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Cardio vascular syst

Animal medicines WK16

QuestionAnswer
Cardiovascular Controls - Autonomic Nervous System - Hormones Kidneys and Fluid Balance Mechanisms
sympathetic nervous system (SNS) Initiated in “fight or flight” situations Norepinephrin (noradrenaline) released at neuromuscular junctions in heart, blood vessels and adrenal glands. Increases stroke volume
sympathetic nervous system (SNS) Causes peripheral vasoconstriction Stimulates adrenaline (epinephrin) release Increases HR and arteriole change (vasoconstriction of periphery and kidneys, dilation at lungs, muscles & heart)
Parasympathetic Nervous System (PSNS) “rest and digest” Acetylcholine released at heart slows heart rate
Autonomic Control of Blood Pressure signal sent to cardio and vasomotor centres in brain - efferent signals cause vasodilation or constriction, and change heart rate change in BP BP registered by baroreceptors
Blood pressure = Cardiac Output x Systemic Vascular Resistance
Cardiac output = Stroke Volume x Heart Rate
Hormones are used by the body to lower or raise blood pressure by: Vasoconstriction Vasodilation Altering blood volume
Adrenaline and Noradrenaline produced by adrenal medulla
Renin-angiotensin system Controlled/produced by the kidney
Aldosterone produced by adrenal cortex
Antidiuretic hormone (vasopressin) produced by the posterior pituitary
renin angiotensin aldosterone system (look at diagram)
fluid homeostasis in the kidney Aldosterone – acts on the DCT and collecting duct resulting in reasboprtion of water, this process involves the exchange of Na and K (leading to loss of K+ and retention of Na+)
ADH – acts on the collecting ducts to increase their permeability to H2O – increases water retention.
Cardiovascular Drugs - Modes of Action -increase the contractile strength - positive inotropes - alter the heart rate - chronotrope (pos + neg) - improve peripheral circulation, Vasodilation, correct fluid balance Protect against arrhythmias
contractile agents Glycosides Calcium Sensitisers Xanthine derivatives
glycosides increases calcium stored in intracellular vesicles in muscle fibres Increases calcium stored in intracellular vesicles in muscle fibres Does this indirectly by inhibiting myocardial Na-K ATPase enzyme
glycosides More calcium exposes more binding sites for myosin, producing more forceful contraction Easily absorbed Excreted by kidney Narrow safety margin between therapeutic and side effects E.g. digoxin No veterinary licence in UK
glycosides side effects - Vomiting - Anorexia - Life threatening arrhythmias Hypokalaemia increases the risk of arrhythmia Some diuretics cause K+ loss
Calcium sensitisers Enhance the effect of existing intracellular calcium on myosin binding sites Also: Vasodilatory action through calcium effects on vascular smooth muscle mild chronotropic effect
Calcium sensitiers side effects Very strong effect for severe heart failures in dogs Vomiting can be a rare side effect E.g. pimobendan
Xanthine Derivatives Related to caffeine Mild positive ionotropic effects Mild diuretic Releases adrenaline so also increases HR
Xanthine Derivatives mostly used bronchial smooth muscle relaxation or improved cerebral blood flow E.g. theophylline
Chronotropes Glycosides Beta blockers Calcium channel blockers Xanthine derivatives
Digoxin was first used medicinally to affect heart rate How does it work It has a negative chronotrope effect on the electrical conducting system of the heart via stimulation of the parasympathetic nervous system
Negative chronotrope = decreased heart rate
Beta Blockers Cardiac β adrenergic receptor antagonists Negative chronotrope Doesn’t slow a normal heart, but blocks SNS stimulation of rate Also has mild negative ionotrophic effects
Can interact with functions of other drugs Increase bradycardia from digoxin ↓HR - ↓BP - potentiates hypotension from anaesthetics, diuretics etc. Overdose can lead to BP collapse E.g. propranolol (no veterinary licence)
Calcium Channel Blockers Inhibit cellular Ca+ uptake Nerve cells in cardiac conducting system Vascular smooth muscle (vasodilation) Heart muscle cells Leads to reduced heart rate and reduced blood pressure. Two drugs licenced for vet use; amlodipine and diltiazem
Calcium Channel Blockers Side effects Vomiting in cats Bradycardia in dogs (not licensed in dogs) Overdose can cause hypotension
Xanthine Derivatives Related to caffeine These are positive chronotropes Effects heart rate not really used for this reason
Drugs affecting Peripheral Circulation ACE Inhibitors Diuretics Vasodilators
Pathophysiology of Congestive Heart Failure Poor cardiac output + poor oxygenation stimulate responses in the body that are designed to respond to blood loss Peripheral vasoconstriction Increased heart rate Fluid retention
Pathophysiology of Congestive Heart Failure responses compound the heart failure (diagram) Peripheral vasoconstriction, Increased pressure to pump against = poor contraction = poor cardiac output Increased heart rate, Increased oxygen consumption of heart muscle cells = poor contractions = poor cardiac output
Pathophysiology of Congestive Heart Failure responses compound the heart failure Fluid retention Increases lung fluid = poor oxygenation
ACE Inhibitors ACE inhibitors block the RAAS system, blocking vasoconstriction and fluid retention (DIAGRAM)
ACE Inhibitors Block the conversion of angiotensin I to angiotensin II Prevent vasoconstriction Reduce fluid retention via ADH and aldosterone
ACE Inhibitors side effects Vomiting Examples; enalapril, benazepril
Diuretics will hace action on the water balance systems within the kidney (DIAGRAM)
Diuretics Loop diruetics Inhibit sodium resorption in the ascending loop of Henle Decreases solute concentration in the medulla lower water
Diuretics Reduced volume in circulation = reduced hydrostatic pressure = reduced fluid in lungs Better oxygenation reduces respiratory distress and reduces heart rate
Diuretics Mechanism of sodium retention involves inhibition of the sodium/potassium/chloride transporter, so K+ is also lost in the urine  can cause hypokalaemia E.g. frusemide
Diuretics Potassium-sparing diuretics Interfere with aldosterone action in the DCT Aldosterone causes Na+ resorption Does not require K+ exchange
Diuretics Weaker than loop diuretics Most water resorption takes place before the DCT Often used in conjunction with loop diuretics E.g. spirinolactone
Vasodilators Eg. Nitro-glycerine Also key ingredient of dynamite Absorbed across the skin Vasodilation reduces pressure against which heart is attempting to pump
Vasodilators improves cardiac output and returns normal circulation to the lungs BUT reduces blood pressure Ideally used only for emergencies and when BP is high Other drugs eg. ACE inhibitors have more controlled, predictable vasodilatory effects.
Membrane stabilisers - Arrhythmia protectants Na+ channel blockers Eg. Lignocaine Also a local anaesthetic Slows passage of nerve impulses from atria to ventricles
Membrane stabilisers - Arrhythmia protectants β blockers Reduce sympathetic stimulation of membranes Reduce risk of ectopic foci These drugs are mostly used in emergency situations (eg. anaesthetic induced arrhythmias)
Created by: lucy.fox
 

 



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