Cv2_Maloney_Agents For Heart Failure

Front 1

CO= ____ x______

Back 1

HR x SV

Front 2

A 57 year old male began taking a drug to dilate his arteries. Which of the following parameters will DECREASE?

-Preload
-Afterload
-Myocardial Contractility

Back 2

Afterload

Front 3

If you increase preload, you _______ CO

Back 3

increase

Front 4

This is described as the amount of myocardial stretch at the end of diastole

Back 4

preload

Front 5

under steady state conditions, CO and Venous Return are ________.

Back 5

equal

Front 6

CO= ____ x______

Back 6

HR x SV

Front 7

A 57 year old male began taking a drug to dilate his arteries. Which of the following parameters will DECREASE?

-Preload
-Afterload
-Myocardial Contractility

Back 7

Afterload

Front 8

If you increase preload, you _______ CO

Back 8

increase

Front 9

This is described as the amount of myocardial stretch at the end of diastole

Back 9

preload

Front 10

under steady state conditions, CO and Venous Return are ________.

Back 10

equal

Front 11

This is defined as Resistance the ventricles must overcome
to empty its contents

Back 11

Afterload

Front 12

Increase PVR--> _______ afterload

Back 12

increased

Front 13

What effect will afterload have on the heart? (Starling Curve)

Back 13

Lowers the curve

Front 14

This is defined as the ability of the heart to develop contractile force

Back 14

Contractility

Front 15

Changes in contractility shift the Starling Curve _____________

Back 15

up or down

Front 16

what effect will myocardial damage from an MI have on the Starling Curve?

Back 16

Shifts curve down

Front 17

A 65 yr old man with HF is started on a β blocker. What does this do to his Staling curve?

Back 17

Raises it!!

Remember, his HF originally lowered it!

Front 18

What happens to CO when a person excercises? What about a person with HF?

Back 18

In a healthy person the CO increases to meet physiological needs

A person with HF can not increase their SV and thus CO to meet physiological needs

Front 19

With systolic and/or diastolic dysfunction, you have a _________ CO

Back 19

decreased

Front 20

What happens to blood pressure and perfusion of vital organs if CO is decreased?

Back 20

↓BP

↓Perfusion --> organ failure

Front 21

What is the body's response to ↓CO?

Back 21

Increase RAAS

Increase SNS

Both will INCREASE BP

Front 22

How does activating the RAAS increase BP?

Back 22

Kidneys: Increased Na+ and water retention

Arteries and veins: Vasoconstriction

Front 23

In the long-run, the body's compensatory actions to incease BP and CO cause ________ and ________

Back 23

**more damage (↑afterload, ↑HR, ↑Force of contraction)

**edema (↑preload)

Front 24

In patients with heart failure, ↑ preload causes

Back 24

little effect on CO, instead it causes MORE EDEMA

Front 25

Excess neurohormones such as NE, Ang II and Aldosterone cause _________

Back 25

cardiac remodeling
(hypertrophy, ventricular dilation, fibrosis, ect...)

Front 26

Heart failure patients at home are said to have _________ chronic heart failure

Back 26

Stable chronic heart failure

Front 27

Patients experiencing worsening HF and being admitted to a hospital have __________

Back 27

Acute Decompensation

Front 28

What are the two types of heart failure?

Back 28

Stable Chronic Heart Failure

Acute Decompensation

Front 29

A patient whose symptoms of heart failure can be controlled by drugs has __________________.

Back 29

Stable Chronic HF

Front 30

A patient whose HF progresses, or something triggers a "relapse". Symptoms of pulmonary congestion and/or low CO

Back 30

Acute Decompensation

Front 31

What are the goals of treating HF?

Back 31

Improve EF

Symptomatic relief of pulmonary edema

Reduce Cardiac Remodeling

REDUCE MORTALITY

Front 32

How can you ↑EF in a patient with Heart Failure?

Back 32

↑Contractility (+ionotropic drugs)

Reduce afterload (arterial dilators)

Front 33

What drug classes can you use to reduce preload?

Back 33

Diuretics

Venous Dilators

Front 34

List the stages of Heart Failure

Back 34

Stage A
-High risk of developing HF but no structural disorder

Stage B
-Structural Disorder but no symptoms

Stage C
-Symptoms of HF assoc. w/ underlying heart disease

Stage D
-End stage disease who requires specialized support

Front 35

A 68 year old female patient has high risk for developing HF (atherosclerosis, diabetes mellitus), but does not have a structural disorder (eg. no LVH). What will we use to treat her HF?

