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1. Cardiology Review:Heart Failure and Valve DiseaseMarch 30, 2009 Dr. Lisa Mielniczuk
Assistant Professor Medicine
University of Ottawa Heart Institute
2. Outline Heart Failure
Causes
Symptoms
Treatments
Approach to valve disease
Aortic stenosis and regurgitation
Mitral stenosis and regurgitation
4. HF Prevalence in Canada -HF is a growing problem across North America, including Canada the overall prevalence of HF is estimated at 1%, but clearly regional variation exists
-highest prevalences in regions where CAD also high southern ONT and Quebec, new brunswick and manitoba.
-HF is a growing problem across North America, including Canada the overall prevalence of HF is estimated at 1%, but clearly regional variation exists
-highest prevalences in regions where CAD also high southern ONT and Quebec, new brunswick and manitoba.
5. Majority of HF Patients Treated by GPs/FPs -fanily doctors take a leading role in the care of HF across Canada the majority of patients admitted with HF are looked after by GP (data from CIHI from 99-2000 demonstrating MRP in hospital. Younger patients, men and those living in urban areas are more likely to be cared for by specialist. -fanily doctors take a leading role in the care of HF across Canada the majority of patients admitted with HF are looked after by GP (data from CIHI from 99-2000 demonstrating MRP in hospital. Younger patients, men and those living in urban areas are more likely to be cared for by specialist.
6. Why Heart Failure?
7. Definition Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body
Clinically
Ventricular dysfunction
Reduced exercise capacity
Impaired quality of life
Shortened life expectancy
8. Cardiomyopathy Characterized by ventricular
Dilatation
Hypertrophy
Frank Starling: CO = SV x HR
Laplace: Tension = Press x rad/ 2 x thick
-indpt of the cause of the damage there are several responses to injury for the heart the most common is dilatation of a chamber and hypertrophy. (fibrosis can occur but more specifically in myocardial infarcts)
-hypertrophy refers to increase muscle cell mass to to cellular hypertrohpy implies that the weight of the heart is increased usually reflects an increased afterload or preload
-dilatation refers to increase in size of the chamber due to increased pre load or volume overload-indpt of the cause of the damage there are several responses to injury for the heart the most common is dilatation of a chamber and hypertrophy. (fibrosis can occur but more specifically in myocardial infarcts)
-hypertrophy refers to increase muscle cell mass to to cellular hypertrohpy implies that the weight of the heart is increased usually reflects an increased afterload or preload
-dilatation refers to increase in size of the chamber due to increased pre load or volume overload
9. -enlargement of all 4 chambers, heart assumes a more spherical shape-enlargement of all 4 chambers, heart assumes a more spherical shape
11. Gross Pathologic Findings Enlargement of all 4 chambers
Normal valves with regurgitation
Enlargement and distortion of the subvalvular apparatus
Intracavitary thrombi
12. Heart Failure -in a normal heart, cardiac output increases as a function of preload. Decreased LV contractility is characertized by a heart that is shifted downward. Point a is normal person at rest. Point B is the same person after developing systolic dysfunction. , stroke volume has fallen (decreased LV emptying) and the LVEDV has increased. This increase in EDV is compensatory (on the ascending part of the curve) because it will increase SV for the next beat. BUT further augmentation in LV filling in the heart puts patients on C where SV is not increased but symptoms of pulmonary congestion develop-in a normal heart, cardiac output increases as a function of preload. Decreased LV contractility is characertized by a heart that is shifted downward. Point a is normal person at rest. Point B is the same person after developing systolic dysfunction. , stroke volume has fallen (decreased LV emptying) and the LVEDV has increased. This increase in EDV is compensatory (on the ascending part of the curve) because it will increase SV for the next beat. BUT further augmentation in LV filling in the heart puts patients on C where SV is not increased but symptoms of pulmonary congestion develop
13. Classification of Cardiomyopathy Multiple ways to consider classification:
Etiologic
Systolic vs. Diastolic
Right vs. Left
Pathologic
14. General Causes of HF Coronary artery disease
Myocardial infarction
Valve disease
Idiopathic cardiomyopathy
Hypertension
Myocarditis / pericarditis
Arrhythmias
Thyroid disease
Pregnancy
Toxins (alchohol, chemotherapy)
15. Dilated Cardiomyopathy CAD is the most common cause of systolic dysfunction
What are the other non-ischemic causes of a dilated cardiomyopathy? Idiopathic (50%)
Familial
Substance abuse
Myocarditis
Infiltrative disease
Peripartum
HIV
Chemotherapy
Electrolyte imbalance
Nutritional: thiamine,scurvy
16. Mechanisms and Causes of HF
17. Mechanisms and Causes of HF
19. Functional Classification The ACC defined 4 stages of heart failure in the last consensus guidelines. (ref:ACC/AHA 2005 Chronic Heart Failure Guideline Update, Journal of the American College of Caridiol, 2005;46:1116-1143 ) This highlights the point that we should think of HF in those who are at risk (stage A and B) even before they have developed symptomatic HF. The NYHA functional classification is a well-accepted definition of exercise capacity in the setting of HF. The ACC defined 4 stages of heart failure in the last consensus guidelines. (ref:ACC/AHA 2005 Chronic Heart Failure Guideline Update, Journal of the American College of Caridiol, 2005;46:1116-1143 ) This highlights the point that we should think of HF in those who are at risk (stage A and B) even before they have developed symptomatic HF. The NYHA functional classification is a well-accepted definition of exercise capacity in the setting of HF.
