Heart Disease and Blood Pressure Flashcards

Question

Atenolol

Answer 1

Beta 1 selective antagonist Decreases heart rate and contractility Reduces renin release and peripheral vascular resistance Used more in cats with SHT and hypethyroidism Used in dogs as adjunct for refractory SHT with reflex tachycardia

Answer 2

Non-selective beta antagonist Decreases heart rate and contractility Reduces renin release and peripheral vascular resistance

Answer 3

Excessive bradycardia

Answer 4

Injectable mix of alpha and beta antagonists. Used to manage severe acute hypertension promotes vasodilation and prevents associated tachycardia The use has been explored in dogs undergoing craniotomy or adrenalectomy

Answer 5

Promotes vasodilation by altering smooth muscle intracellular metabolism. works primarily on arteries Causes vasodilation, afterload reduction and lowering of blood pressure The mechanism is not entirely understood but the end result is smooth muscle relaxation and decrease in peripheral vascular resistance. It is not used as a first-line drug but used as an adjunct in chronic management. Injectable form used in urgent/emergent treatment due to its potent vasodilatory effects, and rapid onset.

Answer 6

Arteriolar vasodilator excessive or irreversible hypotension reflex tachycardia sodium and water retention GI upset

Answer 7

Arteriolar vasodilator promotes potent vasodilation through release of nitric oxide. Nitric oxide diffuses to vascular smooth muscle decrease influx of calcium, activation of actin/myosin chains and overall contractile forces Effects: smooth muscle relaxation and decreased vascular tone and peripheral vascular resistance The injectable form has a short half-life and is easy to titrate, so it is ideally used for hypertensive crises. Administer as CRI. Used to treat acute hypertensive crises or fulminant CHF Contraindicated in hypotensive patients

Answer 8

promotes potent vasodilation through release of nitric oxide. Nitric oxide diffuses to vascular smooth muscle decrease influx of calcium, activation of actin/myosin chains and overall contractile forces Effects: smooth muscle relaxation and decreased vascular tone and peripheral vascular resistance The injectable form has a short half-life and is easy to titrate, so it is ideally used for hypertensive crises. No risk of cyanide poisoning

Answer 9

generation of cyanide and thiocyanate at high doses and prolonged use. Patients with kidney and liver disease have decreased metabolism, therefore greater risk of cyanide toxicity. Clinical signs of toxicosis: metabolic acidosis, depression, stupor, seizures

Answer 10

Selective agonist of dopamine 1 receptor. Promotes peripheral and renal vasodilation and natriuresis Increases glomerular filtration rate Injectable has a short half life. Good potential for application in hypertensive crisis, but needs further investigation in vet med.

Answer 11

Sodium channel blockers Interferes intracellularly with sodium conduction through sodium channels Subclassification determined by potency of effects on sodium channel, activated/inactivated blockade and effects on other channel receptors.

Answer 12

Quinidine and procainamide Effective against ventricular and supraventricular arrhythmias. fast sodium channel blocking effects and moderate blockade of rapid component of the delayed rectifier potassium current resulting in action potential elongation.

Answer 13

Class 1 A antiarrhythmic Sodium channel blocker Depresses conduction velocity and prolongs refractory period in a variety of tissues, including atrial and ventricular myocardium Administer slowly IV over 5-10 minutes to prevent hypotension Adverse effects more commonly associated with cats and humans; include anorexia, nausea, and vomiting

Answer 14

Inhibits fast sodium channels, primarily in the open and inactivated state, with rapid onset. Sodium current is also inhibited, resulting in the shortening of action potential in normal myocardial tissue Lidocaine and mexiletine

Answer 15

Class IB antiarrhythmic Sodium channel blocker. The ability of lidocaine to block sodium currents is better during acidosis. Benefit: minimal hemodynamic, SA, AVN affect at standard doses Hepatic clearance determines serum concentration Heart failure, hypotension, and severe hepatic disease can decrease lidocaine metabolism and predispose patients to lidocaine toxicity. Adverse effects: higher incidence in cats Nausea, vomiting, lethargy, tremors, seizure activity (usually symptoms stop when lidocaine is discontinued) Dosing: Bolus 2mg/kg over 20-30 seconds; bolus can be repeated up to 8mg/kg within 10 minute period barring adverse effects CRI: 25-75mcg/kg/min

