Agents for treating HF Flashcards
(139 cards)
1
Q
What is Afterload?
A
The resistance from the arteries when the heart is trying to pump blood through them
2
Q
What is Cardiac Output?
A
The amount of blood that is being pumped out by the heart.
3
Q
What is Cardiomegaly
A
Enlarged heart
4
Q
What is Cardiomyopathy?
A
A group of heart conditions that can lead to Cardiomegaly, Muscle failure or death
5
Q
What is Dyspnea?
A
Difficulty breathing, usually paired with anxiety
6
Q
What is Heart Failure?
A
When the heart has poor cardiac output. May be caused by various factors.
7
Q
What is Hemoptysis?
A
Coughing up blood
8
Q
What is Nocturia?
A
Needing to urinate during the night. In HF this is usually caused by gravity depending edema
9
Q
What is Orthopnea?
A
Difficulty breathing when laying down. Patient usually needs to be propped up to a 45 degree angle, but this varies from person to person.
10
Q
What is Positive inotropic?
A
Drugs that causes a strong muscle contraction.
11
Q
What is Preload?
A
Blood that come back to the heart to be circulated again.
12
Q
What is Pulmonary edema?
A
Fluid buildup in the lungs.
13
Q
What is Tachypnea?
A
Fast shallow respirations.
14
Q
Explain the 4 stages of congestive heart failure
A
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)
15
Q
Explain the 4 classifications of heart failure
A
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).
16
Q
What are some causes of Congestive Heart Failure?
A
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.
17
Q
What do we look for in the blood when we suspect that someone has had a heart attack?
A
Troponin. This is a substance that the heart muscles release when they are damaged due to lack of oxygen and a buildup of toxins.
18
Q
Name 3 ways the body compensates for decreased cardiac output.
A
By sympathetic stimulation
Positive inotropic effect (heart beats harder) and by the release of renin.
19
Q
What are the long term effects of the compensation mechanisms of decreased cardiac output?
A
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.
20
Q
When does compensation start?
A
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.
21
Q
What happens when there is decreased blood flow to the kidneys?
A
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.
22
Q
What are some symptoms of CHF?
A
- 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.
23
Q
What are the drug catergories used for treatment for CHF?
A
****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
24
Q
What lifespan considerations should be taken into account when it comes to Cardiotonic agents in children?
A
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.
25
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)
26
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.
27
What is the drug that we need to know for Cardiac Glycosides?
Digoxin
28
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.
29
What is the overall desired effect of Digoxin?
Increased cardiac output.
30
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.
31
Why would we give Digoxin to patients?
To treat HF, atrial fibrillation, atrial flutter (due to action on the AV node) , paroxysmal atrial tachycardia.
32
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).
33
What symptoms will be worsened by Digoxin due to its slowing effect of the AV node?
Heart block and Sick Sinus Syndrome
34
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)
35
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.
36
What is the name of the Digoxin toxicity antidote and how does it work?
DigiFab.
Binds to Digoxin molecules and inactivates them.
37
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.
38
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
39
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.
40
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.
41
What is the drug we need to know for Phosphodiesterase Inhibitors?
Milrinone
42
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.
43
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.
44
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.
45
When would we be extra cautious of giving Phosphodiesterase Inhibitors to a patient?
When they are pregnant or breastfeeding (no studies)
46
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)
47
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.
48
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
49
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.
50
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.
51
What is the drug that we need to know for Hyperpolarization-Activated Cyclic
Nucleotide–Gated Channel Blockers (HCN blockers) ?
Ivabradine
52
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.
53
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.
54
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)
55
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)
56
What are some known adverse effects of HCN blockers?
Bradycardia (lowering HR too much), hypertension, atrial fibrillation (due to effects on SA node), and luminous
phenomena (sudden changes in brightness in parts of the visual field, colored bright lights, image decompensation, multiple images due to action potential affecting the retina).