20. Stages of Heart Failure
21. Diagnosis of HF Constellation of symptoms and signs
CXR
Alternative Methods
Invasive hemodynamic studies
Echocardiogram
Serum BNP testing
22. Symptoms and Signs of HF
23. Evaluating the JVP Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal
http://cal.fmc.flinders.edu.au/gemp/ClinicalSkills/clinskil/year1/cardio/cardio04.htm
24. Congestion Left-Sided
Symptoms
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue
Signs
S3 gallop
Displaced apex
MR
Pulmonary rales
Loud P2 Right-Sided
Symptoms
Peripheral edema
Abdominal bloating
Nausea
Anorexia
Signs
Elevated JVP
Hepatomegaly
Ascites
Edema
25. Assessing Perfusion Symptoms
Fatigue
Confusion
Dyspnea
sweating Signs
Hypotension
Tachycardia
Cool extremities
Altered mental status
Rising creatinine
Liver enzyme abnormalities
26. Pulmonary Edema General Considerations
Increase in the fluid in the lung
Generally, divided into cardiogenic and non-cardiogenic categories.
Pathophysiology
Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg)
Further accumulation occurs in the interstitial tissues of the lungs
Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more)
27. Cardiogenic vs. Noncardiogenic pulmonary edema Cardiogenic pulmonary edema
Heart failure
Coronary artery disease with left ventricular failure.
Cardiac arrhythmias
Fluid overload -- for example, kidney failure.
Cardiomyopathy
Obstructing valvular lesions -- for example
Myocarditis and infectious endocarditis
Non-cardiogenic pulmonary edema -- due to changes in capillary permeability
Smoke inhalation.
Head trauma
Overwhelming sepsis.
Hypovolemia shock
Acute lung re-expansion
High altitude pulmonary edema
Disseminated intravascular coagulopathy (DIC)
Near-drowning
Overwhelming aspiration
Acute Respiratory Distress Syndrome (ARDS)
Re-expansion
By drainage of a large pleural effusion with thoracentesis
Of the lung collapsed by a large pneumothoraxRe-expansion
By drainage of a large pleural effusion with thoracentesis
Of the lung collapsed by a large pneumothorax
28. CXR Findings of Pulmonary Edema cardiogenic pulmonary edema
Kerley B lines (septal lines)
Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface
Pleural effusions
Usually bilateral, frequently the right side being larger than the left
If unilateral, more often on the right
Fluid in the fissures
Thickening of the major or minor fissure
Peribronchial cuffing
Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls Non-cardiogenic pulmonary edema
Bilateral, peripheral air space disease with air bronchograms or central bat-wing pattern
Kerley B lines and pleural effusions are uncommon
Typically occurs 48 hours or more after the initial insult
Stabilizes at around five days and may take weeks to completely clear
On CT
Gravity-dependent consolidation or ground glass opacification
Air bronchograms are common
Collectively, the above four findings comprise pulmonary interstitial edema
The heart may or may not be enlarged
When the fluid enters the alveoli themselves, the airspace disease is typically diffuse, and there are no air bronchograms \
-cuffing is fluid in the bronchial wall looks like donuts
Correlates with LAP
Normal (5-10)
Cephalizatioin 10-15, kerly b 15-20, pulmonary interstital edema 20-25, alveloar edema >25
Collectively, the above four findings comprise pulmonary interstitial edema
The heart may or may not be enlarged
When the fluid enters the alveoli themselves, the airspace disease is typically diffuse, and there are no air bronchograms \
-cuffing is fluid in the bronchial wall looks like donuts
Correlates with LAP
Normal (5-10)
Cephalizatioin 10-15, kerly b 15-20, pulmonary interstital edema 20-25, alveloar edema >25
30. Goals of Therapy Identify and Treat the Underlying Cause
