212 Week 10 Notes PDF

REVIEW OF KEY POINTS: Closed system where the blood flows from high to lower pressure The kidneys and heart are sensitive to the quantity and consistency of the blood’s volume. Too little water in plasma results in dehydration. Too much water in plasma causes edema and hype...

REVIEW OF KEY POINTS: Closed system where the blood flows from high to lower pressure The kidneys and heart are sensitive to the quantity and consistency of the blood’s volume. Too little water in plasma results in dehydration. Too much water in plasma causes edema and hypertension (HTN). Various organs help to maintain normal fluid balance, including the kidneys, gastrointestinal tract, and skin Systemic veins and the Pulmonary vessels are distensible (stretchable) with thin walls Systemic arteries are elastic with thicker (smooth muscle) walls The CV system also complements the autonomic NS, pulmonary, and renal systems. Central Perfusion (cardiac output) : Regulation of Cardiac Output Formula: CO = HR x SV Systole: pumping pressure (top number of BP) Diastole: resting pressure (bottom number of BP) Cardiac Output (CO): The heart’s job as a pump. About 5 L/min of blood out of the ventricles. Heart rate: number of beats per minute (AKA pulse) ○ Increased pulse (to a certain maximum effect) should increase cardiac output, but compensatory mechanisms may prevent this. Insufficient filling time with tachycardia causes decreased CO. Stroke volume: amount of blood pumped by a ventricle in a single contraction. impacted by preload, afterload, and contractility Preload: left ventricular end-diastolic pressure. Amount of stretch in the ventricle at the end of the diastole. amount of stretch in the ventricle and the end of the diastole. ○ Cardiac venous return impacts preload (increased return = increased preload) ○ Increased blood volume = increased venous return ○ Peripheral Vasoconstriction INCREASES venous return = increased SV and CO ○ Peripheral Vasodilation DECREASES venous return = DEcreased SV and CO Afterload: systemic vascular resistance. force that ventricles must pump against. the systolic pressure in the aorta that must be overcome for blood to be ejected from the left ventricle. Increased afterload decreases the cardiac stroke volume (and thus CO) ○ Increased afterload causes: —----> Decreased SV + CO Hypertension causes increased cardiac workload Antihypertensive drugs create less afterload, increase stroke volume, and result in less workload for the heart (Adams et al., 2022, p. 473). Contractility: strength (force) of contraction. Should be proportional to the muscle fiber length (stretch). forcefulness of the heart’s pump.  Mean arterial pressure (MAP) or perfusion pressure is the average pressure in the arteries during ventricular contraction and relaxation. MAP determined by three elements: Heart rate Stroke volume, or the amount of blood that is pumped out of the ventricle with each heartbeat Total peripheral vascular resistance (PVR) MAP = CO × PVR [understand the factors composing AMP don’t memorize it] [2xDBP+SBP]/3 Cardiac Contractility: Increased right ventricular DIASTOLIC filling pressure of the right heart is communicated to the left heart and results in increased filling pressure for both ventricles. The increased filling pressure, results in increased CO if the myocardium is not stretched too much. In HF, the muscle tension is decreased. Thus, increased filling pressure doesn’t result in the expected amount of increased CO. Other heart failure key terms include: Cardiomegaly: cardiac enlargement secondary to chronic hypertension, valvular disease, heart failure, and other causes Cardiomyopathy: disease of the heart muscle that leads to a weakened heart and can eventually lead to complete heart muscle failure and death (Tucker, 2022, p. 769). Dyspnea: difficulty breathing or discomfort; often present with left-sided heart failure. Heart failure (HF): ineffective cardiac output/ pumping ability due to structural and/or functional issues. This results in blood/fluid backup or congestion of blood in the pulmonary system or systemic fluid backup (peripheral and dependent edema). Causes or exacerbating factors include coronary artery disease (CAD)/atherosclerotic