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heart failure is when ventricles unalbe to fully ____ or ____ completely
heart failure is when ventricles unalbe to fully fill or empty completely
what is the most common cause of RV failure?
LV failure
what is the etiology of HF?
-Impaired myocardial contractility ▪Typically either cardiomyopathy or ischemic heart disease -Cardiac valve abnormalities -Systemic hypertension -Pericardial disease -Pulmonary hypertension MOST COMMON CAUSE OF RV FAILURE IS LV FAILURE
Ultimately – ___ forms will lead to high ventricular end diastolic pressure
Ultimately – All forms will lead to high ventricular end diastolic pressure
why all forms of HF lead to high ventricular end diastolic pressure?
▪Secondary to altered ventricular function and neurohormonal regulation.
what are characteristics of systolic HF?

  • Decreased contractility
  • “Disease dependent”
  • Middle Aged Men (50-70)
  • Decreased EF <40%
how is decreased contractility affects EF and SV in systolic HF?
  • Decreased ejection fraction
  • Stroke volume can be normal (Compensatory mechanisms)
what are the characteristics of distolic HF?

  • Reduced compliance/relaxation
  • “Age Dependent”
  • Elderly Women
  • Preserved EF >40%
  • Common Causes: (Long standing essential HTN,Ischemic Heart Disease,Progressive aortic stenosis)
"age dependent" diastolic failure, what ages does it effect?
  • <45 years – 15% of HF
  • 50-70 years – 35% of HF
  • > 70 years –  50% of HF
what characteristics differ acute from chronic failure?

  • Requires emergency therapy
  • Hypotension
  • No peripheral edema
  • Three clinical entities: (New-onset, Worsening chronic, Terminal failure (non-responsive to therapy)
what characteristics differ chronic from acute failure?

  • Persistent; long-standing disease
  • Normotensive
  • Venous congestion
  • Severity varies greatly throughout the course of the disease
what are the characterisctics of left sided HF?

Pulmonary venous congestion (May develop pulmonary edema, effusions, HTN)
what are the causes of left Hf?
  • Systemic HTN
  • left-sided MI
  • Valvular disease
what are the s/sx of left HF?
Respiratory:
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
what are characteristics of right sided HF?
systemic venous congetion
what are the causes of right sided HF?
  • Pulmonary HTN/disease
  • Right-sided MI
  • Valvular disease
  • Left-sided failure (most common)
what are the s/sx of right sided HF?
Symptoms (systemic/GI):
  • Peripheral edema
  • Congestive hepatomegaly (Abd pain, nausea, etc.)
  • JVD/Hepatojugular reflex
what are characteristics of high output HF?

  • CI greater than normal (>3.5 L/min/m-2)
  • Increased  tissue demand (Failure because of hemodynamic burden)
  • Also see myocardial toxicity (thyrotoxicosis, beriberi, and anoxia)
what are the causes of high output HF?
  • Anemia
  • Pregnancy
  • Hyperthyroidism (Severe)
  • Paget’s disease
what are the characteristics of low output HF?

  • CI less than normal(<2.2 L/min/m-2)
  • Difficult to diagnose (Patient can have a normal CI at resting state, but fail to respond to increased demand)
what are the initiating mechanisms to cause HF?
  • Pressure overload
  • Volume overload
  • Infarction/Ischemia
  • Inflammatory disease
  • Restricted diastolic filling
what are the adaptive mechanisms to cause HF?
  • Frank-Starling Relationship
  • Activation of the SNS
  • Hemodynamic Alterations (contractility, HR, afterload)
  • Humoral-Mediated Responses
what mechanism contributes to myocardial remodeling?
ALL
describe frank-starling relationship
“The force or tension that develops in a muscle fiber depends on the extent that it is stretched before contraction” (Often compared to a RUBBER BAND)
what's "patho" behind frank-starling relationship?

As preload (LVEDP) increases, there is a greater stretch of the myocardium àincreases force of contraction à increased stroke volume (SV).
(according to F-S relationship) Over distension of ventricle can lead to _____ SV
decreased
(according to F-S relationship) Decreased contractility – _____ increase in SV as LVEP increases
(according to F-S relationship) Decreased contractility – small increase in SV as LVEP increases
(according to F-S relationship) Increased contractility – ______ response in SV to increased LVEDP
(according to F-S relationship) Increased contractility – larger response in SV to increased LVEDP

SNS Activation promotes _____ and _____ constriction

SNS Activation promotes venous and arteriolar constriction
how does venous constriction take place during SNS activation?
▪Blood is shifted from peripheral to central circulation ▪Result -> increased blood return to heart (increased preload)-Remember Frank-Starling?
how does arteriolar constriction take place during SNS activation?
  • Constriction causes increased afterload
  • Shunts blood flow to heart and brain
  • Decreased renal blood flow = RAAS activation
Decreased renal blood flow = RAAS activation, which means....... ­
  • Increases Na+/H2O retention
  • Result -> increase blood volume (increased preload) Again…..Frank-Starling
what is the difference btw short and long term SNS activation?
Short Term:
  • Effective at increasing and maintaining C.O
Long Term:
  • Worsening heart failure due to increased work
  • Increased wall tension à increased myocardial O2 demand
Contractility of the heart is reflected by _____ of _____
Contractility of the heart is reflected by velocity of contraction.
Max velocity is called ____
Max velocity is called “Vmax” ▪See decreased Vmax with impaired contractility (heart failure)
SV is relatively fixed in systolic heart failure (SHF)…so… Cardiac Output ____ are dependent on increases in heart rate.
SV is relatively fixed in systolic heart failure (SHF)…so… Cardiac Output increases are dependent on increases in heart rate.
what about HR and CO in SHF?
­In SHF, tachycardia is expected and should maintain C.O.
what about HR and CO in DHF?
­In DHF, tachycardia can decrease CO due to decreased filling time.
what is a target therapy in patients with DHF?
HR
why is afterload increased in HF?
Increased due to arterial constriction and hypertension
how can forward SV in HF pts can be optimized?
decreasing afterload with vasodilators (exNTG)
name the nuerohumoral pathways that cause HF
  • RAAS (Na+/H2O retention & Vasoconstriction)
  • SNS Activation (Catecholamine release à unopposed vasoconstriction)
  • Vasopressin Release (Anti-diuretic à fluid retention)
  • Release of Inflammatory Mediators (include endothelin and cytokines)
what is the fx of naturetic peptides?
Promote BP control, protection from volume/pressure overload.
how do naturetic peptides work?
  • Anti-hypertrophy/anti-inflammatory properties
  • Inhibition of RAAS/SNS (Naturesis, diuresis, vasodilation)
what are 2 types of NP's?
ANP and BNP
where is ANP stored and when is it released?
Stored in atrial muscle – released with increased atrial pressure.
what part of the heart secretes BNP?
-Secreted by atria and ventricles with increased stretch. -In HF, it is secreted primarily by the ventricles.
There is a ____ BNP that can be administered in acute heart failure.
There is a synthetic BNP that can be administered in acute heart failure.
what is myocardial remodeling?

Compensatory changes to the size, shape, and function of the ventricular myocardial tissue.
what drugs have been shown to promote reversal of remodeling changes to the myocardium?
ACEI's
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