Acute Heart Failure presentation slides

1. BY: NKRUMAH JEPHTAH BEJNAMIN
NAANA BOATEMAA KUFUOR
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2. Introduction/Overview
Epidemiology
Etiology
Pathophysiology
Signs & Symptoms
Investigations and Diagnosis
Complications
Management -Pharmacological & Non-Pharmacological
Counselling Points
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3. Heart failure(HF) is “a complex clinical syndrome that results from any
structural or functional cardiac impairment of ventricle filling or ejection of
blood (AHA/ACC)
It results from inability of the heart to adequately pump blood sufficient to
meet the metabolic needs and adequately perfuse body cells
 Heart failure is a progressive condition with complex possible causes, and mortality
varies according to etiology and severity of symptoms.(Roger Walker,5th edition)
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4. PRELOAD
 This is the loading condition of the heart at the end of its relaxation and filling
phase(diastole) just before contraction(systole)
 Preload represents the extent of dilation of the ventricles in diastole(end-diastolic
fiber stretch) and the volume of blood the dilated ventricles can hold(end-diastolic
volume)
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5. After load
 the tension developed in the ventricular wall as contraction (systole) occurs.
 It is determined by the chamber pressure in the LV and the thickness of the
myocardium
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6. CARDIAC OUTPUT
 This is the volume of blood being pumped by the heart(ventricles),per unit time
 Normal CO in a healthy heart is about 5-6L/min.
 Co=Heart rate(HR) × Stroke volume(SV)
 where HR is the number of heart beats per minute and
 SV is the volume of blood pumped out the LV during systolic cardiac contraction.
 (i.e. EDV-ESV)
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7. EJECTION FRACTION
 Is the ratio of stroke volume to the end diastolic volume
 EF=
𝑆𝑉
𝐸𝐷𝑉
∗ 100
 It represent the percentage of blood that that was pumped out during systole
 The normal ejection fraction of a healthy heart ranges from 50-70%
 Anything lower than 40% indicates a failing heart
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8. SYSTOLIC DYSFUNCTION
 Reduction in muscle mass
 Dilated cardiomyopathies
 Ventricular hypertrophy
 Restrictive cardiomyopathy
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9. DIASTOLIC DYSFUNCTIONS
 Increased ventricular stiffness
 Ventricular hypertrophy
 Myocardial ischemia and infarction
 Mitral or tricuspid valve stenosis
 Pericardial disease (e.g., pericarditis, pericardial tamponade)
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10. OTHER FACTORS
 Hypertension
 Viral illness
 Thyroid disease
 Excessive alcohol use
 Pregnancy-related heart disease
 Familial congenital disease
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11.  Heart Failure with reduced Ejection Fraction HFrEF – Ejection fraction ≤ 40% .
 In HFrEF, the LV poorly contracts and empties inadequately leading to increased diastolic
volume and pressure with reduced ejection fraction.
 Heart Failure with Preserved Ejection Fraction HFpEF – Ejection Fraction ≥50%
 In HFpEF,LV filling is impaired resulting in an increase in LV end diastolic pressure at rest
or during exertion usually with normal EF
 Heart failure with mid-range ejection fraction(HFmrEF)-Ejection fraction,41-49%
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12.  HIGH OUTPUT FAILURE
 The heart functions normally (or increased) but unable to meet up with the
increased metabolic demand of the body
 Eg.in anemia,hyperthyroidism,pregnancy
 LOW OUTPUT FAILURE- – Heart fails to generate adequate output to meet normal
metabolic demands of the body.
 E.g. .in dilated cardiomyopathy, valvular heart disease, tamponade and bradycardia.
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13.  Right sided heart failure is characterised by the presence of peripheral oedema,
raised JVP and hypotension and congestive hepatomegaly.
 Left sided heart failure – pulmonary oedema is the striking feature. Other signs are
tachypnoea, tachycardia, third heart sound, cardiomegaly.
 Congestive Cardiac Failure – Characterised by combination of both left and right
sided heart failure.
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14.  It describes the relationship between preload and cardiac performance.
