Trigger - HF 1 Flashcards
RUQ pain, SOB, Orthopnea, and PND are symptoms of what
ACUTE heart failure
Edema, Anorexia, Abdominal distention and fatigue are common symptoms of what
CHRONIC heart failure
can be caused by thyrotoxicosis, severe anemia and sepsis
high output HF
what type of HF is EF of 46%
Type a - HFpEF borderline
Type I - HFrEF (EF </=40%)
Type II - HFpEF (EF >/= 50%)
Type a - HFpEF, borderline (EF 41-49%)
Type b - HFpEF, improved (EF >40%)
JVD, hepatic congestion, ascites, LE edema
R sided HF s/s
when do you see isolated R sided HF
rare, only when lung disorder is present!
DOE, PND, Orthopnea, fatigue, cyanosis
Left sided HF
These classes quantify functionality
NYHA
These classes CANNOT change and describe the evolution of HF
ACC/AHA
How would you classify someone with structural HF that has symptoms occasionally
AHA classification
Class C
A = At risk but no disease or symptoms.
B = Structural disease but no S/S.
C = Structural dsease with prior or current S/S
D = Refractory HF that requires specialized interventions (Usually class IV patients)
what causes RAAS system activation in HF
poor renal perfusion d/t poor CO.
leads to fluid retention and sodium dilution -> hyponatremia
increases ventricular contractility of the heart and HR.
also leads to vasoconstriction and enhanced venous tone, increasing preload
NE release. (d/t activation of SNS)
how does plasma concentration of NE correlate with HF severity
inversely correlated
kidney rxn to HF
Increased proximal tubular sodium reabsorption, which contributes to sodium retention in HF.
stimulated by increased beta - q adrenergic activity
RAAS system
also stimulated by decreased glomerular filtration
this peptide rises in early HF
ANP
this is released in response to high ventricular filling pressures
BNP
this Reduces SVR and central venous pressure and increases natriuresis to reduce afterload.
BNP
effects of angiotensin II and catecholamines
promote myocyte loss and result in cardiac remodeling
venous return and EDV (end-diastolic volume) is considered what
preload
force generated at any given EDV
contractility
aortic impedance, SVR, and wall stress
Afterload
4 common PE findings in HF
Resting sinus tach
narrow PP (< 25 mm Hg)
Diaphoresis
Peripheral vasoconstriction
What causes myocytes to develope more AT receptors and therefore result in apoptosis
RAAS system
