Amanda Bartlett, PA-C Dustin Bartlett, PA-C Andrea Applegate, PA-C Leslie Yearta Brown, NP CHF Round Table Discussion Objectives ANDREA- Discuss the definition and different categories of CHF DUSTIN- Define how Starlings low affects CHF/ structural changes associated with CHF LESLIE- Discuss counter regulatory/ compensatory mechanisms associated with CHF CHAD- Discuss NYHA classification of CHF and the most common symptoms associated with systolic vs diastolic CHF AMANDA- Discuss the standard therapy modalities for CHF as well as new medications/ devices available. Pre-discussion questions
All of the following are symptoms of left sided heart failure except: a. Dyspnea b. Orthopnea/PND c. Elevated Pulmonary Capillary Wedge Pressure d. Peripheral edema 10 Systolic and Diastolic heart failure both cause loss of: 0% a. Stroke volume 0% b. Cardiac output c. Preload 10 A 58 year old male with h/o EF 30%, currently on Lisinopril and Coreg gets SOB when walking >3 blocks and up hill. Denies PND or orthopnea. His NYHA functional class would be classified as: a. Class I b. Class II c. Class III d. Class IV 10
Reduction of mortality risk in patients with HFrEF occurs with standard therapy of the following except: 0% a. ACEi 0% b. Beta Blockers 0% c. Mineral corticoid antagonists d. Digoxin 10 Andrea Applegate, PA-C CHF definition and categories Heart Failure Occurs when the body s need for blood and oxygen cannot be met by the heart muscle s ability to pump or may be met only with an elevated diastolic filling pressure. Causes include myocardial injury or high demand states. Heart failure causes circulatory compromise and can lead to circulatory failure.
Left sided Heart Failure Systolic failure: loss of ability to squeeze. This prevents adequate blood flow forward from the LV into circulation HFrEF: Heart failure with reduced EF Diastolic failure: loss of ability to relax. This prevents adequate blood filling into the LV. HFpEF: Heart failure with preserved EF. Systolic and diastolic HF both reduce stroke volume. Right sided Heart Failure RV failure reduces blood return from the venous system due to myocardial injury, poor perfusion, or increased pulmonary pressures. May be caused by valvular disease, but the RV compensates to volume overload better than pressure overload, and may be minimally symptomatic.
Dustin Bartlett, PA-C Cardiac Hemodynamics Cardiac hemodynamics (Cliff s notes version) Cardiac output (CO) = Stroke volume (SV) x HR -CO= SV x HR or CO = (LVEDV-LVESV) x HR Normal CO value: 4-6 L/min LVEDV= Left ventricular end diastolic volume LVESV= Left ventricular end systolic volume Cardiac Index = Cardiac output/ Body surface area Normal Cl value: 2.2-4.0 L/min/m2 Stroke volume Blood volume ejected with each heartbeat Normally 50-100cc RVSV=LVSV SV reflects EF HR Stroke Volume affected by Preload Afterload Contractility Tachyarrhythmmia! inadequate filling time Bradyarrhythmia! inadequate forward output
Cardiac hemodynamics Preload refers to the left ventricular end-diastolic volume. Assessed by: ECHO (LV volumes PA Catheter (PCWP estimates LVEDP) Central venous catheter (CVP estimates RVEDP) Preload of the LV- normal 8-12mmHg (PADP 10-15mmHg) Preload of the RV normal 2-8mmHg Increasing preload Blood transfusions Fluid Aortic stenosis and insufficiency (LV preload) Pulmonic stenosis and insufficiency (RV preload) LV systolic failure Gravity- lying flat Reduced heart rate which increases ventricular filling time Decreasing preload Diuretics Vasodilators Diastolic heart failure Mitral or tricuspid valve stenosis Gravity- standing Cardiac hemodynamics Afterload refers to the left ventricular wall tension at the start of systole. This tension must be overcome to allow ejection of blood from the ventricle. Systemic Vascular Resistance and Preload (assessed by PA catheter) Normal range 800-1200 dyne-sec/cm5 SVR = (MAP-CVP)80! CO Cardiac hemodynamics Increases Afterload Alpha agonists Neosynephrine midodrine Alpha + Beta agonists Epinephrine Norepinephrine dopamine Aortic stenosis Systemic HTN Decreases Afterload Beta blockers Calcium channel blockers ACE inhibitors Alpha blockers Direct vasodilators Milrinone Intraaortic balloon pump Mitral regurgitation
Frank- Starling Law Frank-Starling law of the heart: Increased venous return= Increased LVEDP=increased Preload= Increased SV Increased Afterload= Decreased SV Decreased Afterload= Increased SV Leslie Yearta-Brown, NP counter regulatory/ compensatory mechanisms associated with CHF Compensatory Mechanisms In order to compensate for the failing heart: Cardiac output is increased via Frank-Starling law. The sympathetic nervous system is activated in response to decreased cardiac output as well as neuro-hormonal systems. This results in tachycardia, vasoconstriction and and redistribution of blood flow away from the skin and splanchnic beds to the heart and central nervous system. - RAAS - Elevated levels of arginine vasopressin and endothelin also may contribute to vasoconstriction and volume expansion. - Natriuretic peptides act as counter-regulatory hormones resulting in diuresis, natriusesis, vasodilation, and aldosterone/endothelin antagonism. Initially beneficial, all compensatory mechanisms eventually lead to worsening heart failure.
