Heart failure teatment

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Heart failure teatment
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2013-12-09 22:40:42
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  1. Medical Nutritional Therapy in Heart Failure
    • - Should promote a diet to control sodium and fluid retention, maintaining a healthy body weight, and providing a diet adequate in vitamins, minerals, and proteins
    • - —May have other comorbidities such as diabetes, hypertension, obesity, or kidney failure
  2. nutrition
    • —Sodium should be restricted
    • - If preserved or depressed EF, restrict to 2-3 gm/day
    • - —Moderate to severe with a very low EF, <2 gm/day

    ——Should be taught major sources of dietary sodium, not adding salt, where to find sodium content on labels, and to choose foods low in sodium

    —DASH (dietary approaches to stop hypertension)

    —Salt substitutes , spices, and low sodium marinades and sauces may be good substitution but watch for potassium in patients with kidney failure
  3. food with a lot of sodium
    canned, processed, frozen lean cuisines, etc.
  4. what else does the hospital restrict when the hospital puts the patient on sodium restrcition?
    restriction on fluid intake
  5. foods high in K
    • potato's 
    • tomato's
    • oranges
    • bananas
  6. weight monitoring
    • weight yourself at the same time everyday, wearing the same thing
    • keep record
    • if gain 2 lbs in one day or 5 lbs in a week, call provider
  7. cardial cachexia
    • means wasting away
    • weight loss of more then 6% of the previous normal weight over 6 months associated with heart failure
    • occurs in 10-15% of clients with heart failure 
    • seen in advance Dx
    • under nutrition due to one or a combination of 
    • --inc. nutirnt losses
    • --unmet inc. nutritional req.
    • --dec. nutritional intake
    • --malabsorption
  8. medical treatments
    • efect preload, afterload, contractility, RAAS system
    • diuretics 
    • inhibitors of RAAS system
    • beta blockers
    • digoxin
  9. diuretics
    • first line drug for patient with signs of volume overload
    • reduce blood volume and therefor dec. preload and afterload, edema, and cardiac dilation
    • must watch blood pressure
  10. diuretic: Thiazides
    • ex: hydrochlorothiazide
    • produce moderate diuresis
    • used for long term therapy
    • ineffective when GFR is low - in your CO is low, kidney blood flow dec., dec. filtration rate
    • also used for HTN, should dec. preload and after load
    • adverse effect: hypokalemia, hyponatremia
  11. diuretics: loop diuretics
    • ex. furosemide [lasix]
    • produce profound diuresis
    • also called high ceiling agents
    • promotes fluid loss even with low GFR
    • used for severe heart failure, pulmonary edema
    • oral or IV
    • adverse effects: hypokalemia, dehydration, ototoxicity [occurs when given with gentamycin]
  12. diuretics: loop diuretic drug interactions
    • digoxin
    • ototoxic drugs: aminoglycoside antibiotics
    • potassium sparing diuretics
  13. aldosterone
    • promotes ventricular remodeling
    • promotes myocardial fibrosis [make the heart non-compliant and stiff]
    • activation of SNS and suppression of norepinephrine uptake in the heart
    • promotion of vascular fibrosis
    • acts to promote sodium uptake in exchange for potassium excretion
  14. diuretics: potassium sparing diuretics
    • ex. spironolactone [aldoactone - nonselective]
    • eplerenon [inspra] - selective
    • promote small amounts of diuresis
    • used to counteract K loss caused by thiazide and loop diuretics
    • adverse effects: Hperkalemia, gynecomastia
    • be cautious if combined with an ACE l or ARB - can cause kidney failure which can cause elevated K+
    • pregnancy category C - should not be given to pregnant women
  15. non-selective potassium sparing diuretics
    block not only aldosterone but also other endocrine hormones as well
  16. selective potassium sparing diuretic
    blocks only aldosterone
  17. spironolactone
    • prolongs survival in patients with HF primarily by blacking receptors for aldosterone 
    • guidelines recommend adding to standard therapy in patients with moderately severe or severe HF
  18. Drugs that inhibit RAAS