57
Are there any drug-drug interactions that we need to be aware of with Ivabradine, and if so, which ones?
CYP3A4 inhibitors or inducers (Azal antifungals, macrolide antibiotics, HIV protease inhibitors, calcium channel blockers & grapefruit juice) - drug levels of Ivabradine may be altered.
Negative chronotropic drugs - may cause severe bradycardia.
58
What assessments should we do prior to prescribing Ivabradine to patients?
Assess for contraindications or cautions
Perform a physical assessment:
Assess pulse and blood pressure; auscultate heart sounds; obtain the patient’s weight and a baseline ECG.
Inspect skin and mucous membranes for color, and check capillary refill.
Assess voiding patterns and urinary output.
Monitor serum electrolyte levels, complete blood count, and renal and hepatic function tests.
59
What are some nursing diagnoses that can be made prior to giving Ivabradine to patients?
Altered cardiac output related to development of arrhythmias or hypotension.
Injury risk related to visual changes.
Altered tissue perfusion (total body) related to hypotension or bradycardia.
Knowledge deficit related to drug therapy
60
What are some nursing implementations that should be made when and after giving Ivabradine to patients?
Monitor heart rate and blood pressure regularly
Monitor input and output and record daily weight
Provide safety measures if visual disturbances occur - fall risk prevention should be put in place.
Provide comfort measures
Provide thorough patient teaching
61
What medications do we need to know for Angiotensin Receptor Neprilysin Inhibitor (ARNI)?
Sacubitril / Valsartan - combination
62
How does ARNIs work?
By decreasing the effect of the RAAS. The drugs prolong the loss of sodium and therefore water which decreases blood volume and cardiac workload.
63
Why would we give Sacubitril / Valsartan to a patient?
To reduce the risk of CV death and hospitalization in adults with chronic HF
It is most effective in patients with low left ventricular ejection fraction and may be used in pediatric patients 1+ years old.
Angiotensin Receptor Neprilysin Inhibitor (ARNI)
64
When should we absolutely not give Sacubitril / Valsartan to patients?
Allergy
History of angioedema (a swelling of the skin and mucous membranes and may lead to swelling in the mouth, throat, lips and tongue - its an allergic reaction ) with ACE inhibitors or ARBs medications may increase the risk of angioedema.
Concurrent use with ACEI
Concurrent use with aliskiren - may cause renal impairment in patients with lower renal function.
Pregnancy and lactation (absolute contraindication)
Angiotensin Receptor Neprilysin Inhibitor (ARNI)
65
What are the most common adverse effects when patients are taking Sacubitril / Valsartan?
Due to the effect on the RAAS, ARNIs may cause hypotension, hyperkalemia, cough, dizziness, renal
impairment.
Angiotensin Receptor Neprilysin Inhibitor (ARNI)
66
Are there any drug-drug interaction with ARNIs that we should be aware of, and if so, what are they?
There are numerous.
ARNIs should not be used with ARBs or ACE inhibitors
Use with Lithium may increase Lithium toxicity.
Should also not be taken with other nephrotoxic drugs due to the increased risk of renal damage.
67
what should we assess for prior to prescribing ARNIs ?
Assess for contraindications or cautions
Perform a physical assessment:
Assess pulse and blood pressure; auscultate heart sounds; obtain the patient’s weight and a baseline ECG.
Inspect skin and mucous membranes for color, and check capillary refill.
Assess voiding patterns and urinary output.
Monitor serum electrolyte levels, complete blood count, and renal and hepatic function tests.
68
What nursing diagnoses can be made prior to administering ARNIs?
Altered cardiac output related to development of arrhythmias or hypotension.
Injury risk related to visual or CV effects.
Altered tissue perfusion (total body) related to hypotension or bradycardia.
Knowledge deficit related to drug therapy.
69
What nursing implementations should we be prepared to make during and after administration of ARNIs?
