heart failure

1. Odyss Gladney S. Obuyes, MD
First Year Fellow

2. Learning Objectives
• Understand Heart Failure: signs and symptoms, diagnostics and
classification
• Discuss clinical manifestations and diagnosis of HFpEF and its
management
• Discuss clinical manifestations and diagnosis of HFrEF and its
management
• Learn the different types of Cardiomyopathies and its anesthesia
management

3. References

4. Heart Failure
• is a complex clinical syndrome identified by presence of current
or prior characteristic symptoms, such as dyspnea and fatigue,
and evidence of cardiac dysfunction as a cause of these
symptoms.
• can result from any structural or functional cardiac disorder that
impairs the ability of the ventricle to fill with or eject blood.

5. Batman, et Al Hear Failure, JAMA. 2020;324(10):1015.
doi:10.1001/jama.2020.13310

6. Identification of symptoms of HF is a key step in diagnosing
HF
Acute and subacute presentations (days to weeks)
shortness of breath, at rest and/or with exertion
orthopnea
paroxysmal nocturnal dyspnea,
right upper quadrant discomfort (right HF)
palpitationswith or without lightheadedness (tachyarrhythmias)
Chronic presentations (months)
fatigue
anorexia
abdominal distension
peripheral edema
dyspnea (more subtle and exertional in nature)

8. Classification of HF by LVEF

9. Possible Treatment

10. Heart failure with preserved
ejection fraction (HFpEF)
is a clinical syndrome in patients with current or
prior symptoms of HF with a left ventricular
ejection fraction (LVEF) ≥50 percent and evidence
of cardiac dysfunction as a cause of symptoms (eg,
abnormal LV filling and elevated filling pressures)

11. Heart failure with preserved ejection
fraction (HFpEF)
• Diagnosis: limited to patients with current or prior symptoms of
HF (American College of Cardiology/American Heart Association
[ACC/AHA] stages C and D HF)
• Excludes: patients with stage A (at high risk for HF but without
structural heart disease or symptoms of HF) or stage B HF (structural
heart disease but no symptoms or signs of HF)

12. Clinical Manifestations of HFpEF
Patients with HFpEF and those with HFrEF have similar
symptoms and signs.
Dyspnea and fatigue are by far the most common
symptoms.
Signs of HF (such as elevated jugular venous pressure,
pulmonary rales, and lower extremity edema) may or may
not be present.

13. Comorbidities commonly associated with
HFpEF
oAging
oCardiovascular disorders: systemic hypertension,
coronary artery disease, AF
oMetabolic Disorders: diabetes and metabolic
syndrome, obesity
oRespiratory Disorders: sleep-disordered breathing,
chronic obstructive lung disease
oKidney disease
oAnemia

