CHF I Flashcards
What is a good diagnostic tool for CHF?
distended EJV
What is heart failure?
a systemic disease of result of deficiency of the heart to supply blood flow to vital tissues leaving from under perfused
What disease could impair forward flow from the heart to the tissues without damage to the myocardium?
- HTN
- Valve disease
- Pulmonary disease
- many more
What system is turned on when the kidneys don’t get sufficient blood flow?
the renin system, resulting in angio II release and salt and water retention (due to aldosterone) and probably is directly toxic to the heart (some ACE is present in the heart)
What does angio II do?
causes increased resistance, which increases afterload
Name 3 neurohumoral I systems that are activated in heart failure?
- renin system
- sympathetic system (nor)
- ANP
What are the major detriments of increased afterload?
- systolic BP
- size of the left ventricle
Name 3 contraindications to heart transplant.
- being too old
- lack of money
- drug addicts
- people with malignancies
T or F. HF is common with men
T, although women’s incident rises with age post-menopause
How is a HF-Class I defined?
those with low ejection fraction who are asymptomatic and live normally
How is a HF-Class II defined?
during normal activities, these patients become symptomatic (angina, dyspnea)
How is a HF-Class III defined?
symptoms with minimal activity
How is a HF-Class IV defined?
these people are always experiencing symptoms regardless of activity
What are some myocardial adaptations to reduced cardiac function?
- dilation, common with MI and viral infections (eccentric hypertrophy)
- heart muscle thickening (concentric hypertrophy) seen in HTN and vaulter disease
What is ejection fraction?
SV/EDV, normally 50+%
What are some things that ejection fraction don’t predict?
- CO
- renal blood flow
- RAAS activation
- salt and water retention
Where is angiotensinogen made? Renin? Aldosterone
- the liver
- the kidneys (juxtaglomerular apparatus in response to renal perfusion or hyperkalemia)
- the kidneys
Where is angio I converted to angio II by ACE?
the lungs
Quick overview of CHF
the kidneys respond to CHF as if the body was hemorrhaging. Thus, it works to retain blood volume by activating the renin system which leads to edema and mainly of the symptoms associated with CHF
What is the relationship between renin release and body position?
renin (even in normal people) is consistently elevated in upright people compared to when supine
thus, some treatment of CHF relies on bedrest for long periods of time
What percentage of CO do the kidneys receive normally?
20% at all times to maintain GFR
How does the renin system respond to increased thermal stress?
plasma aldosterone increased (resulting in decreased urine output)
How does decreasing the size of the heart help in CHF?
reduced afterload
What is ‘compensated’ heart failure?
have a reduced ejection fraction but the ANP and brain peptides balance out the activation of the renin system well
urinary sodium: potassium ratio is more than 1.0 here
What is ‘decompensated’ heart failure?
have a reduced ejection fraction and the ANP and brain peptides DO NOT balance out the activation of the renin system well so fluid retention is increased
urinary sodium: potassium ratio is less than 1.0 here
What levels of fluid retention does it take to develop pitting edema in the ankles and EJV distention? Edema at the knee then thigh? Anasarca?
3L
10-20L
30L
Using diuretics, how much of the volume overload do we typically want to reduce per day?
about 1 L because more will exacerbate the kidney under-perfusion leading to renal failure
What does spironolactone do?
aldosterone antagonist. Not prescribed unless the patient is symptomatic (class III usually)
What does aldosterone do specifically?
reabsorbs sodium (water follows) and excretes potassium
Side effect of spironolactone ?
hyperkalemia
Note on cachexia in CHF
Inappropriate activation of RAAS is accompanied by oxi-/nitrosative stress in the failing heart, skeletal muscle, skin, etc. leading to an increased inflammatory state (TNF-a and IL-6) resulting in a wasting of soft tissue and bone
