Agents for treating HF Flashcards
What is Afterload?
The resistance from the arteries when the heart is trying to pump blood through them
What is Cardiac Output?
The amount of blood that is being pumped out by the heart.
What is Cardiomegaly
Enlarged heart
What is Cardiomyopathy?
A group of heart conditions that can lead to Cardiomegaly, Muscle failure or death
What is Dyspnea?
Difficulty breathing, usually paired with anxiety
What is Heart Failure?
When the heart has poor cardiac output. May be caused by various factors.
What is Hemoptysis?
Coughing up blood
What is Nocturia?
Needing to urinate during the night. In HF this is usually caused by gravity depending edema
What is Orthopnea?
Difficulty breathing when laying down. Patient usually needs to be propped up to a 45 degree angle, but this varies from person to person.
What is Positive inotropic?
Drugs that causes a strong muscle contraction.
What is Preload?
Blood that come back to the heart to be circulated again.
What is Pulmonary edema?
Fluid buildup in the lungs.
What is Tachypnea?
Fast shallow respirations.
Explain the 4 stages of congestive heart failure
Stage A. High risk of HF but no structural heart disease or symptoms.
Stage B. Structural heart disease but no signs or symptoms of heart failure (heart starts to enlarge)
Stage C. Structural heart disease with prior or current symptoms of HF. (heart is enlarged and patient is starting to experience fatigue, shortness of breath and/or fluid retention)
Stage D. Refractory HF requiring specialized interventions.(patient have all the above symptoms and symptoms are no longer responsive to treatment)
Explain the 4 classifications of heart failure
Class 1. No limitation of physical activity (able to function as normal).
Class 2. Slight limitation of physical activity ( start to have symptoms with average physical activity).
Class 3. Marked limitation of physical activity (comfortable at rest, but normal activities makes them experience symptoms).
Class 4. Unable to perform any physical activity without symptoms or symptoms at rest (having symptoms whether they are resting or not and any physical activity makes them feel short of breath or fatigued).
What are some causes of Congestive Heart Failure?
Coronary artery disease : There is plaque and cholesterol buildup in the heart, which inhibits enough blood and oxygen to the heart and the heart isn’t operating well. May lead to an MI.
Cardiomyopathy : structural muscular changes and less effective pumping of the heart.
Hypertension : Will lead to cardiomegaly if left untreated because the heart works against pressure.
Valvular Heart Disease : Valves may leak and then the heart is working twice as hard to pump the blood through.
What do we look for in the blood when we suspect that someone has had a heart attack?
Troponin. This is a substance that the heart muscles release when they are damaged due to lack of oxygen and a buildup of toxins.
Name 3 ways the body compensates for decreased cardiac output.
By sympathetic stimulation
Positive inotropic effect (heart beats harder) and by the release of renin.
What are the long term effects of the compensation mechanisms of decreased cardiac output?
Over time, compensation mechanisms increase the hearts workload and the muscles of the heart may stretch and/or thicken. This results in the chambers not being able to effectively pump blood which leads to increased heart failure.
When does compensation start?
When the heart begins to be less effective at getting the blood where it needs to go. This may be caused by conditions such as hypertension or coronary heart disease.
What happens when there is decreased blood flow to the kidneys?
The RAAS is activated. This increases blood pressure, output and aldosterone levels.
Aldosterone increases sodium reabsorption which will increase fluid volume in the body and excrete more potassium. Increased fluid volume will increase BP.
All of this is hard on our hearts.
What are some symptoms of CHF?
- Fluid retention : Pitting edema, tachypnea, jugular vein distension, splenomegaly and nocturia.
- Long term compensation will cause cardiomegaly, S3 sounds and tachycardia. Distal pulses may become weaker and hypoxic and patients may feel weak and fatigued.
What are the drug catergories used for treatment for CHF?
****Cardiotonic (inotropic) drugs: **
Cardiac glycosides -Digoxin
Phosphodiesterase Inhibitors - Milrinone
HCN Blocker - Hyperpolarization-activated cyclic nucleotide-gated - Ivabrandine
Combination drugs ( work on both the inotropic and the RAAS) :
*Angiotensin Receptor Neurolysin Inhibitor (ARNI) - Sacubitril/Valsartan
What lifespan considerations should be taken into account when it comes to Cardiotonic agents in children?
Digoxin may be given. but NOT Phosphodiesterase inhibitors due to unknown severity risk and high potential for adverse effects in children. HCN blockers may be used for stable heart failure in children 6 months +
Dosage should always be double checked by another nurse.
