NURS 331 Unit II PDF

Regulation of Cardiac Performance (week 6) ○ Cardiac Output: the measurement of cardiac performance Cardiac Output (CO) = HR x SV HR = beats per minute SV = volume ejected during systole ○ SV is further divided int...

Regulation of Cardiac Performance (week 6) ○ Cardiac Output: the measurement of cardiac performance Cardiac Output (CO) = HR x SV HR = beats per minute SV = volume ejected during systole ○ SV is further divided into preload, afterload, contractibility Normal CO = 4-6 liters/minute Cardiac Output is the volume of blood the heart pumps through circulatory system within one minute If HR decreases, SV will increase to compensate; if SV increases, HR will decrease ○ Ejection Fraction (EF): The % of blood that is pushed out of the left ventricle with each beat EF is influenced by myocardial contractility (inotropic force) ○ ↑ SNS stimulation = ↑ contractility ○ ↓ Ventricular function/failure = ↓ contractility EF is determined by echocardiography (an ultrasound probe that goes on the chest and looks at blood flow) ○ Is used to evaluate the prognosis of people with heart disease or heart failure Normal EF = 55-75% ○ Preload (VEDV or CVP): Preload is the volume & pressure inside the ventricle at rest (just before contraction). AKA: ventricular end-diastolic volume (VEDV) —> venous return during diastole, central venous pressure (CVP) Think about Preload as “how much fuel is in the tank”-- how much vascular volume is returning to the right side of the heart? Higher volume = higher pressure Lower volume = lower pressure High Preload:  High preload refers to excessive ventricular filling that stretches the myocardium beyond what is normal (fluid volume overload). ○ ↓ SV is due to poor contraction ○ ↑↑ Preload = ↓ CO (from decreased SV) Excessive high preload → chronically leads to heart failure (HF) (from decreased contractility) ○ Think about how a balloon loses integrity when it is constantly being blown up excessively over and over. ↑ Pressure in the ventricle at rest will cause backup of blood ○ Left: lungs – pulmonary edema ○ Right: rest of the body (systemic) – peripheral edema (jugular venous distention) Low Preload: Poor ventricular filling will lead to no myocardial stretch ○ ↓ SV ○ ↓ Preload = ↓ CO Example: ○ Dehydration ○ Blood loss Hypovolemia ○ Afterload: Afterload is ventricular resistance – the pressure that the ventricles must overcome in order to contract Ventricular pressure must exceed aortic pressure in order to open the aortic/pulmonic valve and eject blood ↑ afterload is caused by narrowed arterial lumens from plaques, obstructions, vascular remodeling and vasoconstriction, valvular stenosis High arterial pressure = high afterload Slowed contraction; higher workload; ventricular hypertrophy Vasoconstriction  Low arterial pressure = low after load Heart contracts more; rapidly & efficiently Vasodilation ○ Contractility: Contractility is the force of contraction Contractility refers to ability of myocardial fibers to shorten and recoil effectively ○ Muscle fibers need to stretch a little bit to achieve maximum force/contractility ○ Muscle fibers need to rest to reach optimal contractile strength Changes in the stretching of the ventricular myocardium = preload ○ Where excessive preload will impair SV because of inadequate rest periods ○ ↑ venous return/preload will distend the ventricle ○ ↑ volume/preload = ↑ SV & CO Frank Starling’s Law ○ Other Factors that Impact Contractility: CHEMICALS: Inotropic Stimuli: ○ Positive (↑ contractility) or negative (↓ force of contraction) Epi/norepinephrine (SNS) = positive Acetylcholine (PSNS) = negative ○ Profound inflammation: Cytokines (TNF) = negative ○ Oxygen supply: mild/moderate ↓O2 (SNS) = positive Compensatory Arterial oxygen saturation 7.45 ; HCO3 > 26 ↑ in HCO3 and pH → excess H+ ion loss or HCO3 gain Causes: Decrease in acids (HCl) from vomiting (losing significant amount of acid) or gastric suctioning Excessive diuretic usage (H+ and K+ loss from kidney) Increase in base from using antacids (excessive use) Hyperaldosteronism (NaHCO3 retention & H+/K+ loss in the urine) Patient Presentation: Neurologic – may experience