs Right sided HF
Left Right
 Due to stress on left heart chambers
 Causes are; systemic HTN, mitral or
aortic Valvular stenosis; Ischemic heart
disease; myocarditis; restrictive
pericarditis
 Pulmonary congestion(dyspnea);
reduced tissue perfusion(kidney, brain,
skeletal muscles)
 More as consequence of left sided HF
 Also due to intrinsic lung disease
,Pulmonary or tricuspid valvular
disease, Pulmonary HTN 2 to
thromboembolism, Myocardial
disease, Congenital heart disease(left-
right shunt)
 Present systemic venous
congestion(edema), cyanosis, coldness
of extremities
Backward Vs Forward HF
Backward Forward
 The ventricles fail to eject blood
normally so there is increase in end-
diastolic volume and increase in atrial
volume and pressure that is
transmitted to backward to the veins.
 Manifestations result from failure of
heart to pump blood causing
hypoperfusion of tissues like kidney
which activates the RAAS
Presentation:
Infants and young children
 Respiratory distress with rapid respiration, cyanosis,
 wheezing, subcostal, intercostal, and sternal recession
 Rapid pulse, gallop rhythm, excessive sweating
 Tender hepatomegaly
 Difficulty with feeding
 Cardiomegaly
Presentation
Older children and adults
 Palpitations, shortness of breath, exercise intolerance
 Fatigue, orthopnea, exertional dyspnoea, wheezing
 Rapid pulse, gallop rhythm
 Raised jugular venous pressure (JVP)
 Dependent oedema, enlarged tender liver
 Basal(fine) crepitations only in inspiration course r in both esp in
pneumonia
Presentations continued…
 Renal failure
 Orthopnea
 Paroxysymal nocturnal dyspnea(PND)
 Third heart sound(S3)
 Atrial fibrillation
 Hypoxic encephalopathy (irritability, restlessness, stupor and coma)
Complications
 Renal failure
 Portal hypertension
 Hypoxic encephalopathy(stupor, coma)
 Splenomegaly
 Arrhythmias
 Angina and heart attack
 Pulmonary edema
 Ascites
 Anasarca
 embolism
Examination
 Inspection of the patient
 Radial pulse, HR, BP(both sides)
 Neck examination for jugular vein pulse
 Palpation of anterior chest wall
 Auscultation of heart
 Percussion and auscultation of the lung bases
 General;
 systemic(general appearance)
Investigations
 Chest x-ray (cardiac dilation, pleural effusion)
 Echochadiogram (dilatation, hypertrophy, valvular diseases)
 Electrocardiogram (arrhythmias, MI,)
 Radionuclide angiography(MI)
 CT angiography (CAD)
 MRI (MI,CAD,myocarditis, cardiomyopathies)
Investigations continued:
 Biochemical investigations
 Cardiac enzymes(creatinine kinase) and structural proteins(troponin T,I)
 Renal functional tests
 Electrolyte measurements
 Blood Glucose and lipid profile
 Bacteriology (blood culture, serology)
Management of heart failure
 Bed rest with head of bed elevated
 Prop up patient in sitting position
 Reduce salt intake and limit fluid intake(1-1.5L/day)
 Surgery e.g. coronary artery bypass, valve repair/replacement, heart
transplant
 Medical devices e.g. VADs, Implantable cardioverter-defibrillators (ICDs),
Cardiac resynchronization therapy (CRT), or biventricular pacing
 Manage other underlying causes accordingly
Drugs used
 ACE inhibitors ; inhibit formation of angiotensin ll and diminish the
inactivation of bradykinin e.g. captopril, fosinopril, enalapril
Dose; enalopril(2.5mg once daily), captopril(6.25-12.5mg 8-12hourly)
Contraidicated in pregnancy
 Angiotensin receptor blockers ; competitive antagonists of angiotensin ll type
l receptor e.g. valsartan, losartan. (Are contra indicated in pregnancy)
 Aldosterone antagonists; e.g. spironolactone, eplerenone. Indicated in
patients with severe HFrEF
Dose; spirinolactone(25-50mg/day) k+ greater than 5(contraindicated)
all Prolong survival
Drugs cont’d…
 Beta- blockers e.g. bisoprolol, carvedilol, metoprolol succinate. Decrease
HR, remodelling and cell death
Dose: carvedilol (3.125mg 12hourly)
 Diuretics; reduce pulmonary congestion and peripheral oedema (reduce
orthopnea and PND). loop diuretics (furosemide) are commonly used
Dose; furosemide (20-40mg oral/IV 12hourly)
 Positive Inotropic drugs e.g. digoxin. Low drug concentrations are used
in severe HFrEF
Dose; 125-250microgram/daily
 Vaso dilators e.g. nitrates and venodilators e.g. hydralazine or
hydralazine/isosorbide dinitrate.