Back 35

Stage A

ACE INHIBITOR/ ARB

Front 36

"-pril"

Back 36

ACE INHIBITORS

Front 37

What effect will ACE Inhibitors have on arteries?

Back 37

Vasodilation --> ↓Afterload --> ↑SV -->↑CO

Front 38

What effect will ACE Inhibitors have on plasma volume?

Back 38

↓Plasma volume by ↓Aldosterone

↓Ang II
↓
↓Aldosterone
↓
↓Na+ and water retention
↓
↓preload

Front 39

What's the problem with ACE Inhibitors and the edema associated with HF?

Back 39

Na+ and water loss with ACE Inhibitors is not sufficient to reduce edema assoc. w/ HF

Front 40

After several months of tx with ACE Inhibitors, what happens to aldosterone levels?

Back 40

They increase

Front 41

High levels of Ang II lead to _______

Back 41

Cardiac Hypertrophy and Remodeling

Front 42

What drugs prevent or reverse cardiac hypertrophy and remodeling?

Back 42

ACE Inhibitors

Front 43

What are the benefits of using ACE Inhibitors in heart failure?

Back 43

- ↓ afterload
-may ↓ preload
**PREVENT CARDIAC REMODELING**

Front 44

All patients with heart failure due to LEFT VENTRICULAR SYSTOLIC DYSFUNCTION should receive __________

Back 44

ACE Inhibitors

Front 45

What stages of HF can ACE Inhibitors treat?

Back 45

Stages A-D

NYHA I-IV

Front 46

What symptoms and lab tests would prevent you from using an ACE Inhibitor in a patient with HF?

Back 46

HIGH creatinine

Low BP (hypotension)

Front 47

Adverse Effects

What are the biggest concerns when using an ACE Inhibitor in a pt. with HF?

Back 47

Hypotension

Worsening Renal Fxn

Hyperkalemia

Front 48

"-sartan"

Back 48

Angiotension Receptor Blockers

Front 49

MOA: ARBs

Back 49

Inhibit formation of Ang II

DOES NOT EFFECT Bradykinin

Front 50

Advantages of using ARBs to treat HF?

Back 50

No/less cough or angioedema

Front 51

A female patient recently had an echocardiogram and unfortunately, she now has LVH and a reduced ejection fraction. Otherwise, she feels good. What would you use to treat her HF?

Back 51

Stage B

Still use ACE Inhibitors

ADD A β BLOCKER

Front 52

Which β- BLOCKERS are used to treat HF?

Back 52

Metroprolol
Bisoprolol
Carvedilol

These have been proven in clinical trials!!

Front 53

Metoprolol and Bisoprolol are what?

Back 53

β1- BLOCKERS

"BEAM"

Front 54

What receptors does Carvedilol block?

Back 54

β1, β2, α1

Front 55

MOA: β- BLOCKERS for HF

Back 55

unknown

Front 56

With the use of β- BLOCKERS, ________________ is thought to contribute to mortality

Back 56

Over stimulation of SNS

Front 57

Overstimulation of the SNS can ultimately lead to what?

What other things can happen?

Back 57

CARDIAC REMODELING

-Down regulation of β1 receptors
-Increased renin release
-Na+ and water retention
-Tachycardia and arrythmias

Front 58

MOA in HF:

Prevent or reverse cardiac remodeling

Prevent atrial/ventricular arrythmias

Back 58

β- BLOCKERS

Front 59

Are β- BLOCKERS negative ionotropic or positive ionotropic?

Back 59

negative ionotropic

Front 60

These agents:

-↑ LV Ejection Fraction**
-↓ Ventricular volume
- ↓ symptoms of HF
-↓ Hospitalization for worsening HF
-↓mortality

Back 60

β- BLOCKERS

Front 61

This drug should be used in:

-Pt's with asymptomatic LV systolic dysfunction

-Stage B

-All patients with a hx of MI

-All patients with a reduced Ejection Fraction

Back 61

β- BLOCKERS

Front 62

Should you start a patient with Acute Decompensation a β- BLOCKER?

Back 62

NO!

Only use β- BLOCKERS in Stable Chronic HF

Front 63

What stages and classes of HF can β- BLOCKERS be used in?

Back 63

Stages B-D

NYHA Class I-IV

Front 64

Can β- BLOCKERS be used in all stage D patients?

Back 64

NO

Patients with severe HF might not tolerate β- BLOCKERS

They are negative ionotropes and will cause more harm than good

Front 65

You are about to start a β- BLOCKER in a patient with Stable Chronic HF. How would you dose it?