disorientation (less frequent) Musculoskeletal– weakness, tetany, hypocalcemia (because Ca2+ will bind to albumin) Respiratory – depression, bradypnea, hypoventilation (compensation) Treatment: Difficult to treat → isotonic fluids for hypochloremia, maybe iatrogenic ○ Respiratory Acidosis: pH < 7.35; CO2 > 45 Acute or chronic Compensation: kidneys will try and eliminate H+ and retain HCO3 People with chronic respiratory acidosis will have chronically high levels of HCO3 Causes: Alveolar hypoventilation; hypercapnia Depression of the respiratory center ○ Drugs, head injury, post op sedation OSA (obstructive sleep apnea) Problems with the chest wall ○ Pain, injury, abdominal distention Disorders of lung parenchyma ○ PNA, atelectasis, COPD Patient Presentation: Pulmonary – slower RR, decreased TV (tidal volume) Neurologic – H/A, disorientation Integumentary – warm & flushed (increased CO2 concentration → causes pink skin) Treatment: Increase ventilation ○ Oxygenation alone will not solve problem *ventilation must be the first problem to solve, then oxygen second ○ Respiratory Alkalosis: pH > 4.5 ; CO2 < 35 Can be acute or chronic Compensation: kidneys will try and retain H+ ions and eliminate HCO3 Causes: Alveolar hyperventilation Anxiety; pain; fear  Hypocapnia, hypoxemia, pulmonary disease, HF ○ Poor perfusion → hyperventilation to compensate Hypermetabolic state → fever, sepsis, thyrotoxicosis (via compensation) Patient Presentation: Neurologic – numbness; tingling; dizziness; disorientation; cerebral vasoconstriction (low PaCO2) MSK – hypocalcemia; tetany; carpopedal symptoms Treatment: Look for the cause Monitor for repository fatigue/failure  Hypertension (week 7) ○ The most significant risk factor for CV disease ○ The leading cause of morbidity and mortality (worldwide) ○ HTN → increases risk for: MI, HF, cerebral infarction, hemorrhage, renal disease ○ Definitions: Normal → SBP = < 120 mmHg; DBP = < 80 mmHg Stage 1 → SBP = 130-139 mmHg; DBP = 80-89 mmHg Stage 2 → SBP = >140 mmHg; DBP = >90 mmHg Hypertensive Crisis → SBP = >180 mmHg; DBP = >120 mmHg ○ Classifications: Primary → 90-95% : Genetics Obesity smoking/alcohol Insulin resistance High salt intake (salt-sensitive people) Aging Sedentary lifestyle Stress Secondary → caused by other diseases: Renal disease (not filtering and eliminating fluids) Endocrine diseases (e.g., thyroid issues) CNS (e.g., stress hormones) ○ May be cured by managing underlying issue ○ Regulation: Blood pressure → force exerted on arterial walls by blood flow Cardiac Output (HR x SV) → systolic pressure Peripheral vascular resistance (PVR) → diastolic pressure ○ Autoregulation:  Ability of tissues to regulate its own blood flow (homeostatic) → constriction or dilation Will depend on the nutritional needs of the tissue Changes in regulation are determined by: Lack of O2 Cellular metabolism byproducts ○ Key chemical mediators: Histamine ○ Mast cells & tissue injury SNS → stimulated when SNS is blocked/withdrawn and causes vasodilation ○ Bradykinin Dilate the arteries/arterioles & constrict veins/venules ○ Serotonin Released from aggravating platelets (vasoconstriction) ○ Prostaglandins Responds to tissue injury and vasodilates ○ Neural Regulation: SNS (fight or flight): ↑ HR = ↑ CO Vasoconstriction = ↑ vascular resistance Activation of RAAS Procoagulation effects hypercoagulopathy Over time, vascular remodeling will occur and ↑ insulin resistance from SNS stimulation → hyperglycemia ○ RAAS: Renin = enzyme synthesized/stored in the kidneys and respond to decreased BP, SNS stimulation (decreased Na+ concentration) Compensatory: ○ Restores blood pressure and blood flow to tissues  ○ Renin released from the kidneys: Decreased blood flow, SNS stimulation, decreased Na+ concentration ○ End result: ↑ preload and vasoconstriction = ↑ BP ○ Endothelial Cells → BP control: Produce vasoconstricting substances: ○ Angiotensin II ○ Endothelin I ○ Thromboxane II Produce vasodilating substances: ○ Nitric oxide (NO) ○ Prostacyclin Balance between vasoconstriction and vasodilation will contribute to atherosclerosis, HTN and other diseases ○ Vessel injury = ↑ vasoconstrictors (thrombus formation) ○ Long Term Regulation → Natriuresis Natriuretic hormones (protective) play an important role in renal sodium excretion ○ Normal functioning → hormones will respond to ↑ BP by promoting vasodilation and Na+ excretion, leading to decreased BP Opposite effect when overwhelmed ○ System can become overwhelmed when: Electrolyte disturbances occur (decrease K+, Ca+, MgSO4) Too much volume (wont have protective function) ○ Largest Contributors to HTN: Increased vascular resistance: ○ Angiotensin II (potent vasoconstrictor) ○ ↑ PVR  ○ Arteriolar vasoconstriction Increase in circulating volume: ○ Aldosterone (RAAS) ○ Sodium and water retention (renal system) ○ K, Ca, Mg loss Loss of natriuretic function ○ Other contributors to HTN: Inflammation ○ Endothelial damage, decrease NO, smooth muscle contraction, insulin resistance Insulin resistance ○ Decreased NO, renal function leading to Na/H2O retention, SNS hyperactivity Obesity ○ Adipokine dysfunction leading to ↑ appetite and decreased metabolism, growth factors leading decreased NO and vessel narrowing Inflammation, insulin resistance and obesity all lead to vascular remodeling ○ Potential complications of HTN: Profoundly alters CV function: ○ ↑ workload causing myocardial hypertrophy → HF Initially asymptomatic, where symptoms will eventually reflect target end-organ damage (heart, brain, kidneys, eyes)  Pharmacologic Management of HTN (week 7): ○ Autonomic Nervous System (ANS): SNS & PSNS PSNS → rest & digest Cholinergic receptors: Stimulation releases Acetylcholine → facilitates physiologic response ○ Eyes → constrict (miosis) ○ SA node → rate decreases ○ Bronchial muscle → constriction ○ Arterioles → dilation ○ Gastric motility → increased ○ Increased bodily secretion → ↑ lacrimal secretions or foaming at the mouth ○ “Tropes” Inotropic: Force of contraction Chronotropic: Rate of conduction of SA node (+ or -) Dromotropic: Rate of conduction of AV node ○ Epinephrine Nonselective adrenergic agonist: Activates beta 1 or beta 2, and alpha 1 Sympathomimetic (SNS) → vasoactive catecholamine vasoconstrictor /vasopressor IND: Cardiac life support, pulseless electrical activity, asystole, bradycardia (↓ CO), anaphylaxis, severe asthma ○ Medication Management of HTN: Is initiated when lifestyle modification is unsuccessful  SBP → >140 mmHg or DBP → >90 mmHg Multiple Groups → will decrease CO or PVR: ACE inhibitors ARBS CCBs Anti-adrenergic Diuretics Direct vasodilators Key Considerations: Antihypertensives: Recommendations → stage I: ○ Lifestyle modifications ○ Monotherapy First Line Medications: ○ ACEi, ARBS, or CCBs, or thiazide diuretics Recommendations → stage II: ○ Lifestyle modifications ○ Combinations therapy with two different classes of antihypertensives Ethnicity: ○ African Americans: More likely to have severe HTN and need multiple medications. Will have decreased Renin, increased Na sensitivity and increased rate of obesity ○ Asian Americans: Generally require much smaller doses of beta blockers due to slow metabolism and excretion (increased risk of toxicity) General Teaching Guidelines: Patients may need several visits to providers to figure out the best medications and combinations as well as best dose.  Do not stop taking HTN medications abruptly (unless angioedema occurs). Routinely monitor BP at home at the same time everyday (log in a journal) Steps to avoid dizziness: ○ Change positions slowly, wear elastic stockings, avoid prolonged standing and hot baths (heat will cause dilation) ○ Discuss persistent dizziness with the provider. Dyslipidemia (week 8): ○ Imbalance of lipid components of the blood ○ Triglycerides: Used in energy metabolism 3 FA + 1 glycerol ○ Phospholipids: Structural: Lipoproteins, blood clotting, myelin, cell membrane ○ Cholesterol: Created from FAs Activities are similar to other lipids ○ Hyperlipidemia: Interchangeable with dyslipidemia → elevated levels of one of all of the above (triglycerides, phospholipids, cholesterol) ○ Lipoproteins: Cholesterol + triglyceride → combine with H2O soluble proteins Travel through plasma Chylomicrons: Carry triglycerides to GI tract for absorption Very low density lipoproteins (VLDL): Carries large