Lecture 9: Heart Failure & Endocrine Disorders

Lecture 9: Heart Failure & Endocrine Disorders Heart Failure · HF can result from any functional or structural disorder of the heart in which the ventricles cannot adequately fill or eject blood to meet the bodies demands · Any condition that decreases the hearts ability to pump blood can cause HF: ↳ coronary artery disease (CAD) → cardiac muscle is starved and dysfunctional ↳ hypertension → chronic, increases afterload and decreases CO ↳ arrhythmias (v-fib, a-fib, bradycardia) → decreases perfusion and CO ↳ cardiac tamponade → expansion of heart impacted ↳ renal disease → increase in blood volume leads to HTN and increased CO ↳ cardiomyopathy → disease of the heart muscle that makes it harder to pump blood 1. dilated: heart is loose & stretched out, issues contracting 2. hypertrophic: muscle of heart proliferates and becomes thick & non-pliable, difficult to contract 3. restrictive: similar to hypertrophic, but also limited volume in ventricles & atria ↳ congenital heart disease Diagnosis: health history, physical Cardiac Output (CO) exam, vital signs, echocardiogram, · CO = HR x Stroke volume BW (ABG lactic acid) · stroke volume is affected by: ① Preload: the degree of stretch of the heart ② Afterload: the force the heart must overcome to contract and eject blood ③ Contractility: the strength of the contraction of the heart a e i - - - Right Sided HF "Right Ventricular Dysfunction" · impaired ability of the heart to pump deoxygenated blood from the body to the lungs · blood ends up backing up into systemic circulation · peripheral & tissue edema! **A · S&S: JVD, peripheral edema, enlarged liver (or abdomen b/c weight gain), fatigue - - Left Sided HF "Left Ventricular Dysfunction" · impaired ability of the heart to pump oxygenated blood from the lungs to the body · blood backs up into pulmonary circulation · S&S: pulmonary edema, SOB, crackles, fatigue, LOC effects - - Low Output Failure · results from left or right HF · low CO leads to hypotension and hypoxemia ↳ compensation to increase BP and CO Compensation · SNS activation worsens CO (tachycardia, water retention) · release of endothelial enzymes induce smooth muscle cell and fibroblasts to proliferate, leading to hypertrophy of the smooth muscle and fibroblasts (thick & stiff cardiac wall) · risk of arrhythmias (v-fib, a-fib, v-tach, bundle branch block) Diastolic Dysfunction: Systolic Dysfunction: · relaxation of heart is · decrease in contractility, abnormal, cannot fill, decline in ejection fraction - reduced preload (less than 40%, normal is 65%) Bundle Branch Block eclass Video: · the left and right ventricles cannot contract equally to pump blood due to an interruption in the electrical pulses of the heart · can be a LBBB or a RBBB due to a block of the electric stimulus ↳ this causes a delay of conduction, and the heart pumps Heart Failure Tx: unequally which weakens the heart · ACE inhibitors · Tx: CRT device is placed under the collarbone and connects to · ARBs the heart with 3 wires to ensure the electrical signals are equal · Beta Blockers Note: there is another testable video but I am not adding the notes here · Phosphodiesterase inhibitors · Diuretics · ARNIs · Cardiac Glycosides Pharmacotherapy of HF: ① Reduce Preload ② Reduce Afterload ③ Improve Contractility E ARB-Neprilysin Inhibitors (ARNIs) · Neprilysin is an enzyme that breaks down natriuretic peptides (NPs) which are endogenous vasodilators (like NO) · inhibition of neprilysin allows for high NPs causing vasodilation ↳ HOWEVER, NPs Stimulate the RAAS system so we must combine with an ARB to inhibit RAAS · drug: Entresto (sacubitril/valsartan) Cardiac Glycosides · MOA: blocks Na/K ATPase which blocks exit of Na. High Na activates