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what is the normal cardiac output?
4-5 L/min
what is stroke volume?
the amount of blood pumped out of the left ventricle with each heartbeat
heart failure with reduced ejection fraction (HFrEF) is a _____________ issue
contractility
heart failure with preserved ejection fraction (HFpEF) is a _______ issues
muscle stiffness & preload
what are the avaialble pharmacological treatments available for heart failure?
ACE inhibitors
Angiotensin Receptor Blockers
Angiotensin receptor/neprilysin inihibitors
Mineralocorticoid receptor antagonist (MRAs)
Beta-blockers
Sodium-glucose cotransport inhibitors (SGLT2Is)
Diuretics
how does ACE inhibitors work to help with heart failures?
it reduces the cardiac workload in that it dilates the arteries which reduces the arterial pressure the heart would have to overcome to push the blood so essential the heart would work less to push the same amount of blood to the body
if ARBs is similar to ACEIs with fewer side effects (less risk of angioedema and no nagging dry cough), why are ACEIs still used today?
People still use ACE inhibitors because they are often the first choice for certain conditions, like heart failure and after a heart attack, due to more extensive clinical data showing benefits in preventing death and cardiovascular events. While ARBs have fewer side effects like cough and are a good alternative for those who can't tolerate ACE inhibitors, the quality of evidence for ACE inhibitors is more robust for specific outcomes
what is the therapeutic effects of ARBs for heart failure?
very similar to ACEIs → decrease the pressure in the arteries by causing vasodilation -? which decrease the blood pressure and the afterload which in turn decrease the cardiac workload
what is one lab value that the nurse should pay attention for patient using ARBs and why?
enzymes concerning the liver as since the medication is metabolized by the liver, it can cause liver toxicity or liver failure
what are the nursing considerations for ACEIs and ARBs?
avoid high-potassium food → because these medications can cause accumulation of potassium (ARBs - angiotensin II is blocked so aldosterone cannot be release to get rid of sodium, and ACEIs block the creation of angiotensin II)
report side effects like swelling of the face and lips and difficulty breathing
discontinue if pregnant, trying to become pregnant, or breastfeeding (they are teratogenic!!!)
report signs and symptoms related to low blood pressure or stroke
what are the first-line medications for heart failure?
ACE inhibitors
beta-blockers
angiotensin receptor/neprilysin inhibitors (ARNIs)
what is angiontensin receptor/neprilysin inhibitor (ARNIs)? how does it work? what are the adverse effect and drug interactions?
basically an ARB and neprilysin inhibitor combined (e.g., sacubitril + valsartan (Entresto)
Neprilysin inhibitor prevent the breaks down BNP (brain natriuretic peptide) to prolong vasodilation, decreasing afterload and preload (BNP help create vasodilation as a mechanism by the brain to reduce the workload on the heart)
adverse effects: angioedema, hypotension, renal impairement, hyperkalemia, fetal toxicity, cough
drug interactions: potassium-sparing diuretics, NSAIDs, ACEIs, ARBs,
do not take ARNIs with what medications?
ACE inhibitors & ARBs
what kind of beta-blocker do we use for hypertension and what kind do we use for heart failure?
hypertension: non-selective beta-blocker (sometimes selective can also be use)
heart failure: cardio-selective beta-blocker (e.g., bisprolol and metoprolol)
which beta-blocker that are not cardio-specific but are known to work well with heart failure?
carvedilol
true or false: different from the cardio-selective beta-blocker, non-selective beta-blockers can also affect the lung, causing bronchoconstriction
TRUE!!!!! that why non-selective for not recommended for patient with breathing issues like asthma!!!!
are beta-blockers recommended for patients with asthma? Why or why not?
Non-selective beta-blockers (β₁ + β₂ blockers) are NOT recommended → they can block β₂ receptors in the lungs → bronchoconstriction and asthma attack risk.
Selective (β₁-only, cardioselective) beta-blockers like metoprolol, atenolol may be used with caution if necessary → lower risk of bronchospasm but still monitor breathing.
Always assess lung sounds, breathing difficulty, oxygen saturation, and history of severe asthma before giving.
what should a nurse monitor before giving a beta-blocker? When should they hold it?
Monitor before/during administration:
Heart rate (HR) → hold if < 50–60 bpm (or per doctor order)
Blood pressure (BP) → hold if systolic < 90–100 mmHg
Signs of heart block → check ECG, dizziness, syncope
Breathing (especially if COPD/asthma)
Blood glucose in diabetics
Do not stop abruptly → risk of rebound hypertension / tachycardia
Nursing judgment → HOLD if:
✔ HR too low
✔ BP too low
✔ New wheezing or bronchospasm
✔ Severe dizziness or signs of heart block
how do beta-blockers affect patients with diabetes?
Beta-blockers can mask symptoms of hypoglycemia (like tachycardia, tremors) → patient may not feel low blood sugar coming.
They block β₂ receptors in liver, which reduces glycogen → glucose release → risk of prolonged hypoglycemia.
Nurses should:
Monitor blood glucose more frequently
Teach patients to look for other signs of hypoglycemia (sweating, confusion, hunger)
Use β₁-selective agents if needed (safer than non-selective)
a patient is taking valsartan, carvedilol, and spironolactone daily, what monitoring should the nurse educate the patient about to ensure safe medication administration?
electrolytes, because two of the medications cause an elevation in potassium
electrolytes, because two of the medications cause a decrease in potassium
glucose, because the combination of the medications can lower blood glucose
uric acid because the combination of the medication can increase uric acid
electrolytes, because two of the medications cause an elevation in potassium
true or false: some beta-blockers can increase potassium so the nurse should keep that level in mine when judging whether the patient should take the beta-blocker or not
true! Beta blockers work by blocking the effects of adrenaline (epinephrine) and noradrenaline (norepinephrine). This can lead to: Reduced potassium uptake into cells, Increased release of potassium from cells, and Decreased excretion of potassium in the urine.
which type of heart failure/antihypertensive medications have been found to reduce the risk of all-cause mortality in patients with heart failure?