Order of therapy
Loop duiretics
ACE inhibitors/ARBs and beta-blockers
Digoxin,spironolactone,hydralazine/isosorbide dinitrate
Management of chronic heart failure
• Periodic monitoring of body weight, BP, respiratory rate and O2
saturation
• Salt and fluid restriction
• Limit alcohol intake
• Regular exercise within limits of symptoms
• Continued treatment with medicines listed above
Refernces:
 Uganda clinical guidelines 2016.
 Davidsons Principles and Practice of Medicine, 22nd edition, pg
 Harsh Mohan - Textbook of Pathology, 6th Edition

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Congestive heart failure

  • 1. Nanokha Dan Namutyaba Najiba Ssenoga Dickson Namutebi Sarah Tutor: Dr. Kwarisiima Levi
  • 2. objectives  To define HF  To classify HF  To discuss clinical presentation and complications of HF  To discuss examination and investigations  To discuss management of HF
  • 3. DEFN  Heart failure is defined as the pathophysiologic state in which impaired cardiac function is unable to maintain an adequate circulation for the metabolic needs of the tissues of the body.  It may be acute or chronic.  The term congestive heart failure(CHF) is used for the chronic form of heart failure in which the patient has evidence of congestion of peripheral circulation and of lungs.  CHF is the end-result of various forms of serious heart diseases.
  • 4. CAUSES OF HEART FAILURE  Intrinsic pump failure. (weakening of heart muscle) due to Ischemic heart disease, myocarditis, metabolic disorders, fibrillations, flutter)  Increased workload which increases myocardial demand. May be pressure load (systemic/pulmonary arterial HTN, valvular stenosis, lung diseases) or volume load(valvular insufficiency, severe aenemia, thyrotoxicosis, arteriovenous shunts, hypoxia in lung disease)  Impaired filling of cardiac chambers (cardiac tamponade, constrictive pericarditis)
  • 5. CAUSES  Systolic dysfunction (EF<40%). –ischemia, HTN, drugs(anthracyclines, cyclophosphamide)  Diastolic dysfunction – massive Left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, constrictive pericarditis and restrictive cardiomyopathy. – common in elderly women and diabetics  Valve dysfunction – endocarditis (viral, bacterial rheumatic heart disease, calcifications)  Fluid or pressure overload in a normal heart  Increased demand e.g. hyperthyroidism and anaemia
  • 6. Types of heart failure  Acute or chronic  Right sided or left sided  Forward or backward  HF with reduced EF and HF with reserved EF, MID range
  • 7. Acute vs chronic heart failure Acute Chronic  Sudden and rapid onset  No oedema but has hypotension  Can occur in large MI, valvular rupture, cardiac tamponade, massive pulmonary embolism, acute viral myocarditis, acute bacterial toxaemia  Slow dev’t  Has oedema  Develops compensatory mechanisms like tachycardia, cardiac dilation, hypertrophy to maintain CO  May be due to myocardial ischemia from atherosclerotic coronary artery disease; multivalvular heart disease, systemic HTN; chronic lung disease.
