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S7- Cardiopulmonary > Week 3- Drug Management of Cardiac Disease P1 and P2 > Flashcards

Week 3- Drug Management of Cardiac Disease P1 and P2 Flashcards

1
Q

The heart must carefully balance energy synthesis with immediate energy needs. Why?

A

Inability to do so can result in reduced cardiac function and/or cardiac pathology.

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2
Q

What are the (3) main drug strategies to IMPROVE cardiac function?

A
  1. ) Directly increase cardiac contractility.
  2. ) Reduce workload of the heart i.e. reduce myocardial contractility and O2 demand.
  3. ) Increase myocardial blood flow.
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3
Q

What are (3) ways we can reduce the workload of the heart? Are they direct or indirect?

A
  1. ) Reduce contractility (direct)
  2. ) Reduce afterload (indirect)
  3. ) Reduce preload (indirect)
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4
Q

What are 2 ways we can increase myocardial blood flow?

A
  1. ) Increase blood flow.

2. ) Manage hemostasis.

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5
Q

PART 1: DIRECTLY INCREASE CARDIAC CONTRACTILITY

A

PART 1: DIRECTLY INCREASE CARDIAC CONTRACTILITY

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6
Q
  • What is the purpose of inotropic agents?

- What are the (2) types and the difference between them?

A
  • Inotropic agents are used to alter the force of the hearts contractions.
  • Positive inotropic agents (increase force of contraction), Negative inotropic agents (decrease force of contraction).
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7
Q

When are positive inotropic agents used?

A
  • In instances where there is sudden low CO.
  • Only used in inpatient settings, and only those who have S/Sx of low CO.
  • PT most likely on hold with these patients.
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8
Q

Name the (3) most common positive inotropic agents.

A
  • Dopamine
  • Dobutamine
  • Milrinone
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9
Q

Dopamine:

  • Natural catecholamine that acts as precursor to __________.
  • The hemodynamic effect is _______ dependent.
  • When is it usually used?
A
  • norepinephrine (NE)
  • dose dependent
  • Usually used in severe HF and reserved for patients with moderate hypotension.
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10
Q

Dopamine Dose Dependent:

  • Describe low-dose effects of dopamine.
  • Describe mod-dose effects of dopamine.
  • Describe high-dose effects of dopamine.
A
  • Low-dose = renal/splanchnic vasculature dilation enhancing diuresis (urination).
  • ***Mod-dose = enhance cardiac contractility and HR.
  • High-dose = increase afterload through peripheral vasoconstriction.
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11
Q
  • Is Dobutamine or Milrinone used to improve end organ perfusion i.e improves MAP?
  • Is Dobutamine or Milrinone used in the management of pulmonary hypertension?
A
  • Dobutamine

- Milrinone

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12
Q
  • What is the purpose of Digitalis?

- Is it toxic? What is a sign of toxicity?

A
  • Used to treat impaired cardiac contractility (positive inotropic effect) typically caused by HF.
  • Is toxic, patients are hospitalized while dosage is adjusted. (yellow hues sign of toxicity)
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13
Q

Digitalis:

  • Increased ____ influx into the myocytes.
  • Increases the ______ refractory period, decreasing ventricular responses. (antiarrhythmic)
  • Can cause reflex stimulation of the vagus nerve, which leads to a decrease in what?
A
  • Ca2+
  • AV node
  • decrease in HR and contractility
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14
Q

PART 2: REDUCE WORKLOAD OF THE HEART, i.e. REDUCE MYOCARDIAL CONTRACTILITY AND O2 DEMAND

A

PART 2: REDUCE WORKLOAD OF THE HEART, i.e. REDUCE MYOCARDIAL CONTRACTILITY AND O2 DEMAND

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15
Q

What are (3) ways we can reduce the workload of the heart?

A
  1. ) Directly reduce contractility.
  2. ) Reduce afterload.
  3. ) Reduce preload.
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16
Q

B1 Receptor Agonists:

  • Response when stimulated?
  • Clinical use?
  • Impact on cardiac work?
A
  • ↑HR, ↑Contractility
  • Treat severe cardiac decompensation.
  • INCREASES workload of the heart.
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17
Q

B1 Receptor Antagonists:

  • Response when stimulated?
  • Clinical use?
  • Impact on cardiac work?
A
  • ↓HR, ↓Contractility
  • Treat compromised/diseased hearts.
  • DECREASES workload of the heart, reduces functional capacity.
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18
Q

What are (2) drug classes used to directly reduce contractility of the heart?

