Cardiovascular

Question 1

Parasympathetic response secretes what hormone (negative inotrope)

Answer 1

Acetylcholine ⇒ negative/↓ inotrope/contractility

Question 2

ACE Inhibitors (MOA, “–suffix,” Drug-Drug Interactions)

Answer 2

• MOA: blocks angiotensin I to angiotensin II that usually stimulates vasoconstriction + releases aldosterone that excretes potassium and retains sodium and water to increase body fluid and BP ⇒ so ACE stops angiotensin II and promotes vasodilation + doesn’t release aldosterone ⇒ doesn’t reabsorb sodium and water to decrease body fluid and BP
• “–pril”
• Don’t give to HYPERkalemic pts bc this leaves potassium in instead of it being normally excreted via aldosterone ⇒ potassium would stay in more ⇒ potentiates hyperkalemia
• Don’t give w/ loop diuretics bc this alrdy causes sodium and water excretion ⇒ so if used w/ loop diuretics the pt just loses more fluids ⇒ potentiates fluid loss ⇒ can lead to hypotension
• Don’t give w/ food and antacids ⇒ it reduces bioavailability so give only w/ water
• Don’t give w/ lithium bc it has a narrow therapeutic index ⇒ give them separately
• Don’t give w/ NSAIDs bc it decreases ACE inhibitor effects

Question 3

Angiotensin II Receptor Blockers (MOA, “–suffix,” Drug-Drug Interactions)

Answer 3

• MOA: blocks aldosterone release ⇒ no reabsorption of sodium and water ⇒ ↓ body fluid and BP
• ”–artan”
• Don’t give to HYPERkalemic pts bc this leaves potassium in instead of it being normally excreted via aldosterone ⇒ potassium would stay in more ⇒ potentiates hyperkalemia
• Don’t give w/ loop diuretics bc this alrdy causes sodium and water excretion ⇒ so if used w/ loop diuretics the pt just loses more fluids ⇒ potentiates fluid loss ⇒ can lead to hypotension
• Don’t give w/ food and antacids ⇒ it reduces bioavailability so give only w/ water
• Don’t give w/ lithium bc it has a narrow therapeutic index ⇒ give them separately
• Don’t give w/ NSAIDs bc it decreases ACE inhibitor effects

Question 4

Aldosterone Antagonist (MOA, “–suffix,” Drug-Drug Interactions)

Answer 4

• MOA: competes w/ aldosterone so it doesn’t let aldosterone do its job of sodium and water reabsorption ⇒ ↓ body fluid and BP
• ”–none/one” (ie. spironolactone)
• Don’t give to HYPERkalemic pts bc this leaves potassium in instead of it being normally excreted via aldosterone ⇒ potassium would stay in more ⇒ potentiates hyperkalemia
• Don’t give w/ loop diuretics bc this alrdy causes sodium and water excretion ⇒ so if used w/ loop diuretics the pt just loses more fluids ⇒ potentiates fluid loss ⇒ can lead to hypotension
• Don’t give w/ food and antacids ⇒ it reduces bioavailability so give only w/ water
• Don’t give w/ lithium bc it has a narrow therapeutic index ⇒ give them separately
• Don’t give w/ NSAIDs bc it decreases ACE inhibitor effects

Question 5

Angiotensin Receptor–Neprilysin Inhibitor

Answer 5

• Sacubitril: we have neprilysin enzyme naturally that eats natural peptide that causes diuresis ⇒ water retention BUT sacubitril blocks neprilysin from eating natural peptide ⇒ diuresis ⇒ fluid loss and gives heart congestion a break
• Valsartan: blocks angiotensin II receptors → blocks aldosterone to promote fluid loss + has vasodilatory effects
• Sacubitril + Valsartan: diuresis + blocks aldosterone + vasodilatory effect ⇒ ↓ body fluid and BP
• Drug-Drug Interactions: Hyperkalemia: bc it blocks aldosterone ⇒ aldosterone that usually stimulates K+/Potassium excretion is blocked

