Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
89 Cards in this Set
- Front
- Back
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?
|
High-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
|
Arteriodilator
|
|
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
|
Captopril
Enalapril Lisinopril Ramipril Quinapril |
|
By how much can ACE inhibitor therapy reduce CHF mortality?
|
by 28-40%
|
|
List the common ending for Angiotensin-II receptor Antagonists
|
-SARTAN
|
|
List the common ending for the ACE inhibitors
|
-PRIL
|
|
There are 2 type of Angiotensin II receptors: AT1 & AT2
What receptor do AT-II Antagonists block & where are these receptors predominantly located? |
AT1
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?
|
Nifedipine
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?
|
GI
-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?
|
Headache
Fatigue Malaise Drowsiness 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?
|
Quinidine
Amiodarone Captopril Verapamil Diltiazem Cyclosporin *CDC-VAQ |
|
What increases Digoxin's renal clearance?
|
Thyroxine
|
|
What decreases Digoxin's GI absorption?
|
Cholestyramine
Bran |
|
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?
|
CCA's
-Verapamil -Diltiazem -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?
|
Infants
|
|
What condition predisposes to intoxication of Digoxin by reducing renal clearance to elevate serum Digoxin levels?
|
Hypothyroidism
|
|
List 3 PDE inhibitors used to treat CHF
|
Amrinone
Milrinone Vesnarinone **-RINONE |
|
What do the "-RINONE's" inhibit?
|
type III Phosphodiesterase = inhibit cAMP degradation
|
|
Whta is the mechanism of action of the "-RINONE's"?
-AmRINONE -MilRINONE -VesnaRINONE |
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
|
Dopamine
Beta-1 adrenergic agonists = Dobutamine |
|
What 2 drugs may increase Digoxin toxicity by increasing it GI absorption?
|
1. Erythromycin
2. Omeprazole |