PC3 MOD 6.1

CO

volume of blood pumped by each ventricle per minute

CO= HR (# of bpm) x SV (volume of blood pumped per beat or stroke)

what is HF?

• clinical syndrome resulting from structural/functional impairment of ventricular filling or ejection of blood

• decreased CO

dilated cardiomyopathy

• LV much larger

• weakened myocardium

hypertrophy

• LV decrease in size

• thickened myocardium

risk factors for HF

• hyper/hypothyroidism

• metabolic syndrome

• T2DM

• obesity

• smoking

• alcohol or drug abuse

• certain types of radiation & chemotherapy (anthracyclines= used in breast cancer & leukemias in PEDS pts)

stages of HF

stage A) @ risk for HF= no current or prior S/Sxs of HF & no structural changes or elevated biomarkers of heart disease

stage B) pre-HF= pts w/no current or prior S/Sxs of HF but have one of the following: structural abnormality, abnormal cardiac function, elevated ANP lvls or cardiac troponin lvls

stage C) HF= pts w/current or prior S/Sxs of HF or both caused by structural or functional cardiac abnormality or both

stage D) advanced HF= severe S/Sxs of HF or both @ rest or w/minimal exertion

functional classes of HF

Class I- no limitation of physical activity, regular physical activity does not cause fatigue, palpitation or SOB

Class II- slight limitation on activity, comfortable @ rest, reg activity results in Sxs above

Class III- marked limitation of activity, comfortable @ rest, less than reg activity causes Sxs above

Class IV- Sxs of HF @ rest any activity causes discomfort

HFrEF

• < or = 50%

• systolic dysfunction: heart cannot eject the volume it was once able to

  • decreased contractility

  • increased preload (volume overload)

  • increased afterload (pressure overload)

HFimpEF- pts w/previously reduced EF have increased EF post treatment

HFpEF

• pts w/sxs of decreased CO, but echocardiography measurements stay proportional to normal

• EDV is affected. volume decreased

common pathogenesis of HF

initial cardiac insult→ primary damage→ compensatory mechanisms: tachycard, increased contractility, increased preload, neuroendocrine activation → secondary damage/progression of disease

take home on CCD & HF

CCD accounts for ~2/3 of HF cases

HF affects CO

HF affects SV→ SV decreases→ as a result of this HR has to compensate and increase

things that can impair SV

• increased afterload (increase the workload on the heart)

• decreased preload (reduces EDV)

• decreased contractility