Monitor heart rate and blood pressure regularly
Monitor input and output and record daily weight
Provide safety measures if visual disturbances occur
Provide comfort measures
Provide thorough patient teaching
70
What is a known adverse effect of milrinone?
Thrombocytopenia (abnormally low amount of platelets)
71
What do we call the resistance from the arteries when the heart is trying to pump blood through them?
Afterload.
72
What do we call enlargement of the heart?
Cardiomegaly
73
What is the group name for conditions that can lead to HF?
Cardiomyopathy
74
What is the term for difficulty breathing which is often paired with anxiety?
Dyspnea
75
What is the term used for coughing up blood?
Hemoptysis
76
What is the term for difficulty with breathing when laying down?
Orthopnea
77
What is the term for drugs that cause stronger muscle contraction?
Positive inotropic agents
78
What do we call the blood that comes back to the heart to be circulated again?
Preload
79
What puts pressure on the ventricles?
Preload
80
What do we call fluid buildup in the lungs?
Pulmonary edema.
81
What is the term for fast and shallow respirations?
Tachypnea
82
What does heart failure lead to?
Decreased cardiac output and fluid buildup.
83
What is stage A heart failure?
Risk factors associated with HF but no symptoms or structural changes
84
What is stage B heart failure?
Structure change due to increased strain but no symptoms
85
What is stage C heart failure?
Structural change and symptoms of HF (fatigue, shortness of breath & fluid retention)
86
What is stage D heart failure?
Structural change and symptoms of HF (fatigue, shortness of breath & fluid retention) AND symptoms are no longer responding to treatment.
87
What is class 1 of the functional classifications of HF?
No physical limitations
88
What is class 2 of the functional classifications of HF?
Slight limitation of physical activity
89
What is class 3 of the functional classifications of HF?
Marked limitations of physical activity
90
What is class 4 of the functional classifications of HF?
Unable to perform any physical activity without symptoms or symptoms worsening.
91
Which disease have the following symptoms: 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 ?
Coronary Artery Disease
92
Which disease have the following symptoms: structural muscular changes and less effective pumping of the heart.
Cardiomyopathy
93
Which disease have the following symptoms: Will lead to cardiomegaly if left untreated because the heart works against pressure.
HTN
94
Which disease have the following symptoms: Valves may leak and then the heart is working twice as hard to pump the blood through.
Valvular Heart Disease
95
Which disease presents itself with an S3 sound?
Congestive heart failure.
96
What symptoms does long term compensation of HF cause?
Cardiomegaly, S3 sounds and tachycardia.Distal pulses may become weaker and hypoxic and patients may feel weak and fatigued.
97
Which drug should not be used to treat V-tach or V-fib?
Digoxin have no effect on these rhythms.
98
Which drugs should be used to treat V-tach and V-fib?
Amiodarone, Lidocaine and procainamide.
99
Due to its effect on slowing the AV node, which drug would have a worsening effect on heart block and sick sinus syndrome?
Digoxin.
100
Why would we not give Digoxin in an acute myocardial infarction?
Dye to its effect on making the heart contract harder/stronger because a stronger beat could worsen muscle damage.
101
Why would we not give Digoxin to patients with kidney issues?
Due to risk of toxicity buildup.
102
What is Headache, weakness, drowsiness, GI upset and anorexia common side effects of?
Digoxin, they could also indicate Digoxin toxicity.
103
What are yellow halos around objects a sign of?
Digoxin toxicity.
104
imbalance of what two electrolytes may cause fatal arrythmias?
Sodium and Potassium.
105
Which drug should be at a therapeutic level of 0.5 ng/mm and 2.0 ng/mm
Digoxin.
106
What type of drug class may make digoxin less effective?
Antacids
107
Under what pulse level should we hold the medication Digoxin?
Pulse under 60
108
Which pulse should we check before administering Digoxin and how long should we check it for?
Apical for 60 seconds.
109
What emergency equipment should we have on standby should Digoxin/ Milrinone toxicity occur?