 It states blood contractile performance(represented by SV or CO) is proportional to
preload with the normal physiologic range.
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16. In heart failure, the heart is unable to pump enough blood for tissue metabolic needs
and as a result cardiac-related elevation of pulmonary or systemic venous pressures
may cause organ congestion
This condition can result from abnormalities in the systolic or diastolic function, or
both.
Factors such as change in cardiomyocyte function, cardiac structural defects such as
valvular disorders, rhythm abnormalities and higher metabolic demands due to
thyrotoxicosis can contribute to heart failure
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19.  Endothelins: cause vasoconstriction, potentiation of cardiac remodeling, and
decreased renal blood flow
 Natriuretic Peptides: antagonism of the RAAS, inhibition of sympathetic outflow,
inhibit vasopressin secretion, and ET-1 antagonism decreasing preload and
afterload
 Vasopressin (ADH):
 V1a receptor stimulation: vasoconstriction
 V2 receptor stimulation: free water in the kidneys
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20.  Occurs as a compensatory adaptation to a change in wall stress
 It is largely regulated by neurohormonal activation
 Angiotensin II and aldosterone being key stimuli
 Leads to Ventricular hypertrophy
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23. Left Heart Failure
 Breathlessness
 On exertion
 On lying flat (orthopnoea)
 At night (paroxysmal nocturnal dyspnoea)
 Easy fatiguability
 Cough with frothy blood-stained sputum
 Wheezing
Right Heart Failure
 Pedal/peripheral edema
 Abdominal swelling
 Right hypochondriac pain from an enlarging liver
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25.  FBC
 ECG
 Chest X-ray
 Blood urea, electrolytes and creatinine and eGFR (estimated glomerular filtration
rate)
 Liver function test
 Fasting blood sugar
 Echocardiography
 Thyroid function tests
 Cardiac enzymes, if myocardial infarction is suspected
 Coronary angiography
 Echocardiogram
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26.  Stage A:
 ACE inhibitors/ARBs
 Statins
 Stage B:
 ACE inhibitor or ARB,
 β-blockers
 statin
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27.  Stage C
 ACE inhibitor,
 ARB, or angiotensin receptor-neprilysin inhibitor (valsartan/sacubitril, ARNI)
 β-blocker
 Aldosterone antagonists
 Loop diuretics,
 hydralazine-isosorbide dinitrate (ISDN)
 Digoxin
 Ivabradine
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28.  Stage D: often referred to as advanced, refractory, or end stage HF.
 Diuretics
 Vasopressin antagonists
 Vasodilators
 Inotropes
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31. 31

32. Acute heart failure is the rapid onset of symptoms and signs of heart failure, severe
enough to warrant emergency medical attention
It is a condition with adverse prognosis, characterized by high mortality and
rehospitalization rates especially in individuals aged 65 or older.
Patients with AHF require urgent evaluation with subsequent initiation or
intensification of treatment, including iv. therapies or procedures
Despite the considerable public health and financial burden related to AHF there has
very little progress in the pharmacological management of these patients, as most
drugs that have been investigated failed to improve prognosis.(Tubaro et al,2018)
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33. . AHF is a leading cause of hospitalizations in subjects aged >65 years and is associated
with high mortality and rehospitalization rates.
