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89 Cards in this Set

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When does CHF result?
when the heart can no longer supply oxygenated blood adequately to peripheral tissues during stress or even at rest

*heart is unable to pump blood at a rate sufficient to satisfy the needs of the metabolizing tissues
What does CHF most frequently result from?
Coronary Artery Disease
What is CHF primarily a disease of?
Aging = 75% of existing & new cases occur in people over 65
Among survivors of CHF, the qualiity of life is adversely affected by these 3 things
1. Progressive fatigue
2. shortness of breath
3. functional disability
What is the long-term prognosis of CHF even with treatment?
5-year survival of 37% in men & 57% in women

30-50% of CHF patients with severe symptoms die within one year
What can the mortality of CHF be reduced by?
Drug treatment
What are 4 causes of "high-output" CHF?
1. Hyperthyroidism = upregulation of Beta-1 receptors in heart; increased oxygen consumption & BMR

2. Anemia

3. AV shunts

4. Thiamine deficiency -> wet beriberi
What is the heart work condition in "high-output" CHF?
Healthy heart exhausted by working too hard
What are the main causes of "low-output" CHF?
1. Coronary Artery Disease
2. HTN
3. MI
4. Persistent arrhythmias
5. Rheumatic Heart Disease
6. General Carciomyopathy
What is the heart work condition in "low-output" CHF?
heart is unable to pump enough blood to meet tissue needs
Which one has poor Inotropic drug response, high-output or low output?
Describe the Hemodynamic characeteristic of CHF
1. Subnormal Cardiac Output causing decreased exercise tolerance with rapid muscle fatigue, tachycardia, pulmonary edema, & cardiomegaly

2. Myocardial Hypertrophy to maintain cardiac performance; increased myocardial muscle mass & muscle wall thickness

3. Neurohumoral Reflex compensation arises from increased activity of sympathetic nerves, Renin-angiotensin-Aldosterone system
Describe the normal cardiovascular regulation
-Strong afferent signals from the Carotid & Cardiopulmonary Baroreceptors
-Efferent signals predominantly Parasympathetic & relatively weak sympathetic
Describe the Cardiovascular Regulation in CHF
-generalized SYMPATHETIC activation with reciprocal Parasympathetic withdrawal
-Sympathetic predominance then causes: 1) Arterial constriction 2) increased renin secretion 3) reflex tachycardia
What is Preload?
equivalent to End-diastolic Volume, which is related to Right-Atrial pressure

when venous return increases, End-diastolic volume increases & stretches or lengthens the ventricular muscle fibers
In CHF, what is Preload elevated by?
Increases in Blood Volume & Venous tone
Treatment with __1__ drugs reduces Preload by dilating peripheral veins to retain more blood & keep blood away from the heart

Treatment with __2__ reduces Preload by decreasing blood volume
1. Venodilator

2. Diuretics
Define Afterload
Arterial resistence against which the heart pumps blood which is determined by Aortic impedence & vascular resistance
In CHF why does Afterload rise?
Increases in Sympathetic & Renin-Angiotensin activity which elevate peripheral resistance via Arterial constriction
Treatment with ________ drugs reduces Afterload by decreasing peripheral resistance
Why is Myocardial Contractility reduced in CHF?
Myocardial muscle fibers are stretched beyond their elastic limits as ventricles become dilated
Myocardial contractility is increased by __1__ drugs, but reduced by __2__
1. Inotropic drugs

2. Beta-blockers
What does Reflex Tachycardia result from in CHF?
Sympathetic overactivity due to Baroreflex activation brought about by the reduction in Cardiac Output
_______ drugs reduce cardiac work by slowing the Heart Rate
Beta blockers
What are the "cornerstones" of CHF drug therapy?
1. ACE inhibitors & other Vasodilators to reduce Cardiac workload

2. Diuretics to reduce Preload by correcting salt & water retention
-Loop diuretics prefered b/c of their potency

3. Digoxin = improves cardiac pumping & output
What is a reasonable therapeutic approach in starting treatment for CHF?
Use ACE Inhibitor alone & if the response is inadequate then add a Loop Diuretic & then finally Digoxin if needed

**b/c fo potential Digoxin toxicity
What do ACE Inhibitors counteract in CHF?
counteract the increased Renin-Angiotensin system activity
What are the factors that increase the Renin-Angiotensin activity in CHF?
1. Reduced renal perfusion activating Renal baroreceptors = Renin release

2. Increased Sympathetic activity stimulating Beta-1 receptors on the JG apparatus

3. Anti-hypertensive drugs that stimulate Renin secretion:
-Diuretics by decreasing delivery of Na+ to macula densa
-Vasodilators by reducing Renal perfusion pressure
What 2 drugs specifically counteract the increased Renin-Angiotensin system in CHF? How do they diminish Cardiac Workload?
ACE inhibitors & Angiotensin II Antagonists

1. decrease Afterload = reduce Angiotensin vasoconstriction

2. decrease Preload = reduce Aldosterone release & fluid volume
List some effective ACE inhibitors used to treat CHF
By how much can ACE inhibitor therapy reduce CHF mortality?
by 28-40%
List the common ending for Angiotensin-II receptor Antagonists
List the common ending for the ACE inhibitors
There are 2 type of Angiotensin II receptors: AT1 & AT2

What receptor do AT-II Antagonists block & where are these receptors predominantly located?

