Heart Failure & Autonomic Nervous System Flashcards
define heart failure and congestive heart failure
heart failure is when the heart doesn’t pump blood as well as it should.
congestive heart failure is a weakness of the heart that leads to a buildup of fluid in the lungs and surrounding body tissues.
connect the signs and symptoms related to right side heart failure vs. left side heart failure
right sided: impairment of the ability to move the deoxygenated blood from the systemic circulation into the pulmonary circulation
Sx/Sx: peripheral edema, weight gain, congestion of the viscera, hepatomegaly, abdominal discomfort, anorexia, jugular venous distension
left sided: impairs the movement of blood from the low pressure pulmonary circulation to the higher pressure arterial circulation.
Sx/Sx: elevation in pulmonary venous pressure—>pulmonary edema—>occuring at night,
define systolic failure (systolic dysfunction), including ejection fraction (EF). Recall normal and abnormal EF.
systolic dysfunction is primarily defined as a decrease in myocardial contractility, characterized by an ejection fraction of less than 40%.
A normal ejection fraction is 65%.
briefly explain the Frank-Starling mechanism
The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant.
describe how drugs targeting the RAAS mechanism help with heart failure management
ACE inhibitors: arteriolar dilation, venous dilation, suppression of aldosterone release (to enhance excretion of sodium and water, putting less pressure on the heart)
Angiotensin II Receptor Blockers: very similar effects to ACE inhibitors, but also ARBs improve LV ejection fraction, reduce HF symptoms, increase exercise tolerance, decrease hospitalization, enhance quality of life and reduce mortality.
Angiotensin receptor Neprilysin inihbitor: about the same as Angiotensin II above
Aldosterone antagonists (spironolactone & more): reduce symptoms, decrease hospitalizations, prolong life by blocking aldosterone receptors in the heart. AE: hyperkalemia
differentiate four general classes of drugs for heart failure and how they help on impacting:
CO=HR X SV
Ace inhibitors: decrease HR, decrease stroke volume
ARBs: decrease HR, decrease stroke volume
Beta blockers: decrease HR
Digoxin (inotrope)
up HR and SV
recall adrenergic receptor functions of beta 1 and beta 2
Beta-1 receptors, along with beta-2, alpha-1, and alpha-2 receptors, are adrenergic receptors primarily responsible for signaling in the sympathetic nervous system. Beta-1 receptors are found in the heart, kidney and fat cells. Targeted activation of the beta-1 receptor in the heart increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility. With these two increased values, the stroke volume and cardiac output will also increase.
Beta-2 receptors: Beta 2 receptors are predominantly present in airway smooth muscles, the lungs, and the vasculature. Beta 2 receptors mediate physiologic responses such as smooth muscle relaxation and bronchodilation.
recall nursing implications for Digoxin (“Dizzy Digg”) pt. 2
starting with minimizing AE’s
minimizing AE’s:
Cardiotoxicity: inform outpatients about the danger of dysrhythmias, teach monitoring of pulses for rate and rhythm, and instruct them to notify the prescriber if significant changes occur.
Hypokalemia: teach patients to recognize early signs of it (muscle weakness), and instruct them to notify the prescriber if these develop
Non-cardiac effects: nausea, vomiting, anorexia, fatigue, and visual disturbances can indicate toxicity. Inform patients about these early indications of toxicity and have them notify the prescriber should these signs develop.
minimizing adverse drug interactions:
diuretics: thiazides and loops increase the risk for hypokalemia. If hypokalemia occurs it should be corrected with potassium supplements, a potassium sparing diuretic, or both
ACE inhibitors and ARB’s: can elevate potassium levels and decrease therapeutic response. CAUTION if ACE or ARB is combined with a potassium supplements or a potassium sparing diuretic
Sympathomimetic agents: monitor closely for dysrhythmias when these drugs are combined with digoxin
Quinidine: if employed concurrently with digoxin, digoxin dosage must be reduced as quinidine can elevate plasma levels of digoxin.
recall nursing implications for Digoxin (“Dizzy Digg”) pt. 1–up to enhancing therapeutic effects
Therapeutic goal: treat HF and dysrhythmia
CONTRAINDICATED for pts. experiencing ventricular fibrillation, ventricular tachycardia, or digoxin toxicity.
CAUTION with pts. who are experiencing hypokalemia, partial AV block, advanced HF, or renal impairment
Routes: oral or slow IV injection
if HR less than 60 bpm, hold
IV-monitor cardiac status closely for 1-2 hours after administration
Adherence: digoxin has a small therapeutic range so ensuring that patients take the med exactly is prescribed is critical to obtain a therapeutic outcome. If not taken correctly, toxicity may result.
enhance therapeutic effects:
have patients limit salt intake, only one drink/day, have patients establish and exercise program
briefly explain the baroreceptor reflex as it relates to heart rate and blood pressure
- baroreceptors in the aortic arch and carotid sinus sense BP and relay this information to the brainstem
- IF: BP perceived as too low, brainstem sends signals along sympathetic nerves to stimulate heart vessels.
- THEN: BP becomes elevated by: activation of beta, 1 receptors in the heart–resulting in increased cardiac output AND ALSO activation of vascular alpha receptors, resulting in vasoconstriction
- the reflex switches off when BP has been restored to an acceptable level by stopping sympathetic stimulation of the heart and vascular smooth muscle.
- SENSE
- ACTIVATE
- ELEVATE & FIX
- OFF/RESET