Back 65

Start low, go slow

Since β's are negative ionotropes they might make the pt. worse at first until the body adjusts

Front 66

What is the initial dose for Metoprolol in patients with HF. What would you bump it up to over time?

Back 66

Initial Dose: 25mg

Target Dose: 200mg or highest tolerated dose

Front 67

What would happen if a patient with NYHA Class II heart failure started therapy with 200mg of metoprolol?

Back 67

They would DIE

Start low, go slow

Front 68

Can you use β- BLOCKERS in patients with HF and Diabetes?

Back 68

Yes, diabetes IS NOT a contraindication

Front 69

β- BLOCKERS should be used in conjunction with __________

Back 69

ACEi's

Front 70

Which β- BLOCKERS are FDA approved for HF?

Back 70

Carvedilol and Metoprolol

Front 71

A HF patient has mild symptoms that are controlled with enalapril and furosemide. Should a β- BLOCKER be added to their regimen?

Back 71

YES

Reduce risk of:
-Disease progression
-Clinical deterioration
-Sudden death

Front 72

Your HF patient ran out of β- BLOCKERS two days ago and has yet to re-fill the Rx. Is this a bad thing?

Back 72

YES

Abrupt withdrawal can cause cardiac deterioration

Front 73

Adverse effects of β- BLOCKERS?

Back 73

-Fluid retention and worsening HF
**Initiation of therapy or increasing dose**

-Fatigue
-Bradycardia and Heart Block
-Hypotension

Front 74

If a patient has symptomatic bradycardia or a heart block w/o a pacemaker should you start them on β- BLOCKERS?

Back 74

NO

Contraindicated

Front 75

Are fixed airway diseases (COPD) and diabetes contraindications for β- BLOCKER therapy in HF patients?

Back 75

COPD: not necessarily contraindicated

Diabetes: NOT contraindicated

Front 76

Your HF patient has asthma and uses albuterol. Should you start β- BLOCKER therapy?

Back 76

NO

Contraindicated

Front 77

What do you do when a patient with HF that has been taking β- BLOCKERS presents at the hospital with Acute Decompensation?

Back 77

Keep them on β- BLOCKERS

Stop or reduce β- BLOCKERS ONLY in pt's hospitalized after recent initiation or up titration with marked overload

Front 78

Your patient's HF is getting worse because she just ad an episode of pulmonary edema. Before this, she had LVH and a reduced EF. What will you use to treat her?

Back 78

She is in Stage C

ACEi

β- BLOCKERS

Loop Diuretics

Front 79

What is furosemide's action in HF?

Back 79

Increases Na+ excretion

It counteracts Na+ and water RETENTION that occurs with HF

Front 80

What effect will using a Diuretic in a pt. with HF have on preload?

Back 80

DECREASED PRELOAD

Front 81

if you decrease preload, what happens to edema?

Back 81

EDEMA DECREASES

Front 82

What effect do diuretics have on CO in a pt. with HF?

**EXAM**

Back 82

Little to none

Since the curve is flat in HF, diuretics don't affect CO

Front 83

Which drugs are best to reduce pulmonary and peripheral edema without adversely affecting CO?

Back 83

Diuretics

Front 84

Which class of diuretic is most useful in the tx of edema accosiated with HF?

Back 84

Loop Diuretics

Front 85

Would you use a thiazide or loop diuretic in Stages A or B?

Back 85

No, Stages A and B are asymptomatic and diuretics aren't called for

Front 86

Would you use a diuretic to treat edema in Stages C and D of HF?

Back 86

Yes

Mainly use loops

Add a thiazide if refractory to Loop (potentiate effects)

Front 87

What drugs are the only ones to adequately control fluid retention in HF?

Back 87

Loop and Thiazide Diuretics

Front 88

Adverse effects of Loop and Thiazide Diuretics?

Back 88

-Volume depletion
-Hypotension
-Worsening renal fxn**
-Hypokalemia (esp. in combo w/ Digoxin)

Front 89

What is one of the major problems associated with K+ depletion?

Back 89

Arrythmias

Front 90

How would you prevent hypokalemia associated with Loop and Thiazide diuretics?

Back 90

K+ Sparing Diuretics

Front 91

How does the activation of RAAS effect aldosterone levels

Back 91

aldosterone levels increase

Front 92

Levels of aldosterone can be 20X greater in patients with HF. What should we worry about with high aldosterone levels?