MRAs - mineralocorticoid receptor antagonist
spironolactone is a potassium-sparing diuretics but what specific type of medication is it?
mineralocorticoid receptor antagonists (MRAs)
what is the common suffix for MRAs?
-one
what are the nursing considerations for MRAs?
low potassium diet
monitor serum potassium and renal functions and following dose changes for patient with heart failure or chronic kidney disease (CKD)
contraindicated in preganancy
contraindicated in patient with kidney disease
what is the main differences between loop diuretics and thiazide and thiazide-like diuretics? how do each of them work?
the main differences is where these medications work in the kidney
loop diuretics: block the reabsorption of sodium, chloride and potassium in the loop of Henle, more potent than thiazide diuretics, first choice in treating HF
thiazide and thiazide-like diureticsL block reabsorption of sodium and chloride in distal renal tubule, less potent
which of the four classes of diuretics is the first choice treatment for HF?
loop diuretics
which of the four classes of diuretics is the first choice treatment for hypertension?
thiazide and thiazide-like diuretics
what is a common example of loop diuretics?
furosemide (Lasix)
what is the MOA, indications and adverse effects for furosemide (Lasix)?
MOA: blocks reabsorption of sodium in the loop of Henle, which causes sodium and water to be excreted
indications: HTN, congestion, and/or edema in HF
adverse effects: anaphylaxis, tinnitus/hearing loss, anemia, SJS, ototoxicity, excessive loss of water and electrolytes, decrease in blood pressure, photosensitivity, increase blood glucose level, and decrease potassium
what type of electrolytes imbalances we should watch out for when administering furosemide (Lasix)?
increased glucose
decrease potassium
if furosemide are being pushed IV, wat is one important factor that the nurse should consider? when does the medication peaks and when does it taper off?
pushed it SLOWLY! the medications will peaks after 30 minutes and start to taper off after 2 hours
when does diuresis happened for oral and IV furosemide (Lasix)?
oral: 30-60 minutes after ingestion
IV: 2-5 minutes after infusion
how long does Lasix typically last in the body?
about 6 hours (remember…laSIX!)
what are the first line medications for HFrEF and HFpEF?
HFrEF (a problem with the left ventricle contractility)
ACE inhibitor
ARBs
beta-blockers
mineralocorticoid receptor antagonist (MRAs)
HFpEF (a problem with the left ventricle no filling properly)
diuretics
beta-blockers
sodium-glucose cotransporter-2 (SGLT2)
what is the medication we primarily use for heart failure that is in the cardiac glycoside class?
digoxin
how does digoxin work? how is the dosing/therapeutic range, adverse effects, and toxicity?
Causes more calcium to enter the cardiac cell, leading to stronger contraction (positive inotropic) → also stimulates the parasympathetic nervous system
complicated dosing (loading dose, maintenance dose with considerations of weight, age, renal function, concomitant drugs) → therapeutic range of 0.5-2.0 ng/mL
adverse effects: cardiac arrhythmias, bradycardia, a yellow or green halo around lights, and atrial tachycardia
toxicity can cause anorexia, nausea, vomiting, visual changes, and cardiac arrhythmias
what is the therapeutic range of digoxin?
0.5-2.0 mg/mLbb n
what are one conditions relating to arrhythmia that cannot be treated with digoxin?
ventricular fibrillations
A patient with heart failure who had been taking valsartan recently had the medication switched to sacubitril/valsartan. The patient understands how valsartan works but is confused about sacubitril. The nurse explains that sacubitril:
a. lower heart rate to allow for more oxygen to get to the heart muscle
b, inhibits ACE, which lowers BP
c. helps BNP stays in the system longer, which lowers BPstay
d. causes nitric oxide to be released into the smooth muscle, which lower BP
c. helps BNP stays in the system longer, which lower BP
The nurse is caring for a patient with heart failure who takes digoxin. Which assessment finding should the nurse report to the health care provider prior to administering the drug?
heart rate 54 beats/minute (this is because one of the adverse effects of digoxin is bradycardia)
what is the common suffix for thombolytics?
-plase
how does thrombolytics (AKA fibrinolytics) works? what are the adverse effects, contraindications, and nursing considerations for thrombolytics?
break down a clot very quickly → convert plasminogen to plasmin, which plasmin then performs fibrinolysis (clot breakdown)
adverse effects: bleeding, risk of dysrhythmias
contraindications: bleeding, recent surgery, recent intracranial or intraspinal surgery, or uncontrolled hypertension
nursing consideration: bed rest, neuro checks, skin checks, dedicated IV (established before medical administration), and the timeline of the medications (when can you give it after certain disease happen)?
what are one thigs the nurse should know of their patient before administering thrombolytics?
have they had any recent surgery (e.g., intracranial, intraspinal) as this medications poses a high risk for bleeding
an emergency department nurse is assessing a patient with an acute ischemic stroke prior to administering alteplase. Which finding will the nurse need to discuss with the provider prior to administering alterplase therapy?
total knee replacement surgery 6 months ago
blood pressure of 197/110 mmHg
Glucose level of 168 mg/dL
Past medical history of gastroesophageal reflux disease (GERD)
blood pressure of 197/110 mmHg
not 1 because it is not as of a priority compared to the blood pressure