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PHRM 845: Therapeutics III > Sjogren Heart Failure > Flashcards

Sjogren Heart Failure Flashcards

1
Q

What are the determents that affect Cardiac Output?

A
  • Stroke Volume [End Systolic and Diastolic volume]
  • Heart Rate [Sympathetic and Parasympathetic]
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2
Q

What is preload?

A
  • The amount of blood that comes into the heart, causing the stretching of the ventricles, also known as Ventricular End-Diastolic Volume
    – Decreased by dilation of the veins; A decrease leads to DECREASE in O2 consumption [heart isn’t working as hard] and INCREASE in perfusion [myocytes are able to get more O2]
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3
Q

What is Afterload?

A
  • The arterial resistance that the heart has to overcome to pump the blood to the rest of the body
    – Decreased by dilation of the arteries; A decrease leads to DECREASE in O2 consumption [the heart isn’t working as hard to pump]
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4
Q

How does heart rate affect hemodynamics?

A
  • DECREASED HR will decrease workload
  • DECREASED HR will increase perfusion
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5
Q

What is the Frank-Starling Mechanism?

A
  • Its the mechanism that relates to the contraction of the Myocyte [its related to the Stroke Volume and the Preload]
    – The stroke volume increases as the volume of the heart increases
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6
Q

What is Inotrophy?

A
  • It is the force at which the heart contracts
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7
Q

Explain the Optimum and Failing Heart on the Frank-Starling Curve.

A
  • Optimum Heart: The preload is staying the same BUT the contractility has increased [EX: athletes]
  • Failing Heart: The preload is staying the same BUT the contractility has decreased [EX: heart isnt pumping as strong as it should]
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8
Q

What is Chronic Heart Failure?

A
  • Its a progressive disease composed of compensation and decompensation
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9
Q

What does compensation mean within Heart Failure?

A
  • Compensation: Basically the heart is stable but has the disease, so the heart tries to compensate for that failure
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10
Q

What does decompensation mean within Heart Failure?

A
  • Decompensation: When the Heart really cant compensate for the failure anymore so the there is possible cardiovascular events that may occur.
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11
Q

What are the different type of Chronic Heart Faliure?

A
  • HFrEF and HFpEF
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12
Q

What is HFrEF?

A
  • It is also known as Systolic Failure; it results in a THIN/DILATED heart. [The muscles of the heart are weakened and cant squeeze the heart well]
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13
Q

What is HFpEF?

A
  • It is known as Diastolic Failure; it results in the more STIFF/THICKEN cardiac wall not allowing the muscle to relax.
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14
Q

Describe the action potential of cardiac muscles.

A
  • Phase 0: Rapid Na+ influx causing DEPOLARIZATION
  • Phase 1: Na+ channels close, and K+ channels slightly open; leaving the cell
  • Phase 2: Ca2+ channels open allowing in it and K+ channels open moving it out [balance]
  • Phase 3: Ca2+ close and K+ remain open causing REPOLARIZATION
  • Phase 4: Na+ and Ca2+ channels are closed and K+ channels are open
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15
Q

What is the channel that moves Ca2+ into the cell?

A
  • L Type Ca Channels
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16
Q

What is the important membrane potentials for cardiac cells?

A
  • Starts at -90mV and Ends at 0mV
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17
Q

What is the receptor that moves Ca2+ out of the Sarcoplasmic Reticulum Lumen?

A
  • Ryanodine Receptors (RyR)
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18
Q

What are the other Ca2+ receptors found within the cell?

A
  • Ca2+ ATPase, SERCA, NCX, and Na+/K+ ATPase
19
Q

What does the Ca2+ ATPase channel do?

A
  • It moves Ca2+ out of the cell with the help of ATP [Requires Energy]
20
Q

What does the SERCA channel do?

A
  • Sacro/endoplasmic reticulum Ca2+ ATPase: helps move Ca2+ into the Sarcoplasmic Reticulum and it uses ATP [Require Energy]
21
Q

What does the NCX channel do?

A
  • Sodium Calcium Exchanger: its the main route to get rid of Ca2+
22
Q

What does the Na+/K+ ATPase channel do?