Back 92

Vascular Injury

Cardiac Remodeling

Front 93

It is thought that blocking aldosterone receptors in the heart/blood vessels is _________

Back 93

Cardioprotective

Front 94

Your patient is on drugs that gives him an increased risk of developing hypokalemia. What drug can you add that has been proven to reduce the risk of hypokalemia?

Back 94

Spironolactone DECREASES RISK OF HYPOKALEMIA

Decreases Mortality

Decreases hospitalization for HF

Front 95

When adding Spironolactone to a pt.'s HF regimen what 2 things must you monitor?

Back 95

Renal Function

K+ concentrations --> Hyperkalemia

Front 96

What Stages and NYHA classes is spironolactone recommended in?

Back 96

Stage C

NYHA III-IV

Front 97

Levels of aldosterone can be 20X greater in patients with HF. What should we worry about with high aldosterone levels?

Back 97

Vascular Injury

Cardiac Remodeling

Front 98

It is thought that blocking aldosterone receptors in the heart/blood vessels is _________

Back 98

Cardioprotective

Front 99

Your patient is on drugs that gives him an increased risk of developing hypokalemia. What drug can you add that has been proven to reduce the risk of hypokalemia?

Back 99

Spironolactone DECREASES RISK OF HYPOKALEMIA

Decreases Mortality

Decreases hospitalization for HF

Front 100

When adding an ALDOSTERONE RECEPTOR BLOCKER to a pt.'s HF regimen what 2 things must you monitor?

Back 100

Renal Function

K+ concentrations --> Hyperkalemia

Front 101

What Stages and NYHA classes are ALDOSTERONE RECEPTOR BLOCKERS recommended in?

Back 101

Stage C

NYHA III-IV

Front 102

These drugs should be used in pt's with moderately severe to severe HF and recent decompensation or with LV dysfunction early after an MI

Back 102

ALDOSTERONE RECEPTOR BLOCKERS

Spironolactone

Eperlenone

Front 103

A pt has Stage C, NYHA Class III HF. If their serum creatinine is >2.5 mg/dl (normal 08.-1.2mg/dl) would you use an ALDOSTERONE RECEPTOR BLOCKER?

Back 103

NO

Creatinine is too high

Front 104

A pt has Stage C, NYHA Class III HF. If their serum K+ is >5.0 mEq/L (normal 3.5-5.0) would you use an aldosterone blocker?

Back 104

NO

K+ is too high

Front 105

When using an aldosterone receptor blocker, what are the guidelines to minimize the threat of hyperkalemia?

Back 105

Serum Cr < 2.0 female, < 2.5 male

Serum K+ < 5.0

Front 106

What is an advantage of using eperlenone vs. spironolactone

Back 106

Eperlenone doesn't block androgen/progesterone receptors

Front 107

Adverse affects of this drug class include:

Fluid depletion
Renal dysfxn
Hperkalemia
Gynomastasia

Back 107

Aldosterone Receptor Blockers

Note: Use of spironolactone can cause gynomastasia, not eperlenone

Front 108

You have a HF patient that complains of being fatigued with short walks. She has had to go to the hospital several times for her HF. She is on an ACEi, β- BLOCKER, Loop Diuretic, and Aldosterone Blocker. What drug will you add to help?

Back 108

She's in Stage C

Add Digoxin

Front 109

What drug class is Digoxin in?

Back 109

Digitalis Glycosides

Front 110

What does digoxin inhibit?

Back 110

It inhibits the Na/K ATPase in the cardiomyocyte

Front 111

What type of ionotropic effect does digoxin have?

Back 111

Positive Ionotropic Effect

Front 112

MOA: Digoxin

Back 112

Inhibits Na/K ATPase

Higher [Na+] causes less Ca++ to be lost from the cell by the Na/Ca exchanger

More Ca++ taken up by SR

Larger Ca++ gradient created

Increased force of contraction

Front 113

If a patient has hyperkalemia, Digoxin is _________________

Back 113

Less likely to bind to Na/K ATPase

It is thought that K and Digoxin compete for the same receptor

Front 114

Hypokalemia will (increase/decrease) Digoxin's effect/toxicity

Back 114

Increase

Front 115

What class of drugs can cause hypokalemia?

Back 115

Loop and thiazide diuretics

Front 116

What are Digoxin's indirect effects (2)? What do they cause?

Back 116

1) increases vagal activity

2) Sensitizes baroreceptors and decreases SNS

These 2 effects DECREASE ACTIVITY of SA and AV Nodes

Front 117

What effect does digoxin have on neurohormonal activity in HF patient?