Eliminate the acute precipitant
Manage HF symptoms
Modulate the neurohormonal response
Improve long-term survival -treating underlying cause may be difficult can require surgical valve or coronary repair, treatement HTN, cessation of alcohol
-modulating the neurohormonal response to help prevent adverse ventricular remodeling in oder to slow progression of LV dysfunction-treating underlying cause may be difficult can require surgical valve or coronary repair, treatement HTN, cessation of alcohol
-modulating the neurohormonal response to help prevent adverse ventricular remodeling in oder to slow progression of LV dysfunction
31. Precipitants of HF Increased metabolic demands
Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy
Increased circulating volume
Excessive salt or fluid in diet
Renal failure
Increased afterload
Hypertension
PE
Impaired contractility
Negative inotropes
Ischemia
Failure to take medications
32. Pharmacotherapy
33. Management Strategy
34. Beta Blockers The MERIT-HF trial randomized 3991 patients with NYHA class II to IV heart failure who were treated with digoxin, angiotensin converting enzyme inhibitors, and digoxin to metoprolol CR/XL or placebo. Kaplan-Meier curves show a significant reduction in total mortality at 12 months with metoprolol (7.2 versus 11 percent for placebo, p = 0.006). Data from The MERIT-HF Study Group, Lancet 1999; 353:2001
In the MERIT-HF trial of 3991 patients metoprolol CR/XL reduced the number of patients requiring hospitalization for any reason by 18 percent compared to placebo (p = 0.004), the number admitted for a cardiovascular cause by 25 percent (p<0.001), and the number admitted for worsening heart failure by 35 percent (p<0.001) (panel A). There was an equivalent reduction in the number of hospital days (panel B). Data from Hjalmarson, A, Goldstein, S, Fagerberg, B, et al. JAMA 2000; 283:1245. The MERIT-HF trial randomized 3991 patients with NYHA class II to IV heart failure who were treated with digoxin, angiotensin converting enzyme inhibitors, and digoxin to metoprolol CR/XL or placebo. Kaplan-Meier curves show a significant reduction in total mortality at 12 months with metoprolol (7.2 versus 11 percent for placebo, p = 0.006). Data from The MERIT-HF Study Group, Lancet 1999; 353:2001
In the MERIT-HF trial of 3991 patients metoprolol CR/XL reduced the number of patients requiring hospitalization for any reason by 18 percent compared to placebo (p = 0.004), the number admitted for a cardiovascular cause by 25 percent (p<0.001), and the number admitted for worsening heart failure by 35 percent (p<0.001) (panel A). There was an equivalent reduction in the number of hospital days (panel B). Data from Hjalmarson, A, Goldstein, S, Fagerberg, B, et al. JAMA 2000; 283:1245.
35. Beta Blockers and Functional Class In the SOLVD-prevention trial of 4223 patients with mostly asymptomatic left ventricular (LV) dysfunction, those receiving a beta blocker and enalapril had a significantly lower all cause mortality compared to those receiving beta blocker or enalapril alone (relative risk 0.7); this was due to a significant reduction in death from arrhythmia or pump failure. Data from Exner, DV, Dries, DL, Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916.
Kaplan-Meier analysis of survival in patients with chronic heart failure (HF) who were maintained on digoxin, diuretics, and an angiotensin converting enzyme inhibitor and then treated with carvedilol or placebo. Therapy with carvedilol was associated with a significant improvement in survival (p<0.001). Data from Packer, M, Bristow, MR, Cohn, JN, et al for the US Carvedilol Heart Failure Study Group, N Engl J Med 1996; 334:1349.
