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N216 A/B > Perfusion Part 6 - > Flashcards

Perfusion Part 6 - Flashcards

1
Q

Why is chronic stress an issue?

A

Chronic stress = chronic cortisol secretion = no purpose for extra cortisol = adrenal insufficiency (overall depletion due to perceived overproduction).

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2
Q

Cortisol _____ _____ glycogen to prevent ______.

A

breaks down; starvation.

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3
Q

What are 4 common signs & symptoms of adrenal insufficiency?

A
  1. Salt cravings due to a excess Na+ excretion.
  2. Fatigue due to lack of glycogen breakdown.
  3. Hypoglycemia (post-exercise) due to lack of refill mechanism.
  4. Hyponatremia.
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4
Q

What is the danger of a non-physician monitored Keto diet?

A

Metabolic acidosis: breakdown of adipose tissue for energy > triglycerides > fatty acids > decline in cellular function/necrosis

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5
Q

Why are diabetics prone to metabolic acidosis?

A

They lack insulin to break down glucose, so fatty acids are used for energy.

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6
Q

What’s the difference between primary and secondary pulmonary hypertension?

A

Primary: related to organ function.
Secondary: due to diagnosed disease.

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7
Q

What do we use to treat pulmonary hypertension? What route of admin is used?

A

Nipride (DAV): endotracheal for pulmonary vasodilation.

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8
Q

What is a potential secondary injury that can result from pulmonary hypertension?

A

Cor pulmonale (right-sided heart failure) due to backlog affecting the heart.

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9
Q

What is the difference between an MI and heart failure (HF)?

A

MI: injury to cardiac cells due to lack of O2.
HF: ANY condition decreasing the heart’s ability to pump enough blood to meet metabolic demands.

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10
Q

What’s the difference between systolic & diastolic HF?

A

Systolic: contraction is affected due to muscle atrophy.
Diastolic: filling is affected due to hypertrophy decreasing chamber space.

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11
Q

List some major risk factors for HF.

A 
Basically anything that can lead to decreased functional ability.
CAD
HTN
Large MI
Cardia tamponade
Electrolyte imbalance (K+, Ca2+ for contraction)
Arrhythmias (a. fib, bradycardia)
Cardiomyopathy
Diabetes
Vascular dysfunction
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12
Q

What regulates HR, CO & BP? (4)

A

CNS
ANS (peripheral vascular resistance & BV)
Baroreceptors
Hormonal regulation of BP (ex: aldosterone, ADH, renin-angiotensin)

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13
Q

Where does the back-up occur in right-sided heart failure?

A

Systemic circulation (specifically: venous system).

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14
Q

Right-sided heart failure causes ______ pressure to build, leading to fluid shifting _________.

A

capillary; into cells.

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15
Q

What are 3 symptoms of right-sided heart failure?

A
  1. Peripheral edema (pitting due to fluid accumulation)/weight gain.
  2. Organ congestion: liver, renal, GI.
  3. Ischemia: LoC changes, fatigue.
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16
Q

Where does the back-up occur in left-sided heart failure?

A

Pulmonary circulation.

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17
Q

What are 3 signs & symptoms of left-sided heart failure?

A
  1. Pulmonary edema: hypoxia, hypoxemia, cyanosis.
  2. SoB, crackles on auscultations & coughing.
  3. Exercise intolerance.
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18
Q

Briefly describe how SNS activation leads to compensation and ultimately, worsening of CO.

A

Induces muscle hypertrophy of surrounding smooth muscle/fibroblast (not heart cells) > decrease in ventricle volume > CO decreases more.

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19
Q

What 2 substances does the SNS release to initiate compensation?

A
  1. Endothelial enzymes.

2. Cytokines (inflammatory mediators).

20
Q

What are our 3 goals for pharmacotherapy of HF?

A
  1. Decrease cardiac workload.
  2. Increase O2 supply.
  3. Increase contractility.
21
Q

What are 3 ways to either decrease cardiac workload or increase O2 supply?

A
  1. Decrease preload/afterload (decrease blood volume & vasodilate).
  2. Decrease HR.
  3. Oxygenate the patient.
22
Q

Which 5 classes of drugs can we use to decrease preload/afterload or decrease HR to targets?