AHF predominant in males (Dimitrios et al,2015)
Majority of subjects (65–75%) have a known history of heart failure. Other comorbid
conditions include arterial hypertension in about 70% of patients, documented CAD in
50–60%, and AF in 30–40%. Non-cardiovascular comorbidities include diabetes mellitus in
about 40% of patients, renal dysfunction in 20–30%, COPD in 20–30%, and anemia in 15–
30%
 In-hospital mortality ranges from 4% to 10%.Post-discharge 1-year mortality can be 25-
30% with up to more than 45% deaths or readmission rates.(EHJ,2021)
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35.  ECG [ Arrhythmias, Myocardial Ischemia ]
 Chest X-ray [ Congestion, Lung infection ]
 Lung Ultrasound [ Congestion ]
 Echocardiography [Congestion, Cardiac dysfunction ]
 Natriuretic Peptides [ Congestion ]
 Serum Troponin [ Myocardial injury(ACS) ]
 Serum Creatinine [ Renal dysfunction ]
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36. INVESTIGATIONS
 Serum Electrolytes [ Electrolyte disorders ]
 Iron status [ Iron depletion ]
 Thyroid Stimulating Hormone [ Hypo and hyperthyroidism ]
 Procalcitonin [ Pneumonia ]
 Lactate [ Lactic Acidosis ]
 Pulse Oximetry and Arterial Blood gas [ Respiratory failure ]
 D-dimer [ Pulmonary Embolism ] 36

37. 37

38. According to the 2021 ESC Guidelines for the diagnosis and treatment of acute and
chronic heart failure, Acute heart failure may present as 4 major complications;
 Acute Decompensated Heart Failure
 Acute Pulmonary Oedema
 Isolated Right Ventricular Failure
 Cardiogenic Shock
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39.  Most common presentation of Acute Heart Failure ( 50%-70% of hospital
presentations)
 Gradual onset (days)
Main Cause
 Sodium and water retention
 Left ventricular dysfunction with or without hypoperfusion
Main Clinical Presentation
 Wet and warm
 Dry and cold 39

40. ACUTE DECOMPENSATED
HEART FAILURE
Treatment Objectives
 Identification of precipitating factors
 Decongestion with Diuretic therapy
 Hypoperfusion correction with Inotropes and Vasopressors
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41. 41

42.  Rapid onset( Hours)
Clinical criteria;
 RR> 25 breaths/min
 Dyspnea with Orthopnea
 Respiratory failure
 Tachypnoea
Main Clinical Presentation;
 Lung congestion ( Wet and warm)
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43. ACUTE PULMONARY OEDEMA
Treatment Objectives;
 Oxygen given as continuous positive airway pressure or high flow nasal
cannula
 IV Diuretics
 IV Vasodilators( If SBP is high to reduce afterload )
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44. a
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45.  Onset may be gradual or rapid
Main clinical presentation;
 Associated with increased right ventricular and atrial and systemic congestion
 Impairs left ventricular failing ultimately reducing Cardiac output
 May present as wet and warm or dry and cold
Treatment Objectives;
 IV Diuretics( for Venus systemic congestion)
 Vasopressor and/or Inotropes (For low cardiac output and hemodynamic
instability)
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46. s
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47.  Cardiogenic shock is a syndrome due to primary cardiac dysfunction resulting in an
inadequate cardiac output, comprising a life-threatening state of tissue hypoperfusion,
which can result in multi-organ failure and death
 Onset may be gradual or rapid
Main Clinical Presentation is associated with Hypoperfusion;
 Cold sweatered extremities
 Oliguria
 Mental confusion
 Dizziness
 Narrow pulse pressure 47

48. CARDIOGENIC SHOCK
Relevant Biochemical Markers;
 Elevated serum Creatinine
 Metabolic acidosis ( Elevated blood pH)
 Elevated serum lactate
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49. Treatment Objectives;
 Identification and treatment of underlying cause
 Hemodynamic stabilization
 Management of organ dysfunction
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50. g
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51. 1. Oxygen Therapy and/or Ventilatory Support ;
 Oxygen should not be used routinely in non-hypoxemic patients, as it causes
vasoconstriction and a reduction in cardiac output.
 Oxygen Therapy is recommended in patients with AHF with SpO2<92% to
correct hypoxemia, increase oxygenation and pH and decreased work of
breathing.
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52.  During oxygen therapy, acid base balance,SpO2 and BP should be monitored
regularly.
 Intubation is recommended for progressive respiratory failure in spite of oxygen
administration
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53. 2. Diuretics
 Intravenous diuretics are the cornerstone of AHF treatment. They increase renal
excretion of salt and water and are indicated for the treatment of fluid overload
and congestion in the vast majority of AHF patients.
 Loop diuretics are commonly used due to their rapid onset of action and efficacy.