Answer 16

Class 1B antiarrhythmic most common oral class in dogs Highly protein-bound and excreted by the kidneys Use and adverse effects similar to Lidocaine (rarely used in cats because of adverse effects)

Answer 17

Class 1B antiarrhythmic Similar to lidocaine, rarely used in small animals because of high incidence of serious adverse effects including renal failure and corneal dystrophy

Answer 18

Potent blockade of the open state fast sodium channel with greater effects as the depolarization rate increases These agents prolong the refractory period in atrial and ventricular tissues Propafenone and Flecainide

Answer 19

Class 1C antiarrhythmic used to treat narrow complex tachyarrhythmias usually combined with diltiazem also has mild beta blocking properties

Answer 20

Class 1C antiarrhythmic potent negative inotropic properties Side effects include GI, but not commonly seen Rarely used in veterinary medicine Monitor heart rate, blood pressure and ECG when administering

Answer 21

Beta-adrenergic antagonists or beta-blockers are the most used cardiovascular drugs. Must be cognizant of animals' underlying disease when prescribing. Beta-blockers contraindicated in patients with evidence of sinus nodal dysfunction, AVN conduction disturbances, pulmonary disease or CHF (must be evaluated for fluid retention and condition must be stabilized before implementing beta-blockade). Reduces heart rate and myocardial oxygen demand and increases atrioventricular conduction time. Inhibits pacemaker current I(f) that promotes proarrhythmic depolarization in damaged cardiomyocytes Inhibits calcium current by decreasing tissue cyclic adenosine monophosphate levels ; the magnitude of effects depends on the sympathetic state. Greater effect with higher adrenergic states Beta-adrenergic antagonists slow AVN conduction in SVT by slowing sinus discharge rate in inappropriate sinus tachycardia and suppresses ventricular tachycardia that may be exacerbated by increased sympathetic tone. Used to treat supraventricular and ventricular arrhythmias. Also used in HCM to control heart rate and decrease myocardial oxygen demand Can cause hypotension due to decreased heart output. Extremely low dosages must be used with patients with systolic myocardial dysfunction. Because of that, beta blockers are not generally first choice for acute anti-arrhythmic therapy because the amount required is not well tolerated.

Answer 22

Non-selective beta receptor antagonist (targets both beta-1 and 2 receptors). Function: decrease heart rate and contractility. Decrease renin release and peripheral vascular resistance

Answer 23

Class II Antiarrhythmic Short-acting Beta-1 blocker that can help control sympathetically driving ventricular tachycardia . Administered as a CRI on telemetry. Side effects: Negative inotropic effects may be too pronounced in some patients and cause cardiovascular collapse. Requires blood pressure monitoring.

Answer 24

Class II antiarrhythmic. The most common oral beta blocker in small animals. Relative beta 1 selectivity and long half-life compared to propranolol. Water soluble and eliminated by the kidney.

Answer 25

Class II antiarrhythmic. Common oral beta blocker in small animals. Long half-life compared to propranolol. Metabolized and eliminated through the liver.

Answer 26

Block the repolarization of I(k) resulting in prolongation of action potential durations and effective refractory period. Blocks rapid component of I(k) instead of the slow component -- therefore effects are accentuated at slower heart rates rather than at the problematic tachyarrhythmic rates. Puts patients at risk of early afterdepolarization (accounts of proarrhythmic effects of class III AA drugs) - risk is increased in patients with hypokalemia, bradycardia, intact females, increasing age, macrolide antibiotic therapy/other drug therapies

Answer 27

Class III Antiarrhythmic Alpha and Beta blocking properties. Effects on sodium, potassium, and calcium channels. Broadest spectrum exhibiting properties of all 4 AA classes. Makes action potential durations more uniform throughout the myocardium and has the least reported proarrhythmic activity of any of the class III agents. Used for refractory tachyarrhythmias, both atrial and ventricular Significant side effects in dogs, including hepatopathy and anaphylaxis. Monitor heart rate, blood pressure and ECG with administer. Available as oral or injectable. Major drawback: associated with a host of multi-systemic adverse side effects that do not occur with sotalol. Adverse side effects (more common with higher maintenance doses): vomiting, anorexia, hepatopathies, thrombocytopenia Two brands: Cardarone IV, Nextarone

Answer 28

IV formulation of amiodarone Serious side effects attributed to vasoactive solvents in the formulation. Side effects include life-threatening hypotension, anaphylaxis, bradycardia, acute hepatic necrosis, and death.