Na/Ca exchanger which then increases contractility ↳ secondary effect: slows electric conduction at AV node and decreases HR · drugs: Digoxin (Lanoxin), Digitoxin ↳ digitalization = starting on digoxin (loading dose) ↳ narrow TI, monitor HR (do not give if apical pulse < 60) ↳ TOXIC: N&V → Tx: Digibind Beta-1 Agonists (Catecholamines) · potent, IV continuous administration (Directly stimulates beta-1 receptors of the heart to increase · Short t 1/2, requires continuous monitoring myocardial contractility and stroke volume, resulting in increased CO) · drugs: Dobutamine, Dopamine HCL ↳ Dobutamine: direct sympathomimetic, high B1 specificity ↳ Dopamine: precursor to norepi, non-selective beta (Causes increased HR and contractility) Acute HF: · O2 · Furosemide (Lasix), IV · Nipride, IV/ET · increase contractility: ↳ phosphodiesterase inhibitor: milrinone ↳ B1 agonist: dobutamine ↳ 35% EF → CRT Chronic HF: (use longer acting less potent drugs) · ACE inhibitors/ARBs instead of direct acting vasodilators ↳ except may use hydralazine · Beta adrenergic blockers · combination diuretics · cardiac glycosides instead of B1 agonists Endocrine Disorders Expected Knowledge: * Thyroid and Parathyroid Glands · The thyroid controls metabolism (basal metabolic rate) · The thyroid has 2 different cell types: ↳ parafollicular cells: secrete calcitonin ↳ follicular cells: secrete T3 and T4 · The parathyroid gland secretes PTH · Calcitonin decreases calcium levels, whereas PTH increases calcium levels (negative feedback loop) - - Thyroid Hormones · iodine is essential for hormone synthesis as iodine binds to tyrosine to create T3 and T4 · T4 is a precursor to T3, and T4 is converted to active T3 by the tissue cells · T3 has a short t1/2 and is immediately active, whereas T4 has a long t1/2 and needs to be converted - - Further Calcium Homeostasis · Calcitriol is an active form of Vitamin D which helps to support calcium absorption in the GI ↳ calcitriol works alongside Calcitonin and PTH in calcium homeostasis · When sunlight hits the skin 7-dehydrocholesterol is converted into Cholecalciferol (Vitamin D3) which is then converted by the liver into 25-hydroxyvitamin D3 (calcidiol) and finally the kidneys convert it into 25-dehydroxyvitamin D3 (calcitriol) which is the active form of Vitamin D for the body TSA ADit ACH FSH LH PR Hypothyroidism · Dx: S&S, BW, TSH & T4 · Common causes: ① Congenital ② Autoimmune (Hashimoto Disease) ③ Iodine Absence in Diet · S&S: low BMR, low sensitivity to SNS, bradycardia, decreased CO, hypoventilation, cold, weight gain, decreased appetite/constipation, depressed CNS, Goiter, myxedema coma (emergency!) ↳ everything slows down · Tx: hypothyroid agents (synthetic hormone) drugs: Levothyroxine (Synthroid, Eltroxin) → synthetic T4 Liothyronine (Cytomel) → synthetic T3 · T3 is for emergencies, whereas T4 is preferred ↳ high PPB, long t 1/2, slow onset ↳ qd (on empty stomach), renal excretion ↳ hepatic metabolism (CYP3A4), active metabolite (T3) Hyperthyroidism · "Graves Disease" · autoimmune thyroid hypersecretion · S&S: goiter, bulging eyes, sweating, tremor (Makes it harder for the body · Tx: to produce thyroid hormone) ① Thioamides eg. Methimazole ② Radioactive isotope eg. sodium iodide ↳ single dose and monitor w - - SIADH · "syndrome of inappropriate ADH" · S&S: "soaked inside" ↳ water retention (no excretion) ↳ low osmolality (too dilute) ↳ high BP ↳ bounding pulses, edema · Tx: diuretics (Lasix, IV), sodium (3% NaCl), fluid restriction DI · "diabetes insipidus" · too little ADH · S&S: "dry inside" ↳ high urine output ↳ high thirst ↳ high osmolality ↳ low BP · Tx: fluids! + synthetic ADH drug: desmopressin ↓ alsouseasends disease (Damages the thyroid gland to bring activity down to normal)