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NU 600
Exam 4 - Vasodilators and Antidysrhythmics
| Question | Answer |
|---|---|
| What are the 4 uses of peripheral vasodilators? | Tx HTN, hypotensive technique, increase stroke volume, reduce preload |
| Nitro- based vasodilators produce their effects by producing what substance? | nitric oxide |
| What does nitric oxide stimulate? | guanylate cyclase |
| What does guanylate cyclase increase? | Intracellular concentrations of cGMP |
| What is the effect of cGMP? | Vascular relaxation |
| What are 6 roles of NO? | 1)chemical messenger 2)vascular homeostasis 3)platelet regulation 4)CNS neurotransmitter 5)GI relaxation 6)immune response |
| Where does NO synthesis occur? | Endothelial cells |
| NO is produced in endothelial cells from _________ by the enzyme _________. | L-Arginine; NO synthase |
| In the presence of decreased tissue oxygenation, endothelial cells (increase/decrease) NO production. | increase |
| NO has (negative/positive) inotropic and chronotropic effects. | Negative |
| What does the inhibition of NO suggest? | CV system is continuously exposed to NO dependent vasodilator tone |
| Where in the lungs are the bronchodilatory effects of NO achieved? | Areas of pulmonary circulation which supply blood to ventilated areas |
| How does NO influence platelets? | Inhibits platelet actiivty, aggregation, and adhesions |
| How does NO inhibit adhesions? | Activates guanylate cyclase, which increases cGMP, and decreases intracellular calcium |
| Stimulation of the _______ receptor leads to the release of NO. | NMDA |
| What are two neurologic functions that NO is involved in? | Memory, antinociception |
| What effect does NO have in the GI tract? | Causes relaxation of the peripheral nerves in the GI tract |
| Essential hypertension is a reflection of decreased levels of ________. | NO |
| What amino acid decreases BP in patients with essential hypertension? | L-arginine |
| What class of anti-hypertensives stimulate the production of NO? | ACE inhibitors |
| What inactivates NO? | Hemoglobin in systemic circulation |
| NMDA is an (inhibitory/excitatory) neurotransmitter. | excitatory |
| What effect do VAAs have on NO? | Suppress NO formation, resulting in decreased neurotransmission and increasing GABA |
| What class of medications can be used to decrease MAC requirements? | Nitric oxide synthase inhibitors |
| What nitric oxide synthase inhibitor can be purchased OTC? | L-arginine |
| The effects of NO are rapidly terminated by binding to what blood product? | Hgb |
| In what scenarios is NO given through vent delivery systems? | After bypass, newborn hypertension, prematurity w/respiratory distress |
| NO toxicity leads to what three conditions? | Methemoglobinemia, rebound pulmonary hypertension, NO2 toxicity |
| What is Silo Filler’s disease? | Occupational lung disease associated w/the inhalation of toxic gas (NO2) |
| How does Silo Filler’s Disease present? | ARDS, pulmonary edema, |
| What are the 3 clinical uses for peripheral vasodilators? | 1)Tx of HTN 2)controlled HTN 3)Increase LV SV w/regurgitation |
| What are 3 clinical uses for nitro-based vasodilators? | 1)Tx symptomatic LV dysfxn 2)decrease preload 3)decrease effects of peripheral vasoconstrictors |
| What are three meds that produce direct vasodilation? | Sodium nitroprusside, nitroglycerin, hydralazine |
| Identify which Rx produces vasodilation of arteries, veins, or both: Nipride, nitroglycerin, hydralazine. | Nipride=both, nitroglycerin=veins, hydralazine=arteries |
| What is the primary mechanism of action of nipride, nitroglycerin, and hydralazine? | Production of nitric oxide |
| What is the composition of nipride? | Ferrous ion center w/5 cyanide and 1 nitrosyl sodium group |
| What blood product does SNP interact with? | Oxyhemoglobin |
| What occurs when SNP interacts w/oxyhemoglobin? | Dissociates to form methemoglobin along with releasing cyanide and NO. |
| What enzyme does NO inhibit and what does this result in? | Inhibits adenylate cyclase and increases cGMP (vasodilation) |
| What enzyme does NO activate? | Guanylate cyclase |
| What is the mechanism of action of cGMP? | Inhibits calcium entry into vascular smooth muscle cells and increases calcium uptake into the endoplasmic reticulum (vasodilation) |
| What initially occurs in the metabolism of SNP? | An electron is transferred from the iron of oxyhemoglobin to yield methemoglobin and an unstable SNP radical |
| What occurs with breakdown of the unstable SNP radical? | All 5 cyanide ions are released |
| What happens to the 5 cyanide ions that are released w/SNP metabolism? | 1 ion reacts with methemoglobin to form cyanomethemoglobin; the remaining 4 ions are catalyzed by rhodanese to form thiocyanate |
| Cyanomethemoglobin is (toxic/non-toxic). | Non-toxic |
| What type of toxicity results from the use of SNP? | Cyanide toxicity |
| Increased concentrations of what product is found with high rates of SNP infusions? | Thiocyanate |
| Cyanide toxicity with SNP occurs with rates greater than ____________. | 2mcg/kg/min |
| Increase tissue cyanide produces what effects? | Anoxia, anaerobic metabolism, lactic acidosis |
| When should cyanide toxicity be suspected? | When hypotension exists despite treatment |
| What are 4 medications utilized in the treatment of cyanide toxicity? | Sodium bicarbonate, sodium thiosulfate, sodium nitrate, hydroxocobalamin (Vit B12a) |
| Besides administering medications, what are two immediate actions to take with cyanide toxicity? | D/c gtt and give 100% O2 |
| Why is sodium bicarbonate given in cyanide toxicity? | Tx the metabolic acidosis |
| How does sodium thiosulfate work to treat cyanide toxicity? | Converts cyanide to thiocyanate |
| What is the dose of sodium thiosulfate for cyanide toxicity? | 150mg/kg over 15min |
| Thiocyanate is (more/less) potent than cyanide in its harmful effects. | More |
| How does sodium nitrate work to treat cyanide toxicity? | Converts hemoglobin to methemoglobin, and methemoglobin acts as an antidote to convert cyanide to cyanomethemoglobin |
| What is the dose of sodium nitrate in the treatment of cyanide toxicity? | 5mg/kg |
| How does hydroxocobalamin work to treat cyanide toxicity? | Binds cyanide to form cyanocobalamin (Vit B12) |
| What is the dose of hydroxocobalamin for cyanide toxicity? | 25mg/hr up to 100mg |
| What is the infusion rate of SNP? | 0.3-20mcg/kg/min |
| What is the maximum amount of time you can infuse SNP at a max rate of 20mcg/kg/min. | 10min |
| _______ accounts for a decrease in SVR, while _______ accounts for a decrease in venous return. | Arterial vasodilation; venodilation |
| What receptors respond to venous pooling and decreased R atrial pressure as seen w/Nipride? | Baroreceptor reflexes respond and cause tachycardia |
| The administration of Nipride results in a net (increase/decrease) in CO. | Increase |
| Why is there an increase in CO w/Nipride? | Increase in peripheral SNS tone combined w/decreased ventricular resistance |
| What negative effect can SNP have on the heart in regards to blood flow. | May cause intracoronary steal, diverting blood away from ischemic areas to areas that are perfused |
| SNP (increases/decreases) CBF and blood volume. | Increases |
Created by:
philip.truong
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