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39 Cards in this Set
- Front
- Back
What is low output heart failure?
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Decreased cardiac output
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What causes congestion?
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Pathologic elevation of preload
- fluid retention - venous vasoconstriction |
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What is high output heart failure?
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Increased cardiac output - but increased blood flow demand from tissues, or decreased oxygen carrying capacity
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How would you develop LCHF due to mitral valve insufficiency?
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Left ventricle would need to eject more blood to keep up with the right ventricle
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Increased left ventricular preload is synonymous with what?
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pulmonary venous congestion
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What are 4 causes of LV volume overload?
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1. mitral insufficiency
2. aortic insufficiency 3. VSD 4. PDA All of these result in a decrease SV so the heart will compensate by increasing preload so that SV can equal that of the RV |
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What are 3 causes of RV volume overload?
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1. tricuspid regurgitation
2. pulmonic regurgitation 3. atrial septal defect |
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What causes pressure overload of the LV?
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Aortic stenosis
Systemic hypertension |
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What are the results of pressure overload of the LV?
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Heart needs to generate excessive high pressure to maintain forward CO
Concentric hypertrophy - relative ischemia, loss of compliance, dysdynamic myocardial failure Compensatory mechanisms - abnormal loading, high HR, autonomic imbalance - pulmonary congestion |
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What are common causes of pressure overload of RV?
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Heartworm - anything that elevates pulmonary pressure
LCHF - pulmonary congestion causes RV pressure overload |
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What is the result of RV pressure overload?
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loss of compliance, RV concentric hypertrophy, muscular outflow obstruction
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What are the causes and clinical signs of myocardial disease that cause loss of inotropy?
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toxic, metabolic, viral, genetic etc
LCHF and RCHF - Left predominates |
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What type of disfunction results from myocardial diseases which cause loss of inotropy or loss of compliance?
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Inotropy = systolic
Complaince = diastolic |
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What is the prototypical example of a myocardial disease that causes loss of inotropy OR loss of compliance?
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Inotropy - Idiopathic dilated cardiomyopathy
Compliance - hypertrophic cardiomyopathy |
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What is the role of the SNS in heart failure?
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1. Compensatory - Diminished distention of arterial, thoracic baroreceptors of the carotid sinus and great vessels activates SNS
2. Maladaptive - b receptors down regulated, increased myocardial O2 consumption, depleted catecholamines and increased NE |
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How does the PNS contribute to heart failure?
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PNS efferent withdrawal - increased HR and HR variability
Normally baroreceptors decrease SNS and increase PNS in response to high pressure - blunted in CHF |
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What are three stimulators for renin release?
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1. decreased renal afferent arteriole distention
2. increased renal sympathetic stimulation 3. decreased Na+ |
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What are 5 effects of angiotensin on the heart?
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1. catecholamine release
2. increased inotropy 3. cardiac vasoconstriction 4. impaired diastolic relaxation 5. myocyte hypertrophy |
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What are 4 effects of ANF?
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1. Kidney - increase GFR - diuresis, natriuresis
2. suppresses aldosterone + ADH 3. coronary vasodilation 4. sympathoinhibitory effect |
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What happens to ANF in CHF?
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First it is elevated by atrial distention
Eventually heart is unresponsive to ANF |
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What is the most important feature of BNF?
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Can be used as a biomarker for CHF
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What are 3 stimulants for AVP release?
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1. increase osmolarity
2. decreased BP 3. decreased blood volume |
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What happens to AVP in CHF?
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Activated in severe CHF by nonosmotic mechanisms - retention of water, hyponatremia, hypochloremia
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What does the plasma ET level tell you about CHF?
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Correlates HF functional class + severity of pulmonary hypertension
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What are 3 functions of ET?
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1. vasoconstriction
2. positive inotrope - causes reflex bradycardia 3. neuroendocrine release - ANF, PGs, renin, aldosterone, AVP |
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Name stimulators of ET release.
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ATII, EPI, AVP, Thrombin, IL1, OFR, TGF-B
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What might be a contributory factor to cardiac cachexia in late stage CHF?
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TNF
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Why does hypertrophy of heart occur? What are different types that occur?
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compensatory -return forces needed to be generated by the myocardium to normal
Volume overload - dilation of heart w/ proportional ventricular wall thickness Pressure overload - dysproportional ventricular hypertrophy |
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What are 3 consequences of hypertrophy?
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1. myocardial failure - muscle dysfuction = HF
2. coronary insufficiency - coronary can't keep up demand by myocardium 3. increased preload - decrease compliance makes increase preload necessary |
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How does the kidney response to high ATII levels?
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vasoconstriction of efferent arteriole - decrease blood flow, peritubular capillary pressure, increased capillary pressure, GFR, fluid resorption
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What are the levels of ATII and aldosterone in CHF? What is the result?
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abnormally increased
decreased ability to excrete Na+ |
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What are 3 reasons peripheral vascular resistance increases in CHF?
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1. increased sympathetic tone
2. increase in circulating vasoconstrictor neurohormones 3. impaired NO |
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What are three results of venous vasoconstriction?
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1. elevation of venous pressure
2. increased cardiac preload 3. increased CO |
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What is the result of pathologic elevation in venous pressure?
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Definition of congestion!
Organ dysfunction, damage, edema |
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What are 5 consequences of LCHF?
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1. pulmonary congestion
2. increased pulmonary vessel size 3. interstitial then alveolar pulmonary edema 4. pleural effusion (in cat - drained by visceral pulmonary lymphatics) 5. Respiratory problems - orthopnea, nocturnal dyspnea, cardiac asthma |
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What is Cheyne-Stokes respiration?
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alternating phates of apnea and hyperventilation - lengthening of circulation time between lungs and respiratory centers due to decreased CO
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How can LCHF be diagnosed?
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cardiac catheterization - elevation of pulmonary venous pressure
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What is the cardinal feature of RCHF?
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Systemic venous engorgement
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What are 3 clinical signs of RCHF?
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1. jugular venous distention
2. hepatomegaly/splenomegaly 3. ascites, pleural effusion, pericardial effusion |