Cardio1/2- Cardiac Dysfunction

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  1. Characterize DCM relative to:
    a- main functional abnormality 
    b- ejection/shortening fraction
    c- EDV and pressure
    • DCM:
    • a- decreased inotropy
    • b- decreased EF/SF due to decreased contractility
    • c- for any given EDV, peak wall tension and SV are depressed compared to a ventricle with norma inotropy (Frank-Starling law down and to right)
  2. Characterize hypertrophic cardiomyopathy relative to:
    a- main functional abnormality
    b- ejection/shortening fraction
    c- EDV and pressure
    d- mitral inflow profiles (Doppler) compared to a normal heart.
    • HCM:
    • a- impaired ventricular relaxation and decreased compliance caused by hypertrophy and intercellular fibrosis [DIASTOLIC DYSFUNCTION]
    • b- EF is normal to high
    • c- EDV is lower (for any given EDV, higher intraventricular pressure is required to force it out)
    • d- Doppler- delayed ventricular relaxation causes filling to shift to later in diastole--> E wave is smaller and A wave is larger due to a more vigorous atrial contraction
  3. Describe the primary pathophysiology of outflow tract stenosis.
    systolic pressure gradient across obstruction: high velocity ejection across obstruction, post-stenotic dilation due to turbulent flow and dissipation of kinetic energy
  4. Describe the auscultation of an outflow tract stenosis.
    systolic heart murmur
  5. Describe the response of the left ventricle to aortic stenosis.
    • aortic stenosis- discrete narrowing of LVOT--> concentric hypertrophy of ventricle and dilation of ascending aorta
    • LV has to generate more pressure then normal in systole and sends RBCs across the valve at a higher than normal velocity--> concentric LV hypertrophy
  6. Describe the abnormal path of bloodflow with mitral regurgitation.
    blood flows back into the LA from the LV during systole
  7. Describe the abnormal path of bloodflow with aortic regurgitation.
    blood flows back into the LV from the aorta during diastole (once LV pressure drops below 80)
  8. Describe the abnormal path of bloodflow with ventricular septal defect.
    blood flows from the LV to the RV during systole (when pressure in the LV is very high)
  9. Describe the abnormal path of bloodflow with patent ductus arteriosus.
    blood flows from the aorta to the pulmonary trunk throughout the entire cardiac cycle (pressure is always higher in the aorta)
  10. Which chambers and great vessels carry extra blood volume with patent ductus arteriosus?
    shunt causes increased pulmonary blood flow--> increased LA and LV filling--> increased LV EDV/preload--> increased total SV (enough to still perfuse tissue and feed the shunt.... until the ventricle eventually starts to fail)
  11. Which chambers and great vessels carry extra blood volume with ventricular septal defect?
    shunt increases blood to RV--> increased blood flow to pulmonary artery
  12. Characterize mitral regurgitation relative to:
    a- the functional abnormality
    b- EF
    c- EDV and pressure
    • mitral regurgitation:
    • a- regurgitation across incompetent valve sends blood in the wrong direction, into the lower pressure chamber--> increased blood volume in ventricle during diastole, overloading that chamber
    • b- EF????
    • c- backward flow increases LA pressure--> increased LV filling and preload--> increased EDV and pressure (causes compensatory eccentric hypertrophy)
  13. Mitral regurgitation causes what compensation?
    compensatory eccentric hypertrophy and increased SV
  14. Hypertrophic cardiomyopathy is __________ dysfunction.
    diastolic
  15. Dilated cardiomyopathy is __________ dysfunction.
    systolic
  16. What are causes of DCM? (5)
    genetic predispositions, prior myocardial injury, diffuse myocardial inflammation, taurine deficiency (cats), relentless tachycardia
  17. When there is delayed ventricular relaxation, how is diastolic function affected as seen by PW Doppler echo?
    filling shifts to later in diastole and the E wave becomes small and the A wave larger due to a more vigorous atrial kick
  18. When there is high LA pressure, how is diastolic function affected as seen by PW Doppler echo?
    early E wave becomes especially prominent
  19. What is an especially prominent E wave on PW Doppler echo indicative of? What disorder is this characteristic of?
    increased LA pressure; congestive heart failure
  20. When there is a stiff, noncompliant ventricle, how is diastolic function affected as seen by PW Doppler echo?
    abbreviated ventricular filling- short E wave; the atrium cannot generate enough pressure to further fill the ventricle- small A wave
  21. Describe how concentric hypertrophy affects wall thickness, myocardial relaxation, compliance, and EDV.
    increased thickness, decreased myocardial relaxation, decreased compliance, decreased EDV
  22. What disorders of the heart cause concentric hypertrophy? (2)
    chronic high BP, obstruction of the ventricular outflow tract (aortic or pulmonary stenosis)
  23. With mild diastolic dysfunction, there is impaired __________, reduced __________, and prominent ____________.
    relaxation; rapid early filling; atrial filling
  24. With severe diastolic dysfunction, there is decreased _____________, and for any given EDV, ________ must be ________.
    LV compliance; intraventricular pressure; higher to eject blood
  25. What 3 problems generally lad to ventricular overloads?
    congenital shunt, vascular disease, hypertension
  26. The heart respond to pressure overload by ___________; it respond to volume overload by ___________.
    concentric hypertrophy; eccentric hypertrophy
  27. Causes of pressure overload. (2)
    high arterial BP, stenosis of ventricular outflow tract
  28. Causes of volume overload. (2)
    congenital shunt, valve regurgitation
  29. Describe the compensatory responses that develop secondary  to a loss of myocardial contractility as would occur in DCM.