Review of the RAAS Renin is released in response to decreased renal perfusion and activation of the SNS. Renin mediates the conversion of angiotensinogen to angiotensin I. Angiotensin I is converted to Angiotensin II (AII) by angiotensin-converting enzyme (ACE) Angiotensin II is a potent vasoconstrictor. AII stimulates aldosterone release. Aldosterone stimulates sodium reabsorption in the distal tubule. The nervous system increases circulating catecholamines to increase heart rate and contractility, vasoconstriction, and redistribution of the of blood flow away from the skin and splanchnic beds. Beta blockers are used to block effects of excessive catecholamine response. Elevated levels of circulating angiotensin II results in systemic vasoconstriction. Treat with ACEI/ARB to block the production of AII. Aldosterone increases blood pressure and volume by increasing water retention, sodium conservation and potassium secretion. Treat with mineral corticoid receptor antagonist (spironolactone/eplerenone). Dustin Bartlett, PA-C NYHA Classification of Heart Failure
Symptoms of Heart Failure, Systolic and Diastolic Dyspnea Orthopnea Chest pain or Discomfort Fatigue Edema Palpitations NYHA Functional and Objective Classification FUNCTIONAL Class I- No limitation of physical activities. Ordinary physical activity does not cause symptoms Class II- Mild symptoms and slight limitation during ordinary activity. Comfortable at rest Class III- Marked limitation of physical activity. Comfortable at rest. Class IV Unable to carry on any physical activity without symptoms. Symptoms at rest * Source American Heart Association OBJECTIVE Class A- No evidence of cardiovascular disease. No symptoms or limitation in ordinary physical activity Class B- Objective evidence of minimal cardiovascular disease. Mils symptoms and limitations during ordinary activity. No rest sx. Class C- Objective evidence of moderately severe cardiovascular disease. Marked limitation in activity due to symptoms. No rest sx Class D- Objective evidence of severe cardiovascular disease. Severe limitations. Rest sx. Examples Patient A- Patient with no shortness of breath, chest discomfort, or fatigue at rest or with exertion. Recent echo shows moderate to severe aortic stenosis, anterior wall motion abnormality, and EF of 25% Functional Class I, Objective Assessment D Some mild shortness of breath with daily activities. No chest discomfort. Had recent heart cath with nonobtsructive CAD and EF of 45% on ventriculogram. Functional Class II, Objective Assessment B
Amanda Bartlett, PA-C Standard Therapies for CHF Standard Therapy for CHF ACE inhibitors/ ARB Beta Blockers when added to ACEi, 30-35% Long term tx with Enalapril decreased relative risk of death by 16% among pt with mild to mod symptoms Mineral corticoid antagonists- 22-30% Diuretic Neprilysin (Entresto) Neutral endopeptidase Degrades several endogenous vasoactive peptides Natriuretic peptides, bradykinin, adrenomedullin Combined inhibition of renin-angiotensin system and neprilysin had effects superior to those of either approach alone Clinical trials, combined inhibition of ACE and neprilysin associated with serious angioedema Pt s NYHA II-VI symptoms, EF</40% (10,521 pt) Neprilysin and Angiotensin II receptor inhibition more effective in reducing death from cardiovascular causes or hospitalization for CHF than was ACEi
Corlanor Approved in US by FDA in 2015 Decreases cardiovascular death rate and risk of CHF hospitalization Decreases rate without decreasing contractility Indicated in CM pt s with EF <35% in combination with beta blockers and whose HR exceeds 70 bpm CardioMEMs device Small wireless sensor implanted with catheter based procedure, no battery or replaceable parts CHAMPION trial, HFrEF pt already on guideline directed medical therapy Pulmonary artery pressure guided management reduced CHF hospitalization 43% and mortality by 57%. CardioMEMs device
Post discussion questions All of the following are symptoms of left sided heart failure except: a. Dyspnea b. Orthopnea/PND c. Elevated Pulmonary Capillary Wedge Pressure d. Peripheral edema 10 All of the following are symptoms of left sided heart failure except: Dyspnea 27% Orthopnea/PND 33% ary Capillary Wedge Pressure 20% 30% Peripheral edema 20% First Slide Second Slide
Systolic and Diastolic heart failure both cause loss of: 0% a. Stroke volume 0% b. Cardiac output c. Preload 10 Systolic and Diastolic heart failure both cause loss of: Stroke volume 37% 37% Cardiac output 40% 40% Preload First Slide Second Slide A 58 year old male with h/o EF 30%, currently on Lisinopril and Coreg gets SOB when walking >3 blocks and up hill. Denies PND or orthopnea. His NYHA functional class would be classified as: a. Class I b. Class II c. Class III d. Class IV 10
A 58 year old male with h/o EF 30%, currently on Lisinopril and Coreg gets SOB when walking >3 blocks and up hill. Denies PND or orthopnea. His NYHA functional class would be classified as: Class I 20% 40% Class II 13% Class III 20% 20% Class IV 17% 47% First Slide Second Slide Reduction of mortality risk in patients with HFrEF occurs with standard therapy of the following except: 0% a. ACEi 0% b. Beta Blockers 0% c. Mineral corticoid antagonists d. Digoxin 10 Reduction of mortality risk in patients with HFrEF occurs with standard therapy of the following except: ACEi 17% 20% Beta Blockers 10% corticoid antagonists 37% 47% Digoxin First Slide Second Slide
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