1. Umer Ahmed, MS III Daniel Mehrhoff, MS III Tazeen Al-Haq, MS III
CHF
Umer Ahmed, MS III
Daniel Mehrhoff, MS III
Tazeen Al-Haq, MS III

2. Definitions
Forward Heart Failure – heart unable to maintain adequate cardiac output to meet systemic demands and/ or able to do so only by elevating filling pressure.
Backward Heart Failure – Heart unable to accommodate venous return resulting in vascular congestion (systemic or pulmonary)
Heart Failure can involve left side of heart, right side of heart or both(biventricular failure)
Components of ineffective filling (diastolic dysfunction)and/or emptying-systolic dysfunction
Most cases of HF are associated with poor cardiac output(low-output HF);however HF may not be due to intrinsic cardiac disease,but due to increased demand-HOP

3. Pathophysiology
Primary insults (myocyte loss,overload) -> pump dysfunction, which leads to remodeling (dilation, hypertrophy) and neurohumoral activation->necrosis and apoptosis.
Both pathways result in further damage (re-starting the cycle), edema, tachycardia, vasoconstriction, congestion
Compensatory response to myocardial stress –
increased end-systolic ventricular pressure(pressure overload) e.g. aortic stenosis-> hypertrophy.

4. Pathophysiology
Increased end-diastolic ventricular volume (volume overload) e.g. aortic regurgitation ->cardiac dilation Systemic response to ineffective circulating volume results in activation of sympathetic nervous and renin-angiotensin-alsosterone systems which causes -Salt and water retention with intravascular expansion - increased heart rate and myocardial contractility - increased afterload

5. Classification of Heart Failure by Hemodynamic Abnormality
Diastolic Heart Function About 30% of heart failure Characterize by impaired LV relaxation The hemodynamic abnormality is an elevated LVEDP – normally it should relax down to around 5-10 mmHg The elevated LVEDP causes increased left atrial and pulmonary capillary pressures

6. Diastolic Heart Failure
Fluid is transudated across the pulmonary Capillaries causing intestitial edema and dyspnea Systolic performance is initially normal or hyperdynamic, but later fails. Examples include hypertensive heart disease, HCM, and diabetic cardiomyopathy

7. High Output Systolic Heart Failure
Pure forms of systolic heart failure are uncommon and are characterize by: A low LVEDP Normal or hyper dynamic left ventricular function Tachycardia And increased cardiac output

8. High Output Systolic Heart Failure
Occurs with peripheral shunting with large
AV fistulas, large hepatic hemangiomas, and Paget’s disease
Occurs with decrease peripheral resistance, as in Gram negative sepsis
Other causes are hyperthyroidism, beriberi,
Carcinoid, anemia and pregnancy
Note: it is either due to a dramatic decrease in after load or an increase in preload. Basically High output heart failure- differs from the usual heart failure in that the heart may pump out its usual amount of blood, but that still may not be enough to meet the body's needs

9. Low Output Systolic Heart Failure
The vast majority of systolic failure involves both decreased systolic dysfunction and an elevated LVEDP Decreased forward output causes weakness, fatigue, fluid retention. Note: which leads to increased LVEDP

10. Causes of Low Output Systolic HF
Coronary artery disease – 40%
Dilated cardiomyopathy – 30%
Valvular heart disease – 15%
Hypertensive heart disease – 10%
Restrictive cardiomyopathy - < 1%

11. Pathophysiology of Heart Failure
Decreases Stroke Volume -> Decrease cardiac output – > decrease Renal perfusion –> increase Renin –> increased Angiotensin- >increased Angiotensin II –> increased Sodium retention –> increased water retention –> increased Preload –> increased Ventricular filling pressures –> Exacerbation of heart failure –>

12. Morbidity and Mortality
50% die with progressive heart failure, 40% of sudden death due to VT/VF
LVEF is closely associated with prognosis!
Other markers of poor outcome include low sodium, high BUN, low potassium, high or low magnesium, high catecholamine levels
Exercise tolerance does not predict outcome

13. Classifications of Heart Failure by Myocardial Abnormality
Myocardial Abnormalities Ischemic Hypertensive Dilated Restrictive Hypertrophic

14. Ischemic Cardiomyopathy
Caused by coronary disease
By far the most common cause of heart failure
Characterized on echo by segmental wall motion abnormalities. .

