Cardiovascular Flashcards
Lidocaine class and MOA
1b: Na channel blocker (inactive state - depolarized), shortens action potential
Procainamide class and MOA
1a: fast Na channel blocker, slows phase 0, prolongs action potential
Atenolol class and MOA
Class II: beta1 blocker
Propranolol class and MOA
Class II: beta 1 & 2 blocker
Esmolol class and MOA
Class II: beta 1 blocker
Sotalol class and MOA
Class III: potassium blocker
Also beta blocker
Amiodarone class and MOA
Class III: potassium blocker
Also I, II, and IV
What is the most common primary cardiac tumor in dogs?
hemangiosarcoma (69%)
Aortic body tumors are most common in which breeds?
Boxer, Bostons, English bulldogs, and also German shepherd dogs
Capillary endothelium can be damaged by (6)?
- Endotoxin
- cytokines (TNFa, IL-6)
- Arachidonic acid metabolites
- complement components (C3a, C5a)
- Vasoactive peptides (bradykinin, histamine)
- chemokines (macrophage inflammatory protein 1 alpha)
What is the Gibbs-Donnan effect?
Describes the behavior of charged particles in solution separated by semipermeable membrane, which does not allow some particles to pass. For example, albumin is not permeable and its negative charge will attract cations like sodium.
What contributes the most to COP? What else contributes?
Albumin 65-80% of COP. Also: globulins, fibrinogen, hemoglobin, RBCs
Describe the activation of RAAS in detail.
Decreased renal blood flow & decreased Na deliver to distal portion of nephron–> renin release from macula densa–> angiotensinogen to angiotensin I–> angiotensin II (via ACE) in pulmonary vasculature
Effects of angiotensin II via RAAS system?
Increased thirst, vasoconstriction, cardiac and vascular remodeling and fibrosis, renal sodium & water retention, myocardial apoptosis, production of aldosterone
Effects of chronic sympathetic nervous system activation?
Adrenergic Rc downregulation, persistent tachycardia, increased myocardial oxygen demand, myocyte necrosis
Two main hormones that induce natriuresis, diuresis, and vasodilation?
Atrial natriuretic peptide (ANP)
B-type natriuretic peptide (BNP)
Both are increased in in dogs and cats with heart disease, roughly in proportion to disease severity
What is the function of ANP & BNP ?
To serve as a counter-regulatory system to RAAS and SNS, but ANP & BNP are overwhelmed in later stages of heart disease
What is the function of endothelin I?
Potent vasoconstriction produced by vascular endothelial cells in response to sheer stress, angiotensin II, and other various cytokines; alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes
Describe normal calcium ion handling
During systole calcium ions enter the myocardial cell; this triggers release of additional calcium ions from the main storage area of calcium (sarcoplasmic reticulum). Calcium stored in the SR flows through the ryanodine channel and binds to troponin C. Binding to troponin C causes SR contraction, then release of calcium from troponin C initiates relaxation cycle. Ca++ ions are then moved back into the SR
What happens to cells that have abnormal intracellular Ca distribution?
Electrical abnormalities, apoptosis, necrosis
What does the Frank-Starling mechanism state?
That an increase in the initial volume or pressure within a ventricle increases the strength of subsequent ventricular contractions. Up to a physiologic limit, preload and contractility are positively associated
What happens to the Frank-Starling curve during increased adrenergic drive?
Up and leftward; causes further improvement in cardiac performance
What happens to the Frank-Starling curve during disease?
Shifted down and to the right; contraction is less vigorous despite increased preload and fluid retention
What happens to the Frank-Starling curve with administration of diuretics?
Shifted to the left