  • 8. Left Vs Right sided HF Left Right  Due to stress on left heart chambers  Causes are; systemic HTN, mitral or aortic Valvular stenosis; Ischemic heart disease; myocarditis; restrictive pericarditis  Pulmonary congestion(dyspnea); reduced tissue perfusion(kidney, brain, skeletal muscles)  More as consequence of left sided HF  Also due to intrinsic lung disease ,Pulmonary or tricuspid valvular disease, Pulmonary HTN 2 to thromboembolism, Myocardial disease, Congenital heart disease(left- right shunt)  Present systemic venous congestion(edema), cyanosis, coldness of extremities
  • 9. Backward Vs Forward HF Backward Forward  The ventricles fail to eject blood normally so there is increase in end- diastolic volume and increase in atrial volume and pressure that is transmitted to backward to the veins.  Manifestations result from failure of heart to pump blood causing hypoperfusion of tissues like kidney which activates the RAAS
  • 10. Presentation: Infants and young children  Respiratory distress with rapid respiration, cyanosis,  wheezing, subcostal, intercostal, and sternal recession  Rapid pulse, gallop rhythm, excessive sweating  Tender hepatomegaly  Difficulty with feeding  Cardiomegaly
  • 11. Presentation Older children and adults  Palpitations, shortness of breath, exercise intolerance  Fatigue, orthopnea, exertional dyspnoea, wheezing  Rapid pulse, gallop rhythm  Raised jugular venous pressure (JVP)  Dependent oedema, enlarged tender liver  Basal(fine) crepitations only in inspiration course r in both esp in pneumonia
  • 12. Presentations continued…  Renal failure  Orthopnea  Paroxysymal nocturnal dyspnea(PND)  Third heart sound(S3)  Atrial fibrillation  Hypoxic encephalopathy (irritability, restlessness, stupor and coma)
  • 13. Complications  Renal failure  Portal hypertension  Hypoxic encephalopathy(stupor, coma)  Splenomegaly  Arrhythmias  Angina and heart attack  Pulmonary edema  Ascites  Anasarca  embolism
  • 14. Examination  Inspection of the patient  Radial pulse, HR, BP(both sides)  Neck examination for jugular vein pulse  Palpation of anterior chest wall  Auscultation of heart  Percussion and auscultation of the lung bases  General;  systemic(general appearance)
  • 15. Investigations  Chest x-ray (cardiac dilation, pleural effusion)  Echochadiogram (dilatation, hypertrophy, valvular diseases)  Electrocardiogram (arrhythmias, MI,)  Radionuclide angiography(MI)  CT angiography (CAD)  MRI (MI,CAD,myocarditis, cardiomyopathies)
  • 16. Investigations continued:  Biochemical investigations  Cardiac enzymes(creatinine kinase) and structural proteins(troponin T,I)  Renal functional tests  Electrolyte measurements  Blood Glucose and lipid profile  Bacteriology (blood culture, serology)
  • 17. Management of heart failure  Bed rest with head of bed elevated  Prop up patient in sitting position  Reduce salt intake and limit fluid intake(1-1.5L/day)  Surgery e.g. coronary artery bypass, valve repair/replacement, heart transplant  Medical devices e.g. VADs, Implantable cardioverter-defibrillators (ICDs), Cardiac resynchronization therapy (CRT), or biventricular pacing  Manage other underlying causes accordingly
  • 18. Drugs used  ACE inhibitors ; inhibit formation of angiotensin ll and diminish the inactivation of bradykinin e.g. captopril, fosinopril, enalapril Dose; enalopril(2.5mg once daily), captopril(6.25-12.5mg 8-12hourly) Contraidicated in pregnancy  Angiotensin receptor blockers ; competitive antagonists of angiotensin ll type l receptor e.g. valsartan, losartan. (Are contra indicated in pregnancy)  Aldosterone antagonists; e.g. spironolactone, eplerenone. Indicated in patients with severe HFrEF Dose; spirinolactone(25-50mg/day) k+ greater than 5(contraindicated) all Prolong survival
  • 19. Drugs cont’d…  Beta- blockers e.g. bisoprolol, carvedilol, metoprolol succinate. Decrease HR, remodelling and cell death Dose: carvedilol (3.125mg 12hourly)  Diuretics; reduce pulmonary congestion and peripheral oedema (reduce orthopnea and PND). loop diuretics (furosemide) are commonly used Dose; furosemide (20-40mg oral/IV 12hourly)  Positive Inotropic drugs e.g. digoxin. Low drug concentrations are used in severe HFrEF Dose; 125-250microgram/daily  Vaso dilators e.g. nitrates and venodilators e.g. hydralazine or hydralazine/isosorbide dinitrate.
  • 20. Order of therapy Loop duiretics ACE inhibitors/ARBs and beta-blockers Digoxin,spironolactone,hydralazine/isosorbide dinitrate Management of chronic heart failure • Periodic monitoring of body weight, BP, respiratory rate and O2 saturation • Salt and fluid restriction • Limit alcohol intake • Regular exercise within limits of symptoms • Continued treatment with medicines listed above
  • 21. Refernces:  Uganda clinical guidelines 2016.  Davidsons Principles and Practice of Medicine, 22nd edition, pg  Harsh Mohan - Textbook of Pathology, 6th Edition

Editor's Notes

  1. Presenting complaint Review of other systems Medical history Socio– family history Examinations (cvs, rs, cns)