Answer 29

Premixed aqueous solution of IV amiodarone. No adverse hemodynamic effects of other adverse cllinical effects in healthy research dogs.

Answer 30

Calcium channel antagonist Slow AVN conduction and prolong the effective refractory period of nodal tissue Effects are more notable at faster stimulation rates and in depolarized fibers. Effective in slowing the ventricular response rate to atrial tachyarrhythmias and can prolong AVN's effective refractory period to terminate AVN-dependent tachyarrhythmia. It is mainly indicated to reduce the rate of arrhythmias passing through the AV node, such as supraventricular arrhythmias. Major negative inotropic effects due to interactions with calcium in the smooth muscles. Causes vasodilation Limit amount of calcium available in cardiac contractility. Diltiazem is the most widely used IV antiarrhythmic drug

Answer 31

Class IV antiarrhythmic Calcium channel blocker. Minimal negative inotropic effects. Used in dogs to immediately terminate a severe AVN-dependent tachyarrhythmia or slow ventricular response rate to an atrial tachyarrhythmia. Adverse side effects: hypotension and bradyarrhythmia. Administer IV slowly over 2-3 minutes. Oral diltiazem administered TID.

Answer 32

Class V anti-arrhythmic (other) Effects occur indirectly through the autonomic nervous system by enhancing central and peripheral vagal tone. Used as an antiarrhythmic due to its ability to slow AV conduction time and have parasympathomimetic effects Treats SVT to slow AV nodal conduction and reduce ventricular rate Positive inotrope that will increase cardiac contractility in systolic disease The risk of toxicity manifests as neurological, GI, and cardiac involvement. Predisposed to toxicity if the patient has renal dysfunction, hypokalemia, elderly, chronic lung disease, hypothyroidism.

Answer 33

1st line treatment for torsades de pointes Used to treat hypomagnesemia Administer slowly IV @ 30mg/kg over 5-10 minutes Adverse effects: CNS depress, weakness, bradycardia, hypotension, hypocalcemia and QT prolongation

Answer 34

Used in humans to terminate AVN dependent tachyarrhythmias. No study to date has shown effectiveness in dogs and cats.

Answer 35

Transvenous radiofrequency catheter ablation Permanent pacemaker implantation Implantable cardioverter defibrillators

Answer 36

Identify reentrant circuit or automatic focus for ablation Deliver radiofrequency energy via electrode causing thermal desiccation of small volume tissue to interrupt tachycardia circuit

Answer 37

Manage bradyarrhythmias

Answer 38

experimental in dogs

Answer 39

class of drugs taht block the action of acetylcholine (ACh), a neurotransmitter that sends signals between cells that affect a bodily function. By blocking ACh at synapses in the central and peripheral nervous system, anticholinergics inhibit the parasympathetic nervous system.

Answer 40

Anticholinergic inhibit acetylcholine at muscarinic receptors Clinical effects include increasing heart rate, resolving vagally mediated bradycardia, decreasing GI motility, pupillary dilation, bronchodilation, urinary retention and drying or secretion Most commonly used to treat vagal-mediated bradycardias and toxicities Able to pass the placental barrier.

Answer 41

Anticholinergic inhibit acetylcholine at muscarinic receptors Clinical effects include increasing heart rate, resolving vagally mediated bradycardia, decreasing GI motility, pupillary dilation, bronchodilation, urinary retention and drying or secretion Most commonly used to treat vagal-mediated bradycardias and toxicities Glycopyrrolate is associated with more stable cardiovascular system with fewer arrhythmias Glycopyrrolate has a stronger anti-saliva secretion effect than atropine It does not pass the placental barrier and, therefore, is the agent of choice for pregnant animals.

