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Pharmacology -- Test #3 > Pharmacology of CHF drugs > Flashcards

Pharmacology of CHF drugs Flashcards

1
Q

Two main factors influencing cardiac output

A

Stroke Volume and Heart Rate

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2
Q

Preload is..

A

Left ventricular end diastolic volume

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3
Q

Afterload is…

A

force that the ventricle has to push against to eject blood

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4
Q

Increasing contractility will increase….

A

SV for a given preload

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5
Q

How do optimized and failing hearts compare to normal hearts in Frank-Starling curves

A

Optimum hearts have a steeper curve where small changes in preload result in major SV changes. Failing hearts do not respond well to increased preload, as might be seen in a CHF patient.

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6
Q

Relationship btw SV and afterload?

A

Inverse

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7
Q

What might make a patient very sensitive to afterload changes?

A

Heart Failure

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8
Q

Effect of inotropy on SV at a given afterload

A

Increases it

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9
Q

What is compensation (CHF)?

A

When heart fxn is stable. There i still underlying disease, but patient can participate in most normal activities.

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10
Q

What is decompensation (CHF)?

A

When the heart/CV cannot compensate adequately for reduced effectiveness of the CHF heart. Patient is often hospitalized. Basically – Acutely worsening CHF.

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11
Q

In early heart failure, how does afterload, SV, preload

A

Afterload – Potentially high
SV – Reduced a bit
Preload – Starts to increase

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12
Q

How does the body maintain SV in early heart failure (3)

A
  1. Sympathetic Discharge
  2. RAAS Activity
  3. Cardiac remodeling
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13
Q

How does a CHF ventricular wall compare to a healthy one

A

Thicker walls and increased deposition of connective tissue

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14
Q

How is Calcium related to CHF hypertrophy response

A

When the heart has more rounds of calcium enry/exit, the expression of hypertrophic memodeling genes is upregulated.

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15
Q

What endocrine condition can exacerbate hypertrophic CHF?

A

Hyperthyroidism

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16
Q

How does late stage heart failure change the starling curve and force-tension curve?

A

Starling – Preload continues to rise,
FT – Afterload increases
SV goes down

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17
Q

What does it mean when I say that CHF patients are afterload sensitive?

A

Increases in afterload bring about sharp reductions in stroke volume

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18
Q

Two main categories of CHF treatment strategies? Do them improve mortality rates?

A 
Manipulate Hemodynamics (No)
Inhibit Compensation (Yes)
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19
Q

What does someone do for a CHF patient under the “Manipulating hemodynamics” strategy

A

Alleviate extreme pressure problems of CHF to improve overall heart fxn. Mainly only treats symptoms.

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20
Q

What does someone do for a CHF patient under the “Inhibit compensation” strategy

A

Use agents to reverse cardiac remodeling

ACE inhibitors and beta-blockers

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21
Q

Four drug classes used to manipulate hemodynamics of CHF patients

A

Vasodilators, Diuretics, Angiotensin inhibitors, inotropic agents

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22
Q

Why use a vasodilator? Examples?

A

Dilate veins, decrease preload

Organic nitrates, hydralazine

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23
Q

Why use a diuretic?

Examples of diuretics?

A

Decrease blood volume

Furosemide, Bumetanide, Torsemide

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24
Q

Why use an angiotensin inhibitor?

Examples of angiotensin inhibitors?

A

Decrease pressure and volume

ACE inhibitors, ATII rec antag., Renin inhibitors

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25
Q

Why use an inotropic agents?

Examples of inotropic agents?

A

Stimulates contractility

Digoxin, PDE3 inhibitors, beta-arrestin agonists

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26
Q

Examples of chronic inotropic therapy?

A

Glycosides (digoxin)

27
Q

Examples of acute inotropic therapy?

A

PDE inhibitors and beta agonists

Typically only used in decompensated, hospital/ER patients

28
Q

Risk associated with PDE inhibitors?

A

Inducing arrhythmias long term

29
Q

Problem with long term beta agonists?

A

Desensitization

30
Q

How does Calcium move in myocyte contraction

A

Ca enters through L TYPE channel, triggers internal release through RYANODINE receptors.

31
Q

How does Calcium move in myocyte relaxation?

A
  1. Ca ATPase pumps it out of the cell.
  2. SERCA pumps Ca into the SR
  3. NCX (Na/Ca exchanger) trades Ca out of the cell
32
Q

What is oubain?

A

A blocker of Na/K ATPase

33
Q

Oubain has what effect on Ca? Contractility? (After 25 minutes)

A

Increased release of Ca during contraction, increase in contraction.

34
Q

Why does blocking a sodium pump jack up the Calcium levels?

A

Decreased Ca extrusion by NCX. This leads to more being reloaded by SERCA for intracellular stores, and thus more release in response to stimulation.