cardiovascular disease (ASCVD), mitral stenosis, myocardial infarction (MI), chronic hypertension (HTN), diabetes mellitus (DM). Hemoptysis: blood-tinged sputum. This can occur in left-sided heart failure due to pulmonary congestion (fluid volume overload) when fluid backs up into the lung tissue. Pink frothy sputum is characteristic of pulmonary edema (regardless of cause). Nocturia: nighttime urination. In heart failure, this is due to increased renal perfusion with fluid shifts in the supine position when a person has gravity-dependent edema related to heart failure or other medical conditions, including urinary tract infection, increasing the need to get up and void (Tucker, 2022, p. 769). Orthopnea: dyspnea when lying down, often referred to by the number of pillows required to allow a person to breathe comfortably Tucker, 2022, p. 769). Pulmonary edema: increased fluid in the lung tissue that can be due to left-sided heart failure. Note the tissue itself holds the fluid. Thus, it cannot be removed with a with a needle/drainage tube like a pleural effusion (fluid sits inside the lung’s pleural cavity rather than the tissue) can.  INOTROPES: NEGATIVE INOTROPIC DRUGS: Inotropic effect = increased cardiac contractility Decrease cardiac contractility Positive inotropic drugs Quinidine and beta-adrenergic antagonists such epinephrine, norepinephrine, thyroid as propranolol (Inderal) hormone (T3, T4), and dopamine. Alpha 1 adrenergic receptor agonists cause vasoconstriction Beta 1 agonists Alpha 2 adrenergic receptor agonists decrease BP through central effects on the vasomotor center. What about BLOOD PRESSURE? BP = (CO + resistance) INDIRECT MEASUREMENT OF TISSUE PERFUSION Tissue and organ perfusion are dependent upon mean arterial pressure (MAP) DISCUSSION QUESTIONS: What is the effect on BP if preload increases? What is the effect on BP if afterload increases? What is the effect on afterload if preload decreases…if BP is to remain the same? Drugs can act on arterial vascular smooth muscle. Drugs that cause vasoconstriction increase BP Drugs that relax smooth muscle = vasodilation = opening the lumen and lowering blood pressure ENDOCRINE + NS BP Control: Reflexes: BARORECEPTORS: can sense PRESSURE within large VESSELS → Reflex Tachycardia [baroreceptors notice a change in pressure and up the BP] + Atrial Reflex [excessive right atrium stretching triggers reflex, increasing CO + HR until backlog of venous blood is well  distributed] CHEMORECEPTORS: recognize blood levels of O2, CO2, + pH. ○ Chemoreceptor Reflex: activation of the sympathetic NS to increase these values when they get abnormally low. Hormonal Control: [AUTONOMIC NS] Catecholamines: can be endogenous or exogenous epinephrine or norepinephrine - raise blood pressure ADH: released for BP drop or increased osmotic pressure = vasopressin [exogenous ADH is prototype drug desmopressin (DDAVP, Nocdurna)] ADH causes the kidneys to conserve water and increase blood volume, thereby causing blood pressure to increase. Kidneys release the enzyme renin when BP drops. Renin goes through a two-step pathway to create angiotensin II → increases CO + constricts arterioles to raise BP. Promotes the release of aldosterone from the adrenal gland, which causes sodium and water retention. Atrial Natriuretic Peptide (ANP) - NA, H2O, ADH, Aldosterone, ect. ○ Atrial wall stretch stimulates right atrial secretion of ANP ○ Increased renal sodium and water excretion ○ Suppresses ADH and aldosterone release ○ reduces CNS sympathetic outflow, resulting in dilation of peripheral arteries Renin-Angiotensin-Aldosterone System (RAAS): Renin released with BP drops → Angiotensin II causing vasoconstriction + increased CO Indicates/promotes the release of aldosterone → NA & H2O retention RAAS Impacting Drug Classes: affect the reflexes that control BP levels angiotensin-converting enzyme (ACE) inhibitors, which block the conversion of angiotensin I to angiotensin II ARBs, which block the angiotensin receptor site on the blood vessels renin inhibitor, which blocks the reflex at the beginning by inhibiting renin. aldosterone antagonists also alter the RAAS ACEi and ARBs: Both drug classes work by reducing the effect of angiotensin II. BP Classification: (from 2017) NORMAL: or equal to 90  Hypertension: Chronic, progressive disorder More prevalent in older adults, African Americans, Mexican Americans, postmenopausal women, obese patients Antihypertensives treat the symptom to prevent long term adverse consequences – DO NOT CURE HTN ETIOLOGY: neurostimulation, increased blood volume or genetic, environmental, idiopathic SECONDARY HTN: develops in 10% of all people with HTN Etiology: Cushing’s, primary aldosteronism, hyperthyroid, CKD, OSA, pheochromocytoma. ETOH, nicotine, caffeine, decongestants, corticosteroids, estrogen/OC, NSAID, erythropoietin Treat or remove the cause Effects: Increased myocardial demand, O2 consumption, vessel inflammation, atherosclerotic cardiovascular (ASCVD) CV: left ventricular hypertrophy (LVH), CAD, angina, MI; Brain: transient ischemic attacks/stroke (CVA/TIA); Renal: CKD; Eye: retinopathy [vision impairment] CRUCIAL to manage HTN well – especially in chronic kidney disease or DM Treating Hypertension: Lifestyle Modification for mild HTN See Heart Healthy Lifestyle Interventions Slide Meds for Stage 2 HTN and Stage 1 with 10-year ASCVD risk >10% NEVER use ARB with an ACE inhibitor If African American start thiazide diuretic or CCB before ACEi or ARB Non-African American use thiazide or CCB or ACEi or ARB If >18 years and CKD start with ACEi or ARB Calcium Channel Blocker CCB TYPES  BOTH kinds are used to TX angina + HTN CCB: Very Nice Drugs Very verapamil (Isoptin SR, Calan SR – and non SR forms); non dihydropyridine Nice nifedipine (Procardia XL – and non XL); dihydropyridine Drugs diltiazem (Cardizem) non dihydropyridine —-------------------------------------------------------------------------------------------------------------------------------------- Nondihydropyridine CCB nondihydropyridine CCBs – diltiazem (Cardizem) and verapamil (Calan) only significant sinoatrial (SA) and AV node depressant effects, more direct negative inotropic (less heart pumping force) than the dihydropyridine calcium channel blockers more negative chronotropic (lower heart rate) effects than the dihydropyridine calcium channel blockers lesser amounts of peripheral vasodilation more dangerous to use for patients with HF due to potentially decreasing heart muscle function diltiazem (Cardizem): Extended-release diltiazem is used for adult HTN and angina Immediate release diltiazem is used for angina and arrhythmias (rapid atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia-PSVT) Antianginal doses are LOWER than antihypertensive doses verapamil (Calan) Extended-release verapamil is used for HTN only Immediate release verapamil is used for arrhythmias (rapid atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia-PSVT) —---------------------------------------------------------------------------------------------------------------------------- Dihydropyridine CCB – ALL CCB EXCEPT for diltiazem and verapamil, amlodipine (Norvasc), nicardipine (Procardia), nifedipine primarily peripheral vasodilatory actions → More peripheral vasodilation, Less negative inotropic, Less rate effect, Less risk with HF (CCB) nifedipine (Adalat CC, Procardia XL): Used as monotherapy or adjunct for adult HTN and angina nimodipine, nifedipine, amlodipine (Norvasc) —---------------------------------------------------------------------------------------------------------------------------- Atherosclerotic CardioVascular Disease ASCVD Events: Angina pectoris > ACS > MI Transient ischemic attack (TIA) Ischemic stroke (CVA) Peripheral Arterial Disease (PAD) Dyslipidemia and CVD Risk Factors for Major Adverse Cardiovascular Events (MACE): Obesity, CKD, HTN, Male, >65 yrs old, DM, Smoking, Race, family Hx CAD or hyperlipidemia, BP, ASA, BP meds, Labs Heart Healthy Lifestyle Interventions: No tobacco and more exercise Less saturated fats & cholesterol and low fat dairy & lean meat Less sodium and alcohol More fruits, veg, whole grains Treat Anyone with HLD if ASCVD Risk is: LDL-C greater than 190 mg/dL 40 to 75 years + LDL 70-189 mg/dL + 10-year risk 7.5% or more 40 to 75 years + LDL 70-189 mg/dL + DM Documented Clinical ASCVD —---------------------------------------------------------------------------------------------------------------------------- Cardiac