15. Hypertensive Cardiomyopathy
Chronic HTN causes LVH, which increases LV stiffness and elevates LVEDP
Systolic function may be normal, hyperdynamic, or eventually, decreased
Characterized on echo by concentric LVH

16. Dilated Cardiomyopathy
50% are idiopathic, presumably post viral
Other causes include alcohol, cocaine, inhaled glue, chemotherapy, late hemochromotosis, and selenium and carnitine dificiencies
Characterized on echo by four chamber cardiac enlargement

17. Peripartum Dilated Cardiomyopathy
Occurs from the beginning of the third trimester to six months postpartum
There is predilection of older women in African Americans
About two thirds resolve spontaneously
There is increased risk of occurrence with subsequent pregnancies

18. Dilated Cardiomyopathy and Embolization
About 2% of patients form mural thrombi and can have arterial embolization
Pulmonary emboli can arise from the RV
Anticoagulation is indicated even if no mural thrombi can be detected

19. Restrictive Cardiomyopathy < 1%
Caused by infiltrative diseases, such as amyloid, sarcoid, hemochromotosis, and lipid storage diseases
Presents with left and right heart failure, initially from diastolic dysfunction, but later from systolic failure also. HF from due to restrictive cardiomyopathy usually presents as refractory left and right sided heart failure.

20. Restrictive Cardiomyopathy
Characterized an echo by normal sized ventricles, huge atria, and (in Amyloidosis) by a “sparkling” appearance of the LV myocardium.
The venticles cannot enlarge, because they have already been enlarged.

21. Hypertrophic Cardiomyopathy
There are disordered myocytes in the region of the hypertrophy, especially in the region of the upper ventricular septum
Areas other than the septum can be affected; Asians frequently have an apical form
Occasionally there is a concentric LVH
Sudden death is probably due to ventricular arrhythmias

22. Hypertropic Cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is associated with sudden cardiac death, especially in exercising young people with the familial form
The severity of the LV outflow gradiant is not related to the risk of sudden death
There is no cure except heart transplant .

23. New York Heart Association (NYHA) Functional Classification of Heart Failur
Class I: ordinary physical activity does not cause symptoms of HF
Class II: comfortable at rest, ordinary physical activity results in symptoms
Class III: marked limitation of ordinary activity; less than ordinary physical activity results in symptoms.
Class IV: inability to carry out any physical activity without discomfort; symptoms may be present at rest.

24. Acute Versus Chronic Heart Failure
Acute heart failure is the patient who is entirely well but who suddenly develops a large myocardial infarction or rupture of a cardiac valve.
Chronic heart failure is typically observed in patients with dilated cardiomyopathy or multivalvular heart disease that develops or progresses slowly

25. Acute Versus Chronic Heart Failure
Acute heart failure is usually largely systolic and the sudden reduction in cardiac output often results in systemic hypotension without peripheral edema.
In chronic heart failure, arterial pressure tends to be well maintained until very late in the course, but there is often accumulation of peripheral edema .

26. Backward versus forward heart failure
Forward heart failure-Is the inability of the heart to pump enough blood to meet the needs of the body for oxygen during exercise or at rest.
Backward heart failure-Is the inability of the heart to meet the oxygen needs of the body when heart filling pressures are too high

27. Redistribution of Cardiac Output
Finally, the redistribution of cardiac output is an important compensatory mechanism when cardiac output is reduced. This redistribution is most marked when a patient with HF exercises, but as heart failure advances, redistribution occurs even in the basal state.

28. Demographics The most expensive medical problem in the US
The most common diagnose in hospitalized elderly patients
Note: It is the most expensive medical problem, because in the later stages patient are hospitalized over and over again as the disease progressed with frequent exacerbations and remissions.