 It is appropriate that when starting diuretic treatment, to use low doses, to assess
the diuretic response and increase the dose when that is insufficient.
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54.  Diuretic treatment should be started with an initial iv. dose of furosemide, or
equivalent dose of bumetanide or torsemide at a starting dose of;
 0.5-1 mg/kg or 20-40mg IV Furosemide over 1-2min every 8-12 hrs. which may be
increased to 80 mg if there is no adequate response within 1 hour without
exceeding maximum dose of 160-200mg/dose.
 10-20 mg IV Bolus Torsemide daily
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55.  If the diuretic response remains inadequate, e.g. <100 mL hourly diuresis despite
doubling loop diuretic dose, concomitant administration of other diuretics acting
at different sites, namely thiazides or metolazone or acetazolamide, may be
considered. However, this combination requires careful monitoring of serum
electrolytes and renal function.
 Transition to oral treatment should be commenced when the patient’s clinical
condition is stable. It is recommended that, after achievement of congestion
relief, oral loop diuretics are continued at the lowest dose possible to avoid
congestion
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56. PHARMACOLOGICAL
MANAGEMENT OF AHF
3. Vasodilators;
 Intravenous vasodilators, namely nitrates or nitroprusside dilate venous and arterial
vessels leading to a reduction in venous return to the heart, less congestion, lower
afterload, increased stroke volume and consequent relief of symptoms.
 Nitrates act mainly on peripheral veins whereas nitroprusside is more a balanced
arterial and venous dilator hence may be more effective than diuretics in those
patients whose acute pulmonary oedema is caused by increased afterload and fluid
redistribution to the lungs in the absence or with minimal fluid accumulation and also
in patients with SBP>/= 110 mmHg.
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57. PHARMACOLOGICAL
MANAGEMENT OF AHF
 Sodium Nitroprusside should be given at an infusion rate of 0.3mcg/kg/min
monitoring for BP at least 5 min before titrating to higher or lower dose to
achieve desired BP.
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58. PHARMACOLOGICAL
MANAGEMENT OF AHF
4. Inotropes;
 Inotropes are still needed for treatment of patients with low cardiac output and
hypotension and should be reserved for patients with LV systolic dysfunction, low
cardiac output and low SBP (e.g. <90 mmHg) resulting in poor vital organ
perfusion.
 Phosphodiesterase III inhibitors ( Amrinone, Milrinone ) may be preferred over
dobutamine for patients on beta-blockers as they act through independent
mechanisms. Excessive peripheral vasodilation and hypotension can be major
limitations of type-3-phosphodiesterase inhibitors especially when administered
at high doses.
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59. PHARMACOLOGICAL
MANAGEMENT OF AHF
 IV Amrinone ; 0.5mg/kg IV bolus over 2-3 mins, then 5-10 mcg/kg/min IV not
exceeding a total daily dose of 10 mg/kg/day.
 IV Milrinone ; 50mcg/kg loading dose IV over 10 mins then 0.375-0.75 mcg/kg/min
IV with a maintenance dose of 1.13mg/kg/day.
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60. PHARMACOLOGICAL
MANAGEMENT OF AHF
5. Vasopressors;
 Among drugs (Norepinephrine, Epinephrine, Dopamine, Dobutamine ) with a
prominent peripheral arterial vasoconstrictor action, norepinephrine may be
preferred in patients with severe hypotension. The aim is to increase perfusion to
the vital organs.
 However, this is at the expense of an increase in LV afterload. Therefore, a
combination of norepinephrine and inotropic agents may be considered,
especially in patients with advanced HF and cardiogenic shock and patients with
SBP<90 mmHg with hypotension and/or hypoperfusion.
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61. PHARMACOLOGICAL
MANAGEMENT OF AHF
 IV Norepinephrine ; 0.2-1.0 mcg/kg/min
 IV Epinephrine ; 0.05-0.5 mcg/kg/min
 IV Dobutamine ; 2-20 mcg/kg/min
 IV Dopamine ; 3-5 mcg/kg/min
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62. PHARMACOLOGICAL
MANAGEMENT OF AHF
5. Digoxin ;
 It is indicated in AHF with fast atrial fibrillation or in sinus rhythm with systolic
dysfunction.