In the COPERNICUS trial of 2289 patients with class IV heart failure and a left ventricular ejection fraction carvedilol significantly reduced the risk of death by 38 percent compared to placebo (P = 0.0001). The drug also reduced the combined end point of death and hospitalization by 24 percent (P< 0.001). Data from Packer, M, Coats, AJ, Fowler, MB, et al. N Engl J Med 2001; 344:1651. In the SOLVD-prevention trial of 4223 patients with mostly asymptomatic left ventricular (LV) dysfunction, those receiving a beta blocker and enalapril had a significantly lower all cause mortality compared to those receiving beta blocker or enalapril alone (relative risk 0.7); this was due to a significant reduction in death from arrhythmia or pump failure. Data from Exner, DV, Dries, DL, Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916.
Kaplan-Meier analysis of survival in patients with chronic heart failure (HF) who were maintained on digoxin, diuretics, and an angiotensin converting enzyme inhibitor and then treated with carvedilol or placebo. Therapy with carvedilol was associated with a significant improvement in survival (p<0.001). Data from Packer, M, Bristow, MR, Cohn, JN, et al for the US Carvedilol Heart Failure Study Group, N Engl J Med 1996; 334:1349.
In the COPERNICUS trial of 2289 patients with class IV heart failure and a left ventricular ejection fraction carvedilol significantly reduced the risk of death by 38 percent compared to placebo (P = 0.0001). The drug also reduced the combined end point of death and hospitalization by 24 percent (P< 0.001). Data from Packer, M, Coats, AJ, Fowler, MB, et al. N Engl J Med 2001; 344:1651.
36. ACE Inhibitors and Survival Decreased mortality in patients with advanced NYHA class III or IV heart failure after treatment with enalapril compared to placebo (p = 0.003). Data
-from The CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429.
-consensus one of the first RCT for ACE I very sick population look at placebo mortality rateDecreased mortality in patients with advanced NYHA class III or IV heart failure after treatment with enalapril compared to placebo (p = 0.003). Data
-from The CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429.
-consensus one of the first RCT for ACE I very sick population look at placebo mortality rate
37. ACE Inhibitors and Heart Failure A meta-analysis of five trials involving 12,763 patients with left ventricular dysfunction who were followed for 35 months found that therapy with an angiotensin converting enzyme (ACE) inhibitor significantly reduced mortality (23 versus 26.8 percent, odds ratio 0.80, p<0.0001). There is continuing divergence in the mortality curves during the follow-up that exceeds four years. Data from Flather, MD, Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575
-
-curves separate beyond one yearA meta-analysis of five trials involving 12,763 patients with left ventricular dysfunction who were followed for 35 months found that therapy with an angiotensin converting enzyme (ACE) inhibitor significantly reduced mortality (23 versus 26.8 percent, odds ratio 0.80, p<0.0001). There is continuing divergence in the mortality curves during the follow-up that exceeds four years. Data from Flather, MD, Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575
-
-curves separate beyond one year
39. Valvular Disease
40. Mitral Stenosis Restriction and narrowing of mitral valve
Impairment of left ventricular filling
41. Mitral Stenosis - Causes Rheumatic Fever (>90% cases)
50% patients will have known history
Average 20 years prior to clinical symptoms
Congenital stenosis of MV
Extensive calcification
endocarditis
42. MS - Pathophysiology LA pressure increases
Increased pulmonary pressures
LA dilatation
Atrial fibrillation
Stagnation of blood in LA
thromboembolism
43. MS - Clinical Presentation Natural history variable
10 year survival (symptoms)
50-60%
Early onset
Dyspnea and reduced exercise capacity
Advanced
SOB at rest
Pulmonary congestion (orthopnea, PND etc)
Pulmonary HTN (RHF)
Hoarseness from laryngeal nerve compression
-natural history depends on the extent of symptoms, mean survival 3 years once pulmonary HTN develops
-the more severe the MS the more symptoms related to high atrial and pulmonary venous pressures
-early on once exercise and shorten DFP more symptoms-natural history depends on the extent of symptoms, mean survival 3 years once pulmonary HTN develops
-the more severe the MS the more symptoms related to high atrial and pulmonary venous pressures
