C19: Module 5 Flashcards
Definition:
a measure of the degree of the ventricular stretch when the heart is at the end of diastole (filling)
Preload
List of things that Increased Preload may lead to:
- CHF => Backward failure (congestion)
- Further RAAS activation (via increased SNS and atrial stretch) - further Na+ & H2O retention => increase venous pressure
- increase venous & capillary pressures => edema and cavity effusions
Clinical Problem: Increased Preload
How do diuretics reduce preload?
They reduce preload by increased formation of urine
- Increase renal elimination of Na+/Cl-/K+/Mg2+ & H2O -> contraction of plasma volume -> decrease venous & capillary hydrostatic pressures -> decrease formation of edema & effusions
- Important drug used & reliable!
- Main indication: CHF
- given orally => standard home therapy
- acute situations: Parenteral
- CRI
Clinical Problem: Increased Preload
Diuretics:
- Strong
- Block 2Cl-/Na+/K+ symporter
- Furosemide
- Torasemide (more agressive)
- Hypochloremia may occur but is NOT a problem
- Indicates if the drug is working
Loop Diuretics
Clinical Problem: Increased Preload
Diuretics:
- Block Na+Cl- co-transporter
- Hydrochlorothiazide (second choice) -> oral
- less potent, longer acting
- negative effect on kidneys
Thiazides
- Diuretic acting on the Distal Nephron
Clinical Problem: Increased Preload
Diuretics:
- Weak but spares potassium
- do not have to deal with hypokalemia
- Spironolactone = Antagonizes effects of aldosterone in the distal nephron
Aldosterone Receptor Blockers
What are the most effective of all diuretics?
Loop diuretics
(T/F) All but spironolactone reach the side of action intraluminally after drug excretion in the proximal convoluted tubule
True
Problem: Diuretic resistance
Due to excessive neurohormonal activation (renin),
decrease enteral drug reabsorption, comorbidities, or end-stage heart disease
What are some strategies?
- Increase dose
- Switch to Torasemide
- Add SC. injections
- Sequential nephron blockade => Combination of several diuretics with different anatomical locations of action
Definition: Nitrates
Potent mixed vasodilation via stimulation of guanylate cyclase + cGMP production
Nitric Oxide (NO)
- Most effect in Veins & Coronaries (less in systemic arteries)
- reduces preload (due to redistribution of volume from the chest into the splanchnic area), relieves vasoconstriction & decreases afterload due to vasodilation
- Fast tolerance -> therefore given for one day
- Used as an ointment in acute, severe CHF for ventilation & preload reduction
Clinical Problem: Increased Afterload
List the clinical context:
- Hypertrophic obstructive cardiomyopathy
- Aortic |pulmonary stenosis
- Systemic hypertension
- “Relative” hypertension (= high normal to normal systemic blood pressure in animals with advanced myocardial disease -> = “afterload mismatch” – BP too high for the failing heart)
- Pulmonary hypertension
Definition:
The amount of pressure that the heart needs to exert to eject blood during ventricular contraction
Afterload
In increased afterload “situations”, what are the drug classes used?
- Beta receptor blockers (-lols)
- Calcium channel blockers
- ACE inhibitors
- Specific pulmonary arterial vasodilators
- Nitrates
List beta-Blocker Effects:
- decrease SAN discharge
- decrease AVN conduction velocity
- decrease Contractility
- decrease Myocardial oxygen demand (anti-ischemic)
Anti-arrhythmic
(beta-blockers have the opposite effects of beta-agonists)
Excess beta-adrenergic Signals in CHF:
What does excess stimulation lead to?
-
Downregulation and Desensitization (uncoupling) of cardiac cardac beta-receptors
=>autoprotective process to avoid cell death - decrease contractility & decrease chronotropy
- Muscle weakness (Beta2) decrease Exercise tolerance