A
  • B1 Antagonists

- Ca+ Channel Blockers

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19
Q

B1 Antagonists:

  • Affect the _____ primarily.
  • Are called “___________”.
  • Have negative chronotropic/inotropic effects thus __________ workload of the heart.
  • What is the difference between Non-specific Beta Blockers and Cardioselective Beta Blockers?
A
  • heart
  • “beta-blockers”
  • reducing
  • Non-speific Beta Blockers have + effect on heart, but - effect on bronchial smooth muscle.
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20
Q

How do we typically identify B1 Antagonists (“beta-blockers”)?

A

-lol

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21
Q

What are some common AE of B1 Antagonists (“beta-blockers”)? (4)

A
  • Bronchoconstriction (becomes problem in those with pulmonary disease i.e. cor pulmonale).
  • Can cause excessive depression of cardiac function (too much of a good thing).
  • OH
  • Depression, lethargy, and sleep disorders (long term use).
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22
Q

What is the biggest thing we should be mindful of when treating patients who are on B1 Antagonists?

A

REDUCED PEAK HR

-HRmax = 164-0.7*age

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23
Q

Ca+ Channel Blockers:

  • Reduces _____ flux into myocytes.
  • ____ contractility and energy demands on the heart.
  • Also ↓ _____.
A
  • Ca+
  • ↓
  • CO
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24
Q

What are the (3) main AE of Ca+ Channel Blockers?

A

Results in peripheral vasodilation leading to:

  • Decreased BP
  • Dizziness
  • Bradycardia
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25
Q

What are (4) drug classes used to reduce afterload?

A
  • A1 Blocker
  • Direct Vasodilators
  • B1 Blocker
  • Centrally Acting Agents
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26
Q
  • When thinking about reducing afterload, think ___!!!

- ↑ radius = __ resistance

A
  • BP!!!

- ↓

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27
Q

What is the purpose of A1 Blockers?

A

Decrease BP by preventing norepinephrine from tightening muscles in the walls of small arteries/veins.

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28
Q

Alpha 1 Receptors:

  • Located on ________ _______ muscle.
  • Stimulation causes smooth muscle contraction and results in ____________.
  • Blockade results in smooth muscle relaxation, _________ and decreased TPR.
A
  • vascular smooth muscle
  • vasoconstriction (↓r)
  • vasodilation (↑r)
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29
Q

What is TPR/SVR?

A

Total Peripheral Resistance/ Systemic Vascular Resistance

-The resistance to blood flow offered by all of the systemic vasculature beds to blood flow.

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30
Q

What are some common AE of A1 Blockers?

A
  • Systemic drug = systemic effects
  • Reflex tachycardia secondary to hypotension
  • OH
  • Edema of LE, syncope, and SOB
  • Weakness, N/V
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31
Q

What is the function of Direct Vasodilators?

A

Act directly on smooth muscle cells to cause relaxation. (↑r)

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32
Q

What specific Direct Vasodilator is most commonly known for its effects on hair growth?

A

Minoxidil

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33
Q

B1 Antagonists (Beta-Blockers):

  • Mainstay of anti-HTN therapy.
  • May produce a general decrease in sympathetic tone or outflow thus _______ vascular smooth muscle contraction.
  • Decrease _____ release from kidney → decreased amount of angiotensin II → decreased blood volume.
  • HOWEVER, these drugs act primarily on the ______.
A
  • reducing
  • renin
  • heart
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34
Q
  • What are the (2) biggest AE of Beta-Blockers?

- How do we estimate HRmax of patients on Beta-Blockers?

A
  • Bradycardia, Dizziness

- 164-(0.7*age)

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35
Q

What is the function of Centrally Acting Agents?

A

Inhibit sympathetic outflow from the brainstem.

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36
Q

Centrally Acting Agents:

  • __ HR, Contractility, TPR
  • Act like __ _________
  • Often given with a diuretic
A
  • ↓

- A2 antagonists

37
Q

What are common AE of Centrally Acting Agents?

A
  • Dry mouth
  • Dizziness
  • Drowsiness
  • Hypotension
38
Q

What are the (4) drug classes used to reduce preload?

A
  • Diuretics
  • ACEi (Ace inhibitors)
  • ARBs (Angiotensin II Receptor Blockers/Antagonists)
  • Aldosterone Antagonists
39
Q

What is the purpose of Diuretics?

A

Act directly on kidneys to increase water/Na+ excretion. This increased diuresis helps to decrease blood volume i.e. preload.

40
Q

What are the (3) types of Diuretics?