Question 6

Alpha-1 Blockers

Answer 6

• MOA: blocks alpha-1 receptors that causes vasoconstriction so this med causes vasodilation
• “–osin”

Question 7

Beta-Blockers

Answer 7

• Beta-1 Blocker: in heart blocks beta-1 receptor that ↑ HR (pos chronotropy) + ↑ inadequate cardiac contraction (neg inotropy) + ↑ renin release ⇒ ↑ BP ⇒ SO this med blocks that to result in ↓ HR (neg chronotropy) + ↓ adequate cardiac contraction (pos inotropy) + ↓ renin release ⇒ ↓ BP
• Beta-2 Blocker: in lungs blocks beta-2 receptor that causes bronchodilation and vasodilation ⇒ SO this med blocks that to result in bronchoconstriction and vasoconstriction
• Selective Beta Blockers: blocks either beta-1 or beta-2 receptors
• Nonselective Beta Blockers: blocks both beta-1 and beta-2 receptors
• “–lol” / “–ol”

Question 8

Calcium Channel Blockers

Answer 8

• MOA: blocks Ca+ production ⇒ ↑ adequate heart contractility (pos inotropy) + ↓ HR (neg chronotropy)
• Nondihydropyridines: cardiac tissue focused
  
  • Verapamil & Diltiazem
• Dihydropyridines: blood vessel/vasculature vasodilation focused
  
  • Nifedipine & Amlodipine

Question 9

Digoxin

Answer 9

• MOA: blocks re-entry of Ca+ into cell w/ sodium-potassium ATPase pump ⇒ slows HR ⇒ allows for better filling ⇒ adequate heart contractility (pos inotropy) + ↓ HR (neg chronotropy)
• Lanoxin
• Drug-Drug Interactions: If pt HYPOkalemic: potentiates digoxin toxicity bc it works by competing w/ digoxin for sodium-potassium pump ⇒ digoxin binds to pump more ⇒ potentiates digoxin toxicity

Question 10

Nursing considerations for anti-hypertensive medication administration (specifically, alpha-1 blockers)

Answer 10

• Hold when BP ≤90/60
• Can cause postural blood pressure/orthostatic hypotension ⇒ pts are fall risks + make sure that whenever they move they move slowly
• If pushing IV ⇒ push slowly, set it on pump course over hours
• Hypotension (1st dose) ⇒ pt are fall risks + make sure that whenever they move they move slowly
• Urinary Sxs

Question 11

Adverse effects of ACE-Inhibitors

Answer 11

• Cough bc med stimulates bradykinin accumulation ⇒ stimulates fluid build up in tissues ⇒ triggers coughing
• Angioedema bc bradykinin encouraging fluid build up in tissues can lead to edema
  
  • Can constrict airways so if pt shows airway obstruction signs ⇒ stop med + give epi
• Hyperkalemia bc it blocks aldosterone that usually excretes potassium ⇒ potassium stays
• Hypotension (1st dose)

Question 12

Nursing considerations for modifiable risk factors for hypertension

Answer 12

• Manage blood sugar
• Control cholesterol
  
  • Lipoproteins:
    
    • “L” for lousy LDLs: if you have constant vasoconstriction and ↑ LDL lvls ⇒ ↓ HDLs
    • “H” for healthy HDLs: ↓ LDL lvls
• Manage BP
• Healthy diet
• Physical activity
• Healthy sleep
• Smoking cessation
• Manage weight:
  
  • Pts w/ metabolic trifecta that puts them at risk for cerebrovascular or vascular disease…
    
    • Obesity
    • Dyslipidemia
    • HTN

Question 13

Clinical Manifestations of LEFT HF

Answer 13

• “L” for lung issues bc left side of heart pumps to lungs ⇒ if blood backs up and congests left side ⇒ signs of lung problems
• Pulmonary Edema
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Signs of hypoxia, cyanosis
• Cough w/ frothy sputum