29. CHF Diagnosis
Tazeen Al-Haq

30. CHF Diagnosis Four components involved in the diagnosis of CHF History
Physical
Labs
Imaging

31. History Classical manifestations of heart failure include
Fatigue
Dyspnea on exertion
Orthopnea
Paroxysmal nocturnal dyspnea
Fluid retention
Older patients with heart failure often present with nonspecific symptoms
Nocturia
Insomnia
Irritability
Anorexia

32. Physical Examination Left heart failure Low cardiac output (forward)
Fatigue
Syncope
Systemic hypotension
Cool extremities
Slow capillary refill
Peripheral cyanosis
Pulsus alternans
Mitral regurgitation
S3 aka Kentucky gallop
Occurs at the beginning of diastole after S2 and is lower in pitch than S1 and S2
Will increase on expiration

33. Pulsus Alternans
Is a physical finding with arterial pulse waveform alternating strong and weak beats
Almost always indicative of left ventricular systolic impairment and also occurs in aortic and mitral valve stenosis, hypertrophic and congestive cardiomyopathy, pericarditis and use of general anesthesia
Carries a poor prognosis
EF is decreased in left ventricular dysfunction which causes an increase in EDV
In the next cycle of systolic phase, the myocardial muscles are stretched more than usual causing an increase in muscle contraction and a stronger systolic pulse

34. Physical Examination Left heart failure Venous congestion (backward)
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Cough
Crackles

35. Physical Examination Right heart failure Low cardiac output (forward)
Can mimic most of the symptoms of forward left heart failure if decreased right ventricle output leads to left ventricle underfilling
Tricuspid regurgitation
S3 (right-sided)
will increase on inspiration

36. Physical Examination Right Heart failure Venous congestion (backward)
Peripheral edema
Elevated JVP with abdominal jugular reflex
Kussmaul’s sign
Rise in JVP with inspiration
Usually JVP falls with inspiration due to reduced pressure in the expanding thoracic cavity
Suggests impaired filling of the right ventricle
Hepatomegaly
Pulsatile liver
Signifies severe tricuspid regurgitation or constrictive pericarditis

37. Investigation
Identify and assess precipitating factors and treatable causes of CHF
HEART FAILED
HTN (common)
Endocarditis
Anemia
Rheumatic heart disease and other valvular disease
Thyrotoxicosis
Failure to take meds (very common)
Arrhythmia (common)
Infection/Ischemia/Infarction (common)
Lung problems (PE, pneumonia, COPD)
Endocrine (pheochromocytoma)
Dietary indiscretions (common)

38. Investigations Blood work CBC Electrolytes BUN and Creatinine TSH
Ferritin
Cardiac biomarkers
B-type/Brain natriuretic peptide (BNP)
Secreted by ventricles due to LV stretch and wall tension
Sensitive marker of ventricular pressure and volume overload
Higher levels are suggestive of heart failure
Lower levels (<100 pg/mL) is most useful for ruling out heart failure

39. Cardiac Biomarkers Provide diagnostic and prognostic information
Identify increased risk of mortality in acute coronary syndromes
Troponin I and T
Peak at 1-2 days and remain elevated up to 2 weeks
DDx: MI, CHF, acute pulmonary embolism, myocarditis, chronic renal insufficiency, sepsis, hypovolemia
CK-MB
Peak at 1 day and remain elevated for 3 days
DDx: MI, myocarditis, pericarditis, muscular dystrophy, cardiac defibrillation

40. Investigations Chest X-Ray HERB-B Heart enlargement/Cardiomegaly
Pleural Effusion
Re-distribution (alveolar edema)
Kerley B-lines
Bronchiolar-alveolar cuffing

41. Chest X-Ray

42. Chest X-Ray
Cardiomegaly

43. CHF Treatment
Umer Ahmed

44. General Principals in the Treatment of CHF
No one simple treatment regimen is suitable for all patients.
The following are a general guideline, but the order of therapy may differ among patients and/or with physician preferences.

45. General Principles in the Treatment of CHF
Mild CHF (NYHA Class I to II)
Mild restriction of sodium intake (no-added-salt diet of <4 g sodium) and physical activity (aka Lifestyle Changes).
Start a loop diuretic if volume overload or pulmonary congestion is present.
Use an ACE inhibitor as a first-line agent.
Systolic dysfunction
- Sodium restriction: <4 g/day (initially)
- Diuretics
Most effective means of providing symptomatic relief to patients with moderate to severe CHF
Have not been shown to reduce mortality or improve prognosis
Loop diuretics: furosemide (Lasix)—most potent
Thiazide diuretics: hydrochlorothiazide—modest potency
Spironolactone (Aldactone)—low potency
- ACE inhibitors
Cause venous and arterial dilation, decreasing preload and afterload
The combination of a diuretic and an ACE inhibitor should be the initial treatment in most symptomatic patients.
ACE inhibitors reduce mortality (Cooperative North Scandinavian Enalapril Survival Study[CONSENSUS] and Studies of Left Ventricular Dysfunction [SOLVD] trials), prolong survival, and alleviate symptoms in mild, moderate, and severe CHF.
All patients with systolic dysfunction should be on an ACE inhibitor even if they are asymptomatic.
Always start at a low dose to prevent hypotension.
Monitor BP, potassium, BUN, and creatinine.
- Angiotensin II receptor blockers (ARBs)
Used in patients unable to take ACE inhibitors due to side effect of cough, but should not replace ACE inhibitors if patient tolerates an ACE inhibitor
- Hydralazine and isosorbide dinitrates
Can be used in patients who cannot tolerate ACE inhibitors
The combination of hydralazine and isosorbide dinitrate has been shown to improve mortality in CHF. But not as effective as ACE inhibitors and require inconvenient dosing schedules.

