Cardiac, Renal, Pulmonary Physiology and Irregularities PDF

Cardiac, Renal, Pulmonary Physiology and Irregularities Path of Blood – Basic Anatomy Start: Inferior and superior vena cava (used blood from tissues) Right atrium via IVC and SVC Right ventricle through tricuspid valve Lungs through pulmonic valve and through pulmonary arteries Left...

Cardiac, Renal, Pulmonary Physiology and Irregularities Path of Blood – Basic Anatomy Start: Inferior and superior vena cava (used blood from tissues) Right atrium via IVC and SVC Right ventricle through tricuspid valve Lungs through pulmonic valve and through pulmonary arteries Left atrium via pulmonary veins Left ventricle via mitral valve Aorta via aortic arch Cardiac Terminology End Diastolic Volume (EDV) ○ Blood in ventricles at end of diastole (relaxation) End Systolic Volume (ESV) ○ Blood in ventricles at end of systole (contraction) Venous Return ○ Total blood returned to right atrium ○ Should equal cardiac output Total Peripheral Resistance ○ Resistance to blood flow from peripheral structures ○ Increases with vasoconstriction; decreases with vasodilation Stroke Volume ○ SV = EDV - ESV Ejection Fraction ○ EF = SV/EDV Cardiac Output ○ CO = SV x HR Blood Pressure Systole ○ Determined by stroke volume Diastole ○ Determined by TPR Cardiac Output CO = SV x HR Rises to meet demands ○ Stress, exercise etc Increases with HR Increases in HR mean a decrease in SV ○ Due to decreased diastole/filling time Pathologic settings such as tachycardia and arrhythmias can increase HR so much that CO decreases Determined by ○ Preload ○ Afterload ○ Contractility ○ HR Preload Amount of blood loaded into LV Also how much stretch is on fibers prior to contraction More preload = increased CO More preload = more work and more O2 consumed Increased with more volume and more relaxation/filling time/diastole and vein constriction (pushes blood back to heart) ○ Decreased with opposite of each above Review Question: What group of arteries supply cardiac mm.? Afterload Forces that resist outflow of blood out of left ventricle Increases with HTN and Aortic Stenosis Decreases with hypotension Contractility How intensely the heart mm. Squeezes Key regulator is the SNS ○ Increases contractility and HR ○ Increased catecholamines (epi and norepi) bind to beta 1 heart adrenergic heart receptors ○ This increases calcium release from sarcoplasmic reticulum and this increases cardiac mm. Contractility Increased with sympathomimetics ○ Dopamine, dobutamine, epi, norepi Increased with Digoxin ○ Inhibition of Na/K pump; calcium builds up in heart muscle; stronger contraction Decreased with beta blockers -olol Decreased with calcium channel blockers ○ Verapamil and diltiazem Heart Rate is also increased with sympathomimetics and decreased with beta and calcium channel blockers Path of Conduction SA node fires and this stimulates the atria to depolarize These signals travel to AV node and the signal gets delayed ○ This delay allows for all blood to exit atria and enter ventricles Eventually, signal travels to His bundle, then bundle branches and purkinje fibers for ventricular contraction Cardiac Pacemaker Cells Spontaneously create action potentials to initiate hear contraction Influenced by sympathetic and parasympathetic NS Phase 4 “Funny Current” (If) ○ Spontaneous flow of Na ○ Allows for threshold potential of -40 mV to be reached to action potential occurs Phase 0 is rapid depolarization ○ Fast influx of Ca2+ Cardiac Myocytes Receive signals from pacemaker cells and they contract Phase 0 allows for rapid depolarization Phase 1-3 allows for repolarization Phase 4 allows for achieving a resting potential Action potentials spread to nearby myocytes via gap junctions HR and Arrhythmia Tachycardia > 100 BPM ○ Calcium channel blockers and beta blockers can help to slow pacemaker cells Beta blockers decrease Phase 4 slope so harder to reach potential Calcium channel blockers help to slow the calcium release so Phase 0 happens slower Bradycardia < 60 BPM ○ Sympathomimetics can speed up the heart rate EKG Basics Atrial Fibrillation Most common arrhythmia Palpitations, dyspnea, fatigue Loss of distinct P wave ○ Start to see fibrillatory F waves Decreases preload ○ Atria can’t fill ventricles properly Risk for stroke ○ Cardiac embolism formation from blood becoming turbulent in atria Atrial Flutter Similar to Afib Notice the “saw tooth” pattern on EKG Endocarditis S. viridans group ○ S. mutans ○ S. mitis ○ S. sanguis ○ Mitral/bicuspid valve S. aureus ○ Commonly infects the tricuspid valve ○ IV Drug Users “Tri Before You Bi” Heart Failure Left Side HF ○ HTN, MI, damage to heart muscle, increased afterload are common causes ○ Left ventricle and atria cannot pump blood as efficiently This causes blood to backup and pool into lungs Pulmonary congestion and therefore pulmonary edema ○ Leads to dyspnea Can cause intra alveolar hemorrhage Right Side HF ○ Most commonly due to left side HF Right heart cannot pump blood into backed up lungs Can cause jugular venous distension (blood backed up into veins) Hepatosplenomegaly ○ Blood from liver and spleen cannot drain into vena cava cause right heart is backed up Renal Main function is to maintain fluid levels, electrolyte balance, and absorption and secretion of nutrients and/or metabolites/toxins This in turn allows for BP regulation, pH balancing, and filtration of byproducts the body does not need ○ Stuff not needed gets excreted in urine Makes Erythropoietin (EPO) which helps to produce erythrocytes in anemic and hypoxic states Renal–Volumes and Pressure Kidneys have a big effect on effective circulating volume (ECV) Low ECV = low blood pressure ○ This activates SNS and RAAS ECV regulation is needed to maintain tissue perfusion to avoid hypoxic and ischemic injuries Hydrostatic pressure = essentially a pressure of fluid pushing against capillary walls ○ Will push fluid out of capillary if too high inside capillary Oncotic pressure = essentially a pressure of solutes like proteins such as albumin ○ High oncotic pressure = lots of proteins/solutes inside the capillary This will draw fluid into the capillary to “Dilute”/decrease solute concentration Glomerular Filtration Rate Blood enters through afferent and exits through efferent ○ Liquid that passes through glomerulus eventually turns into urine How much and how quickly blood is filtered through glomerulus = GFR Dilating Afferent = increase GFR ○ More blood will pass over glomerulus Constricting Efferent = increase GFR ○ Allows for blood to pool up in glomerulus to increase GFR GFR Continued Measure GFR using Inulin ○ Inulin is neither secreted nor reabsorbed ○ Good measurement of GFR Creatinine is closest naturally occurring substance to inulin ○ Therefore this is used to measure GFR clinically Worsening renal function/lessening GFR ○ High blood creatinine level This is because it cannot be filtered through glomerulus so it stays and increases in blood Proximal Tubule Proximal Tubule Diabetes Mellitus ○ Insulin deficiencies ○ High blood glucose = hyperglycemia ○ glucose/Na cotransporter gets hypersaturated and cannot function properly Glucose ends up in urine Should be 100% reabsorbed in proximal tubule and not be in urine Hartnup Disease ○ Amino acids end up in urine ○ Should be 100% reabsorbed in proximal tubule Fanconi syndrome ○ Complete dysfunction of reabsorption of bicarb, glucose, amino acids, phosphate Polyuria (increased urination) and polydipsia (thirst) Bicarbonate Proximal Tubule Allows for for H+ to be excreted in acidosis and bicarbonate to be reabsorbed/released into blood to adjust acidosis CA inhibitors are weak diuretics ○ H+/Na exchanger cannot work and Na stays in urine and water follows so blood pressure decreases Thin Descending Loop of Henle Impermeable to NaCl Concentrates Urine Reabsorbs water Water drawn out by hypertonicity of urine Thick Ascending Limb Dilutes urine through NaCl reabsorption Distal Convoluted Tubule Essentially a last portion of final solute reabsorption ○ Na/K/Ca Collecting Duct Reabsorption of Na and Water Secretion of H+ and K+ Aldosterone Steroid/Mineralocorticoid hormone Increases Na/K-ATPase proteins Increases ENaC/Na channels of principal cells ○ Increases Na reabsorption Promotes K+ and H+ excretion Stimulated by ATII, Hyperkalemia ADH Promotes free water retention Two receptors: V1 and V2 ○ V1 for vasoconstriction ○ V2 for antidiuretic response V2 promotes aquaporin migration to membrane for water reabsorption ○ Two methods for raising blood pressure RAAS Renin release stimulated by ○ Low perfusion pressure by afferent arteriole ○ Low NaCl delivery ○ Sympathetic activation Cushing Syndrome Increased ACTH Leads to increased cortisol HTN, bone loss, type 2 diabetes, metabolic alkalosis can develop Fatty hump between shoulders from excess fat development, rounded face, pink/purple stretch marks Addison's Disease Adrenal Insufficiency Aldosterone deficiency Less sodium and water reabsorption = more excretion Keep more K Hyponatremia and hyperkalemia Cna give corticosteroid drugs for maintenance Conn’s Disease Hyperaldosteronism Hypernatremia and hypokalemia This can lead to HTN ○ Too much sodium therefore more water and higher ECV Small Cell Carcinoma and SIADH Tumors can lead to ectopic production of ADH and ACTH Symptoms of excess of these hormones Syndrome of Inappropriate ADH Too much water retention and eventual brain swelling if severe enough Hyponatremia Can lead to hypervolemia but usually self resolves Respiratory Acidosis and Alkalosis Acidosis ○ Increased CO2 and therefore increased H+ and decreased pH ○ Renal compensation with increased bicarbonate release to buffer and make pH more basic