Answer 42

Loop diuretics Osmotic Diuretics Potassium sparing diuretics Thiazide diuretics Carbonic anhydrase inhibitors Aldosterone Antagonist Aquaretics (new)

Answer 43

Enhanced excretion of retained water, solutes and toxins Promote urine flow decrease urine concentration of solutes and toxins

Answer 44

Oligoanuric acute renal failure decompensated kidney disease Congestive heart failure ascites from liver failure other fluid and electrolyte disorders

Answer 45

Only when fluid retention is caused by an increase in hydrostatic pressure. When vascular permeability is increased, further depletion of vascular volume with diuretics is rarely indicated and often detrimental

Answer 46

May activate RAAS by reducing intravascular volume and ventricular filling and may subsequently decrease tissue perfusion. Therefore, diuresis requires therapeutic monitoring

Answer 47

pressure natriuresis osmotic diuresis

Answer 48

A negative feedback in hypervolemic hypertensive states

Answer 49

Diuretics at the loop of Henle are the most effective because of the large amount of filtrate delivered to this site and the lack of efficient distal reabsorption region.

Answer 50

Elevated plasma osmolality hypovolemia hypotension (lesser extent) nausea increased concentration of angiotensin II

Answer 51

passive mechanism due to abnormal urine concentration of osmotically active solutes such as glucose and sodium

Answer 52

functional renal tubular system medullary concentration gradient of sodium and urea functional ADH receptor system without any one of these factors will result in inappropriate diuresis

Answer 53

Diuretics that work on proximal tubule can modulate a greater bulk of sodium, but their efficacy may be overcome by distal compensatory increases in sodium reabsorption.

Answer 54

Diuretics operating on distal tubule may be limited by small amount of sodium reaching distal tubule

Answer 55

hyperosmolality causes water shift from the intracellular fluid compartment to extracellular space, causing ECF expansion Used to contract ICF in cases with cerebral edema associated with an increase in ICF and elevated intracranial pressure Contraindicated for patients in or at risk of heart failure. Effective in patients with anuric or oliguric rental disease, cerebral edema and increased intraocular pressure eg. Mannitol

Answer 56

osmotically active non reabsorbed sugar alcohol filtered by the glomerulus; does not undergo tubular reabsorption, thereby increasing tubular flow rate and osmotic diuresis An increase in tubular flow rate reduces urea absorption, resulting in increased urinary clearance and serum urea concentration. Potential benefits of mannitol: Prostaglandin-induced renal vasodilation reduced tendency of erythrocytes to aggregate reduced renal vascular congestion reduced hypoxic cellular edema protection of mitochondrial function reduced oxidative damage renoprotectant when administered before toxic or ischemic event *No data supports above benefits in renal failure cases At high doses, mannitol can cause renal vasoconstriction and tubular vacuolization Use cautiously with oliguric animals to avoid volume overload, hyperosmolality and further renal damage.

Answer 57

Clinical application of carbonic anhydrase inhibitors - mainly used to treat elevated intraocular pressure in glaucoma. Work by suppressing the activity of carbonic anhydrase, an enzyme in red blood cells that converts carbon dioxide into carbonic acid and bicarbonate ions. CAIs can reduce secretion of H+ ions by the kidney tubule and can also impair the reabsorption of sodium, chloride and bicarbonate. eg. Acetazolamide Carbonic anhydrase also located on other organs. Blockade of ocular and brain CA decreases the production of aqueous humor and CSF. Blockade of red blood cell CA hampers carbon dioxide transport Gastric CA - minimally affected by inhibitors.

Answer 58

Carbonic anhydrase inhibitor Function: diuretic Inhibits mostly the type II (cytoplasmic) and IV(membrane) proximal tubular carbonic anhydrases, decreasing the reabsorption of sodium bicarbonate. Results in metabolic acidosis and natriuresis - minimal and self-limiting because progressively less bicarbonate is filtered as the proximal tubule becomes less responsive to carbonic anhydrase inhibition and the distal sodium reabsorption increases to compensate for the proximal losses.