A
  • It works with the NCX to help remove Na+ from the cell with the help of ATP [Requires Energy]
23
Q

Explain what what Dopamine [Norepi & Epi] does within a myocyte?

A
  • Dopamine/Norepi/Epi will bind to the Beta receptor, causing GDP to GTP activating Adenylyl Cyclase. The activation of AC will active the HCN channel via cAMP allowing Na+ in. cAMP binds to PKA activating the L-Type Ca2+ Channel allowing Ca2+ in
24
Q

What are the drugs that are used to manipulate hemodynamics in CHF?

A
  • Vasodilators, Diuretics, Angiotensin Inhibitors, Inotropic Agent
25
Q

What do the Inotropic agents do in CHF?

A
  • They will increase inotropy [increase contractility] without increasing or decreasing the PRELOAD
26
Q

What are the Inotropic agents that are used?

A
  • Cardiac Glycosides, Phosphodiesterase Inhibitors, Beta-Adrenegic Agonists
27
Q

What is the mechanism of action for the Cardiac Glycosides?

A
  • They are going to inhibit the Na+/K+ ATPase, causing an INCREASE in Na+ retention inside the cell, causing an increase of intracellular Ca2+
28
Q

What is the chemical structure that is related to the Glycosides?

A
  • Very similar to the Steroid molecule
29
Q

What are some of the Toxic Effects and Interactions for Glycosides?

A
  • Toxicities: Fatigue Confusion, Nausea, Vomiting, Abdominal Pain
  • Interactions: Beta-Blockers, CCBs & K+ Diuretics
30
Q

What do the Beta-Blockers and CCBs do for the Interactions of Gylcosides?

A
  • They will depress the heart [causing the heart rate to decrease] resulting in an opposed digoxin action
31
Q

What do K+ Diuretics do for the interaction of Glycosides?

A
  • They will decrease K+, causing a promotion in Digoxin action [INCREASING the risk for arrhythmias]
32
Q

What is the mechanism of action for the Beta Agonist?

A
  • They will activate the B1 receptor, causing the activation of AC and cAMP, promoting constriction
33
Q

What are the Beta Agonists?

A

-Dobutamine and Dopamine

34
Q

What is the mechanism of action of the Phosphodiesterase 3 Inhibitors?

A
  • These will stop the break down of cAMP to AMP, resulting in constriction
35
Q

What are the PDE3 inhibitors?

A
  • Milrinone and Amrinone
36
Q

What do the Inotropes do for the Frank-Starling Curve?

A
  • They ONLY increase the Inotrope and NOT the preload [Increase in Constriction]
37
Q

What are the drugs used in inhibiting compensation?

A
  • Renin/Angiotensin System Inhibition, Diuretics, Beta-Blockers
38
Q

Simply describe the Renin-Angiotensin-Aldosterone System?

A
  • The liver releases Angiotensinogen
  • Renin [Released from the Kidney] converts Angiotensin I
  • ACE [Released from the Lungs] converts Angiotensin I to Angiotensin II
    -Angiotensin II activates a lot of things
39
Q

What is the importance toward the Renin/Angiotensin System Inhibition?

A
  • It will help alleviate pressure and volume problems [Reducing preload and afterload]
  • Can also help stop/reverse remodeling
  • Decrease mortality
40
Q

How do the ACE Inhibitors affect the Frank-Starling Cruve?

A

-It will increase Inotropy [Increasing Contraction] and decrease preload

41
Q

What is the mechanism of action for the Aldosterone Analogues?

A
  • They inhibit the release of Aldosterone from Angiotensin II, causing a decrease in preload [Decrease blood volume]
42
Q

How do the Diuretics affect the Frank Staring Curve?

A

-They just DECREASE the preload and NO affect on the Inotrope

43
Q

What is the mechanism of action for the Beta-Blockers?

A
  • They will inhibit the Beta receptor causing a decrease in AC, resulting in a decrease in cAMP, causing more relaxation than contraction.
  • Slow the pacemaker cells in the heart: DECREASING heart rate [contractility]
44
Q

What are the three beta-blockers that are used in HF to help decrease Morality?

A
  • Metoprolol, Carvedilol, Bisoprolol

PHRM 845: Therapeutics III (25 decks)

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