05 - Cardiorenal Drugs

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

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

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 dissolve clots and prevent embolism.

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

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.

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

Loop diuretics such as Bumetanide and Furosemide.

Platelets.

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

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

Diltiazem and verapamil.

Hypercalcemia and hyperkalemia, along with hydration.

Blood vessels constrict to prevent blood leakage.

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

Dizziness, headache, fatigue, and peripheral edema.

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.

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

To assist in platelet aggregation and stabilize platelet plug formation.

Cardiac glycosides, beta blockers, vasodilators, and diuretics.

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

Water reabsorption.

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

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

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

Used for AV node arrhythmias.

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

Digoxin.

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

Increased digoxin toxicity if the patient has hyperkalemia.

Na, Cl, and K.

Atorvastatin, Rosuvastatin, Simvastatin.

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

Digitalis-induced arrhythmias and Torsades de pointes.

Cholestyramine, colesevelam, and colestipol hydrochloride.

Trauma.

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

It has a low therapeutic index and may cause toxicity.

Potassium status and blood glucose levels.

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

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

Monitor for rebound hypertension due to abrupt withdrawal.

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

They inhibit the conversion of angiotensin I to angiotensin II.

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

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

Decreases ectopic pacemakers.

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

Internal damage to the internal layers of blood vessels.

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

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

It causes the kidneys to produce renin.

Clonidine, as it can worsen CNS depression.

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

Captopril and Enalapril.

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

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

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

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

Losartan and Valsartan.

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

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

Bradycardia, nausea, vomiting, and diarrhea.

It is a potent vasoconstrictor that increases blood pressure.

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

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

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

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

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

They can increase bleeding tendencies when taken with anticoagulants.

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

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

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

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

The heart and the blood vessels.

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

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

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

Digifab.

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

Prazosin and Doxazosin.

Pregnancy, as they are teratogenic.

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

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

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

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

Hypotension and reflex tachycardia.

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

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

They are teratogenic.

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

Hyperkalemia, gastric upset, and gynecomastia in males.

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

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

WBC and differential counts, as well as potassium levels.

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

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

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

Stress.

The kidneys, ureters, bladder, and urethra.

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

Inhibits renin production.

The interatrial septum.

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

Bruising, hematoma formation, skin necrosis, and thrombocytopenia.

Record weight each morning after voiding and before breakfast.

They inhibit the conversion of angiotensin I to angiotensin II.

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

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

The SA node (pacemaker).

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

Pre-infarction or crescendo angina.

Nephrons.

To treat peripheral edema.

Aliskiren.

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

Fondaparinux.

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.

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

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

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

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

Metoprolol, Atenolol, and Bisoprolol.

Back pain, fatigue, abdominal pain, and pharyngitis.

Relax vascular smooth muscles, decreasing afterload and cardiac workload.

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

Chlorothiazide, Indapamide, Metolazone, and Hydrochlorothiazide.

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

Antiplatelets and NSAIDs.

Blood accumulates in the pulmonary circuit.

Protamine sulfate.

They cause vasodilation and reduce myocardial oxygen demand.

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

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

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

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

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

Effects usually decrease when dosage is reduced.

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

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

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

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

Inhibits Vitamin K synthesis in the liver.

It initiates the heartbeat.

It decreases systemic arteriolar resistance and reduces afterload.

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

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

Asthma.

Increased QT interval, torsades de pointes, thrombocytopenia.

Go to the emergency department.

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

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

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

The ability to spontaneously develop action potentials.

The patient's apical pulse.

Hyperkalemia, as it enhances digitalis toxicity.

Alcohol.

Acetazolamide and Methazolamide.

Hemorrhage, prolonged bleeding time, hepatitis.

Alteplase, Reteplase, Tenecteplase, Urokinase, Streptokinase.

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

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

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

Metabolic acidosis, hypokalemia, and renal stone formation.

Phytomenadione (Vitamin K).

Bleeding, arrhythmias, urticaria, fever, hemorrhage.

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

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

Arrests platelet aggregation, thereby preventing thrombolytic events.

Aminocaproic acid.

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

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

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

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

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

Ventricular arrhythmias.

CNS toxicity.

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

Last drug for refractory ventricular arrhythmias.

Forms new forms of arrhythmias.

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

SVT, post-MI, arrhythmia prophylaxis.

Impotence, bradycardia, depression, worsens asthma.

Prolongs phase 3 repolarization and increases effective refractory period.

Atrial flutter (AF), ventricular arrhythmia.

Bradycardia, torsades de pointes, photosensitivity, hypotension.

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

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