15. H2FPEF score — developed and clinically validated at the
Mayo Clinic. The score is the sum of points assigned to the
following clinical variables (score range 0 to 9):
●Heavy – Body mass index >30 kg/m2 (2 points)
●Hypertensive – Hypertensive and treated with two or more
antihypertensive medicines (1 point)
●Atrial Fibrillation (AF) – Paroxysmal or persistent (3 points)
●Pulmonary hypertension (PH) – Pulmonary artery systolic pressure >35
mmHg using Doppler echocardiography (1 point)
●Elder – Age >60 years (1 point)
●Filling pressure – Doppler echocardiographic E/e' >9 (1 point; E is the
peak velocity of early LV filling; e' is the peak early diastolic velocity of LV
myocardium adjacent to the mitral annulus by tissue Doppler)
HFA-PEFF score — is based upon assessing criteria in three
domains (functional, morphologic, and biomarker). Each
domain can contribute a maximum of 2 points (score range 0
to 6):
●Functional – These parameters are measured by Doppler echocardiography.
•Major criteria (2 points if ≥1 of the following is present):
-Septal e’ <7 cm/s
-Lateral e’ <10 cm/s
-Average E/e’ ratio ≥15
-Peak tricuspid regurgitation velocity >2.8 m/s (pulmonary artery systolic pressure [PASP] >35
mmHg)
•Minor criteria (1 point if ≥1 of the following is present):
-Average E/e’ 9 to 14
-Global longitudinal strain (GLS) <16 percent
●Morphologic – These parameters are measured by echocardiography (or cardiovascular magnetic
resonance [CMR] if not adequately measured by echocardiography) and indexed to body surface area in
m2.
RWT = LVPW X 2 / LVIDD
in which RWT is relative wall thickness, LVPW is the LV posterior wall thickness measured at end-
diastole, and LVIDD is the LV internal end-diastolic diameter.
•Major criteria (2 points if ≥1 of the following):
-Left atrial volume index (LAVI) >34 mL/m2
-LV mass index (LVMI) ≥149 g/m2 (men) or ≥122 g/m2 (women) and RWT >0.42
•Minor criteria (1 point if ≥1 of the following):
-LAVI 29 to 34 mL/m2
-LVMI >115 g/m2 (men) or >95 g/m2 (women)
-RWT >0.42
-LV wall thickness ≥12 mm
●Biomarker – Different threshold serum natriuretic peptide levels are used based on whether the patient
is in sinus rhythm or AF.
•Major criteria (2 points if either of the following):
-In sinus rhythm: NT-proBNP (N-terminal pro-B-type natriuretic peptide) >220 picograms/mL or BNP (B-
type natriuretic peptide) >80 picograms/mL
-In AF: NT-proBNP >660 picograms/mL or BNP >240 picograms/mL
•Minor criteria (1 point if either of the following):
-In sinus rhythm: NT-proBNP 125 to 220 picograms/mL or BNP 35 to 80 picograms/mL
-In AF: NT-proBNP 365 to 660 picograms/mL or BNP 105 to 240 picograms/mL

16. Management of Patients with HFpEF
Goals of therapy
reduce HF symptoms
increase functional status
reduce the risk of hospital admission
There is no clear evidence that pharmacologic therapy, diet, or
other therapies reduce the risk of mortality in patients with HFpEF.

17. Management of Patients with HFpEF
Exercise, diet, weight loss, and cardiac rehabilitation
• participation in structured exercise programs, cardiac
rehabilitation, and dietary interventions is safe and can lead to
small improvements in exercise tolerance.

18. Preferred pharmacotherapies for symptomatic patients
Patients with volume overload
• require diuretic therapy before
initiating other pharmacologic
therapies.
Patients with HF symptoms and elevated
BNP
• treatment with both a sodium-glucose
co-transporter 2 (SGLT2) inhibitor and
a mineralocorticoid receptor
antagonist (MRA) is suggested rather
than no HFpEF-specific therapy (Grade
2B).
• use of both agents rather than either
drug alone or treatment with other
agents is suggested (Grade 2C).

19. Secondary pharmacotherapies
•For patients with HFpEF who have poorly controlled
hypertension and persistent HF symptoms despite optimal SGLT2
inhibitor and MRA therapy, we suggest adding sacubitril-
valsartan (Grade 2C).
•For patients with comorbid diabetes and chronic kidney disease
(CKD), ACE inhibitors and ARBs may be used as first-line therapy
Device-based therapies: not routinely use

20. HF with reduced
ejection fraction
(HFrEF)
is defined as HF with left
ventricular ejection fraction
(LVEF) ≤40 percent.
Goals of management:
reduce morbidity
reducing symptoms
improving health-related quality
of life and functional status
decreasing the risk of
hospitalization
reduce mortality

21. Management of HFrEF
• Includes management of the cause of HF (eg, coronary artery
disease) and the management of associated conditions (eg,
diabetes)

22. PHARMACOLOGIC THERAPY
Goals:
improve symptoms (including risk of
hospitalization)
slow or reverse deterioration in myocardial
function
reduce mortality

