05 - Cardiorenal Drugs

Loop diuretics such as Bumetanide and Furosemide.

BP medication for patients with DM, angina, supraventricular tachyarrhythmias, migraine, and cluster headache.

The diameter of the vessels and the force of contraction exerted in the smooth muscles.

To dissolve clots and prevent embolism.

Diltiazem and verapamil.

To reduce the ability of the blood to clot or promote hemostasis.

Platelets.

They cause the body to convert hepatic cholesterol to bile acids, decreasing hepatic cholesterol levels and increasing the number of LDL receptors to clear LDL-cholesterol in the blood.

Treatment of Type IIA hyperlipoproteinemia (familial hypercholesterolemia) in patients unable to lower LDL levels through dietary changes.

Vital signs, specifically SBP < 90 mmHg and HR < 60 bpm.

Combining with niacin, mycin, or fluoroquinolones can increase myopathy or rhabdomyolysis, which may lead to renal failure.

Inhibits aldosterone secretion and blocks angiotensin II from binding to receptor sites, preventing vasoconstriction.

Hypersensitivity, early myocardial infarction, severe anemia, angle-closure glaucoma, orthostatic hypotension, cardiac tamponade.

Bradycardia, nausea, vomiting, and diarrhea.

They can increase bleeding tendencies when taken with anticoagulants.

The heart and the blood vessels.

Vasodilation, flushing, hepatotoxicity, nausea, vomiting, diarrhea, and epigastric pain.

DVT, Pulmonary embolism, DIC, unstable angina, post MI, cerebral thrombosis, heart failure, atrial fibrillation.

Record weight each morning after voiding and before breakfast.

Compete with beta-adrenergic receptor sites in the heart and inhibit renin release in kidneys.

Blood collects in the SVC and IVC, enters the right atrium, passes through the tricuspid valve to the right ventricle, and then goes to the pulmonary circuit.

Metoprolol, Atenolol, and Bisoprolol.

To reduce blood pressure by decreasing circulatory blood volume through increased urine output.

They cause vasodilation and reduce myocardial oxygen demand.

Effects usually decrease when dosage is reduced.

It occurs as a consequence of left-sided heart failure, leading to increased pressure in pulmonary arteries and workload on the right ventricle.

The ability to spontaneously develop action potentials.

They prevent the passage of Ca ions into the cell membrane of myocardial smooth muscle, resulting in arteriolar vasodilation, decreased cardiac workload, blood pressure, afterload, and O2 demand of the heart.

Blood vessels constrict to prevent blood leakage.

Water reabsorption.

Increased digoxin toxicity if the patient has hyperkalemia.

It has a low therapeutic index and may cause toxicity.

Weight, blood pressure, and electrolyte imbalances, especially potassium levels.

Clonidine, as it can worsen CNS depression.

Heparin, Warfarin, Antiplatelets, Factor XA inhibitors, Thrombolytic drugs.

Nitrates, beta-adrenergic blockers, and calcium channel blockers (CCB).

They compete with beta-adrenergic receptors and inhibit renin release in kidneys.

The kidneys, ureters, bladder, and urethra.

Pre-infarction or crescendo angina.

A condition where the heart cannot pump enough blood to meet the myocardial oxygen demand.

Relax vascular smooth muscles, decreasing afterload and cardiac workload.

Antiplatelets and NSAIDs.

Asthma, tachycardia, cardiogenic shock, second or third-degree heart block, and heart failure.

Carbonic Anhydrase Inhibitors, Loop Diuretics, Osmotic Diuretics, Thiazide Diuretics, and Potassium-sparing Diuretics.

Increased QT interval, torsades de pointes, thrombocytopenia.

Alcohol.

Phytomenadione (Vitamin K).

Cardiac output (CO) = Stroke volume (SV) x Heart rate (HR).

The sum of the formed elements and plasma volume in the vascular system.

Hypercalcemia and hyperkalemia, along with hydration.

The resistance of fluid to flow; increased viscosity leads to increased flow resistance.

A state of elevation in systemic arterial blood pressure caused by an increase in peripheral vascular resistance.

Essential hypertension (most common, cause unknown) and secondary hypertension (5%, caused by other diseases).

They inhibit the conversion of angiotensin I to angiotensin II.

It causes the kidneys to produce renin.

Increases osmotic pressure of glomerular filtrate, inhibiting sodium and water reabsorption.

It decreases triglyceride and apolipoprotein B-100 levels while increasing HDL levels by inhibiting hepatic synthesis of lipoproteins.

Systolic blood pressure greater than 180 and diastolic blood pressure greater than 120, requiring immediate hospitalization if there are no signs of organ damage.

Digifab.

Hypotension and reflex tachycardia.