Signs of toxicity is nausea, vomiting, confusion, visual disturbance and arrythmias.
What lifespan considerations should be taken into account when it comes to Cardiotonic agents in adults?
Should be instructed to check their own pulse & weigh themselves daily.
Changes in GI or dietary should be reported (may have a change in electrolyte balance and may lead to decreased effect or toxicity).
Avoid switching between brands of Digoxin.
Should be avoided in pregnancy and lactation (benefit vs. risk)
What lifespan considerations should be taken into account when it comes to Cardiotonic agents in older adults?
More susceptible to digitalis toxicity.
Dose should be adjusted in renal impairments.
Should be instructed to take their own pulse abd weight.
What is the drug that we need to know for Cardiac Glycosides?
Digoxin
How does Digoxin work on the body?
It increases the force of myocardial contraction, cardiac output and renal perfusion and output. It DECREASES blood volume to slow heart rate and conduction velocity through the AV node.
What is the overall desired effect of Digoxin?
Increased cardiac output.
What is the action of Digoxin?
Allows more calcium into cells during depolarization, which creates a stronger muscle contraction.
They also have a diuretic effect which decreases blood volume and they causes the heart rate to slow down due to the slower repolarization.
All of this increases cardiac output.
Why would we give Digoxin to patients?
To treat HF, atrial fibrillation, atrial flutter (due to action on the AV node) , paroxysmal atrial tachycardia.
When would we absolutely not give Digoxin to patients?
Allergy to Digoxin, Ventricular Tachycardia or Ventricular fibrillation (digoxin have no effect of these rhythms which are fatal if not treated immediately with correct medication - amiodarone or lidocaine).
Heart block or sick sinus syndrome (worsened due to slowing of the AV node)
Idiopathic hypertrophic subaortic stenosis (when the heart thickens right below the aortic valve. can obstruct flow - digoxin make the heart contract harder could further obstruct flow)
Acute MI.
AVOID in patients with renal insufficiency (toxicity) & electrolyte abnormalities (alter mechanisms of drug).
What symptoms will be worsened by Digoxin due to its slowing effect of the AV node?
Heart block and Sick Sinus Syndrome
What are some adverse reactions of Digoxin?
*Headache, weakness, drowsiness (these could also indicate toxic digoxin levels), and vision changes(yellow halos around objects)
*GI upset and anorexia
*Arrhythmia development
*Digoxin toxicity (DigiFab is the antidote)
What should the therapeutic levels of Digoxin be?
Between 0.5 - 2 nanograms
Anything over 1.2 nanograms pr ml more likely to result in adverse effects.
Anything over 2 nanograms per ml is likely to result in toxicity.
What is the name of the Digoxin toxicity antidote and how does it work?
DigiFab.
Binds to Digoxin molecules and inactivates them.
Are there and drug-drug interactions that we need to be aware of with Digoxin, and if so, what are they?
Yes, there are many.
Diuretics that affect potassium and thyroid medication and antacids can make digoxin less effective.
What assessments are important to make before considering giving patients Digoxin?
- contraindications or cautions
- physical assessment: weight, pulse & blood pressure, heart sounds,ECG.
Inspect the skin and mucous membranes, check capillary refill.
Monitor affect, orientation, and reflexes.
Respiratory rate and lung sound.
Examine abdomen for distension, bowel sounds, voiding patterns & urinary output.
Labs : Digoxin levels, serum electrolyte levels, and renal function tests
What nursing diagnoses should we consider prior to administering Digoxin?
Altered heart rate r/t cardiac effect.
Impaired comfort due to GI upset (anorexia, nausea).
Risk of altered tissue perfusion due to dysrhythmias.
Injury risk due to CNS effects (fatigue, weakness).
Knowledge deficit r/t drug therapy.
What implementations should we be prepared to make after and when giving patients digoxin?
Count apical pulse for 60 sec before giving drug - hold if less than 60 bpm.
Monitor the pulse for any change in quality or rhythm.
Check the dose and preparation carefully; check the pediatric dose with extreme care.
Administer IV doses slowly over at least five minutes; avoid IM administration (IM is very painful).
Arrange for the patient to be weighed at the same time each day in the same clothes.
Avoid administering the oral drug with food or antacids.
Maintain emergency equipment on standby: potassium salts, lidocaine (may help treat potential arrythmias) phenytoin (treats seizures), atropine (increases HR if needed), and a cardiac monitor.