A
  1. Diuretics (ex: Spironalactone): decreases preload.
  2. ACE inhibitors.
  3. Adrenergic antagonists (receptor-specific).
  4. DAVs.
  5. Calcium channel agonists/blockers.
23
Q

Besides decreasing preload/afterload, what is another benefit of using diuretics to treat HF?

A

Decreases sodium retention.

24
Q

Which 3 drug classes are used to increase contractility?

A
  1. Cardiac glycosides.
  2. P inhibitors.
  3. Adrenergic agonists.
25
Q

What is the mechanism of action of cardiac glycosides?

A

Affects electrolyte transport: blocks exit of Na+ > high intracellular Na+ prompts NA+/Ca2+ exchanger > brings in Ca2+ > increased contractility.

26
Q

If a patient is on cardiac glycosides, we should prioritize monitoring their ____ because:

A

HR; cardiac glycosides slow conduction pathway at AV node.

27
Q

Name 2 cardiac glycosides.

A

Digoxin (Lanoxin) & Digitoxin.

28
Q

What is notable about Digoxin/Digitoxin in terms of ADME?

A

Narrow TI.

29
Q

What is the mechanism of action for phosphodiesterase (P) inhibitors?

A

Block phosphodiesterase (PDE) > increases cAMP activity

30
Q

Normally, what is the role of phosphodiesterase?

A

Breaks down ATP & recycles its byproducts to create more ATP.

31
Q

What do we consider a “bonus” side effect of phosphodiesterase inhibitors?

A

Vasodilation.

32
Q

Phosphodiesterase inhibitors should only be used for _____/_____ treatments.

A

Acute CHF/short-term.

33
Q

Name 2 meds considered phosphodiesterase inhibitors.

A

Milrinone; amrinone.

34
Q

What 3 things should we monitor for patients taking phosphodiesterase inhibitors?

A

ECGs, HR, BP.

35
Q

Name 2 “rescue meds” considered adrenergic agonists.

A
  1. Dobutamine.

2. Dopamine HCL.

36
Q

Which receptors does Dobutamine affect?

A

Generally: B1 specific.

Some B2 binding, but lower affinity.

37
Q

Why can’t we use epinephrine as a chatacholamine (adrenergic agonist) to treat HF?

A

Generic: affects both alpha & beta 1 + 2.

Will increase afterload.

38
Q

What are 4 things we monitor for patients on adrenergic agonists?

A
  1. Vitals.
  2. Angina.
  3. Tachycardia.
  4. ECGs: watch for arrhythmias.
39
Q

Which 3 classes of drugs should be used to treat acute heart failure?

A
  1. Loop diuretics.
  2. DAVs/organic nitrates.
  3. B1 agonists - catacholamines.
40
Q

List some risk factors for dilated cardiomyopathy.

A 
Genetics
Gender (males)
Age (20-50 years old)
HTN
Diabetes
Cardiac infection (ex: bacterial endocarditis)
MI
CAD
Drugs (ex: cocain, ETOH)
41
Q

In chronic heart failure, which parts of the acute treatment regimen should be subbed out? For what?

A

B1 agonists subbed out for cardiac glycosides.

DAVs subbed out for ACE/ARBs.

42
Q

List 4 factors that affect AV node dysfunction.

A
  1. Ischemia.
  2. Drugs (ex: Digoxin, calcium channel blockers).
  3. Electrolytes (K+).
  4. Inflammation (ex: scar tissue, cardiac surgery).
43
Q

How does PNS stimulation affect cardiac rhythm?

A

Vagus nerve stimulated > bradycardia.

44
Q

What are 2 ways that we can treat arrhythmia?

A
  1. Decrease SA-AV node conduction.

2. Depress ectopy at ventricular level to enhance normal AV conduction.

45
Q

Which drug will decrease SA-AV node conduction?

A

Digoxin.

46
Q

Which 2 drugs will depress ectopy at the ventricular level in treatment of arrhythmia?

A
  1. Lidocaine (Na+ channel blocker).

2. Amiodarone (K+ channel blocker).

N216 A/B (26 decks)

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