Vascular Smooth Muscle
What are 2 important differences between AT-II blockers & ACE inhibitors?
1. AT-II blockers are more specific than ACE inhibitors b/c AT-II antagonists do not affect BRADYKININ metabolism = no coughing or angioneurotic edema

2. AT-II antagonists have more complete inhibition of Antiotensin action b/c enzymes other than ACE can generate Antiotensin II
What are the adverse effects of Angiotensin-II receptor Antagonists?
1. Hyperkalemia

2. reduced renal function (fetal renal toxicity)

"The Sargeant (Sartan) has alot of Potassium & his kid has Fetal Renal Toxicity"
Vasodilator that is infused IV in acute decompensated CHF as long as Cerebral & Renal persusion can be maintained despirte the reduction in systemic BP
Sodium Nitroprusside
Describe the vasodilating effects of Sodium Nitroprusside
Balanced vasodilator = dilates both veins & arteries to produce both Preload & Afterload
What is the most common adverse effect of Sodium Nitroprusside?
excessive Hypotension
Discuss the effects of Nitroglycerin & Isosorbide Dinitrate for CHF treatment
Dilate VEINS > Arteries = lower Preload > Afterload

Tolerance precludes their long-term use
Which Calcium-channel antagonists should not be used for CHF? Why?
Verapamil & Diltiazem b/c their cardiac effects may worsen CHF symptoms & increase mortality
-reduce muscle contractility
Which CCA may be given to treat CHF? Why?

Blocks slow calcium channels to reduce intracellular calcium = relaxes Arteriolar smooth muscles -> Vasodilation
-has little effect on Cardiac L-type Ca++ channels
How do Beta-blockers improve the symptoms of CHF? What do they improve?
1. Slow heart rate
2. slow contraction velocity

1. CO
2. Exercise tolerance
3. Ventricular function
What are the proposed mechanisms of how Beta-blockers have beneficial effects in CHF?
1. Decreased HR & Cardiac Work
2. Attenuation of responses to high catecholamine concentrations
3. Up-regulation of Beta-adrenergic receptors
4. reduced myocardial remodeling
What do Diuretics do to help in the treatment of CHF?
reduce extracellular fluid volume & thereby reduce Preload
What is chronic diuretic treatment only used for?
patients with advanced disease & symptoms
Which diuretics are the 1st choice drug for CHF?
Loop Diuretics
-Furosemide, Bumetanide, Torsemide
-Ethacrynic acid is used only for patients allergic to sulfonamides
What type of CHF are Thiazide diuretics only used for?
Mild CHF
What concurrent treatment may inhibit Diuretic efficacy?
with Vasodilators = reduce renal blood flow
What are the 2 parts of the chemical structure of Digoxin?
1. Algycone or Genin is responsible for all biological activity

2. 3 molecules of sugar (Digitoxose) influence pharmacokinetics including absorption, half-life, & metabolism
What is the mechanical effect of Digoxin?
Positive Inotropy = increased myocardial contractility/Stroke volume
What is the inotropic mechanism of action of Digoxin?
1. inhibition of Na+/K+ ATPase
2. intracellular increase in Na+ & decrease in K+
3. decreased expulsion of intracellular Ca+
4. increased intracellular Ca+
5. increased actin-myosin interaction by IC Ca++
6. increased force of myocardial contraction
What counteracts Digoxin's toxicity & reduces abnormal cardiac automaticity?
Potassium b/c it inhibits Digoxin's binding to Na+/K+ ATPase receptor

Digoxin toxicity should be treated with Potassium
What increases Digoxin's toxicity?
Calcium & hypokalemia
Why is Heart Rate decreased when using Digoxin for CHF?
In untreated CHF, sympathetic activity is already high but upon Digoxin treatment, contractility & CO will be increased thus removing the stimulus for increased Sympathetic tone
Why is Cardiac Output increased in patients with CHF who are on Digoxin?
1. Increased contractility

2. increased CO removes the stimulus for Sympathetic overactivity = reduction in sympathetic tone
-Venodilation = reduced Preload
-Arteriodilation = reduced Afterload
What electrical effects does Digoxin have at therapeutic doses?
1. Decrease automaticity