WBC and differential counts, as well as potassium levels.

Inhibits renin production.

They inhibit vasomotor centers in the brainstem, decreasing sympathetic outflow.

To treat peripheral edema.

To maintain sodium, potassium, water, and other electrolytes regulation through reabsorption and secretion.

Blood accumulates in the pulmonary circuit.

They control arrhythmias by altering myocardial cell membranes and decreasing Na+ influx.

Inhibits Vitamin K synthesis in the liver.

Blocks the action of carbonic anhydrase, preventing the exchange of H+ ions with sodium and water.

Hemorrhage, prolonged bleeding time, hepatitis.

The pressure the cardiac muscle exerts to move blood into the aorta.

Bleeding, pancytopenia, neutropenia, hemorrhage, thrombocytopenic purpura, abnormal stools, pain at injection site.

Impotence, bradycardia, depression, worsens asthma.

A clot that moves inside the blood vessel, which can cause problems in smaller vessels like the brain, potentially leading to ischemic stroke.

Blood volume is directly proportional to blood pressure; a decrease in blood volume results in a decrease in blood pressure.

Acute hypovolemia, hypokalemia, hypomagnesemia, hyperuricemia, and ototoxicity.

Used for AV node arrhythmias.

Digitalis-induced arrhythmias and Torsades de pointes.

Monitor for rebound hypertension due to abrupt withdrawal.

Internal damage to the internal layers of blood vessels.

They reduce cholesterol production early in its formation, mobilize cholesterol from tissues, and increase cholesterol excretion.

It is a potent vasoconstrictor that increases blood pressure.

Insufficient oxygen supply to the myocardium due to coronary artery issues.

Headache, fatigue, dizziness, cough, and symptoms of upper respiratory tract infection (URTI).

Pregnancy, as they are teratogenic.

To pump blood and carry it to the body for oxygenation and nutrients.

Hypersensitivity to nicotinic acid, hepatic or renal dysfunction, active peptic ulcer disease, gout, heart disease, muscle disorder, or arterial bleeding.

They interfere with the coagulation pathway by neutralizing factor Xa, inhibiting thrombin and thrombus formation, especially in newly formed thrombi.

Stroke, peptic ulcer, coagulation disorders, active bleeding, and severe thrombocytopenia.

Chlorothiazide, Indapamide, Metolazone, and Hydrochlorothiazide.

Protamine sulfate.

Bradycardia, hypotension, fatigue, lethargy, and erectile dysfunction.

It initiates the heartbeat.

Prevent pulmonary embolism caused by DVT, MI, prosthetic heart valves, or chronic AF.

Alteplase, Reteplase, Tenecteplase, Urokinase, Streptokinase.

Inhibits Na and Cl absorption in the loop of Henle, increasing Na and water excretion.

Ventricular arrhythmias.

Prolongs phase 3 repolarization and increases effective refractory period.

They compete with beta-adrenergic receptor sites in the heart muscle and inhibit the release of renin in the kidneys, decreasing the availability of angiotensinogen II and aldosterone.

To lower abnormally high blood levels of lipids, such as cholesterol, triglycerides, and phospholipids.

To assist in platelet aggregation and stabilize platelet plug formation.

A mechanism of blood clotting activated by chemicals called clotting factors.

Cholestyramine, colesevelam, and colestipol hydrochloride.

Headache, dizziness, orthostatic hypotension, tachycardia, flushing, palpitation, nausea/vomiting.

By promoting the movement of calcium from extracellular fluid to intracellular fluid.

Both intrinsic and extrinsic pathways activate prothrombin (X) factor, converting it to thrombin, which activates fibrinogen to form fibrin.

Combines with antithrombin III to inactivate thrombin and inhibits the conversion of fibrinogen to fibrin, preventing clot formation.

Teach proper use of sublingual tablets, inform about common headaches, avoid alcohol, and monitor for tolerance.

Hyperkalemia, gastric upset, and gynecomastia in males.

Stress.

They inhibit the conversion of angiotensin I to angiotensin II.

The SA node (pacemaker).

Fondaparinux.

Phase 0: Depolarization; Phase 1: Balanced Na+ ions; Phase 2: Plateau; Phase 3: Rapid repolarization; Phase 4: Resting phase.

Monitor blood cholesterol and lipid levels, check CK levels, and assess for fat-soluble vitamin deficiency.

It decreases systemic arteriolar resistance and reduces afterload.

Thromboembolic disorders such as AMI, acute ischemic stroke, and PAOD.

The end-diastolic pressure and the work imposed on the heart before contraction begins.

Arrests platelet aggregation, thereby preventing thrombolytic events.

CNS toxicity.

Atrial flutter (AF), ventricular arrhythmia.