amounts of triglycerides + cholesterol Have higher protein content than chylomicrons  Low density lipoproteins (LDL): Main carrier of cholesterol 50% + 10% triglycerides High density lipoproteins (HDL): 50% protein Least amount of fat ○ Low-Density Lipoprotein (LDL) → associated with high cholesterol content: Transports 75% of cholesterol to tissues and liver LDL removed by receptor and non receptor mechanisms Most receptors found in the liver → cells regulate cholesterol intake by adding/removing LDL receptors Conditions that decrease LDL receptors → high dietary intake of cholesterol and saturated fat When serum cholesterol is too high, there are less receptors to remove LDLs, and when levels are too high there are more receptors to remove LDLs. Non Receptor removal = macrophages in arterial cell walls attach to LDL and promote accumulation of cholesterol and development of atherosclerosis ○ LDL vs. HDL: LDL: 75% of receptors are located in hepatocytes Can be removed by macrophages ○ ↑ uptake of LDL by macrophages in the arterial wall can lead to atherosclerosis (plaque build up) If the liver has excess amounts of cholesterol: ○ LDL receptors decrease ○ Increase LDL in blood ○ → high cholesterol HDL: Facilitates reverse transcriptase of cholesterol → back to the liver  behavior modification can increase HDL → low cholesterol ○ Dyslipidemia Criteria: ↑ triglycerides ↑ total serum cholesterol ↑ LDL Decreased HDL 12 hour fasting for test to be accurate ○ Hypercholesterolemia → amount of cholesterol in the blood is strongly related to dietary intake of saturated fat Serum cholesterol levels: 240 mg/dL or greater Levels that could contribute to a heart attack, or other cardiovascular event associated with atherosclerosis ○ Classifications: Primary dyslipidemia → genetic: Defective synthesis of apoproteins Lack of defective receptors Cellular deficits in handling of cholesterol Secondary dyslipidemia → behavioral: Dietary factors, excess alcohol Obesity (caused inflammation), hypothyroidism Metabolic changes associated with DM II ↑ adipokines and ↑ macrophages are linked to systemic chronic inflammation ○ Metabolic Syndrome: Group of CV risk factors linked with obesity → need to get back to normal levels ↑ triglycerides Decreased HDL cholesterol ↑ BP  ↑ fasting blood glucose ○ ALL will ↑ CV risk ○ Dyslipidemia Treatment Guidelines: Assess and treat conditions known to ↑ blood lipids Start low-fat diet Eat “mediterranean diet” Increase dietary intake of soluble fiber Dietary supplements and cholesterol-lowering margarines Start weight-reduction diet (if the patient is overweight or obese) Emphasize regular aerobic exercise Smoking cessation Postmenopausal hormone replacement therapy ○ Medication Goals: Decrease blood lipids Prevent or delay atherosclerotic plaque development Promote regression of existing atherosclerotic plaque Reduce morbidity and mortality from CV disease Pharmacotherapy initiated when 6 months of dietary/lifestyle changes fail to decrease dyslipidemia to acceptable levels  Coronary Heart Disease and Pharmacologic Management (week 8): ○ Coronary Heart Disease: Consist of two general categories: Coronary Artery Disease (CAD): ○ Reduction of blood flow to the heart due to build-up of atherosclerotic plaque → can become ischemic and die (MI) Acute Coronary Syndromes (ACS): ○ Unstable angina ○ Myocardial infarction ○ Atherosclerosis: Damage to the intimal arterial lining, leading to a buildup of lipids and fibrous materials Risk factors: Hypercholesterolemia ↑ LDL Family Hx ↑ age Male vs. female HTN Diabetes Obesity Smoking Physical inactivity Stress Elevated hs-CRP ○ Pathogenesis of Atherosclerosis: 1. Endothelial dysfunction/injury Caused by ↑ LDL, smoking, immune mechanisms and mechanical stress (high blood pressure) → adhesion of monocytes and platelets (injury → inflammation)  2. Inflammatory Cell Migration Macrophages engulf LDL & become/morph into foam cells → releases toxic O2 species that will oxidize engulfed LDLs 3. Lipid buildup + SMC Proliferation Accumulation of foam cells = lesion progression (fatty streak); growth factors ↑ SMC and will narrow the lumen. ○ *lots of foam cells = fatty