Essentially a compensation with metabolic alkalosis Alkalosis ○ Decreased CO2 and therefore less H+ and increased pH ○ Renal compensation with bicarbonate erection in urine so less buffer and pH slowly drops Essentially a compensation with metabolic acidosis Metabolic Acidosis and Alkalosis Acidosis ○ Low bicarbonate so therefore pH is low due to high H+ ○ Compensation with hyperventilation blowing off CO2 This shifts to use up H+ and get rid of acidity (high H+) Essentially a respiratory alkalosis compensation Alkalosis ○ High bicarbonate so therefore pH is high due to low H+ (bound in bicarb buffer system) ○ Compensation with hypoventilation to increase CO2 This shifts to increase H+ and drop pH Essentially a respiratory acidosis compensation Respiratory Main purpose ○ O2 and CO2 exchange in alveolar capillaries ○ Oxygenate blood and O2 delivery to tissues ○ Expire CO2 from cellular respiration Respiratory Anatomy/Histology Type I pneumocytes ○ Primary cell for gas exchange Type II pneumocytes ○ Surfactant production Reduces surface tension Prevents alveolar collapse ○ Ion transport ○ Differentiation into Type I pneumocytes after injury Essentially a stem cell Lungs Function Air enters lungs through negative pressure system Negative intrapleural pressure keeps alveoli open and prevents alveolar collapse Negative pressure sucks alveoli open so air enters upon inspiration ○ Negative pressure created when chest wall expands Lung Pressures Transpulmonary pressure = alveolar pressure - intrapleural pressure Chest wall will expand and create a more negative intrapleural pressure so alveoli will suck open Exhalation Lung Pressure Mishaps Normally, a negative intrapleural pressure will suck alveoli open Pneumothorax (from lung injury like a stab wound) ○ Introduces air into the intrapleural space ○ This puts pressure onto alveoli and they collapse Dyspnea Lung Volumes Tidal Volume (TV) ○ Air in and out with normal quiet breathing Expiratory Reserve Volume (ERV) ○ Extra air exhaled with force ○ RV remains Inspiratory Reserve Volume (IRV) ○ Extra air inhaled with force ○ Lungs filled to max capacity Residual Volume ○ Volume of air that cannot be pushed out no matter what Necessary to also help prevent alveolar collapse Lung Volumes Total Lung Capacity ○ Sum of all volumes Inspiratory Capacity ○ Total volume you can inspire Vital Capacity ○ Most you can exhale Ventilation/Perfusion Ventilation = amount of air breathing in and out Perfusion = actual gas exchange into out of capillary with blood flow V/Q Want Ventilation (Q) and Perfusion/blood flow (Q) to “match” ○ Do not want wasted ventilation or under or hyperperfusion Increases in V/Q ○ Exercise Decreases in V/Q ○ Pulmonary fibrosis Obstructive Lung Disease Air gets trapped, cannot exhale properly ○ Low FEV1 (slow initial flow out) ○ Low FVC (less air out) ○ Reduced FEV1/FVC Residual and total lung volumes increase ○ Air is trapped so overall lung volumes increase Emphysema (type of COPD) and Asthma are classic examples Emphysema Classically associated with smokers ○ Increased proteases from inflammation from smoking toxins/pollutants (Polycyclic aromatic hydrocarbons) ○ These toxins overwhelm antiproteases ○ Proteases damage alveoli and macrophages are recruited which further damage alveoli during repair Pts with COPD and Emphysema will exhale slowly to avoid alveolar collapse ○ Pts will want to forcefully exhale which increases intrapleural pressure causing alveoli collapse ○ Slow exhale with pursed lips will help to keep positive alveolar pressure so alveoli don’t collapse Asthma Reversible bronchoconstriction in response to allergen (Type I HSR) Allergens induce TH2 CD4+ T cells ○ TH2 secretes IL-4 (class switch to IgE), IL-5 (attracts eosinophils), and IL-10 (stimulates more TH2 cells) Re Exposure to allergen leads to IgE activation of mast cells ○ Release histamine granules and generation of leukotrienes C4, D4, E4 Bronchoconstriction, inflammation, edema Inflammation from “major basic protein” is from eosinophils and can also damage cells and cause more bronchoconstriction Aspirin induces asthma by upregulating leukotriene production pathways https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.quora.com%2FWhy-may-as pirin-cause-asthma&psig=AOvVaw2eFijP_cXEBeHcyFB7QYA7&ust=1722571646810000 &source=images&cd=vfe&opi=89978449&ved=0CBEQjRxqFwoTCLj22M710ocDFQAAAA AdAAAAABAE Restrictive Lung Disease Cannot get air in, therefore less air out Low low FVC Low FEV1 However a normal or even high FEV1/FVC as air can be exhaled out normally, just in less amounts Pulmonary Fibrosis Fibrosis of lung interstitium Usually from cyclical lung injury Sometimes TGF-beta from injured pneumocytes can cause fibrosis This allows for a decreased amount of ventilation and perfusion ○ Less air in and less air can be processed by alveolar capillaries