Answer 59

Binds to and inhibits Na+-K+-2Cl- cotransporters on the apical membrane of epithelial cells of the thick ascending loop of Henle. Inhibition of reabsorption of both Na and Cl, ions remain in the tubular lumen and water follows, resulting in diuresis and increased Na secretion ○ High sodium concentration later in the nephron results in increased sodium and potassium exchange, which leads to increased potassium secretion as well ○ Increased calcium secretion also occurs ○ Also believed to decrease renal vascular resistance and increase renal blood flow Prototypical loop diuretic: furosemide Torsemide

Answer 60

Loop diuretic Improves renal parenchymal oxygenation by decreasing the energy expenditure of the secondary active Na-K-2Cl transporter Mannitol + furosemide > synergistic in inducing diuresis in dogs with acute renal failure Relative short half-life: 1-1.5 hours in dogs > can result in intermittent rebound sodium retention with loss of efficacy. most commonly used in patients in heart failure.

Answer 61

potent loop diuretic of pyridine-sulfonylurea class longer half-life (8 hours) higher bioavailability (80%-100%) strong diuretic effect than furosemide Large scale study - effective in dogs with mitral valve disease, but high rate of renal adverse events. Additional benefits observed in other species: vasodilation, improved cardiac function, reduction of myocardial remodeling, mineralocorticoid-receptor blockade with anti-aldosterone effect - has not been shown in small animals

Answer 62

exert their action by inhibiting the NaCl cotransporter on distal tubule. Mainly used for anticalciuretic properties to prevent calcium-containing uroliths Managing CHF in conjunction with other diuretics treating ascites associated with right-sided heart failure also used for treating polyuria of diabetes insipidus by inducing a mild hypovolemia and increasing proximal sodium conservation. eg. Hydrochlorothiazide

Answer 63

Antagonize aldosterone by binding to its receptor in the late distal tubule and the collecting duct increases sodium, calcium and water excretion and decreases potassium loss e.g. Spironolactone and eplerenone

Answer 64

concurrent hypernatremia, severe hypokalemia

Answer 65

Aldosterone antagonist potassium sparing diuretic Best used in cases of hyperaldosteronism Main clinical applications in liver and heart failure. Also used as an antihypertensive in hyperaldosteron cases. Usually, it is in combination with a more efficient loop diuretic. Also seems to have a positive effect on myocardial remodeling and the reduction of cardiac fibrosis Commonly added to other diuretics to reduce their potassium-wasting effects Main adverse effect: development of hyperkalemia

Answer 66

Inhibit sodium reabsorption in the distal tubule and the collecting duct; suppressing the driving force for potassium secretion. Only weak diuretic and natriuretic properties Mostly used to counterbalance potassium-wasting effects of proximal diuretics. e.g. Amiloride and triamterene

Answer 67

New class of diuretics that antagonize the vasopressin V2 receptor in the kidney and promote solute-free water clearance Vaptans - vasopressin receptor antagonist Clinical use: free water rention in hypervolemic hyponatremia or normovolemic hyponatremic drugs: conivaptan, tolvaptan and mozavaptan Not used in small animals

Answer 68

Function: positive inotropic and vasodilatory effects Phosphodiesterase III inhibitor Calcium sensitization Used to treat congestive heart failure

Answer 69

increase contractility via increasing binding affinity to the regulatory site on troponin C for calcium sensitizes the myocyte contractile apparatus to calcium without increasing the amount of calcium within the cell. Pimobendan is not dependent on catecholamines

Answer 70

increase contractility by increasing intracellular calcium levels. PDE III inhibition increases cyclic adenosine monophosphate (cAMP), which in turn increases cAMP-dependent protein kinase. Increase in calcium sequestration during diastole and increase in calcium influx during systole - both contribute to positive inotropy PDE III and PDE V are found in vascular smooth muscle. Inhibition of PDE III and PDE V increases intracellular cAMP and cGMP - which facilitates calcium update through intracellular storage sites. Results in reduction of available calcium for contraction > greater vascular smooth muscle relaxation.

Answer 71

undergoes hepatic demethylation

Answer 72

Pimobendan is highly protein bound with greater than 90% bioavailability. Maximal cardiac effects at 2-4 hours following oral administration and persists up to 8 hours.

