Sjogren Heart Failure Flashcards
(44 cards)
1
Q
What are the determents that affect Cardiac Output?
A
- Stroke Volume [End Systolic and Diastolic volume]
- Heart Rate [Sympathetic and Parasympathetic]
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]
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]
4
Q
How does heart rate affect hemodynamics?
A
- DECREASED HR will decrease workload
- DECREASED HR will increase perfusion
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
6
Q
What is Inotrophy?
A
- It is the force at which the heart contracts
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]
8
Q
What is Chronic Heart Failure?
A
- Its a progressive disease composed of compensation and decompensation
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
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.
11
Q
What are the different type of Chronic Heart Faliure?
A
- HFrEF and HFpEF
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]
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.
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
15
Q
What is the channel that moves Ca2+ into the cell?
A
- L Type Ca Channels
16
Q
What is the important membrane potentials for cardiac cells?
A
- Starts at -90mV and Ends at 0mV
17
Q
What is the receptor that moves Ca2+ out of the Sarcoplasmic Reticulum Lumen?
A
- Ryanodine Receptors (RyR)
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
What do the Inotropic agents do in CHF?
- They will increase inotropy [increase contractility] without increasing or decreasing the PRELOAD
26
What are the Inotropic agents that are used?
- Cardiac Glycosides, Phosphodiesterase Inhibitors, Beta-Adrenegic Agonists
27
What is the mechanism of action for the Cardiac Glycosides?
- 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
What is the chemical structure that is related to the Glycosides?
- Very similar to the Steroid molecule
29
What are some of the Toxic Effects and Interactions for Glycosides?
- Toxicities: Fatigue Confusion, Nausea, Vomiting, Abdominal Pain
- Interactions: Beta-Blockers, CCBs & K+ Diuretics
30
What do the Beta-Blockers and CCBs do for the Interactions of Gylcosides?
- They will depress the heart [causing the heart rate to decrease] resulting in an opposed digoxin action
31
What do K+ Diuretics do for the interaction of Glycosides?
- They will decrease K+, causing a promotion in Digoxin action [INCREASING the risk for arrhythmias]
32
What is the mechanism of action for the Beta Agonist?
- They will activate the B1 receptor, causing the activation of AC and cAMP, promoting constriction
33
What are the Beta Agonists?
-Dobutamine and Dopamine
34
What is the mechanism of action of the Phosphodiesterase 3 Inhibitors?
- These will stop the break down of cAMP to AMP, resulting in constriction
35
What are the PDE3 inhibitors?
- Milrinone and Amrinone
36
What do the Inotropes do for the Frank-Starling Curve?
- They ONLY increase the Inotrope and NOT the preload [Increase in Constriction]
37
What are the drugs used in inhibiting compensation?
- Renin/Angiotensin System Inhibition, Diuretics, Beta-Blockers
38
Simply describe the Renin-Angiotensin-Aldosterone System?
- 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
What is the importance toward the Renin/Angiotensin System Inhibition?
- It will help alleviate pressure and volume problems [Reducing preload and afterload]
- Can also help stop/reverse remodeling
- Decrease mortality
40
How do the ACE Inhibitors affect the Frank-Starling Cruve?
-It will increase Inotropy [Increasing Contraction] and decrease preload
41
What is the mechanism of action for the Aldosterone Analogues?
- They inhibit the release of Aldosterone from Angiotensin II, causing a decrease in preload [Decrease blood volume]
42
How do the Diuretics affect the Frank Staring Curve?
-They just DECREASE the preload and NO affect on the Inotrope
43
What is the mechanism of action for the Beta-Blockers?
- 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
What are the three beta-blockers that are used in HF to help decrease Morality?
- Metoprolol, Carvedilol, Bisoprolol
