chapter 20- HF Flashcards
Heart Failure
complex syndrome of the heart that results from functional or structural impairment of ventricular filling or ejection of blood into the circulation.
*Assoc. with either a reduced or preserved L Ventricular EF
Compensatory Ability
- how your body pumps just sitting around vs running a marathon
- CO^: Exercise
Cardiac Reserve
how much the heart compensates to increase output during exercise
Myocardial Contractility
(inotrophy)
- the contractile performance of the heart (actin and myosin)
- as contractility ^, CO ^
Preload
Afterload
P- Amt. of blood in ventricles at the end of diastole
A- measure of force that was required to eject the blood from the ventricles
Ejection Fraction
the % of total amount of blood that entered ventricle that is actually moved out. (normal: 60%)
Most common causes of HF
coronary artery disease, hypertension, dilated cardiomyopathy, valvular heart disease
Efficiency of the heart is determined by:
the volume of blood that ejects each minute
Frank Starling Mechanism
*activation of neurohumoral influences: SNS and RAAS,
the naturetic peptides, vasoactive substances, hypertrophy and remodeling of heart
- Firs minutes- hours: SNS keeps heart pumping, RAAS is released to vasoconstrict and retain water
- Weeks: myocardial hypertrophy and remodeling for long-term adaptation to hemodynamic overload.
Heart Failure with reduced EF stimulates:
- RAAS pathway
- body retains water and sodium in kidney which ^ vascular volume and venous return to heart
- causes PULMONARY CONGESTION
Natriuretic Peptides (NP)
- naturally released in body response to overstretching of atria or ventricles (Heart Failure)
- inhibits SNS, RAAS, and ADH
- ANP & BNP levels are ^ in HF patients
A Nat Peptide
B Nat Peptide
A- released from ATRIAL cells in response to stretch, pressure, or fluid overload
B- secreted by VENTRICLES in response to ^ ventricular pressure or fluid overload
Both types of NP are released in response to:
^ chamber stretch and pressure
* promotes rapid and transient natriuretesis and diuretics through an increase in glomerular filtration rate and inhibit tubular sodium and water reabsorption
NP’s inhibit the natural response to heart failure: ___ and ___
SNS and RAAS (antidiuretic hormone and vasopressin)
the activation of SNS releases: ___
Catecholamines
-Epinephrine and Norepinephine to ^ HR and ^ CO
Enodthelins
Vasoconstrictors released from endothelium
Induce myocyte hypertrophy and fibrosis
bolster effects of hypoxic kidneys
-counteract BNP and ANP to encourage water and salt absorption in kidney
myocardial hypertropohy and remodling
cells change size to keep up with the demand
- last step in heart compensation to HF