1. Vasoconstriction 2. Stimulates remodeling 3. Induces aldosterone

Drennan 1 Flashcards by Chris Rodarte

Factors affecting CO

SV*HR

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Consequenes of reduced CO

Tachycardia
Cardiomegaly
Arrhythmia
Fatigue
SOB
Pulm edema
Cyanosis
Orthopnea

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Key thing that happens in CHF

reduction in CO

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Decrease in preload leads to

decrease in O2 consumption

Increase in myocardial perfusion

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Decrease in afterload leads to

decrease in O2 consumption

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Decreased HR will

increase coronary perfusion

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Afterload definition

Force distributed in ventricular wall during systole

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Limit of starling relationship

Stretching passes a certian point >> actin and myosin are not properly aligned >> no further increase in force can be generated

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Optimal length of overlap

2 to 2,2 microns

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In Frank Starling curve, increasing contraction will shift the curve ___

upward

(increased SV per a certain EDV)

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____ and _____ are inversely related.

What relationship is this?

Stroke volume and Afterload

The force-tension relationship

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Failing hearts start to show signs of…

higher sensitivity to afterload for a given stroke volume

Increases in afterload will shift SV down further than normally

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Progessive CHF is a disease of:

compensation and decompensation

Compensation = Stable patient, normal activity

Decompensated = acute worsening of CHF

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Type of CHF with thin/dilated heart

Systolic failure

(Deficit in contraction)

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Thick/stiff walls can’t relax in which type of CHF

Diastolic failure

(Deficit in filling)

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afterload, SV, and preload in early heart failure

afterload = high

SV = reduced somewhat

Preload = starts to increase –> drop off normal curve

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Compensation for maintaining SV in early HF

Increased Sy

Increased volume (RAAS)

Cardiac remodeling

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AT2 effects

Vasoconstriction
Stimulates remodeling
Induces aldosterone

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Increased CT in cardiac remodling is due to

cell death and replacement of dead myocytes with fibroblasts

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Increased ____ in remodeling with CHF

Increase in Ca2+ cycling
Increase in response to Calcium (Ca sensors that will go and mediate Calcium-dependnt genes that play role in hypertrophic response)

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CHF drug strategies (and dothey improve mortality)

Manipulate hemodynamics (NO)

Inhibit compensation (YES)

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Vasodilators

Diuretics

Angiotensin Inhibitors

Inotropic agents

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Inotropic agents

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Cardiac glycosides

PDE inhibitors

B adrenergic agonists

Chronic therapy inotropic agent

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Cardiac glycosides

Acute therapy inotropic classes

PDE inh B agonists

B agonists (inotropic agents)

dobutamine, DA

Pumps calcium into SR lumen

SERCA

Two mechanisms to get calcium out of the cell

1. Ca²⁺ ATPase 2. NCX exchanger = 3 Na in, Ca²⁺ out

Manipulation of _____ enhances cardiac contractility

Na+ gradient

PDE inhiitor risk

arrhythmia (long term)

Beta agonists long term AE

desensitzation

Ca2+ overload is

pro-arrhythmic e.g. overdoses of digoxin

digoxin MOA

1. **Inhibit Na/K+ ATPase** 2. sodium builds up in cell 3. Low Na⁺ gradient 4. NCX is less functional at exchanging Na+ for Ca⁺⁺ 5. **Increases cytoplasmic levels of Ca⁺⁺**

**Increases** = Contractility and AV node refraction **Decreases** = HR (indirect via Vagus) and vascular tone

Glycosides common toxicities

1. Psych 2. GI (N/V, pain) 3. Resp (Increased response to hypoxia) 4. Cardiovascular - Arrhyth., AVBlock

Digoxin interactions

* **BB** and **CCBs** depress heart and digoxin action * **Kaliuretic diuretics** promote digoxin action (via decrease in K+), which raises risk for arrhytmia

PDE3 inhibitors

Milrinone Amrinone

PDE inhibitors risk

Pro arrhyth. Decrease survival

Beta AR agonists risks

prone to desensitization cause hypertension

PDE antagonists block

cAMP--\> AMP

Drugs that act by Inhibiting compensation

RAAS inhibition Aldosterone antagonist BB's

RAAS inhibitors reduce

preload and afterload

Agents for RAAS inhibition

ACEi's (enalapril) AT2R blockers Aliskiren

Aldosterone antagonist that acts as a potassium sparing diuretic

Spironolactone

Arrhythmogenesis and risk of sudden cardiac death

K and Mg loss

Aldosterone effects (6)

1. Increase Na/water retention 2. K⁺ and Mg²⁺ loss 3. Reduced myocardial NE uptake 4. Reduced baroreceptor sensitivity 5. Myocardial fibrosis, FB proliferation 6. Change Na⁺ channel expression (related to arrhythmias)

B-AR blockers are useful in normalizing..

the hyperadrenergic state in CHF

B-AR effect on after/pre load

reduce afterload may increase preload

AT2 stimulates... effects?

Vasopressin secretion (Water retention, Vasoconstrict, enhanced PLATELET aggreg., VSM and myocyte proliferation)

VR antagonists in CHF

Tolvaptan Conivaptan

Indications for tolvaptan and conivaptan

Tx for hyponatremic state in SIADH and HF Acute care setting

VR antagonists AE's and interactions

HoTN, osmotic demyelination CYP3A substrate

Neprilysin MOA

terminates the action of naturetic peptides (neutral endopeptidase) Degrades Naturetic peptides, bradykinin, adrenomedullin

Neprilysin inhibition results in... This Counters...

increased vasoactive peptides counters neurohumoral vasoconstriction, Na+ retention, remodeling

Human Type B naturetic peptide

Activates membrane-bound guanylate cyclase in VSMC and endothelial cells Increased cGMP --\> dephosphorylate MLC --\> Vascular smooth muscle relaxation

Inotropic agents help with...

low output symptoms but not congestive symptoms

ACE inhibitors reduce

both preload and afterload * Preload via volume reduction* * Afterload via BP reduction*

Drennan 1 Flashcards

(57 cards)