2. Prolongs Refractory Period

3. Slow AV node conduction
What can toxic doses of Digoxin cause in the heart?
Arrhythmias by increasing Sympathetic activity & automaticity to form ectopic foci
-slowed conduction may cause Sinus Bradycardia or Heart Block
-may produce almost every variety of arrhythmia
Based on the reduction in Conduction Velocity in the AV node, what is Digoxin used for in the pretreatment of?
Atrial Fibrillation before Antiarrhythmic drugs are used
-antiarrhythmic drugs when given alone may cause paradoxical ventricular tachycardia which can be prevented by pretreatment digoxin which will slow the ventricular rate
What vascular effect does Digoxin have on normal hearts?
contract smooth muscle = Vasoconstriction
What vascular effect does Digoxin have on Failing hearts?
Increase CO -> remove stimulus Sympathetic hyperactivity -> reduced Sympathetic activity -> Vasodilation
What are Digoxin's effects on the Kidney?
Diuresis, but only in CHF patients
-increased GFR is due to Cardiac, not renal actions
-digoxin causes Diuresis only in edematous patients with CHF
-no diuresis in normal subjects or other types of edema
What are the GI effects of Digoxin?
1. Anorexia & diarrhea due to direct irritation
2. Vomiting due to stimulation of the Chemoreceptor Trigger Zone
3. Abdominal pain due to Mesenteric Arteriolar Constriction
Why does Digoxin have a narrow Margin of Safety?

MoS = amount between a therapeutic dose and a lethal dose of a drug
Because the Therapeutic Dose is 50-60% of the Toxic dose & side-effects often occur even with Therapeutic doses; toxicity leads to discontinuing Digoxin in 5-25% of patients
What are the earliest signs of Digoxin intoxication?
-anorexia, NVD, abdominal discomfort
-copious salivation often accompanies the nausea
-vomiting can be harmful as it requires great physical effort
-GI symptoms disappear a few days after discontinuing Digoxin
What are the most dangerous adverse effects of Digoxin?
Cardiac = can simulate almost all arrhythmias including Sinus Bradycardia, Ectopic ventricular beats, AV block, & Bigeminy
What is the most common cause of death due to Digoxin?
Ventricular Fibrillation
How do you monitor the adverse cardiac effects of Digoxin?
1. Routine measurements of ECG

2. Serum Digoxin & Potassium
What are the CNS side effects of Digoxin?
Trigeminal neuralgia
Mental symptoms
Aside from GI, Cardiac, & CNS...what are other adverse effects of Digoxin?
1. Color & Visual Disturbances = Blurry yellow vision
2. Skin rashes
3. Eosinophilia
4. Gynecomastia
5. in severe intoxication, antiarrhythmic drugs may result in cardiac arrest

"Upon DIGGING you find an OX with who has Yellow vision, a skin rash, red cells, & large breasts"
What should treatment of Digoxin intoxication include?
1. discontinue Digoxin
2. oral or IV Potassium (K+)
3. Lidocaine
4. Digoxin antibodies (Anti-Dig Fab fragments)
What drugs enhance Digoxin toxicity by decreasing its Renal Clearance?

What increases Digoxin's renal clearance?
What decreases Digoxin's GI absorption?

What are Digoxin's interactions with Quinidine?
1. Quinidine displaces Digoxin from tissue binding sites

2. Quinidine depresses Digoxin's renal clearance

**may result in sudden death
What diuretics may enhance Digoxin toxicity? Why?
Thiazides & Loop Diuretics

produce Hypokalemia
-Potassium blocks Digoxin's action at the Na+/K+ ATPase
What drugs enhance Digoxin's toxicity by inhibiting SA or AV node activity?
Beta blockers
What drugs enhance Digoxin toxicity by inhibiting myocardial contractility?
-Nifedipine -> but probably not so much
What group of people are mosre susceptible to Digoxin intoxication? Why?
Elderly patients b/c their serum Digoxin levels are elevated by Hypochlorhydria or reduced Renal Clearance
What patients usually require larger doses of Digoxin?
What condition predisposes to intoxication of Digoxin by reducing renal clearance to elevate serum Digoxin levels?
List 3 PDE inhibitors used to treat CHF



What do the "-RINONE's" inhibit?
type III Phosphodiesterase = inhibit cAMP degradation
Whta is the mechanism of action of the "-RINONE's"?
increase Myocardial contractility by increasing cAMP & inward calcium flux in the heart

Inhibit Phosphodiesterase-3 = increase cAMP
-also relax vascular smooth muscles to cause Vasodilation
What are the -RINONE's only used for?
Short-term treatment in advanced heart failure

**long-term trials produce intolerable side effects & increase mortality in CHF patients
These drugs are infused IV to increase Myocardial Contractility only in Acute CHF

Beta-1 adrenergic agonists = Dobutamine
What 2 drugs may increase Digoxin toxicity by increasing it GI absorption?
1. Erythromycin

2. Omeprazole