Ischemia Ideal = myocardial O2 demand = O2 supply Low O2 (supply, pulmonary) Insufficient blood flow | | \/ Inadequate blood flow Hypotension/ severe HTN Hemorrhage, anemia Atherosclerosis | | \/  Myocardial ischemia -> angina Myocardial infarction Disability/death Ischemia occurs DISTAL to the vascular occlusion —---------------------------------------------------------------------------------------------------------------------------- Coronary artery disease (CAD) US- one of leading mortality causes Narrowing or occlusion of one or more coronary arteries. Coronary artery stenosis (narrowing) can result in symptoms of angina pectoris Coronary artery occlusion = MI Most patients who experience an MI have coronary vessel stenosis in other vessels (atherosclerosis) Primary CAD etiology = atherosclerosis secondary to plaque resulting in partial or complete intraluminal occlusion as platelets and fibrin deposits build up on the plaque NORMALLY an increased cardiac workload -> coronary artery dilation (increases myocardial O2 delivery). The fibrous nature of atherosclerosis decreases arterial elasticity = inadequate vasodilation. —---------------------------------------------------------------------------------------------------------------------------- Angina indicates a moderate stage of CAD. Anginal pain characteristics: Retrosternal = behind sternum Typically, not reproducible (i.e., musculoskeletal pain can be “caused” or reproduced) with movement or touch Radiation – sometimes (classic but not necessarily classic in females or diabetics) Left shoulder Left arm Posterior thoracic (esp. if back or inferior vessels/myocardium are affected) Jaw or epigastric region Scary – worried about health and life OR denial “not pain, just pressure” pallor, dyspnea (difficulty breathing) with cyanosis (blue discoloration r/t hypoxia), diaphoresis (sweaty), tachycardia, and elevated blood pressure (may be low! Depending on area affected). Often follows exertion, excitement short duration: May resolve with rest within 5 to 15 minutes. Anginal Treatment goals: 1. Decrease anginal intensity and frequency 2. Improve exercise tolerance and perform ADLs 3. Long term: Prevent ASCVD progression and dysrhythmias, HF, MI Nonpharmacologic CAD/angina/MI prevention includes: Diet, ETOH, tobacco Exercise Weight Pharmacologic MI/Angina Prevention includes: Lipid levels (Statin) BP control (ACE inhibitor) Glycemic control (metformin if DM2, insulin if DM1) Antianginal Treatment (Tx): Restore balance between oxygen supply & oxygen demand Vasodilation + Decrease work of the heart Prevent myocardial ischemia & resultant pain. Prevent myocardial death & infarction. Provide symptomatic treatment, but will not cure underlying pathology of CAD 4 DRUG CLASSES USED TO TREAT ANGINA: Nitrates, beta-adrenergic blockers, calcium channel blockers, and piperazine acetamides [ranolazine (Ranexa)] Angina Prophylaxis (DECREASE FREQUENCY) and/or Abortive (if rate control): MOAa: 1. Negative chronotropic (reduces rate) 2. Vasodilation (reduces preload) 3. Negative inotrope (less contractility/work) 4. Decreases BP (lowers afterload) —---------------------------------------------------------------------------------------------------------------------------- Chronic Kidney Disease (CKD) refers to an alteration in kidney function for a minimum of 6 months CKD is staged from stage 2 (mild) through stage 5 (dialysis needed to live). Decreased GFR* and increased Creatinine labs taken at least 6 months apart indicates CKD. (sometimes called eGFR for estimated) Proteinuria and albuminuria (protein or albumin protein present in the urine) also indicates kidney damage even if the labs are normal. Proteinuria or albuminuria indicate stage 2 (mild) kidney disease. Labs will indicate if the CKD is worse than stage 2. *GFR is the gold standard for kidney function. If a reference book mentions creatinine clearance (CrCl) values, use the GFR in place of the CrCl. A normal GFR is at or above 90 mL/min, but some sources including hospital lab references will list GFRs above 60 (not correct!) CKD is often caused by poor HTN control, especially chronic. Also caused by chronic hyperglycemia (diabetic nephropathy becomes CKD). Some POTENTIALLY