35
Q

Effect of Digoxin?

A

Increase in Contractility

Decreased HR and vascular sympathetic tone

36
Q

How does Digoxin work?

A

Blocker of the Na/K ATPase

37
Q

Important structural components of Glycosides?

A

Steroid Nucleus

Differences defined by sugar/lactone moieties

38
Q

What type of glycoside is digoxin?

A

Cardenolides

39
Q

Whats the problem with treating patients with digoxin?

A

There is a narrow therapeutic window before toxicity.

Because of this loading doses must be monitored closely.

40
Q

Specific types of toxicity commonly associated with digoxin?

A

Psychiatric – Delirium, Fatigue, Malaise, Confusion
GI – Anorexia, Nausea and Vomiting, Ab Pain
Respiratory – Increased response to hypoxia
CV – Pro-arrythmic (atrial tachy, AV block)

41
Q

Pharmacological interaction of digoxin and beta-blockers + Ca Channel Blockers

A

BB+CCB will depress the heart and oppose digoxin action

42
Q

Pharmacological interaction of digoxin and Kaliuretic diuretics

A

Increased K elimination will lower overall K, promoting digoxin action. This will raise the risk for arrythmias.

43
Q

Examples of beta-AR agonists used in CHF patients? Problems with using these drugs?

A

Dobutamine, Dopamine

Prone to desensitization, can cause HTN

44
Q

Examples of Phosphodiesterase 3 inhibitors?

Problems with these drugs?

A

Milrinone, Amrinone

Pro-arrhythmic, decreased survival

45
Q

Three classes of drugs used to inhibit compensation in CHF patients?

A
  1. RAA System Inhibition
  2. Aldosterone Antagonists
  3. beta-AR blockers
46
Q

Pros of RAA drugs?

A

Pro – Alleviated pressure and volume problems (helping preload+afterload). Some stop/reverse remodeling

47
Q

Types of RAA drugs?

A

ACE inhibitors, ATII rec. agonist, Aliskiren (a Renin inhibitor)

48
Q

Pros of Aldosterone antagonists? Example?

A

Decrease blood volume + Reverse hypertrophy

Spironolactone (K sparing)

49
Q

Perks of beta-AR blockers? Examples?

A

Inhibitorn of sympathetic overactivity in CHF. Can decrease remodeling+mortality in CHF.
Carvedilol, Metoprolol, Bisoprolol

50
Q

What does Spironolactone actually do?

A

It blocks the Na+H2O reabsorption caused by aldosterone and inhibits angiotensin IIs ability to increase preload.

51
Q

Six things that aldosterone does that we want to block in CHF

A 
Na/H2O retention
K and Mg Loss
Reduced Myocardial NE uptake
Reduced baroreceptor sensitivity
Myocardial fibrosis, fibroblast proliferation
Alterations in Na+ channel expression
52
Q

Why use a beta-AR blocker in CHF?

A

Counter CHF compensation (increased adrenergic tone, heightened catecholamines, hypertrophic remodeling)

53
Q

Four effects of vasopressin?

A

Water Retention
Vasoconstriction
Enhanced platelet aggregation
VSM and Myocyte Proliferation

54
Q

Two main ADH receptor antagonists used in CHF

What receptors do they block?

A

Tolvaptan (V1A, V2)

Conivaptan (V2 selective)

55
Q

Why would you choose to give a vasopressin receptor antagonist?

A

Hyponatremia in HF and SIADH

Used in Acute Care Settings

56
Q

Adverse effects of Vasopressin Receptor Antagonists in CHF?

A

Hypotension, Osmotic demyelination, CYP3A substrate

57
Q

What is Neprilysin?

A

A synthetic analog for Hyman type B Natriurietic Peptide

58
Q

Human Type B Natriurietic Peptide release is associated with…

A

Increased blood volume and stretch

59
Q

What does human type B Natriuretic Peptide do?

A

Activated membrane bound GC in VSMC+Endothelial cells. This will dephosphorylate MLC, leading the VSMC relaxation.

60
Q

What does Neprilysin inhibition do?

A
  1. Increases levels of vasoactive peptides
  2. Counters neurohumoral vasoconstriction, Na retention, and remodeling.
  3. Investigational for CHF
61
Q

Effect of inotropes on preload problems.

A

They don’t help. They only help with low output symptoms, not congestive symptoms.

62
Q

Effect of ACE inhibitors on a starling curve?

A

Reduction of both preload and afterload (because blood volume and pressure are both reduced).

63
Q

Effect of a diuretic on a starling curve?

A

Only help with congestive symptoms and not low output symptoms. Help pulmonary edema, but not stroke volume.

Pharmacology -- Test #3 (13 decks)

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