23. has been documented with beta blocker, ACE inhibitors (similar with single agent ARB), ARNI, dapagliflozin (an
SGLT2 inhibitor), hydralazine plus nitrate, and MRA. Limited evidence of survival benefit is available for diuretic
therapy.
diuretic, beta blockers, renin-angiotensin system inhibitor (ACE) inhibitor, single agent ARB, or
angiotensin receptor-neprilysin inhibitor [ARNI]), dapagliflozin (a sodium-glucose cotransporter 2
[SGLT2] inhibitor), hydralazine plus nitrate, digoxin, and mineralocorticoid receptor antagonist (MRA).
Improvement in symptoms
Prolongation of patient survival

24. PHARMACOLOGIC THERAPY
Initial therapy
 a combination of:
 diuretic therapy
renin-angiotensin system
inhibitor (ARNI, ACE
inhibitor, or single agent
ARB),
beta blocker
Alternative: hydralazine plus
nitrate
Secondary therapy
consists of a
mineralocorticoid receptor
antagonist and a sodium-
glucose co-transporter 2
inhibitor

25. CARDIAC ELECTRONIC IMPLANTABLE DEVICE
THERAPIES
●Implantable cardioverter-defibrillator: can reduce the risk of SCD
●Cardiac resynchronization therapy (CRT) is indicated in selected
patients with HFrEF with a prolonged QRS duration.
Most patients who satisfy criteria for CRT implantation are also
candidates for an ICD and receive a combined device.

26. Cardiomyopathies
• were originally defined as disorders that were idiopathic.
• ESC working group on myocardial and pericardial diseases
(2008): "A myocardial disorder in which the heart muscle is
structurally and functionally abnormal in the absence of
coronary artery disease, hypertension, valvular disease and
congenital heart disease sufficient to explain the observed
myocardial abnormality"

27. Main cardiomyopathy phenotypes
• Dilated cardiomyopathy (DCM)
• Hypertrophic cardiomyopathy (HCM)
• Restrictive cardiomyopathy (RCM)
• Arrhythmogenic right ventricularcardiomyopathy (ARVC)
• Unclassified cardiomyopathies

28. Dilated cardiomyopathy (DCM)
• is a disease of the myocardium
characterized by impaired
systolic function and dilatation
of the left and right ventricles.
• major cause of heart failure and
arrhythmia in young adults.
Clinical manifestations
• Early stages: asymptomatic.
• As the condition progresses:
most develop signs and
symptoms of heart failure such
as dyspnoea, fatigue, ascites,
peripheral oedema, and
arrhythmias.
• Later stage: Embolic events and
sudden death

29. Echocardiographic features of DCM
• Fractional shortening < 25% and/or EF < 45%.
• LVED >117% of the predicted value of 112% corrected for age and
body surface area.
• Increased sphericity (ratio of the length to the diameter) of the LV.
• Severe impairment of the LV may be associated with the presence of
spontaneous echo contrast which should then prompt a careful
assessment for thrombus.
• Diastolic dysfunction (restrictive or pseudonormal) is associated with a
poor prognosis.
• Tricuspid annular proximal systolic excursion < 14 mm illustrates RV
dysfunction and predicts a poor prognosis.
• MRis frequently seen

30. Dilated cardiomyopathy (DCM):
Preoperative management
Medical therapy: Regular medications should be continued in
all patients and optimized in patients with symptoms of heart
failure.
Arrhythmias: appropriately treated before operation via drug
therapy and/or implantation of devices to achieve rate and
rhythm control.
Echocardiography: assess the extent of ventricular dysfunction
and the presence of valvular abnormality.

31. Dilated cardiomyopathy (DCM)
Goals of anaesthesia management:
Avoid myocardial depression.
Maintain adequate preload and prevent
increases in afterload.
Avoid tachycardia.
Prevent sudden hypotension by careful titration
of anaesthetic agents.

