Flashcards in Acute And Chronic Treatment Deck (45):
Stevenson and colleagues model focuses on what two factors?
diagnoses of HF, focuses on volume status and perfusion
In Stevenson and colleague, patients are characterize into what two categories?
Volume overload/congested related
Perfusion/Output related presentations
What do patients with acute onset of pulmonary Edema usually have⁉️
Marked elevated blood pressure, worsening mitral regurgitation, and myocardial ischemia=> think ischemia of the papillary muscle
What is the standard therapy for acute onset of pulmonary edema?
Supplemental oxygen and intravenous loop diuretic
What is an example of a Venodilator and a arterial vasodilator?
What is a acute treatment for HF patient with ventricular dysfunction? When is nitroprusside appropriate?
Nitroglycerin; hypertensive urgency, severe hypertension, decompensated heart failure related to aortic or mitral regurgitation
In regards to heart failure treatment, what do patients need to be educated about?
Adherence to medical therapy and restriction of dietary sodium and fluid
What disturbance causing HF may require specific therapy?
Atrial fibrillation precipitating decompensated heart failure
What treatment of medical problems may improve heart function?
Sleep disordered breathing in, pulmonary hypertension
What are the non-pharmacological treatments for Heart failure⁉️
Restrict sodium to 2 g per day
Limit Fluid intake
Vascular exercise program
Why is fluid intake limited and weight reduction in obese patients necessary in CHF?
To avoid hyponatremia, and reduce the workload of the failing heart
What is a mechanism that causes volume overload in HF patients?
Activation of RAAS
What do diuretics do or help promote?
Reno excretion of sodium and water providing rapid relief a pulmonary congestion and peripheral Adema
What are the preferred loop diuretics used in hypervolemic HF?
Furosemide, torsemide, or bumetanide
Why are these loop diuretics used in CHF?
Rapid onset, rapid relief of symptoms, decreasing preload, Lowing ventricular filling pressures
What is the mechanism in which diuretics can possibly potentiate the progression of HF?
Activation of RAAS and sympathetic nervous system
What is sequential nephron blockade approach?
When a patient is resistant to loop diuretic monotherapy; drugs block reabsorption at other locations on the nephron
What are examples of reabsorption blockers other than loop diuretics?
Metolazone, Thiazide diuretics, carbonic anhydrase inhibitor, aldosterone receptor blocker, and arginine vasopressin blockers
What patients use sequential nephron blockade strategy?
Intrinsic renal dysfunction or to navigate hyponatremia due to volume overload
What agents are responsible for inhibiting RAAS?
What are the pleiotropic affects of ACEi?
Improved endothelial function, anti-proliferative affects of on smooth muscle cells, neutrophils, and monocytes and that thrombotic effects
What kinds of patients should ACEi be avoided⁉️
Pregnant patients, patient is considering pregnancy, patient with history of Angioedema
Persistent dry cough is a major side effect of what drug? And occurs and what percentage of people? What is the mechanism?
ACEi; 20%, increase bradykinin levels
What are the other possible side effects of ACEi?
Hypotension, hyperkalemia, azotemia
What are the precautions that should be taken when a patient takes ACEi?
Renal function and potassium levels should be checked one week after initiation or after dose titration
What is the mechanism of a ARBs?
Prevent the binding of angiotensin II to his receptor and decrease the release of bradykinin
Why was beta blockers determined to be beneficial in HF patients?
Because unopposed adrenergic stimulation was ultimately found to be deleterious to the myocardium
The beneficial effects of beta blockers are the result of what⁉️
Decrease heart rate, beta receptor upregulation, altering myocardium metabolism, improved calcium transport, and inhibition of RAAS, improvement of endothelial function, and decreased levels of circulating cytokines
What are the three approved beta blockers⁉️
Metoprolol succincatebisoprolol, Carvedilol
When should beta blockers be withheld from patients? Why?
Markedly decompensated acute heart failure, negatively chronotropic and may acutely result in diminished cardiac output
Why should beta blockers be titrated? What are the benefits?
To maximize doses; improve LVEF, reduce or reverse the degree of negative LV remodeling
What beta blocker is the least beta selective?
What are the other traits of Carvedilol?
Antioxidant, alpha blocker (which may lower blood pressure and improve endothelial function)
What are the side effects to Carvedilol?
Hypotension, bronchospasm in patients with underlying lung disease
What is defined as HFrEF? What is recommended for all patients with prior or current symptoms of HFrEF?
LVEF<40%; beta blockers
What are the first line therapy's for CHF? What would be the next class a beneficial agent?
ACEi, B-blocker; Aldosterone receptor antagonist
What are the properties of aldosterone receptor antagonist? What are examples of?
Week diuretics and important and Antifibrotic properties; Spirolactone, Eplerenone
What special combination reduce his mortality in African-American patients with ongoing ongoing symptomatic HF after the institution of the three regimens⁉️
Hydralazine and combination with oral nitrates
When is the hydralazine and nitrate combination given⁉️
When patient is ACEi intolerant or requires additional therapy for blood pressure control
When should combination of hydralazine and isosorbide dinitrate be given?
Current or prior symptomatic HFrEF who cannot be given ACE inhibitor or ARBs because of drug intolerance, hypertension, or renal insufficiency
How does digoxin work?
Inhibit sodium potassium ATPase, increase intracellular calcium, increase contractility
What is proven and not proven for Digoxin?
Mortality is non proven; symptom improvements, exercise tolerance, and health related quality-of-life only in men is proven
What are the the side effects of the Digoxin toxicity?
Nausea, vomiting, Hyperkalemia, heart block, atrial and ventricular arrhythmias, visual color disturbances
What patient are at high risk for the Digoxin toxicity? Why?
Patients with intrinsic renal disease, because the Digoxin is really cleared