46. General Principles in the Treatment of CHF
Mild to Moderate CHF (NYHA Class II to III)
Start a diuretic (loop diuretic) and an ACE inhibitor
Add a β-blocker if moderate disease (class II or III) is present and the response to standard treatment is suboptimal
β-Blockers
Proven to decrease mortality in patients with post-MI heart failure
Reported to improve symptoms of CHF; may slow progression of heart failure by slowing down tissue remodeling
Should be given to stable patients with mild to moderate CHF (class I, II, and III) unless there is a noncardiac contraindication

47. General Principles in the Treatment of CHF
Moderate to Severe CHF (NYHA Class III to IV)
Add digoxin (to loop diuretic and ACE inhibitor)
Note that digoxin may be added at any time for the relief of symptoms in patients with systolic dysfunction. (It does not improve mortality.)
In patients with class IV symptoms who are still symptomatic despite the above, adding spironolactone can be helpful.
Digitalis
Positive inotropic agent
Useful in patients with EF <30%, severe CHF, or severe atrial fibrillation (AFib)
Provides short-term symptomatic relief but has not been shown to improve mortality
Can be added to diuretics and ACE inhibitors in severe CHF
Serum digoxin level should be checked periodically.
Signs of digoxin toxicity
GI: nausea/vomiting, anorexia
Cardiac: ectopic (ventricular) beats, AV block, AFib
CNS: visual disturbances, disorientation

48. Monitoring a Patient with CHF
Weight—unexplained weight gain can be an early sign of worsening CHF
Clinical manifestations (exercise tolerance is key); peripheral edema
Laboratory values (electrolytes, K, BUN, creatinine levels; serum digoxin, if applicable)
The COMET trial compared two β-blockers in the treatment of CHF and showed that carvedilol led to significant improvement in survival compared with metoprolol.
The overall 5-year mortality for all patients with CHF is about 50%.

49. Medical Devices
Ventricular assist device (VAD). When your weakened heart needs help pumping blood, surgeons may implant a VAD into your abdomen and attach it to your heart. These mechanical heart pumps can be used either as a "bridge" to heart transplant or as permanent therapy for people who aren't candidates for a transplant.

51. Medical Devices
Cardiac resynchronization therapy (CRT) device (biventricular cardiac pacemaker). It sends specifically timed electrical impulses to your heart's lower chambers. CRTs are suitable for people who have moderate to severe congestive heart failure and abnormal electrical conduction in the heart.

53. Medical Devices
Internal cardiac defibrillator (ICD). Doctors implant ICDs under the skin to monitor and treat fast or abnormal heart rhythms (arrhythmias), which occur in some people who have heart failure. The ICD sends electrical signals to your heart if it detects a high or abnormal rhythm to shock your heart into beating more slowly and pumping more effectively.

54. Surgery
Heart valve repair or replacement. Cardiologists may recommend heart valve repair or replacement surgery to treat an underlying condition that led to congestive heart failure. Heart valve surgery may relieve your symptoms and improve your quality of life.

55. Surgery
Coronary bypass surgery. Cardiologists may recommend coronary bypass surgery to treat your congestive heart failure if your disease results from severely narrowed coronary arteries.

56. Surgery
Myectomy. In a myectomy, the surgeon removes part of the overgrown septal muscle in your heart to decrease the blockage that occurs in hypertrophic cardiomyopathy. Surgeons may perform myectomy when medication no longer relieves your symptoms.

57. Surgery
Heart transplant. Some people who have severe congestive heart failure may need a heart transplant.

58. Two Questions

62. Thank you 