Cardio. 38. Flashcards
Define heart failure
heart’s inability to meet the metabolic
needs of peripheral tissues, or instances when the heart can only do so in the presence of increased venous filling pressures.
forward failure (poor CO), backwards failure (congestion)
primary trigger for activation of the RAAS
inability to provide normal renal perfusion. Decreased renal blood flow and Cl delivery to DCT induces renin
release from the macula densa.
End result of RAAS activation in CHF
Fluid retention (which promotes development of CHF) and mal-adaptive myocardial and vascular remodeling
SNS acute vs. chronic in heart failure
Acute response adaptive, chronic maladaptive –
SNS activity ultimately leads to further cardiac damage
humans with heart disease, increased NE significant
risk factor for mortality
Myocardial tissue produces two main hormones that induce natriuresis, diuresis, and vasodilation:
produced primarily in response to:
These so-called natriuretic peptides:
atrial natriuretic peptide (ANP)
B-type natriuretic peptide (BNP)
stretch or stress of myocardial tissue
serves as a counterregulatory system to RAAS & SNS
overwhelmed in heart disease
ET-1: name: produced by: in response to (3): causes:
Endothelin 1 is a potent vasoconstrictor
produced by vascular endothelial cells
response to sheer stress, angiotensin II, and CKs
increases cardiac afterload
elevated in dogs and cats with heart failure
> afterload &alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes
Arginine vasopressin ADH MoA:
ADH activation results in:
increases reabsorption of free water within DCT & CT
activation closely resembles that of the RAAS and SNS
fluid overload, CHF, and dilutional hyponatremia
Describe dilutional hyponatremia and the hormone involved:
heightened free water retention to the extent that serum sodium concentrations are decreased, despite an overall excess of body-wide sodium.
ADH
both humans and veterinary patients, dilutional hyponatremia is a marker of severe neurohormonal activation and is a poor prognostic sign
List three maladaptive responses in heart failure following neurohormonal activation :
Myocardial remodeling
ABNORMAL Ca++ handling
ABNORMAL myocyte energy production
response to pressure overload vs response to volume overload:
i.e.
pressure - hypertrophy sarcomeres replicate in parallel
volume - elongate - sacromes replicate in series
SAS, hypertension -conentric hypertrophy
MMVD - eccentric hypertrophy
Cardiac hypertrophy consequences:
concentric: increased myocardial oxygen demand
ischemia, fibrosis, collagen disruption, and injury to small coronary vessels
eccentric: increased myocardial wall stress,
myocyte injury or necrosis, and myocyte slippage
Describe path of Ca++ in an action potential:
- calcium ions enter vis L-type channel in T-tubules (terminal cisterna)
- Ca sensed at feet of RyR receptor triggers release of additional calcium ions from sarcoplasmic reticulum [SR]
- Ca stored in the SRs flows through the RyR ryanodine channel
- binds to troponin C located on the actin and myosin complex (concentration dependant manner)
- conformation change exposing myosin head
- myosin binds to actine - ATP hydrolysis
- “ratcheting contraction”
- ATP dependant release of Ca
- calcium ions are quickly sequestered into the SR
- via ATPase (SERCA) channel
phospholamban
help regulate the reuptake of Ca++ by DECREASING/inhibiting SERCA
myocardial energy source in CHF
heart can utilize both glucose and free fatty acids
In cases of heart failure, the heart preferentially
uses glucose, which requires less oxygen to metabolize
CHF occurs at what pressure?
pulmonary venous congestion (left sided):
systemic venous congestion (right sided):
Pulmonary venous pressures greater than 25 mm Hg
systemic venous pressures greater than 20 mm Hg