-early on once exercise and shorten DFP more symptoms
44. MS - Examination Loud S1
From high pressure gradient from LA and LV
Opening snap
Sudden tensing of chordae and stenotic leaflets on valve opening
Diastolic murmur
Low frequency
Severity relates to duration
--
45. MS - Diagnosis ECG
LAE, RVH
Atrial fibrillation
CXR
LAE, pulmonary vascular redistribution
Prominent pulmonary arteries
Echo
Thickened MV
LAE
46. MS - Treatment Percutaneous balloon valvuloplasty
Surgical repair Antibiotics at time of risk
Diuretics for vascular congestion
Decrease HR if AF
anticoagulation
47. Mitral Regurgitation Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole -normal valve function, requires competent MV such that valve is closed in sytole, coordinated and complex action involving multiple components-normal valve function, requires competent MV such that valve is closed in sytole, coordinated and complex action involving multiple components
48. MR - Causes -causes can be considered by anatomic abnormality-causes can be considered by anatomic abnormality
49. MR - Pathophysiology Portion of the LV stroke volume ejected into LA
Forward CO is les than total LV CO
Elevation of LA volume
Reduction of forward CO
Volume related stress on LV
Severity depends on:
Size of orifice during regurge
SVR opposing LV blood flow
LA compliance
Duration of regurgitation
50. MR Clinical Presentation Chronic
Fatigue
If LV contractile dysfunction heart failure
Acute
Pulmonary edema
hypotension
51. MR - Examination Murmur
Pansystolic murmur heard at apex
S3
Reflects increased volume returning to LV in early diastole
LV displacement
If LV enlargement present
52. MR - Diagnosis CXR
Pulmonary edema if acute
Left atrial and ventricular dilatation
Calcification of MV
Echo
Identifies structural cause of MR
LV /LA size and function
53. MR - Treatment Acute MR
Vasodilators and diuretics
Reduce the resistance to forward flow
Relieve pulmonary edema Chronic
Operative repair once symptoms develop or LV starts to dilate
54. Aortic Stenosis Thickened and restricted opening of aortic valve
Obstruction to LV outflow
55. AS - Causes Age related calcification of valve
Rheumatic heart disease
Congenital bicuspid AV
56. AS - Pathophysiology Blood flow across the AV is impeded
Once AVA reduced by 50%:
Significant LV pressure needed to drive blood into aorta
Results in LV hypertrophy
Reduced LV compliance
Increased end diastolic pressure
57. AS Clinical Presentation Angina
Imbalance b/w myocardial oxygen supply and demand
Syncope
Peripheral vasodilation with inability to augment CO with exercise
HF
Increased LAP from high LVEDP
Contractile dysfunction if longstanding pressure overload
-demand increases bc increase muscle mass, and wall stres increases bc increased pressure
-supply reduced b/c of increased LVEDP (gradient of coronary flow ao pressure LVEDP
-demand increases bc increase muscle mass, and wall stres increases bc increased pressure
-supply reduced b/c of increased LVEDP (gradient of coronary flow ao pressure LVEDP
58. AS -Exam Murmur
Late peaking systolic ejection murmur
Carotid pulse
Weakend (parvus) and delayed (tardus) due to LV obstruction
S4
Atrial contraction into stiff LV -allows estimate of severity-allows estimate of severity
59. AS - Treatment Only effective treatment for severe symptomatic disease is surgical correction
What if asymptomatic?
20% of patients will progress over 20 years if mild disease only
Endocarditis prophylaxis
60. Aortic Regurgitation
61. AR - Causes Abnormalities of valve leaflets
Congenital (bicuspid valves)
Endocarditis
Rheumatic
Dilatation of aortic root
Aortic aneursym
Aortic dissection
syphilis
62. AR - Pathophysiology Severity of AR
Size of regurgitant orifice
Pressure gradient across valve in diastole
Duration of diastole
Acute
LV noncompliant
LVEDP rises quickly pulmonary edema
Chronic
Chronic volume/pressure overload
Dilates well compensated
63. AR Clinical Manifestations SOB on exertion
Fatigue
Decreased exercise tolerance
64. AR - Examination Murmur
Blowing diastolic along LSB
Widened pulse pressure
65. AR - Treatment Asymptomatic disease progresses very slowly
Surgery if:
Symptoms
Impaired LV function
Death occurs within 4 years after angina or 2 years after HF
67. Summary Slide Heart Failure
Understand causes of systolic and diastolic HF
Awareness of the presentation of left vs. right HF
Know treatment priniciples
Valve Disease
Identify the most common causes of 4 common valve lesions
Remember clinical presentations
Surgery treatment of choice any time symptoms present