    • ventricular dilation and hypertrophy
    • increased EDV
    • increased SNS activation (increased alpha and beta--> increased contractility, HR, and vasoconstriction; increased renin, increased NE)
    • systemic arterial vasoconstriction
    • renal retention of Na+ and water (inc plasma volume--> inc venous pressure)
  30. Define cardiac remodeling.
    morphologic changes that develop in the heart as a consequence of a cardiac lesion and the neurohormonal responses to heart failure
  31. Why does chronic heart failure lead to cardiac dilation?
    [dilatation] because dilation activates the Frank-Starling law: increased filling/EDV--> increased SV; however, over dilation also results in loss of compliance
  32. Describe cardiac hypertrophy.
    increased muscle mass that may be primary or may be a secondary response to increased cardiac work; reduces wall stress, maintains SV but impairs ventricular contraction/compliance
  33. Cardiac hypertrophy in heart failure is potentiated by... (3)
    NE, RAAS, and some cytokines
  34. What are the benefits of the ANS-induced cardiac and circulatory changes that occur during compensated heart failure? (7)
    • [SYMPATHETIC ACTIVATION IS COMPENSATORY]
    • increased contractility
    • HR 
    • vasoconstriction/BP
    • increased perfusion and SV
    • hypertrophy decreases wall stress
    • hypertrophy maintains SV
    • dilation activates F-S effect--> increased SV
  35. What are the detriments of the ANS-induced cardiac and circulatory changes that occur during compensated heart failure? (5)
    • [SYMPATHETIC ACTIVATION IS COMPENSATORY]
    • myocardial cell hypertrophy and fibrosis
    • arrhythmias
    • down-regulation of beta receptors--> impaired inotropic response to SNS
    • hypertrophy impairs ventricular relaxation/compliance
    • over-dilation decreases wall compliance, increases wall tension, and predisposes to AV regurg
  36. How is RAAS affected by heart failure? How does it help, and how does it hurt?
    there is increased renin release with HF d/t decreased renal perfusion d/t decreased CO--> helps by increasing plasma volume through water and Na+ retention and causing vasoconstriction--> maintain BP; hurts by causing cardiac hypertrophy and fibrosis and elevated venous BP
  37. List the mechanisms for systemic arterial vasoconstriction that develop in heart failure. (5)
    • SNS alpha activation by NE
    • AngII
    • Arginine vasopressin
    • endothelin
    • decreased vasodilator activity
  38. List the mechanisms for increasing plasma volume in heart failure. (3)
    • increased RAAS--> sodium and water retention
    • increased aldosterone--> sodium and water retention
    • vasopressin--> water retention without sodium
  39. Although vasoconstriction in heart failure helps to maintain normal BP, it can be detrimental because... (2)
    • decreased skeletal muscle perfusion--> exercise intolerance
    • increased afterload--> decreased SV and mitral regurg
  40. What is the difference b/w "low output heart failure" and "congestive heart failure"?
    • Low output heart failure: signs related to decreased BP, peripheral vasoconstriction, and reduced tissue perfusion (pale MMs, exercise intolerance, hypotension)
    • Congestive heart failure: increased venous and capillary hydrostatic pressures--> edema
  41. 3 features of right-sided congestive heart failure.
    hepatomegaly, ascites, SQ edema
  42. 4 features of left-sided congestive heart failure.
    pulmonary edema, dyspnea, pulmonary crackles, cough
  43. Describe the hemodynamic abnormalities that are associated with heart failure. (6)
    • normal to decreased CO
    • normal to decreased BP (depends on whether it is compensated or failing)
    • peripheral vasoconstriction
    • reduced tissue perfusion
    • increased central venous pressure and capillary wedge pressure
    • Left CHF- increased pulmonary a pressure and edema due to backup
  44. What is pulmonary capillary wedge pressure?
    an estimate of left atrial pressure
  45. Explain the genesis of pulmonary edema in left-sided CHF.
    elevated LA pressure--> increased pulmonary venous pressure--> increased capillary hydrostatic pressure--> increased filtration across capillary (leakage)--> increased lymphatic drainage (to a point)--> once lymphatic drainage is exceeded, pulmonary edema
  46. How does right-sided CHF lead to body cavity effusions?
    increased pressure in RA leads to a backup in the venous system--> liver sinusoids are very leaky--> high protein fluid in abdomen [ascites]
  47. PE findings with right-sided CHF. (4)
    • distended jugular/prominent jugular pulse
    • sub-mandibular and brisket edema
    • ascites
    • hepatomegaly
  48. What are some of the radiographic abnormalities that might be expected with left ventricular failure? (3)
    • early LV enlargement
    • late diffuse cardiomegaly
    • pulmonary effusion/interstitial edema--> increased pulmonary densities
  49. How might lymphatic drainage be impeded in heart failure? (2)
    • increased RA pressure (lymphatics drain to venous system)
    • pulmonary hypertension caused by left HF can lead to impaired RV function
  50. Why is ascitic fluid in right-sided CHF higher in protein than pleural effusion in CHF?
    hepatic sinusoids (capillaries) are very leaky (fenestrated), so any ascitic fluid will be relatively high in protein when due to post-sinusoidal pressure elevations (right-sided failure); only fluid can cross the pulmonary capillary endothelial barrier
  51. Survival in CHF is improved by _________ because...
    ACE inhibitors; AngII increases myocardial fibrosis, apoptosis, cell death, and intercellular remodeling
  52. How does DCM affect EDV?
    increased EDV with DCM, which can partially compensate for decreased intropy (F-S law: increased filling--> increased SV).

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Author:
Mawad
ID:
316291
Filename:
Cardio1/2- Cardiac Dysfunction
Updated:
2016-03-27 15:17:13
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vetmed cardio1 cardio2
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vetmed cardio1 cardio2
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