Dizziness, headache, fatigue, and peripheral edema.

Heart failure and AV blocks due to their negative inotropic and dromotropic effects.

Atorvastatin, Rosuvastatin, Simvastatin.

Na, Cl, K, Ca, Mg, and HCO3.

Decreases ectopic pacemakers.

Captopril and Enalapril.

Heart failure (HF) and hypertension (HPN), and they are most effective in treating ascites.

• CCB can cause orthostatic hypotension; + erectile dysfunction drugs and alcohol can lead to hypotension.

Prazosin and Doxazosin.

They are teratogenic.

By decreasing circulatory blood volume through increased urine output, resulting in improved cardiac output.

Bruising, hematoma formation, skin necrosis, and thrombocytopenia.

To inhibit the absorption of cholesterol and related phytosterols from the small intestine.

They block angiotensin II from binding to its receptors, preventing vasoconstriction.

Back pain, fatigue, abdominal pain, and pharyngitis.

It is commonly caused by myocardial infarction (MI), cardiomyopathy, and chronic hypertension.

Reduced blood volume, orthostatic hypotension, hypokalemia, hyperglycemia, and hyponatremia.

They can decrease the effects of levodopa and interact with beta blockers, prazosin, tricyclic antidepressants, verapamil, lithium, and MAOIs.

The patient's apical pulse.

In a cool, dark place in a tightly closed container.

The amount of blood ejected from the left ventricle with each contraction.

Last drug for refractory ventricular arrhythmias.

Blocks Ca channels, slows AV node conduction, and shortens action potential.

Cardiac glycosides, beta blockers, vasodilators, and diuretics.

Digoxin.

Trauma.

They affect collecting ducts and distal tubules, excreting sodium, water, bicarbonate, and calcium while retaining potassium and hydrogen ions.

In rapid atrial fibrillation (AF) and AV nodal reentry.

Selective antagonism of A1 receptors in peripheral vasculature to produce vasodilation.

Increased intracranial pressure, acute renal failure due to shock, drug toxicities, and trauma.

Aldosterone antagonists (e.g., spironolactone, eplerenone) and sodium channel blockers (e.g., triamterene).

Changes in blood pressure are detected by baroreceptors located in the aorta and carotid sinus.

Central-acting sympatholytics, peripheral-acting sympatholytics, calcium channel blockers, vasodilators, and diuretics.

Thiazide and thiazide-like diuretics along with ACE inhibitors and ARBs.

Nephrons.

Depression, drowsiness, edema, dry mouth, and impotence.

They dissolve an existing thrombus by converting plasminogen to plasmin, which lyses thrombi and other plasma proteins.

Go to the emergency department.

Acetazolamide and Methazolamide.

Bleeding, arrhythmias, urticaria, fever, hemorrhage.

Decrease Na influx in ischemic episodes, shorten phase 3 repolarization, and decrease action potential duration.

SVT, post-MI, arrhythmia prophylaxis.

They inhibit HMG-CoA reductase, decreasing hepatic cholesterol synthesis and increasing LDL receptors to reduce plasma cholesterol concentration.

Na, Cl, and K.

Potassium status and blood glucose levels.

Monitor for bleeding, ensure proper dietary management, and advise on fluid intake and reporting severe constipation.

Administer 1 hour before or 4 hours after bile-sequestering drugs like cholestyramine.

Losartan and Valsartan.

Dry cough, fever, altered taste, hypotension, and hyperkalemia.

Active bleeding, thrombocytopenia, severe liver impairment, underlying coagulation disorder, ulcer disease, recent surgery, cancer.

It increases sodium reabsorption in the proximal convoluted tubule (PCT).

Monitor for bruising and bleeding, minimize venipunctures and injections, apply pressure to puncture sites, and monitor hemoglobin, clotting factors, and platelet levels.

ECG for arrhythmias and watch for reflex tachycardia and orthostatic hypotension.

The interatrial septum.

Aliskiren.

Sodium, potassium, glucose, amino acids, bicarbonate, and water.

Asthma.

Hyperkalemia, as it enhances digitalis toxicity.

Metabolic acidosis, hypokalemia, and renal stone formation.

Aspirin, Clopidogrel, Dipyridamole, Ticlopidine, Abciximab, Tirofiban.

Forms new forms of arrhythmias.

Atrial fibrillation (AF), AV node re-entry.

Prevent the passage of calcium ions into cell membranes, resulting in arteriolar vasodilation.

Aminocaproic acid.

Decrease Na influx, slow phase 0 depolarization, slow conduction velocity, and increase QRS duration.

Bradycardia, torsades de pointes, photosensitivity, hypotension.

Decreases SA node automaticity and AV nodal conduction, increases PR interval.