 According to the ACCF/AHA Guidelines a loading dose to initiate therapy in AHF is
not necessary.
 Digoxin ; 0.125-0.25mg PO/IV daily
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63. PHARMACOLOGICAL
MANAGEMENT OF AHF
6. Opiates ;
 Opiates relieve dyspnea and anxiety. They may be used as sedative agents during
non-invasive positive pressure ventilation to improve patient adaptation.
 Dose-dependent side effects include nausea, hypotension, bradycardia, and
respiratory depression.
 Morphine; SC/IM 5-10 mg q4hr PRN (dose range 5-20mg) or IV 2.5-5mg q3-4hrs
PRN infused over 4-5mins (dose range 4-10mg)
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64. PHARMACOLOGICAL
MANAGEMENT OF AHF
7. Thromboembolism Prophylaxis ;
 SC Enoxaparin 1.5 mg/kg daily should be used as prophylactic anticoagulation
against venous thrombosis.
8. Short term Mechanical Circulatory Support ;
 MCS may be necessary to augment cardiac output and support end organ perfusion
in patients presenting with cardiogenic shock.
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65.  Patientswithheartfailureshouldbeadvisedtomake lifestyle changes to reduce the risk
of progression of their heart failure and associated co-morbidities. These include;
 Smoking cessation
 Reducing alcohol consumption
 Increasing physical exercise if appropriate
 Weight control
 Dietary changes such as increasing fruit and vegetable consumption and reducing
saturated fat intake.
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66. NON PHARMACOLOGICAL
MANAGEMENT OF AHF
 Salt and fluid intake should only be restricted if these are high, and a salt intake of
less than 6 g per day is advised.
 Bed rest only( in Acute failure and exacerbation of chronic failure)
 Prop up in bed
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67.  Patient should be counseled on lifestyle modifications to help reduce rate of acute
exacerbations.
 Patients should be counseled and encouraged to adhere strictly to the
pharmacotherapy of their comorbid conditions that predispose the to AHF.
 Patients experiencing side effects and sub optimal therapy from the management of
their co morbid conditions should let their physicians know so as to optimize
therapy and reduce the risk of acquiring AHF.
 Contraception and pregnancy should be discussed with women of childbearing
potential and heart failure. Advice from a heart failure specialist and an obstetrician
should be sought if pregnancy occurs or is being considered.
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68.  Patients should be encouraged to join a personalised rehabilitation programme
including education, psychological support, and exercise when appropriate.
 Reduce salt intake
 Reduce weight in overweight and obese individuals
 Avoid alcohol
 Avoid or quit smoking
 Encourage moderate exercise
 Bed rest (in acute heart failure or exacerbations of chronic heart failure)
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69.  2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure:
Developed by the Task Force for the diagnosis and treatment of acute and chronic heart
failure of the European Society of Cardiology (ESC) With the special contribution of the
Heart Failure Association (HFA) of the ESC, European Heart Journal, Volume 42, Issue 36,
21 September 2021, Pages 3599–3726,
 British National Formulary 80 (September 2020, March 2021). Royal Pharmaceutical
Society of Great Britain. Pages 204-260
 Kode-Kimble & Young (2013). Applied Therapeutics: The Clinical Use of Drugs. 10th edition,
Lippincott Williams & Wilkins, USA. Pages 235-238
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70.  Dipiro J., et al. (2020). Pharmacotherapy: A PathophysiologicApproach. 11TH Edition. McGraw-
Hill, New York. Page 586-673
 Ministry of Health (2017). Standard Treatment Guidelines. Seventh Edition. Yamens Press Limited,
Accra. Pages 133-140
 Zeind, C. & Carvalho, M. (2018). Applied Therapeutics: The Clinical Use Of Drugs. 11th
Edition. Wolters Kluwer, China. Pages 261-278
 Whittlesea C. & Hodson K. (2019). Clinical Pharmacy and Therapeutics. 6th Edition.
Elsevier, China. Pages 357-365
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