nephrotoxic drugs: NSAIDs, ACE inhibitors, ARBs, IV contrast agents used for radiographic tests (i.e., heart catheterization, imaging tests with contrast such as CT scans, etc.). Inappropriate use of diuretics or high doses can be nephrotoxic as well. All diuretics can cause renal failure if given to a patient who is dehydrated All diuretics are contraindicated in acute or complete renal failure and very cautious use in moderate renal failure Acute kidney injury (AKI), also called acute renal failure Most often due to inadequate kidney blood pressure (renal hypoperfusion). Seen if the MAP is below 60 mmHg for longer than the kidney can tolerate (varies based on overall and renal health) Renal hypoperfusion causes: heart failure (HF) Poorly perfusing dysrhythmias Hemorrhage Nephrotoxins Dehydration (hypovolemia) Changes seen with kidney disease include: (Adams et al., 2022, p. 531). Anemia (CKD only). Treated with Epoetin alfa (Epogen, Procrit) to stimulate RBC production. Hyperkalemia (high serum potassium (K) due to inadequate excretion). Treated with polystyrene sulfonate (Kayexalate) with sorbitol – intestinal exchange of potassium for sodium – results in diarrhea Hyperphosphatemia (high serum phosphate (P) due to inadequate excretion). Treated with dietary phosphate restriction, oral phosphate binders (including Tums (calcium carbonate) or prescription). Hypervolemia (volume overload due to ineffective sodium and water excretion causing H2O retention). Treated by dietary sodium restriction, loop diuretics in acute conditions, thiazide diuretics in mild conditions Hypocalcemia (low serum calcium (Ca) due to hyperphosphatemia). Treated by fixing hyperphosphatemia and possibly calcium supplements. Metabolic acidosis (inadequate hydrogen ion and other metabolic acid excretion) Treated with Sodium bicarbonate or sodium citrate. MUST check for altered renal drug dosing if AKI or CKI. —---------------------------------------------------------------------------------------------------------------------------- IMPORTANT FOR TRUE SULFA ALLERGY: all diuretics EXCEPT potassium sparing (triamterene, spironolactone, and amiloride) and the loop diuretic ethacrynic acid are sulfonamide derivatives and contain a sulfa group. Diuretics: Increase urine excretion (diuresis) Increase sodium and potassium excretion and other electrolytes to a lesser extent (Chloride, magnesium, potassium, phosphate, calcium, and bicarbonate)  Decrease edema (peripheral edema and pulmonary edema) Excess fluid excretion improves HTN HF CKD Some signs of hepatic failure (liver failure’s portal HTN causes ascites = fluid collection in the abdomen. Image here: https://tinyurl.com/2s3mafsv) Some diuretics are used to decrease fluid pressure in the eye (intraocular pressure [IOP]), which is useful in treating glaucoma Potassium wasting diuretics are sometimes used to treat hyperkalemia (high serum potassium) Most Common Diuretic MOA: Sodium and the H2O it’s dissolved in are excreted in the urine rather than resorption into blood. block sodium ion (Na+) reabsorption in the nephron increases urinary sodium excretion (called natriuresis) RETAINING 1% of sodium through reabsorption can cause a 4-pound (1.8 L) water weight gain but… EXCRETING more sodium results in increased urine/ fluid excretion which can cause volume depletion and circulatory collapse (hypovolemic shock) Net Effect: Decreased fluid volume Diuretic effect dependent on site of action within the kidney Loop or high-ceiling: furosemide (Lasix), torsemide (Demadex) Prevent sodium reabsorption in the loop of Henle. The loop’s filtrate contains high Na+ amounts = potentially large volume of diuresis with loop diuretics. FUROSEMIDE 3 MAJOR ADEs: severe hypokalemia/electrolyte imbalance (hyperglycemia, hyponatremia, hypocalcemia, hypomagnesemia), hypochloremic metabolic alkalosis, hypovolemia/ dehydration, ototoxicity (tinnitus and reversible or irreversible hearing loss) Thiazides. hydrochlorothiazide (HydroDiuril, Microzide), chlorothiazide (Diuril) act by blocking Na+ in the distal tubule. Because most Na+ was reabsorbed before reaching the distal tubule, thiazides diurese less than loop diuretics. Thiazide like diuretics: chlorthalidone, indapamide, metolazone inhibits distal convoluted tubule sodium and chloride resorption MAJOR ADEs: renal failure, non-melanoma skin CA, Severe hypokalemia/electrolyte imbalance Potassium-sparing: spironolactone (Aldactone) have minimal effect on potassium ion (K+) excretion. Mild diuresis.  