Answer 73

FDA approved to treat CHF with myxomatous mitral valve degeneration or DCM

Answer 74

generally well tolerated but may cause GI upset - inappetence, vomiting, diarrhea and lethargy

Answer 75

Angiotensin-converting enzyme inhibitor Angiotensin receptor blocker aldosterone antagonist calcium channel blocker alpha 1 antagonist beta antagonist arteriolar vasodilator

Answer 76

Family of drugs designed to disrupt the renin-angiotensin-aldosterone system (RAAS). Medications function by inhibiting the conversion of angiotensin I to angiotensin II. ACE inhibitors can decrease proteinuria promote vasodilation, venodilation and reduction in plasma volume with reduction in systolic blood pressure ACE inhibitors can cause decreased metabolism of vasodilatory agent bradykinin --> further reduction in vascular tone Clinical application of ACE inhibitors where systemic hypertension is caused by known or suspected increase in RAAS - most commonly related to chronic kidney disease and or glomerular disease. Most commonly considered 1st line treatment for dogs (not cats). Generally well tolerated. Biggest concern: potential to worsen glomerular filtration rate and renal function through preferential dilation of the efferent arteriole (thereby reducing glomerular filtration pressure) e.g. Enalapril, benazepril, lisinopril

Answer 77

Angiotensin Converting Enzyme Inhibitor

Answer 78

Angiotensin Converting Enzyme Inhibitor

Answer 79

Angiotensin Converting Enzyme Inhibitor

Answer 80

Class of drugs that block angiotensin II from its receptor. **Does not affect the metabolism of bradykinin** ARBs can decrease proteinuria promote vasodilation, vasodilation and reduction in plasma volume with a reduction in systolic blood pressure Side effects: similar side effects as ACEi; avoided or cautiously used in patients with severe dehydration or azotemia. e.g. Telmisartan, losartan

Answer 81

Angiotensin receptor blocker

Answer 82

decrease calcium influx into cardiac tissues (antiarrhythmic properties) and vascular smooth muscles (antihypertensive properties) May cause reflex bradycardia Other side effects could include weakness, lethargy, decreased appetite CCBs promote preferential afferent arteriolar dilation over the efferent arteriole, which increases intraglomerular pressure, which could damage the glomerulus and worsen proteinuria.

Answer 83

Belongs to the dihydropyridines family Calcium channel blocker Relative selectivity for vascular smooth muscles so promotes vasorelaxation and reduces systemic vascular resistance An associated decrease in blood pressure may trigger reflex tachycardia. First-line antihypertensive of choice for managing SHT in cats

Answer 84

Alpha 1 adrenergic antagonist used in hypertensive crisis, specifically as rescue therapy during pheochromocytoma surgery

Answer 85

Alpha 1 adrenergic antagonist commonly used to stabilize patients with pheochromocytoma prior to surgical intervention

Answer 86

Any drug specifically used to cause constriction to blood vessels increase cardiac afterload, produce vasoconstriction, increase vasomotor tone and systemic vascular resistance most common pathway is alpha 1 adrenergic agonism

Answer 87

Any drug specifically used to increase cardiac contractility most common pathway to achieve this is beta 1 adrenergic agonistm

Answer 88

decrease cardiac contractility

Answer 89

Catecholamine and sympathomimetic Primary receptors: dopaminergic, beta-1 and alpha 1 adrenergic agonist different doses = different effects Low range - stimulate urine production in oliguiric or anuric AKI Intermediate range: predominantly positive inotropic effects High doses: vasoconstriction/increase in vascular resistance Effects: increases renal blood flow improves inotropy increases heart rate increases systemic vascular resistance increases blood pressure increases cardiac out put Deliver as a CRI Side effect: arrhythmias, tachycardia, hypertension Continuous ECG, BP monitoring recommended

Answer 90

Sympathomimetic receptors: Beta-1 and Adrenergic-2 agonist Effects: improves inotropy +/- increase in heart rate Increase in cardiac output +/- increase in blood pressure decrease systemic vascular resistance Deliver as a CRI Side effects: arrhythmias, tachycardia, hypertension, bradycardia Monitoring: ECG/BP continuous

Answer 91

catecholamine and sympathomimetic Receptors: Alpha-1 and beta 1 adrenergic agonist Effects: increase in inotropy decrease in heart rate increase in systemic vascular resistance increase in blood pressure Deliver as a CRI Side effects: arrhythmias, hypertension, bradycardia, excessive vasoconstriction

Answer 92

Catecholamine Receptors: alpha 1 and beta 1 adrenergic agonist Lower doses have predominantly beta agonist effect: vasodilation, bronchodilation, increased cardiac contractility and cardiac output, increased heart rate higher doses: more alpha 1 adrenergic effects: vasoconstriction Used to treat anaphylaxis Side effects: arrhythmia Monitoring: continuous ECG/BP Deliver as IV bolus, CRI, IM or intratracheally