streak 4. Plaque Structure Formation of fibrous cap. Rupture may lead to thrombotic occlusion of vessel lumen ○ C-Reactive Proteins: hs-CRP → when elevated, indicates MI Acute phase reactant protein of the inflammatory process Can serve as a general clinical marker of risk for atherosclerotic vascular disease ○ Progression of Atherosclerosis: Inflammation Key determinant of plaque vulnerability ○ Is related to ↑ number of macrophages at the site Rupture of plaque results in endothelial injury Causes platelet aggregation Forms thrombus → may stay there, or break off and travel Releases vasoconstrictive mediators Thrombus occlusion Occludes the artery or detaches and occludes smaller, distal branches ○ Stable Angina → “classic”, “typical”, “exertional” O2 demand > O2 supply = ischemia Precipitated by factors that ↑ myocardial workload Exercise, cold weather, emotional upset (things that ↑ O2 demands)  Clinical Manifestations: Substernal chest pain (elephant foot) Pain radiation (usually to the left arm) Often mistaken as other problems (such as indigestion) N/V, dizziness, dyspnea Men vs. Women Will present differently (e.g., women may not exhibit chest pain and there is a delay in seeking care). Diabetes People with diabetes will present differently Pathogenesis of Stable Angina Ischemia or obstruction → decreased blood flow ○ Myocardial cell injury Disruptions in Na/Ca → electrolyte abnormalities Causes dysrhythmias, mechanical dysfunction, shift from aerobic → anaerobic metabolism (absence of O2) = lactic acidosis = PAIN Usually lasts five minutes or less ○ Variant Angina AKA: prinzmetal or vasospastic angina (not always associated with occlusion) Will occur at rest or with minimal exertion (where stable angina is exhibited with exertion) Often at night and frequently at the same time each day Often people experience variant angina in clusters: 3-6 mos followed by symptom free periods May be linked to dysrhythmias (w/ continuous spasm) or progress to MI ○ Acute Coronary Syndromes Stable Angina and MI ○ Unstable Angina → crescendo, rest, or preinfarction angina  Typically occurs at rest + lasting longer than 20 minutes Clinical Manifestations: Similar to stable angina intensity , timing, and characteristics have ↑ severity Ischemia is not severe enough to cause significant damage to myocardium Will often occur hours or days before an acute MI ○ Electrocardiogram Basics P wave = atrial depolarization QRS complex = ventricular depolarization ST segment = ventricular repolarization Would look at the ST segment for indications of MI T wave = ventricular relaxation ○ Myocardial Infarction – NSTEMI Thrombus formation from plaque disruption → partial occlusion of vessel ST depression, or T wave inversion, or no ECG changes ○ Myocardial Infarction – STEMI Thrombus formation from plaque disruption → full occlusion of vessel ST elevation ○ MI: S/S Manifestations depend on stage and progression Phase One: Classic symptoms of chest pain and dyspnea, generalized discomfort SNS activation (↑ HR/BP) As MI progresses with treatment → decreased CO = decreased HR/BP ○ Ultimately, SV will decrease and HR will ↑ , but as the MI progresses the CO will decrease and thus, SV and HR will decrease  Will present with pallor, duskiness, cool, diaphoretic, pain, SOB, sense of impending doom ○ Serum Biomarker: Troponin Troponins may be elevated with an MI; however, profound elevation of troponins may indicate a MI Troponin assays (Tnl or TnT) have high specificity for diagnosing an ACS As myocardial cells become compromised, their intracellular contents diffuse into the interstitium and blood Levels will rise with in 3 hours after onset of MI and may remain elevated for 7-10 days ○ Goals of Pharmacological Management: To increase perfusion to the heart Coronary artery dilation Decrease O2 demand ○ General teaching guidelines for medications for CHD: Take medications as prescribed → do not increase dosage or stop taking without talking to a provider Keep sublingual nitroglycerin in its original container, keep within reach, but not exposed to body heat Replace nitroglycerin every 6 months Keep a chest pain journal and record use of nitroglycerin