Osmotic: mannitol (Osmitrol) relatively inert drugs that change the osmolality of filtrate, causing water to remain in the nephron for excretion. Crosses the blood brain barrier= used for increased intracranial pressure (ICP), brain edema, and increased intraocular pressure (IOP) very effective but are rarely prescribed because they can produce potentially serious adverse effects. Carbonic anhydrase inhibitors Acetazolamide (Diamox) block the enzyme in the nephron responsible for bicarbonate reabsorption. Weak diuresis = rarely used for diuresis. Are used for open or closed angle glaucoma, altitude sickness, drug induced edema. –----------------------------------------------------------------------------------------------------------------------------- Potassium Balance: Hyperkalemia + Hypokalemia BOTH can cause dysrhythmias Hyperkalemia (K above 5.3 mEq/L) and Hypokalemia (K under 3.5 mEq/L)* This number varies by lab reference. Some labs note normal potassium (K) as 3.3 to 3.5 ranging from 5.0 to 5.5 mEq/L Signs/Sx of Potassium Imbalances Hyperkalemia Hypokalemia can be asymptomatic can be asymptomatic generalized fatigue palpitations (irregular HR/rhythm) muscle weakness muscle weakness or cramping paresthesias paralysis flaccid paralysis constipation palpitations (irregular HR/rhythm) N/V irritability abd cramps nausea, vomiting, diarrhea polyuria, nocturia, or polydipsia abd cramps psychosis, delirium, hallucinations dyspnea depression chest pain dyspnea, respiratory failure hypotension FOODS HIGH IN K+ instant oatmeal, dried apricots dates prunes figs, raw avocado + banana, cooked beets, cooked brussel sprouts, cantaloupe, raw kiwi, lima beans, honeydew melons, fat free skim milk, nectarines, OJ, fresh pears, dry roasted peanuts, baked potato with skin, prune juice, raisins, cooked spinach, tomato products, winter squash, plain yogurt. –----------------------------------------------------------------------------------------------------------------------------- Heart Failure’s (HF) decreased cardiac output (CO) triggers a cycle of compensatory mechanisms that ultimately WORSEN HF. Decreased cardiac output Results in decreased renal perfusion (blood flow) Renin-angiotensin-aldosterone system (RAAS) is activated Water and sodium are retained Increased plasma volume in the blood Causing pulmonary edema and peripheral edema Increased sympathetic activity cause Positive chronotropic (increased rate) and inotropic (increased contractility) effects = increased workload Vasoconstriction = increased afterload The above compensatory mechanisms cause more myocardial dysfunction and worsen the heart failure and accelerate the ventricular remodeling (Adams et al., 2022, p. 608). Two Heart Failure Classification Systems are used: 1. American College of Cardiology and American Heart Association (ACC/AHA) have classified HF in four stages (structural+symptoms): Stage A: At high risk for HF but without structural heart disease or symptoms of HF Stage B: Structural heart disease but without signs or symptoms of HF Stage C: Structural heart disease with prior or current symptoms of HF Stage D: Refractory HF requiring specialized interventions 2. The New York Heart Association (NYHA) has defined functional classifications of HF: Class I: No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF.  Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. Class IV: Unable to perform any physical activity without symptoms of HF, or there are symptoms of HF at rest. Ventricular ejection fraction HF classification: Normal ventricular ejection fraction = 55% to 70% of the left ventricle’s (LV) volume is pumped out with each beat systolic HF – also called HF with reduced ejection fraction (HFrEF) = LV ejection fraction (EF) is ≤40%. Heart has ineffective contractility pumping ability and its shape changes over time – called left ventricular remodeling. diastolic dysfunction HF HFpEF ≥50%. Abnormal relaxation of the heart muscle that