    • RAAS plays important role in hemodynamic changes that occur when cardiac output is low 
    • 4 groups: ACE inhibitors, ARBs, Direct renin inhibitors, aldosterone agonist
  19. ACE inhibitors
    • ex: Cateopril, enalapril
    • block production of angiotensin ll, dec. release of aldosterone, and suppress breakdown of bradykinins
    • results in dilation of arterioles and veins - preload and afterload dec. meaning less work on the heart
    • can prolong life
    • usually combined with beta blocker and diuretic 
    • will start off with a very low dose - can become profoundly hypotensive if treatment beings with a high dose [may have BP in the 80s]
  20. ACE inhibitors benefits
    • improves blood flow to kidneys reduces preload and afterload
    • excretion of sodium and water
    • stops progression of cardiac remodeling
  21. ACE inhibitors adverse effects
    • hypotension 
    • hyperkalemia
    • intractable cough
    • angioedema 
    • renal failure in pts. with bilateral renal artery stenosis - if they have unilateral stenosis they can still get an ACE but cant if they have bilateral stenosis 
    • pregnancy category X
  22. ARBs
    • effect are similar to ACE
    • reserved for those who cannot tolerate an ACE
    • improved ejection fraction, reduce HF symptoms, inc. exercise tolerance, dec. hospitalization, enhance quality of life, and reduce mortality
  23. Direct Renin Inhibitors
    • only 1 available - aliskiren [tekturna]
    • effects similar to ACE l and ARBs
    • acts on renin to inhibit conversion of angiotensin into angiotensin l
    • causes less angioedema and cough then ACE l
  24. beta blockers
    • ex: Carvedilol [coreg], bisprolol [zebeta], sustained release metropolol [toprol XL]
    • can improve left ventricle ejection fraction, inc. exercise tolerance, slow progression of HF, reduce the need for hospitalization, and prolong survival
    • protects the heart from excessive stimulation and dysrhythmias
    • doses initiated at low dose and gradually inc.
    • may take 1-3 months to see benefits
  25. beta blockers adverse effects
    • fluid retention and worsening HF
    • fatigue [initial SE but can get better once you get used to the medication]
    • hypotension
    • bradycardia or heart block [very slow heart rhythms that can be dangerous]
  26. inotropic agents
    • digoxin
    • sympathomimetics
    • increase cardiac output by increasing contractility and reducing neurohormonal activation
    • used more for systolic HF
  27. inotropy
    force of the heart contraction
  28. chronotropy
    the rate of contraction
  29. Digoxin [Lanoxin]
    • its a cardiac glycoside 
    • can be given PO or IV
    • positive inotropic agent
    • inc. CO
    • can alter the electrical activity of the heart
    • second line agent - would be added onto another agent
    • cannot prolong life, it just treats the symptoms at the time
  30. Digoxin and Potassium
    • K ions compete with digoxin on the Na/K ion pump 
    • when K is low, binding of digoxin is inc., causing toxicity [since it has nothing to compete with]
    • when K is high, digoxin is reduced [more K+ to compete with]
  31. Digoxin adverse effects
    • narrow theraputic window
    • nirmal level 0.5-1.5
    • must be monitored closely 
    • dec. dose if renal impairment if present
    • nausea, vomiting 
    • fatigue
    • visual disturbances - yellow tinge 
    • dysrhythmias
  32. digoxin drig interactions
    • diuretic [b/c it dec. your K+]
    • ACE inhibitors and ARBs [affects K+ and renal function]
    • sympathomimetics [makes you tachy]
    • quinide [inc/ dig level by dec. the renal excretion of digoxin]
    • verapamil - can dec. your contractility
  33. pharmokinetics
    • absorption is variable - dec. by foods high in bran
    • eliminated by renal excretion 
    • can take 6 days to reach plateau [unless you do the big IV dose]
  34. treatment od digitalis intoxications
    • stop drug
    • gastric lavage [more severe toxicity] - out an NG tube down the stomach and lavage the stomach
    • activated charcoal - binds to the digoxin
    • hemodialysis
    • digibind - the only antidote that they can  give
    • anti-dysrhythmias - ex: lidocane = for any heart rhythm issues
  35. sympathomimetics: dopamine
    must be given IV in hospital - continuous infusion, weight based [kg]

