Flashcards in 43-44 Mech of HF and Drugs Deck (66)
What are the three cardinal manifestations of HF?
dyspnea, fatigue, fluid retention
[not all patients have fluid overload and thats why they don't call it congestive HF anymore]
T-F-- heart failure can occur when CO is high or low?
What are the 4 causes mentioned of HF when CO is high?
major AV shunts
Increased force of contraction is produced when?
increased sarcomere length during diastole- closely related to end diastolic filling pressure (pre-load)
What is the inotropic state of the heart-
contractile state of the heart determined by its contractile properties and influence of autonomic nerves and circulating catecholamine which can also influence HR
What protein pumps CA into the sarcoplasmic reticulum? out of the SR?
What proteins pump CA out of the cell?
What pumps Ca into the myocyte during the depolarized state.
L-type Ca channel
What happens to the NCX Na/Ca exchanger during depolarization ?
breifly reverses so Ca goes into the cell
In heart failure what is systolic dysfunction? diastolic dysfunction?
1. abnormally weak contraction during systole
2. abnormal relaxation during diastole
[remember they can be individual or in combination]
T-F-- energy delivery, production and storage and energy utilization are thought to be heavily involved in pathogenesis of failure?
What are 5 signs and symptoms of HF?
1. numerous hemodynamic abnormalities
2. dysregulation of Ca homeostasis- impair contraction and relaxation
3. dysreg of contractile proteins and interferes with cross bridge recycling
4. densensitized b adrenergic pathway--> reduced Ca uptake in SR.
5.myocytes lost by cell death-->fibrosis
Reduction in CO does what?
activates SNA and RAS and increases venous volume
Increases in intravascular and ventricular volumes leads to what?
increased diastolic and systolic wall stress, leading to hypertrophic remodeling of the hear and impaired contraction
Neurohumoral mediated increases in arterial and venous constriction increase what?
ventricular after load and preload respectively
Neurohumoral activation (SNA, ANGII, and aldosterone) act directly on the myocardium to promote what?
Unfavorable remodeling via myocyte apoptosis and changes in gene expression and EM composition
Reduced function of both arterial and venous baroreceptors leads to what?
increased activity of SNA, RAS, and vasopressin
T-F--hypertrophied heart operates at a higher inotropic state?
What happens in renal function due to sympathetic- induced vasoconstriction ?
Shunts blood from glomeruli, stimulates renin, -->NA retention, increased blood volume, edema
SNS RAS and vasopressin all react to sustain arterial pressure with low cardiac out put by what? good or bad?
1. increasing peripheral resistance
2. Not beneficial
What is the first thing we must do in the pharmacological treatment of HF?
correct any reversible causative factors
[arrythmias, hypertension, valve defects, anemia, thyrotoxicosis etc.]
AHA stage A and B include who? C and D?
at risk for heart failure
with heart failure
What is stage A? Drugs usually used?
1. at risk but w/out structural heart disease or symptoms
2. ACEI or ARBS
What is stage B? Drugs typically used?
1. Structural heart disease but without signs or symptoms
2.ACEI or ARB and Beta blockers
What is stage C? What drugs typically used/
1. structural heart disease with prior or current symptoms
2. diuretics, ACEI and beta blockers
What is stage D HF? Tx?
1. refractory HF requiring specialized interventions
2. drugs from classes A,B,C, end of life care, and extraordinary measures (transplant, inotropes, mechanical support, experimentals)
What drugs do we use for after load reduction?
ACEI, ARBs, isosorbide dinitrite or hydalazine
What diuresis drugs do we use for HF?
loop diuretics and thiazides, spironolactone
What drugs do we use for positive isotropy?
cAMP phosphodiesterase inhibitors