Obtain digoxin level as ordered; monitor the patient for therapeutic digoxin level (0.5-2 ng/ml).
Provide thorough patient teaching - such as teaching to monitor their own pulse and weight and schedule frequent follow ups.
What is the drug we need to know for Phosphodiesterase Inhibitors?
Milrinone
When would we give a patient Milrinone?
It can be given in acute decompensated heart failure to quickly get the heart to a functional level. Can be given when the heart has not responded to other heart failure treatments such as digitalis, diuretics or vasodilators.
How does Phosphodiesterase Inhibitors work?
They work by stopping the enzyme responsible for getting rid of adenosine monophosphate. By doing this they increase cAMP which increases calcium levels which will cause a stronger contraction of the heart.
The sympathetic stimulation leads to vasodilation and by prolonging it reduces the workload of the heart.
Used in emergency situations.
When would be absolutely not give Milrinone to a patient?
If the patient have an allergy to the drug.
Severe aortic or pulmonary disease (can be exacerbated), acute MI, fluid volume deficit (could cause hypotension) and ventricular arrythmias.
When would we be extra cautious of giving Phosphodiesterase Inhibitors to a patient?
When they are pregnant or breastfeeding (no studies)
What are some known adverse reactions to Milrinone ?
Arrythmias, hypotension (due to vasodilation) and chest pain (increased oxygen demand on the heart) is most common.
GI effect (increased blood flow to other body parts which may lead to decreased GI motility, nausea, anorexia)
Thrombocytopenia
Burning at Injection Site (dilute or inject into larger vein)
Are there any drug-drug interactions that we should be aware of with Milrinone, and if so, what are they?
If combined with Furosemide solid particles may form and cause an IV occlusion or an embolism in the patient. Drugs should not be given at the same time and not in the same IV line.
What assessments should we do prior to prescribing Milrinone to patients?
Assess for contraindications or cautions
Perform a physical assessment:
Assess pulse and blood pressure; auscultate heart sounds; weight; obtain a baseline ECG.
Inspect skin and mucous membranes for color, and check capillary refill.
Examine for abdominal distension; auscultate bowel sounds; assess voiding patterns and urinary output.
Monitor serum electrolyte levels, complete blood count, and renal and hepatic function tests
What nursing diagnoses can be made prior to administering Milrinone to patients?
Altered cardiac output related to development of arrhythmias or hypotension.
Injury risk related to CNS or CV effects.
Altered tissue perfusion (total body) related to hypotension, thrombocytopenia, or arrhythmias.
Knowledge deficit related to drug therapy.
What implementations can be expected to be made when and after administering Milrinone to patients?
Protect the drug from light (will become ineffective)
Ensure that patient has a patent IV access site; monitor IV injection sites and provide comfort measures.
Monitor pulse and blood pressure frequently during administration.
Monitor input and output and record daily weight.
Monitor skin for signs of bruises and petechia as this may be a sign of thrombocytopenia which is a risk with this medication.
Monitor platelet counts before and regularly during therapy.
Provide life support equipment on standby.
Provide thorough patient teaching.
What is the drug that we need to know for Hyperpolarization-Activated Cyclic
Nucleotide–Gated Channel Blockers (HCN blockers) ?
Ivabradine
What is the action of Ivabradine?
These drugs does NOT increase contractility and instead only decreases the rate by slowing action potentials in phase 3.
They do so by blocking the HCNs slows the heart’s SA node, in the repolarizing phase of the action potential.
There is no risk of affecting ventricular repolarization or causing systemic effects such as with beta-blockers.
Why would we give a patient Ivabradine?
We would give this to patients who cannot tolerate a higher dose of beta blockers or in patients who cannot take beta blockers.
And for patients who are stable but with a symptomatic heart failure, to reduce the risk of hospitalization for worsening HF.
When would we absolutely not give Ivabradine to a patient?
This drug should not be used in patients with acute/unstable decompensated HF.
Hypotension, sick sinus syndrome or AV
block, resting heart rate under 60 beats/min (This drug would make these conditions worse)
Patients completely dependent on a pacemaker (due to the effect this drug has on the SA node) and severe hepatic impairment (drug may accumulate in the system)
When would we be extra careful with giving Ivabradine to patients?
Atrial fibrillation or moderate heart block (effect is unpredictable and not shown to be therapeutic)
Pregnancy and lactation (barrier contraceptive and alternative feeding of infants should be highly encouraged)