Potassium salt and lidocaine may help treat arrythmias.
Phenytoin treats seizures.
Atropine will increase heart rate if it drops too low.
110
Which drug(s) should the patients check their own weight and pulse daily?
Digoxin and Milrinone
111
Which drug category is Milrinone?
Phosphodiesterase Inhibitors
112
Which drug is given in acute decompensated HF when the patient are not responding to other medications?
Milrinone
113
Aortic and pulmonic valve problems as well as ventricular arrythmias may be exacerbated by which drug?
Milrinone
114
Why may chest pains occur with the use of Milrinone?
Due to the increased oxygen demand of the heart.
115
Which HF treating agent should Furosemide in IV form NOT be combined with?
Milrinone. Because solid particles may form in the IV line or as an embolism in the patient. Use separate iv lines and take drugs at separate times.
116
Why do you see and increase in GI effect such as decreased motility and anorexia when taking Inotropic agents?
Due to the blood flow increase to other parts of the body and not the GI tract.
117
Which drug must be kept out of the light otherwise it will become ineffective?
Milrinone
118
With whihc drug is the use of a central line preferred?
Milrinone
119
Why should we assess skin for bruising and petechia when a person is taking Milrinone?
To assess for development of Thrombocytopenia.
120
Which drug blocks the HCN and therefore slows the hearts pacemaker & sinus node int he repolarizing phase of the action potential?
Ivabradine
121
Which drug doe we give to reduce the risk of hospitalization for worsening heart failure?
Ivabradine
122
Which drug does not increase contractility?
Ivabradine
123
Which drug works in phase 3 of the action potential?
Ivabradine
124
Which drug specifically work on the SA node
Ivabradine
125
Why is it beneficial to slow the heart rate such as with the use of HCN Blockers/ Ivabrandine?
The ventricles are able to fill more between each contraction increasing cardiac output.
126
Which drug class is good for people that cannot take Beta blockers?
HCN blockers/ Ivabradine
127
Can you give Ivabradine to patients with sick sinus rhythm, AV block, bradycardia or patients with hypotension?
NO. It will worse conditions.
128
TRUE/FALSE
You can give HCN blockers to patients with a fixed rate pacemaker
FALSE
This drug affects the SA node which is the pacemaker region of the heart.
129
Can you give Ivabradine to patients with A-fib?
No. Effects are unpredictable and not shown to be therapeutic.
130
What is a specific adverse effect of Milrinone to be aware of?
Thrombocytopenia.
131
Azal antifungals, macrolide antibiotics, HIV protease inhibitors, calcium channel blockers and grapefruit juice are examples of what and may affect which drug?
CYP3a4 drugs which may alter drug levels of Ivabradine
132
Which drug class has a severe risk for visual changes due to its adverse effect on the retina?
HCN blockers /Ivabradine
133
Which drug blocks the breakdown of natriuretic peptides and inhibits the RAAS?
ARNI's * Sacubitril/valsartan
134
Which drug is used to treat patients from 1+ y.o with systemic left ventricular systolic dysfunction?
Sacubitril/valsartan (ARNI)
135
What is angioedema? Which drug is angioedema a contraindication?
A condition where there are swelling of the skin and mucous membrane which can also lead to swelling in the mouth, throat, lips and tongue.
When using ARNIs with ACE inhibitors or ARBS (Angiotensin 2 receptor blockers) it increases the likelyhood of angioedema.
136
Which drug should Aliskiren not be mixed with as it can call renal impairment in those with lower kidney function?
Sacubitril/valsartan (ARNI)
137
Which drug may cause Hyperkalemia?
Sacubitril/valsartan (ARNI)
138
Can ARNIs be taken with Lithium?
No they should be avoided due to the increased risk of lithium toxicity.
139
ARNIs block the RAAS so the adverse reactions that we should remember are often related to the _______________________
Kidneys