A
  • Loop Diuretics
  • Thiazide Diuretics
  • Potassium Sparing Diuretics
41
Q
  • Which diuretic acts on the distal convoluted tubules to inhibit Na+ reabsorption?
  • Which diuretic acts on the ascending limb of the Loop of Henle, inhibits the reabsorption of Na+ and Cl-, and has a loss of K+?
  • Which diuretic interferes with the Na/K exchange mechanism in the distal convoluted tubules and is less effective at producing diuresis but spares K+?
A
  • Thiazide Diuretics
  • Loop Diuretics
  • Potassium Sparing Diuretics
42
Q

Rank the (3) diuretics by AE.

A

Loop > Thiazide > Potassium Sparing

43
Q

Loop diuretics are used more for _________ than __________.

A

diuresis than hypertension control

44
Q

What are some common AE of Diuretics? (4)

A
  • Fluid depletion (OH, ↑TPR, activate renin-angiotensin system)
  • e- imbalance (hyponatremia/hypokalemia)
  • OH/Falls precaution
  • Urinary incontinence
45
Q

What is the purpose of ACEi?

A

Blocks the conversion of angiotensin I to angiotensin II.

46
Q

Angiotensin II:

  • ________ walls of arterioles.
  • Stimulates ____ reabsorption in the kidneys.
  • Stimulates _______ release from adrenal cortex, causing kidneys to retain Na+/water.
  • What is the net effect of angiotensin II?
A
  • constricts
  • Na+
  • aldosterone
  • vasoconstriction, fluid retention, INCREASED AFTERLOAD
47
Q

What are the (3) net effects of ACEi?

A
  • Decreased vascular smooth muscle tone (vasodilation)
  • Inhibition of aldosterone secretion (reduced Na+ and H2Oresorption/water resorption in kidney and reduced blood volume)
  • Decreased renin activity/production
48
Q
  • Are ACEi well tolerated?

- What are the AE?

A

Yes, generally well tolerated.

  • Allergic reaction
  • GI discomfort
  • Dizziness
  • Chest pain
  • Persistent cough
  • Weakness
49
Q

How do we typically identify ACEi?

A

-pril

50
Q

How do ARBs (Angiotensin II Receptor Antagonists) work?

A

Block renin-angiotensin-aldosterone system.

51
Q

How do we typically identify ARBs?

A

-artan

52
Q

What is the purpose of Aldosterone Antagonists?

A

Block aldosterone binding sites and causes reabsorption of sodium by the kidneys, which encourages water loss, which decreases BP.

53
Q

PART 3: INCREASE MYOCARDIAL BLOOD FLOW

A

PART 3: INCREASE MYOCARDIAL BLOOD FLOW

54
Q

What are the (2) ways we can increase myocardial blood flow?

A
  • Increase blood flow.

- Manage hemostasis.

55
Q
  • What (1) drug class can be used to increase blood flow?

- What is the purpose of them?

A
  • Nitrates
  • Drugs that work more directly at the level of the heart and act as a relaxant of coronary smooth muscle. They act quickly to bring about coronary dilation.
56
Q
  • Venodilator: ↓ venous return and ↓ _________

- Arteriodilator: ↓ ________

A
  • preload

- afterload

57
Q

Organic Nitrates are used in the treatment of angina and produce a general _________ (not specifically a coronary artery dilation).

A

-vasodilation

58
Q

Organic Nitrates MOA:

  • ___ in preload/afterload → ___ in cardiac work and hence ___ in MVO2 (cardiac oxygen use).
  • ↓ in MVO2 is more important than the increased ___ availability
  • Can a tolerance to nitroglycerin be developed?
A
  • ↓, ↓, ↓
  • O2
  • Yes, but can be reversed rapidly by short term withdrawal.
59
Q

What are the ways nitroglycerin can be delivered? (4)

A
  • Oral
  • Sublingual
  • Buccal
  • Transdermal patches
60
Q

Nitroglycerin Patches:

  • NOT effective ________.
  • Must be changed every ___hrs.
  • Change where patch is applied to avoid skin rash.
  • Always use it even if you feel well.
  • Don’t suddenly stop using it.
  • Don’t “______ ___”.
  • Dispose of used patches carefully.
A
  • acutely
  • 24hrs
  • “double up”
61
Q
  • What do we do if blurred vision, dry mouth, skin rash, dizziness, or fainting occurs while treating patients who use Nitroglycerin Patches?
  • What do we need to check frequently in these patients?
A
  • Contact MD

- BP

62
Q

What (3) drug classes can be used to manage hemostasis?

