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24 Cards in this Set
- Front
- Back
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Clinical definition of heart failure
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“Clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or eject blood"
Constellation of signs and symptoms that taken together suggest presence of a specific disease -signs are objective features detected by practitioner -symptoms are subjective features related by the patient |
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Diastolic vs Systolic heart failure: clinical observations
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DHF: EF>50%
SHF: EF<50% Present clinically identically Symptoms -DOE -PND -Orthopnea PE -JVD -Rales -PMI lateral -S3 -S4 -Hepatomegaly -Edema CXR -Pulm edema -Cardiomegaly |
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Diastolic vs systolic heart failure: epidemiology
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DHF:
Older Female SHF: Younger Male |
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Diastolic vs systolic heart failure: remodeling
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DHF:
Concentric remodelling -Increase mass -Volume same -Volume/mass ratio decreases -Systolic function same -Diastolic function decreases SHF: Eccentric remodelling -Increase mass -Volume increase -Volume/mass ratio increases -Systolic function decreases -Diastolic function decreases |
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Heart failure: Pathophysiology downhill cascade
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Myocardial insult
-Ischemia, valvular, HTN, etc... Myocardial dysfunction Reduced system perfusion Organs send out inflammatory signals and hemodynamic defense systems When they are chronically upregulated, heart gene expression is altered, apoptosis happens, remodelling occurs |
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Things that increase and decrease preload
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Increase Preload
Inspiration Exercise Aortic Regurg System Shunt Decrease Preload Valsalva Dehydration Atrial Fibrillation Medications |
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Afterload
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Force that the ventricle must overcome to eject blood
Mean arterial pressure or Aortic Valve/ outflow tract resistance Higher afterload results in longer isovolumetric contraction and slower rate of muscle fiber shortening If preload and contractility does not change this will cause a fall in performance |
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Staging of CHF
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A
High Risk no structural changes B Structural changes without syndrome C Syndrome controlled with therapy D Syndrome uncontrolled despite therapy |
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Major hemodynamic defense systems
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Sympathetic:
Effector -NE Receptor -Beta -Alpha Organs -Cardiovascular innervation -Adrenal gland Cardiac effects -Increase automaticity -Increase contractility -Increase afterload Renin angiotensin: Effector -Angiotensin II Receptor -Angiotensin (1-2) Organs -Kidney -Lungs -Blood vessels Cardiac effects -Increase preload -Increase afterload Aldosterone: Effector -Aldosterone Receptor -Mineralocorticoid Organs -Kidney -Heart Cardiac effects -Increase preload -Increase afterload Under normal circumstances these systems are only transiently upregulated Under chronic upregulation: Sympathetic causes myocyte death and arrhythmia Renin angiotensin causes myocyte hypertrophy and ischemia Aldosterone causes cardiac fibrosis |
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CHF symptom classification
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I
No limitation of activity II Mild limitation activity improves by slowing down III Marked limitation improves with rest IV Severe limitation or symptoms at rest |
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Relationship between systolic performance and functional capacity
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EF and VO2
No relationship |
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Normal vs CHF EDP
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Normal
-heart fills under low pressure -SV increases with exercise CHF -Heart can't relax (decreased lusitropy) -Heart fills under high LA pressure making EDP elevated -SV has small increase with exercise -EDP increased --not tolerated --transmitted back to lungs --cardiopulmonary HTN |
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Physiologic definition of CHF
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The inability of the heart to maintain the circulatory demands of an organism associated with a rise in left ventricular pressure
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Diastolic and systolic CHF cause of symptoms
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DHF
-unable to fill SHF -unable to pump -unable to fill (cause of symptoms) Leads to pulmonary congestion |
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Acute therapy for treatment of CHF
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Stepwise approach as follows:
Reduce congestion -Reduce preload -Reduce afterload Improve performance -Improve contractility Maintain vital organ perfusion -Artificial organ support |
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Clinical profiles in acute heart failure
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Warm and dry
-No congestion at rest -No low perfusion at rest Warm and wet -Congestion at rest -No low perfusion at rest Cold and dry -No congestion at rest -Low perfusion at rest Cold and wet -Congestion at rest -Low perfusion at rest Signs and symptoms of congestion: Orthopnea / PND S3 / Rales JV Distension Hepatomegaly Edema Signs and symptoms of low perfusion: Narrow pulse pressure Cool extremities Sleepy / obtunded Hypotension with ACE inhibitor Low serum sodium Renal Dysfunction |
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Therapies for clinical profiles in acute heart failure
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If congested
-Want to decrease afterload and preload --Vasodilators --Diuretics -Sometimes need to add inotropic effects -Sometimes need to give mechanical support |
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Goals of CHF therapies
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Dependent on which stage patient presents in
Prevent progression of disease Prevent morbidity Prevent mortality |
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Rational for ACE inhibition and ARB receptor blocker for HF
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Kidney senses decreased perfusion, begins renin-angiotensin system
Elicits cardiac and vascular hypertrophy Systemic vasoconstriction Aldosterone |
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Rational for sympathetic nervous system blockade for HF
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When NE is chronically bound to receptors it can cause myocyte death and increased arrhythmias
It also has activity at kidneys activating renin angiotensin system |
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Rational for aldosterone blockade in HF
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Aldosterone released from kidney in response to hypoperfusion
Chronic activation causes hypertension, vascular injury, LVH which all combines to cause ventricular remodelling |
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CHF life prolonging medical therapies
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ACE inhibitors (alternative) ARB (Class I, evidence A) all patients without contraindications or intolerance
-Blockers (Class I, evidence A) all patients without contraindications or intolerance Aldosterone antagonists (Class IIa, evidence A) all patients with Class III-IV HF in past 2 months without contraindications or intolerance |
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Sudden cardiac death (SCD) who and how
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80% have previous CAD
62% with Vtach -#1 risk factor for VT is low EF |
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Guidelines for defibrillator management of heart failure
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Ischemic cardiomyopathy who are at least 40 days post-MI with an LVEF ≤ 35%
Non-ischemic (chronic) ~6 months with an LVEF ≤ 35% High risk of SCA due to genetic disorders such as long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplagia (ARVD) |