    • catecholamine, activates: 
    • - beta adrenergic receptors in the heart [can inc. HR trying to inc. CO]
    • - dopamine receptors in the kidney [increase blood flow to the kidneys = inc. urine output]
    • - alpha adrenerigc receptors in blood vessels [at high doses]

    short term rescue measure for severe acute HF
  36. sympathomimetics: Dobutamine
    given IV in the hospital 

    preferred over dopamine [doesn't inc. vascular resistance]

    • synthetic catecholamine, causes:
    • - selective sctivation of beta agrenergic receptors [inc. HR] does not activate alpha receptors 
    • - does not activate alpha receptors
  37. phosphodiesterase inhibitors
    • ex: Milrinone
    • continuous Iv infusion 
    • inc. contractility and rpmotes vasodilation
    • results from an inc. in cAMP [amessengar between cells] secondary to inhibition of PDE3
    • cAMP should allow your heart to pump more efficiently, inc. contractility 
    • used for patients in acute HF, not responding to traditional Tx
  38. vasodilators
    - isosorbide and hydralizine are usually combined 

    • - can be used as an alternative to ACE or ARB
    • Isosorbide causes dilation of veins, can improving congestive symptoms

    - can cause hypotension tachycardia

    - hydralizone causes dilation of arterioles, improving cardiac output and renal blood flow

    - can cause hypotension, tachycardia  

    • - it decreases preload and afterload 
    • and ACE or/and ARB is preferred unless they can't tolerate it
  39. intravenous vasodilation: nitroglycerin
    • venodilator, dec. venous pressure [de. preload and afterload. dec. workload of the heart]
    • used for acute pulmonary edema
    • this is a late case medication as well
  40. intravenous vasodilators: sodium nitroprusside [nitropress]
    • dilates arteriols and veins, reduces afterload and inc. CO
    • used for short term therapy
  41. intravenous vasodilators: nesitride [natrecor]
    synthetic human BNP

    when your ventricle is stretched, it will release BNP. BNP actually tells the body to try to diuresis itself
  42. Meds to AVOID in heart failure
    • NSAIDs [cause fluid retention]
    • calcium channel blockers [can decrease contractility] 
    • TZD's
    • theophylline [caffeine derivative, can make you tachy]
  43. surgical Tx Heart failure
    • cardiac transplantation is ultimate treatment for end stage heart failure
    • coronary revascularization 
    • mitral valve repair
    • left ventricle reconstruction
  44. device therapy
    • implanted cardioverter defibrollator [trying to rezap the heart to its normal rhythm]
    • cardiac resynchronization [peacemaker]
    • ventricular assist device
  45. VAD
    mechanical devices that can assist and support the circulation 

    • used for 
    • - bridge to transplant: put on the transplant list and waiting
    • - bridge to decision: have't decided or too old for a transplant
    • - destination therapy
  46. PT with VAD - determine if they have a good CO by
    - No fatigue

    - Their pink

    - Their mentating/ urinating

    - No systole or diastole

    - Their warm
  47. exercise training
    • in past, bed rest was recommended 
    • now we know that inactivity is detrimental 
    • exercise can improve clinical status, increase exersie capacity, and improve quality of life
  48. monitoring
    watch for reduction in symptom 

    • - JVD, edema, rales
    • - increased capacity for physical activity 
    • - lower BNP
    • - improved quality of life

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