A
  • Thrombolytic agents
  • Anticoagulants
  • Antiplatelet agents
63
Q

What is hemostasis?

A

Intrinsic process which causes bleeding to stop.

64
Q

Describe the process of hemostasis in (3) steps.

A
  1. ) VESSEL WALL INJURY triggers attachment and activation of platelets and and causes vasoconstriction.
  2. ) PLATELETS become “sticky” and attach at area of vessel wall injury.
  3. ) PLASMA FACTORS interact to convert fibrinogen to fibrin which helps to form a clot.
65
Q

What is the purpose of Thrombolytic Agents?

A

Act by degrading a formed clot.

66
Q

Thrombolytic Agents AE:

  • _________ is the primary and most serious problem with these drugs.
  • Be alert for S/Sx of ______________.
  • No antidote
  • GI distress
A
  • Hemorrhage

- heavy/unusual bleeding

67
Q

What is the purpose of Anticoagulants?

A

Help to prevent/slow coagulation of blood i.e. formation of blood clots.

68
Q

Anticoagulants:

  • Are _____________.
  • Commonly called _______ _________.
  • Act by interfering with the proteins in your blood that are involved with the coagulation process (__________).
A
  • preventative
  • blood thinners
  • (factors)
69
Q

List of Anticoagulants. (5)

A
  • Heparin
  • Coumadin (Dicoumarol, Warfarin)
  • Xarelto
  • Eliquis
  • Lovenox
70
Q

Anticoagulants are used primarily to prevent what?

A
  • Strokes, MI’s, DVT/PE, Hx of clots/post surgery/inactivity, A.fib
  • Anticoagulants are used if you’re at risk for developing blood clots that could potentially block a blood vessel and disrupt the flow of blood around your body.
71
Q

Anticoagulants AE:

  • Excessive _________/__________
  • Bruising, bloody stools, bleeding gums, blood in urine
  • ___________ (decrease in thrombocytes or platelets)
  • ____/_____ pain (bleeding into abdomen or joint)
  • GI distress
A
  • bleeding/hemorrhage
  • thrombocytopenia
  • back/joint pain
72
Q

What are some special concerns for patients on anticoagulants? (4)

A
  • Know why on anticoagulant.
  • Avoid contact sports.
  • DO NOT use with aspirin.
  • Take special care brushing teeth and shaving.
73
Q

Blood clot warning signs. (4)

A
  • Swelling or pain in legs.
  • SOB/Chest pain
  • Sudden difficulty moving limb/side of body
  • Difficulty speaking
74
Q

What is the purpose of Antiplatelet Agents?

A

Prevent platelets from clumping together to form a clot.

75
Q

Antiplatelets:

  • _______ is the classic drug in the class.
  • May also be called ________ ________.
A
  • Aspirin

- blood thinners

76
Q

PART 4: OTHER DRUG CATEGORIES

A

PART 4: OTHER DRUG CATEGORIES

77
Q

What (2) other drug categories are used to improve cardiac function?

A
  • Antiarrhythmics

- Statins

78
Q

What is the purpose of Antiarrhythmics?

A

Antiarrhythmic medications prevent and treat abnormal heartbeats (arrhythmias). Problems with your heart’s rhythm are caused by a disruption in the heart’s electrical system.

79
Q

What are the (3) mechanisms of cardiac arrhythmias?

A
  1. ) Abnormal pulse generation (defects in SA/AV nodes)
  2. ) Abnormal pulse conduction (AV block, Bundle Branch block)
  3. ) Combination of the 2
80
Q

What are the (4) classes of antiarrhythmic drugs?

A
  • Class I: Na+ channel blockers
  • Class II: Beta-blockers
  • Class III: K+ channel blockers
  • Class IV: Ca+ channel blockers
81
Q

1

A

1

82
Q

1

A

1

83
Q

1

A

1

84
Q

1

A

1

85
Q

What is the purpose of Statins?

A

Statins help to lower LDL levels.

86
Q

Statins:

  • Risk factor for ____ disease.
  • _________ lowering drug.
  • ________ atherosclerotic plaque.
A
  • CV disease
  • cholesterol
  • stabilize
87
Q

How do we typically identify hyperlipidemia agents?

A

-statin

88
Q

What are the 2 biggest AE associated with statins?

A

Rhabdomyolysis (destruction of skeletal muscle)
-Patients complain of muscle pain.

Liver Failure

S7- Cardiopulmonary (24 decks)

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