32. Dilated cardiomyopathy (DCM):
Anesthetic Management
Monitoring
Arterial and central venous catheters
TEE: dynamic assessment of the myocardial function
Bispectral index monitoring: titrate anaesthetic agents
Cardiovascular support
Inotropic support: phosphodiesterase inhibitors, levosimendan, dobutamine, and
dopamine.
Noradrenaline: treat hypotension, but care should be taken to prevent sudden
increases in afterload.
Biventricular pacing and intra-aortic balloon pump: considered in those with
severe systolic dysfunction.

33. Dilated cardiomyopathy (DCM):
Anesthetic Management
General anaesthesia
Avoid overdose of induction agents since the
circulation time is impaired.
Etomidate causes least haemodynamic
changes.
Ketamine should be avoided, as it increases
SVR.
Propofol: useful in reducing the SVR.
All volatile anaesthetic agents cause
myocardial depression in high concentration
Opioids: minimal cardiovascular effect and

34. Dilated cardiomyopathy (DCM):
Anesthetic Management
Local and regional anaesthesia
Peripheral nerve blocks: offer minimal haemodynamic changes
Central neuraxial blockade: reduces afterload and improves
cardiac output
*accompanying hypotension resulting in myocardial hypoperfusion must
be prevented
Postoperative care
Intensive care unit: allow invasive monitoring and optimization of
postoperative haemodynamics and fluid therapy.
Adequate analgesia: reduces the deleterious effects of increased
SVR.

35. Hypertrophic cardiomyopathy
• primary cardiac muscle hypertrophy of the left ventricle in the
absence of other structural or functional abnormality.
• is an inherited (autosomal dominant) disease of the
myocardium.
• Pathophysiology: Hypertrophy can be asymmetrical, concentric,
midventricular, and apical. (can also involve the RV)

36. Hypertrophic cardiomyopathy:
Medical therapy
Beta-blockade: first line of treatment for pt with symptoms of
HF
• reduce heart rate and have a negative inotropic effect, thereby
prolonging diastolic time and improving left ventricle filling.
Amiodarone: treat supraventricular and ventricular tachycardia.
Implantable cardioverter defibrillator (ICD): effective in reducing
the risk of sudden death in a subset of high-risk patients.
Invasive treatment options: alcohol septal ablation and surgical
myectomy.

37. Hypertrophic cardiomyopathy
Aims of perioperative care
Adequate preload and afterload
Maintain SVR
Avoid sympathetic activation
Reduce contractility
Avoid tachycardia and maintain sinus rhythm

38. Hypertrophic cardiomyopathy
• Preoperative assessment of fluid status and optimization of medical
therapy reduces perioperative complications
• TEE: is useful in assessing fluid status, biventricular contractility, and LV
end-diastolic and end-systolic volumes.
• Inotropes: used with extreme caution in the presence of high PCWP, as
they can worsen LVOT obstruction and MVR resulting in pulmonary edema
and cardiovascular collapse.

39. Hypertrophic cardiomyopathy:
Anesthetic Management
• Monitors: invasive blood pressure monitoring is essential to recognize
and prevent hypotension.
• IV fluid bolus and alpha-adrenergic agonist (phenylephrine) are
the preferred first line of treatment for hypotension in patients
with LVOTO
• GA vs Regional
• General anaesthesia is considered safer in obstructive HCM
• Regional anaesthesia should be used with caution

40. Restrictive cardiomyopathy
• impairment of ventricular diastolic function due to fibrotic or
infiltrative changes in the myocardium and or subendocardium, which
reduce diastolic ventricular compliance and elevate ventricular end-
diastolic pressure.
• Patients can have normal or near-normal systolic function in the early
stages of the disease.
• can be primary (idiopathic) or secondary to amyloidosis, sarcoidosis,
haemochromatosis, ischaemic heart disease, hypertension, and
valvular diseases.