Avoid OTC decongestants, cold remedies, and diet pills (will stimulate SNS, causes angina, and ↑ O2 demands) Remove nitroglycerin patches/paste at night to prevent tolerance Try to take BP before self-administering nitroglycerin under the tongue Apply nitroglycerin patches/paste at the same time each day to clean, dry, and hairless areas on upper body Dispose of used patches/paste properly. Can be lethal to children and pets. Teach patient how to check pulse rate Beta blockers should be held during bradycardia  Coagulation Modifiers (week 9) ○ Hemostasis Principles Hemostasis is the process that maintains vascular integrity Several interacting activators and inhibitors: ○ Endothelial factors ○ Platelets ○ Blood coagulation factors (produced by the liver) Coagulation modifiers: Prevent clots from forming or becoming larger to restore blood flow to the tissues Anticoagulants, antiplatelets, thrombolytics ○ Coagulation Regulation: Delicate Balance: PRO-coagulation chemicals: Platelets ○ Synthesize thromboxane (TXA 2) Is a potent vasoconstrictor and induce platelet aggregation Von Willebrand factor (factor VIII) ○ Released during vascular injury + activates platelets Activated clotting factors ○ Formed by the liver Tissue thromboplastin ○ Released by damaged endothelial cells, activates factor VIII + X, then converts prothrombin → thrombin Anti-Coagulation chemicals: Prostacyclin ○ Produced by endothelial cells ○ Relaxes blood vessels (vasodilates) ○ Inhibits platelets (will not be activated) Antithrombin III ○ Endogenous heparin  Tissue plasminogen activator – tPA ○ Secreted by endothelial cells ○ Anticoagulants: As a class, anticoagulants will prevent formation of a clot as well as prevent progression of a clot/thrombus Often given for prophylaxis (prevention) or treatment of major thrombotic conditions ○ MI, CVA, DVT, PE, atrial fibrillation, major surgeries, mechanical heart valves, central lines – maintain patency of line DO NOT bust clots ○ Heparin INduced Thrombocytopenia (HIT) Usually see re-exposures (day 4-10) Life threatening complication Immune-mediated drug response ○ Heparin will bind to a protein on inactivated platelets and form a complex Platelets destroyed ○ 50% reduction (type 2) → STOP infusion Paradoxical thrombus formation → “white clot” immune related response ○ Fatal (5-15%) S/Sx: Epistaxis (nose bleed), hematuria, melena (blood in stool), perechia, purpura ○ Common Coagulation Labs → high values = bleeding; low values = clotting Activated Partial Thromboplastin Time (aPTT) (heparin) Desired range is 47-70 seconds Anti-Xa (heparin) Desired range is 0.3-0.7 IU/mL International Normalized Ratio (INR) (warfarin)  Desired range 2-3 ○ Relationship between platelets and the clotting cascade Blood vessel injury Platelets adhere and activate → stimulators: ADP, TXA 2 ○ Causes aggregation and vasoconstriction Anticoagulants work on the clotting cascade, antiplatelet drugs works to prevent platelet aggregation at the site of vascular injury (before cascade) ○ Patient Education for Coagulation Modifiers: Monitor for S/Sx of bleeding: Black, tarry stools Hematuria Epistaxis Petechiae Easy bruising (beyond normal) Avoid trauma: Living environment → no rugs Gently brush teeth/soft bristles Electric razors Avoid these supplements (EGGGOS) E = vitamin E G = ginseng G = ginko biloba G = garlic O = omega 3 S = St. John’s Wart  Heart Failure: Pathophysiology/Pharmacology (week 9) ○ Heart Failure → pump failure The heart cannot pump enough blood to meet tissue needs (O2 and nutrients) Is the leading cause of death in the US and world #1 cause of hospital readmissions 50% mortality with in 5 years of Dx (especially from bad adherence and behavioral modifications) Effective management will ↑ outcomes Etiology: HTN, cardiomyopathy, MI, heart valve disorders, cocaine/meth, dysrhythmias, renal failure, hypo/hyper metabolic states ○ Compensation due to decreased CO: Neurohumoral (catecholamines → epi/norepi) Activations of catecholamines = ↑ HR and vasoconstriction RAAS Activation Vasoconstriction + Na & fluid retention Results in: Vasoconstriction → ↑ afterload → ↑ difficulty with ejection → ↑ preload → ↑ stress/stretching (remodeling) → heart failure ○ Natriuretic Peptide System A-type NP (ANP) = ATRIAL Release stimulated by atrial wall stress and stretch B-type NP (BNP) = BRAIN Release stimulated by ventricular wall stress and stretch ↑ Na excretion by the kidneys, diuresis, direct vasodilation, ↑ GFR, and decreased Renin (will activate RAAS) ↑ BNP is a diagnostic indicator of HF Need to maintain Na and fluid balance Needs adequate K, Ca, and MgSO4 This system is easily overwhelmed and system will not operate ○ Endothelins Released by endothelial cells Vasoconstrictor peptides SMC proliferation → cardiac myocyte hypertrophy (ventricular remodeling) ↑ aldosterone & catecholamines Exert antinatriuretic effects on kidneys ○ Ventricular Hypertrophy & Remodeling Ventricular wall stress →myocardial hypertrophy Symmetric: Width and length increase at the same rate Usually seen with athletes Concentric: Grows from the outside, to the inside Chamber will decrease and muscle will increase Eccentric: Keeps growing & growing → too much volume/stretch Think of a thin balloon (chamber will increase and muscle will decrease) Remodeling: Nonmyocytes initiate fibroblast growth = synthesis of collagen fibers leading to myocardial fibrosis (contractility will decrease) and stiffness ○ Left Heart Failure (systolic) → HFrEF EF < 40% → decreased contractility d/t myocyte dysfunction ↑ preload d/t myocyte dysfunction Heart will stretch (from ↑ workload), BNP (from ↑ stretching) will be released ECCENTRIC hypertrophy ↑ BNP = ↑ dysfunction Diagnostics:  Echocardiogram BNP ↑ ↑ ↑ Patient Presentation: ↑ or decreased BP S3 heart sound → fluid volume overload Pulmonary vascular congestion ○ Pulmonary edema ○ Dyspnea ○ Orthopnea Decreased urine output ○ Left ventricle is not pumping effectively = decreased CO = decreased blood flow to kidneys Inspiratory crackles (from edema) Cyanosis (decreased O2) Pleural effusion (from edema) ○ Left Heart Failure (diastolic) → HFpEF Preserved or normal EF (55%-70%) Impaired relaxation leading to pulmonary congestion Major causes: HTN-induced hypertrophy or prior MI Can not get Ca+ out of the LV myocytes = impaired relaxation ○ Calcium causes contraction, LV smaller at rest ○ CONCENTRIC hypertrophy ○ Ventricular lumen smaller = ↑ pressure Backflow from LV to pulmonary circuit Exacerbated with activity: ↑ HR, shortens ventricular filling time Diabetes will ↑ risk Patient Presentation: S4 heart sound Dyspnea on exertion (DOE) Fatigue  Pulmonary edema → inspiratory crackles Treatment: Focuses on improving ventricular relaxation, increasing diastolic filling times and decreased myocardial demand ○ Pharmacological Management: The goal is to slow or reverse progression of dysfunction, improve symptoms, reduce morbidity and mortality Modulate RAAS, neurohumoral, and natriuretic peptide systems Decrease preload → improve contractility ○ Right Heart Failure Inadequate blood flow to pulmonary circulation Seen with pulmonary HTN Hypoxic pulmonary diseases (COPD) Hypoxic vasoconstriction (of pulmonary vasculature) Remodeling pulmonary endothelium ↑ RV afterload (from constriction at the lungs) Cor pulmonale Progression of left HF to right HF: ↑ LV filling pressure Back flow into lungs (pulmonary congestion) ↑ pressure in the lungs Decreased RV emptying (↑ preload = ↑ resistance) ↑ RV afterload RV dilation & failure from pressure Patient Presentation → s/sx in rest of the body : Venous congestion Peripheral edema Hepatosplenomegaly Dyspnea Fatigue Peripheral edema  Chest pain/palpitations ○ High-output Heart Failure Adequate blood volume & contractility, but there is ineffective tachycardia – unmet metabolic needs Anemia → decreased RBC: Chronic condition Decreased oxygen carry capacity (from decrease HmG, decreased O2 to tissues) Anaerobic metabolism → metabolic acidosis (decreased pH) ↑ HR and SV to maintain CO LV fatigue and failure overtime Sepsis → profound inflammation Acute condition Bacterial toxins = inflammation Profound vasodilation & fever ↑ metabolic needs Anaerobic metabolism → metabolic acidosis (decreased pH) ↑ HR and SV to maintain CO LV fatigue and failure overtime If HR is fast for days → LV will give out