Answer 93

sympathomimetic receptor: alpha-1 adrenergic agonist Effects: decrease in heart rate increase in systemic vascular resistance (marked vasoconstriction) increase in blood pressure May improve blood pressure, but the increase in cardiac afterload may decrease stroke volume and cardiac output Deliver as a bolus or CRI Side effects: arrhythmia, hypertension, bradycardia, excessive vasoconstriction

Answer 94

Sympathomimetic receptors: beta-1 agonist, and alpha 1 adrenergic agonist effects: increase inotropy increase in blood pressure increase in cardiac output +/- Heart rate increase in systemic vascular resistance deliver as a bolus (short duration of effect) or CRI Side Effects: arrhythmias, tachyphylaxis (reduced sensitivity after repeated administration), hypertension, bradycardia, tachycardia

Answer 95

Non-adrenergic hormone AKA anti-diuretic hormone receptors: V1 vasopressin Agonist effects: increase systemic vascular resistance increase blood pressure Increase in cardiac afterload may decrease stroke volume and cardiac output, resulting in decrease oxygen delivery to tissue Alternative or conjunctive therapy to epinephrine in CPCR More effective than epinephrine when patient in acidosis. deliver as a bolus or CRI Side effects: arrhythmias, hypertension, bradycardia, excessive vasoconstriction

Answer 96

- increases in plasma osmolality - central chemoreceptors detect systemic osmolality. Peripheral chemoreceptors in mesenteric and portal veins detect changes in osmolality of ingesta. Afferent impulses ascend via vagus nerve to stimulate vasopressin release. Plasma tonicity sened by hypothalamus to stimulate more vasopressin release. - decreases in blood pressure - shifts osmolality. Baroreceptors in left atrium, aortic arch and carotid sinus sense drops in blood pressure and circulating blood volume. Allows for release of disinhibition of vasopressin release. - drop in circulating blood volume

Answer 97

glucocorticoids low dose opioids atrial natriuretic factor GABA neurotransmitter

Answer 98

found primarily on smooth muscle cells Activation of voltage gated calcium channels, increases intracellular calcium levels allowing for vasoconstriction. V1-R in platelets - facilitates thrombosis because of intracellular calcium V1-R in kidneys decrease blood flow to inner medulla and limit anti-diuretic effects; selective cause contraction of efferent arterials to increase GFR There are species variations in V1R locations.

Answer 99

Found primarily on basolateral membrane of distal tubule and principle cells of cortical and medullary rental collecting duct triggers fusion of aquaporins with plasma membrane of collecting duct --> increasing water absorption. stimulates release of platelets from bone marrow and enhances release of Von Willebrand's factor and Factor VIII from endothelial cells

Answer 100

regulating fast shuttling of aquaporin-2 to cell surface stimulates synthesis of RNA encoding aquaporin 2 hereditary nephrogenic diabetes insipidus have V2-R gene mutations

Answer 101

half life is 24 minutes cleared by renal excretion and metabolized by tissue peptidases

Answer 102

contraction of bladder and gallbladder smooth muscles increase peristalsis decrease in gastric secretions increase in GI sphincter pressure Local irritation at injection site. If extravasated, may cause skin necrosis May increase liver enzymes and bilirubin levels decrease platelet count hyponatremia anaphylaxis/urticaria bronchospams abdominal pain hematuria water intoxication reported with high dose treatment of diabetes

Answer 103

selective for V1R prolong duration - 6 hours half life Used to manage hemorrhagic gastroenteritis increase adverse effects - peripheral cyanosis/ischemia (use with caution)

Answer 104

V1R agonist found to reduce risk of coronary ischemia less adverse effects on mesenteric blood flow and gastric mucosal perfusion effective substitute for maintaining MAP, reducing vascular leak, edema formation and shortening duration of shock. Comparative study with norepi -> no improved outcome

Answer 105

synthetic vasopressin intranasal and injectable form binds primarily to V2R more potent antidiuretic and procoagulant

Heart Disease and Blood Pressure Flashcards

(129 cards)