41. Restrictive cardiomyopathy
• signs and symptoms of
biventricular failure dyspnea
Orthopnoea
Fatigue
Palpitation
Edema
Chest pain
• PE:
audible third heart sound
systolic murmur
raised jugular venous
pressure
ascites
peripheral oedema
Key echocardiographic features: pronounced biatrial enlargement, relatively
little ventricular septal movement during respiration, and very occasional
ventricular septal movement during diastole.

42. Management of Restrictive cardiomyopathy
Aim of the treatment:
reduce and control the symptoms of
heart failure by lowering ventricular
filling pressure without affecting
cardiac output.
Beta-blockers and calcium channel
blockers: prolong ventricular filling
time and improve ventricular
relaxation.
Diuretics: symptomatic relief of
heart failure.
Maintaining sinus rhythm is
essential: Amiodarone, Digoxin,
and Beta-blockers
Permanent pacemakers and ICDs:
indicated in patients with advanced
conducting system dysfunction.

43. Anesthetic Management in Patients with
RCM
• Aims of perioperative anaesthetic management:
maintain adequate preload
maintain SVR
maintain sinus rhythm
• Anesthetic agent: with minimal cardiovascular effect (ketamine
or etomidate)

44. Arrhythmogenic right ventricle cardiomyopathy (ARVC)
• characterized by structural abnormalities and cardiac dysfunction of
the right ventricle (can also involve the LV)
• usually starts as a localized disease with regional wall abnormalities.
As the disease progresses, the right ventricle continues to lose
contractile tissue and becomes thin walled and dilated.
• patients can develop RBBB—before they eventually present with RV
failure between the fourth and fifth decades of life.

45. Signs and
Symptoms
of ARVC
• Young patients
often present with
arrhythmia,
syncope, cardiac
arrest, or sudden
death.
3 clinical phases:
• Phase 1 (concealed disease): patients with
some structural abnormality in the
myocardium in whom sudden cardiac death
can be the first presentation.
• Phase 2 (overt disease): patients with
established structural abnormality of the
myocardium who experience arrhythmias
and syncope.
• Phase 3 (end-stage disease): patients with
severe structural changes, ventricular
dilatation, and right ventricular systolic
dysfunction.

46. Management ARVC
Aim of medical management: prevent or reduce the risk of arrhythmia.
Sotalol, verapamil, and amiodarone: more effective than other anti-
arrhythmic drugs.
Continuous Holter monitoring or an electrophysiological study may be
required.
Catheter ablation: used as a palliative intervention; indicated in
patients with a single-morphology VTACH due to a localized ARVC, with
drug-resistant arrhythmia, or with frequent intervention following ICD
implantation.
Early insertion of an ICD: may be lifesaving
Heart transplantation: may be required in exceptional cases

47. Unclassified cardiomyopathies:
describe disorders that do not readily fit into any of the above
phenotypic categories
Left ventricular noncompaction
• “isolated ventricular noncompaction”
• is a rare unclassified cardiomyopathy with an altered myocardial wall
due to intrauterine arrest of compaction of the loose interwoven
meshwork.
• There is continuity between the LV cavity and deep intratrabecular
recesses that are filled with blood from the ventricular cavity without
evidence of communication to the epicardial arterial system.

48. Unclassified cardiomyopathies:
Stress-induced cardiomyopathy
• also called apical ballooning syndrome, broken heart syndrome,
and takotsubo cardiomyopathy
• generally characterized by transient systolic dysfunction of the
apical and/or mid segments of the LV that is often provoked by
stress.

49. Unclassified cardiomyopathies:
Cirrhotic cardiomyopathy
• defined as an otherwise unexplained chronic cardiac dysfunction
in patients with cirrhosis with impaired contractile
responsiveness to stress and/or diastolic dysfunction
• Electrical abnormalities: QT interval prolongation, electrical and
mechanical dyssynchrony, and chronotropic incompetence.

50. Thank You!