Question 14

Clinical Manifestations of RIGHT HF

Answer 14

• “R” for rest of body issues bc right side of heart pumps to rest of body ⇒ if blood backs up and congests right side ⇒ problems in other body systems/organs
• Dependent Edema
• Liver & Spleen ⇒ hepatosplenomegaly
• JVD
• GI tract congestion

Question 15

Determinants of CO= HR x SV

Answer 15

• Blood Volume & Vascular Resistance
  
  • HTN ⇒ ↑ vascular resistance
  • Low CO ⇒ ↑ HR to compensate ⇒ can’t maintain it ⇒ lowers eventually
  • Blood volume can be replaced by giving fluids

Question 16

Clinical indications for MONA in treating MI; nursing considerations of nitroglycerin administration

Answer 16

• MONA goals: maintaining perfusion + alleviating heart workload
• Morphine: relieves chest pain
• Oxygen: improves oxygen RBC lvls
  
  • Esp for pts w/ low O2 lvls of <90% to increase O2 status and perfusion
• Nitroglycerin: for opening occluded artery via vasodilation ⇒ prevents vasospasms that may happen in arteries
  
  • Nursing Considerations:
    
    • If 1st dose doesn’t work → administer another of same dose 5 mins after
    • Only do so maximum 3X
• Aspirin: prevents platelet aggregation ⇒ doesn’t further cause clots to form

Question 17

Statins

Answer 17

• MOA: HMG-CoA reductase inhibitor ⇒ slows cholesterol production ⇒ ↓ LDLs/triglycerides + slightly increases HDL
• “–statin”

Question 18

Niacin/Nicotinic Acid

Answer 18

• MOA: ↓ release of LDLs/triglycerides + ↑ HDLs
• Vit B

Question 19

Bile Acid Sequestrants

Answer 19

• MOA: binds to cholesterol in bloodstream ⇒ pulls them into liver ⇒ ↓ LDLs
• “Cole–”

Question 20

Cholesterol Absorption Inhibitors

Answer 20

• MOA: blocks absorption of dietary type of cholesterol in small intestine ⇒ ↓ cholesterol blood lvls
• Combined w/ statin, esp for pts not following healthy diet
• Ezetimibe

Question 21

Fibrates

Answer 21

• MOA: ↑ lipoprotein lipolysis ⇒ ↓ triglycerides + ↑ HDLs
• “Fib”

Question 22

Definition + Pathophysiology characteristics of atherosclerosis

Answer 22

• Atherosclerosis: hardening and thickening of arteries
• Endothelial injury ⇒ inflammation of endothelium ⇒ macrophages goes to injury site ⇒ macrophages eat LDLs to form foam cells (lipid-laden cells that form fatty streaks and plaques) accumulation of foam cells ⇒ lipid core formed by foam cells and oxidized LDL becomes surrounded by smooth muscle cells and fibrous tissue to form fibrous cap (stabilizes plaque and separate it from bloodstream) ⇒ fibrous cap weakens/thins bc of increased inflammatory response ⇒ fibrous cap at risk for rupture ⇒ if ruptures ⇒ lipid-rich core of plaque exposed to bloodstream ⇒ triggers thrombus formation ⇒ can lead to complete arterial occlusion or dislodges to other parts of arteries to block it
• S&S:
  
  • Inadequate perfusion to tissues (affected area)
  • ↑ risk for MI, CVA

Question 23

Compensatory mechanism for development of atherosclerosis

Answer 23

• ↑ vascular resistance bc heart is trying to pump harder to get blood thru arteries ⇒ ↑ BP
• Vascular remodeling: blood vessels shrink/expand bc of stiffening/hardening
• Heart hypertrophy

Question 24

Pathophysiology characteristics of Raynaud’s Disease

Answer 24

• Raynaud’s: episodic vasospasms (vasospastic disorder) ⇒ changes in color and sensation of affected body parts due to ischemia (reduced blood flow)
• S&S:
  
  • Sensation changes: tingling, numbness, etc.
  • White skin color ⇒ indicates poor blood circulation
  • Blue skin color ⇒ indicates low oxygenation
  • Very Red skin color ⇒ indicates blood returning to affected area (can be painful)