impairs filling the ventricles with blood. Both types of HF can lead to impaired blood flow, decreased perfusion of tissues, and fluid overload. People can also have a mixture of both systolic and diastolic dysfunction. (Tucker, 2022, p. 770). Where did the 40-50% EF go? There is a VERY rarely discussed midrange HF with mid-range EF (HFmrEF where LVEF is 40–50%) SYMPTOMS of HF: Dyspnea (difficulty in breathing = DIB) Dependent edema Fatigue Orthopnea Ascites (heart failure can cause portal hypertension which can cause ascites over time). Portal HTN is elevated BP in the liver’s portal vein leading to the liver. Heart failure back pressure can cause this. Ascites is fluid collection in the abdominal cavity. Pulmonary edema Nocturia Altered mental status (AMS) – can devolve into a vascular dementia or vascular cognitive impairment Right Sided HF Left Sided HF Elevated jugular venous pressure (JVP, JVD) Tachypnea, dyspnea, orthopnea, hemoptysis, crackles/rales Splenomegaly Anxiety Hepatomegaly Cardiomegaly Decreased renal perfusion when upright S3 Increased heart rate  Increased supine renal perfusion > nocturia GI upset, nausea Abdominal pain Pitting edema Decreased peripheral pulses Weakness/ fatigue Hypoxia Non Pharmacological Adjuncts for HF management: Optimal lipid levels 150 mins of exercise weekly Maintain healthy weight and heart healthy diet Glycemic control Maintain a BP WNL Evidence-Based Drug Therapy for CHF: ARNI/ACEi/ARB + BB + prn diuretic GFR >or equal to 30 an not hyperkalemic add aldosterone antagonist GFR > or more than 30 either dapagliflozin (Farxiga) or empagliflozin (Jardiance) [approved SGLT2] Diuretic if persistent volume overload If African American and on ACE/ARB/ARNI+BB+ aldosterone antagonist add hydralazine +isosorbide dinitrate If on max beta blocker dose and HR > or equal to 70 add ivabradine ARNI: sacubitril/valsartan (Entresto) ARNI = angiotensin receptor blocker/neprilysin inhibitor drug class. ARNI is preferred over ACE/ARB but not seen as often due to cost, kidney concerns, etc. Causes vasodilatation and blood volume reduction increases renal sodium and water excretion Improves cardiac ventricular remodeling Decreases preload and afterload Decreases blood pressure, especially SBP ACE Inhibitors & ARBs decrease preload, afterload, and BP increase cardiac output cause vasodilation Increase sodium and water excretion Slow and may reverse ventricular remodeling prolong life Beta Blockers – 3 approved for use = *carvedilol, metoprolol succinate or bisoprolol  slow progression of HF & improve left heart functioning Minimal effect on preload but do reduce afterload Careful dosage required to maintain perfusion pressure but not work the heart too hard (heart rate under 70 and BP low without signs/symptoms of hypotension/hypoperfusion) FYI: GDMT recommended daily target doses of evidence-based beta-blockers are 200 mg metoprolol succinate; 10 mg bisoprolol; and 50 mg carvedilol Diuretics decrease volume overload (preload) decrease venous return and blood pressure, which decreases afterload, preload, and cardiac workload. aldosterone antagonist (spironolactone) for most patients with HF if GFR ≥ 30 and not hyperkalemic Decreases preload and afterload Improves diastolic function Can reverse LV remodeling SGLT2 Approved for heart failure as of 2022 are: dapagliflozin (Farxiga) and empagliflozin (Jardiance) Improves LV remodeling Decreases preload and afterload Cardiotonic (inotropic) Drugs: cardiac glycosides and phosphodiesterase 3 inhibitors cardiac glycosides [digoxin (Lanoxin)] and phosphodiesterase 3 inhibitors [Amrinone (Inocor), milrinone (Primacor)] affect the intracellular calcium levels in the heart muscle, leading to increased contractility (+ inotropic). Inotropic = increased cardiac output increased renal blood flow and increased urine excretion Increased renal perfusion decreased renin release (inhibiting RAAS) Further urine output = decreased blood volume Beta agonists – reserved for life threatening emergency management (will work the heart harder and cause ischemia!) Beta 1 agonists: dobutamine (Dobutrex), norepinephrine (noradrenaline), dopamine (in high doses). Beta-1 and beta-2 agonists: Epinephrine (adrenaline), isoproterenol (Isuprel).