Back 117

Decreases Neurohormonal Activity

Front 118

TOXIC EFFECTS

Lower doses of Digoxin cause ________________

Back 118

Sinus bradycardia

AV Block

Front 119

TOXIC EFFECTS

Higher doses of Digoxin cause ______________

Back 119

Increased SNS tone

Ca++ overload

Front 120

How does Digoxin cause Ca++ overload?

Back 120

Digoxin prevents Ca++ efflux

Front 121

Calcium overload can lead to what?

Back 121

Arrythmias

Front 122

In a damaged heart, what can excessive SNS tone and Ca++ overload cause?

Back 122

Arrythmias

Front 123

Digoxin has a low therapeutic index. What does this mean?

Back 123

There's not a big difference between effective and toxic doses

Front 124

This drug has NO effect on mortality but is used for symptomatic relief in stages C and D of HF

Back 124

Digoxin

Front 125

This drug treats Atrial fibrillation/flutter

Back 125

Digoxin

Front 126

How does digoxin decrease Atrial Fib/flutter?

Back 126

Increases vagal tone

Slows ventricular rate

**Doesn't get rid of A-fib/flutter but it CONTROLS it**

Front 127

An adverse effect of this drug is arrythmias of any type

Back 127

Digoxin

Front 128

Excessive vagal tone with use of Digoxin can cause __________(2)

Back 128

Sinus bradycardia

AV Block

Front 129

Excessive Ca++ overload and Central SNS tone with use of Digoxin can cause _____________(3)

Back 129

A-tachycardia

PVCs

V-tachycardia & V-Fib

Front 130

What is normally the first sign of digoxin toxicty?

Back 130

GI PROBLEMS
-NVD
-Anorexia

Front 131

Other than GI problems, another early sign of Digoxin toxicity is _________

Back 131

CNS Problems

Headache, Fatigue, Disorientation, Drowsiness, Confusion, Hallucinations

Front 132

This drug may cause visual disturbances and gynecomastia

Back 132

Digoxin

Front 133

What factors enhance Digoxin toxicity?

Back 133

Hypokalemia

Hypercalcemia

Hypomagnesemia
(Mg++ inhibits K+ influx)

Front 134

What is the Digoxin "antidote"?

Back 134

Digoxin Immune Fab
(Digibind)

Fab fragment of digoxin-specific antibody

Front 135

How does Digoxin Immune Fab (Digibind) affect digoxin?

Back 135

Binds digoxin in blood

Decreases amount of Digoxin that can bind and inhibit Na/K ATPase

Digoxin-Digibind complex is excreted by kidney

Front 136

What do you use in life-threatening cases of Digoxin toxicity?

Back 136

Digibind

Front 137

Your Stage C HF patient's serum creatinine has been increasing. Further testing reveals renal artery stenosis. She is on an ACEi, Beta Blocker, Digoxin and a Loop Diuretic. What will you use to treat her HF?

Back 137

remove ACEi --> Renal a. stenosis

ADD a Vasodilator

Front 138

What oral Vasodilators are used for HF?

Back 138

Isosorbide Dinatrate

Hydralazine

Front 139

How does Isosorbide Dinitrate lower preload to treat HF?

Back 139

it Vasodilates Veins

Front 140

How does hydralazine lower afterload to treat HF?

Back 140

Dilates arteries

Front 141

What decreases mortality of african american HF pt's on optimal therapy with a diuretic, ACEi, and Beta Blocker?

Back 141

Isosorbide Dinitrate + Hydralazine

Front 142

Your Stage C heart failure pt cannot tolerate ACEi's or ARB's, what should you use to help decrease mortality?

Back 142

Isosorbide Dinitrate + Hydralazine

Front 143

Is the use of Isosorbide Dinitrate + Hydralazine (BiDil) as effective as ACEi's for Stage C HF?

Back 143

No

Front 144

What is the goal of drug treatment of Acute Decompensated HF?

Back 144

Relieve Pulmonary Edema

Decrease Pump failure (Poor CO)

Front 145

What are two ways CO can be increased?

Back 145

Reduce afterload

Increase contractility

Front 146

what are 2 ways to reduce preload?

Back 146

Decrease Blood Volume

Venous Dilator

Front 147

What can you dilate to reduce afterload?

Back 147

arteries

Front 148

What are the IV drugs for Acute Decompensated HF?

Back 148

-Loop Diuretics
-Nitroglycerin
-Nitroprusside
-Nesiritide

Front 149

When given to treat pulmonary edema in Acute Decompensation HF, what is the MOA of Loop Diuretics?

Back 149

Vasodilation --> Increase SVC --> decrease LVP --> reduce pulm. edema

**when given by IV, Loops Vasodilate**

Front 150

What do you have to be concerned about when using Loop Diuretics for decompensated HF?

Back 150

Excessive diuresis**

Hypotension
Electrolyte disturbances
Worsen renal fxn

Front 151

What is the best choice for treating pulmonary edema in a patient with acute decompensated HF?

Back 151

Loop Diuretic

Front 152

Nitroglycerin increases NO in _____

Back 152

Veins

Front 153

Nitroprusside increases NO in __________

Back 153

Arteries and Veins

Front 154

What will nitroglycerin and nitroprusside do to preload?

Back 154

Decrease preload

Front 155

What effect will nitroglycerine and nitroprusside have on afterload?

Back 155

nitroprusside= Decreased afterload

nitroglycerine= not much of an effect

Front 156

This compound is released by ventricles in response to wall stress, hypertrophy and volume overload

Back 156

B-type natriuretic peptide

Front 157

What types of effects will Nesiritide have when compared to Ang II ?

Back 157

opposite effects

Front 158

MOA: Nesiritide

Back 158

Activates Gaunylyl cyclase on vascular smooth m. cells

Increases cGMP

Dilates arteries and Veins

Front 159

Nesiritide ________ afterload and preload by vasodilating arteries and veins

Back 159

decreases

Front 160

MOA: Nesiritide in Kidney

Back 160

Blocks Na+ reabsorption

Consticts efferent arteriole and Dilates afferent arteriole --> Increased GFR

Front 161

What drugs are added to diuretics for pt's with evidence of severely symptomatic fluid overload in the absence of systemic HYPOtension?

Back 161

IV Drugs for Acute Decompensation

-Nitroglycerin
-Nitroprusside
-Nesiritide

Front 162

What are the side effects of Nesiritide?

Back 162

Hypotension

Headache

Front 163

Is Nesiritde approved for intermittent (weekly) IV infusion?

Back 163

NO

Front 164

In patients with Stage D HF, how can CO be increased?

Back 164

Increase Contractility

Front 165

Inamrinone and Milrinone inhibit what?

Back 165

PDE-3

Front 166

Other than Digoxin, what are some other positive ionotropic drugs you can use for Stage D HF?

Back 166

Dobutamine

Dopamine

PDE-3 Inhibitors

Front 167

What is the end result when using Dobutamine in a Stage D HF patient?

Back 167

Increased force of contraction (+ ionotrope) without significantly increasing HR

Front 168

What is the main MOA in which Dobutamine treats HF?

Back 168

Activates β1 receptors

Increased force of contraction

(+ ionotropic effect)

Front 169

Dobutamine activates which receptors?

Back 169

β1 > β2 > α

Front 170

What receptors does Dopamine activate?

Back 170

Lower dose ------------------High dose
dopaminergic___β________α

Front 171

Low dose Dopamine's MOA in HF?

Back 171

Activates dopaminergic (DA) receptors

Vasodilation of:
-renal a.
-splanchnic a.
-cerebrospinal a.
-coronary blood vessels

Front 172

What is the end result of Dopamine use in the kidneys?

Back 172

Increased renal bloodflow

Increased Urine Output

Front 173

MOA Higher doses of Dopamine to treat HF?

Back 173

Activates β1 receptors on heart

Increases HR (+ ionotropic effect)

Front 174

What drug is useful in episodes of cardiogenic shock where BP and CO are very low?

Back 174

Highest doses of dopamine

Activate α1 receptors ---> VC arteries

INCREASE BP

Front 175

MOA PDE-3 inhibitors in HF

Back 175

Inhibit PDE-3

↑cAMP leads to:
- ↑ force of contraction
- ↑Velocity of relaxation (↑filling)
-Vasodilation

(+ ionotropic drug)

Front 176

Can PDE-3 inhibitors be used chronically?

Back 176

NO!

Increased Mortality with longterm use!!

Front 177

What are some intolerable side effects of PDE-3 inhibitor use?

Back 177

Inamrinone --> thrombocytopenia

Both --> hypotension, arrythmias

Front 178

What are + ionotropic drugs used for in treatment of Stage D HF?

Back 178

+ ionotropic drugs only treat symptoms

Front 179

Should + ionotropic drugs be used longterm?

Back 179

NO

Front 180

Which positive ionotropic drug DOES NOT increase mortality?

Back 180

Digoxin