APP Exam 3 PDF

Osmosis — movement of H2O down concentration gradient Osmolality — concentration of molecules per weight of H2O Normal 275-295 295 = dehydrated Osmotic Forces — amount of hydrostatic pressure required to oppose the osmotic movement of H20 Na most abundant ion in ECF — responsible for osmotic balance...

Osmosis — movement of H2O down concentration gradient Osmolality — concentration of molecules per weight of H2O Normal 275-295 295 = dehydrated Osmotic Forces — amount of hydrostatic pressure required to oppose the osmotic movement of H20 Na most abundant ion in ECF — responsible for osmotic balance of ECF K most abundant ion in ICF — maintains osmotic balance of ICF FOUND IN ICF: K+ P organic ions (-) FOUND IN ECF: Na+ Cl- — follows Na & varies inversely with HCO3 HCO3- Mediated by aldosterone secreted when Na levels are depressed K levels increases, or renal perfusion is decreased leads to Na & H2O reabsoption back into circulation & K & H secretion to be lost in urine Filtration — movement of fluid from capillary into interstitial space Reabsorption — movement of fluid from interstitial space into capillary 4 forces: capillary hydrostatic pressure (blood pressure) — facilitates outward movement of H20 from capillary to interstitial space capillary (plasma) oncotic pressure — attracts H20 from interstitial space back into capillary osmotically interstitial hydrostatic pressure — facilitates inward movement of H2O from interstitial space into capillary interstitial oncotic pressure — attracts H2O from capillary into interstitial space osmotically forces favoring filtration or opposing reabsorption — capillary hydrostatic pressure (BP) & interstitial oncotic pressure (H2O pulling) forces opposing filtration or favoring reabsorption — capillary (plasma) oncotic pressure (H20 pulling) & interstitial hydrostatic pressure major forces for filtration & reabsorption are those within the capillary = capillary hydrostatic pressure (filtration) & capillary oncotic pressure (reabsorption) Accumulation of fluid in interstitial spaces Patho = increase in forces favoring fluid filtration from capillaries or lymphatic channels into tissues localized = limited to site of trauma or specific organ system generalized = dependent edema ANP — produced in atria BNP — produced in ventricles natural antagonist to RAAS — decreases BP & increases Na & H2O excretion released when there is increased atrial pressure (increased volume); ex) CHF decrease in BP decrease atrial pressure therefore inhibiting release of ANP & BNP antidiuretic hormone released when there is an increase in plasma osmolality, decrease in BP which all result in decrease atrial pressure & ultimately secretion of ADH increases water reabsorption interacts with Ca low serum levels cause renal conservation HYPERMAGNESEMIA causes — renal failure manifestations — skeletal muscle depression, muscle wkness, hypotension, respiratory depression, bradycardia HYPOMAGNESEMIA causes — from malabsorption; associated with hypocalcemia & hypokalemia manifestations — neuromuscular irritability, tetany/ convulsions, increased reflexes isotonic alterations = no change in concentration isotonic volume depletion = hypovolemia isotonic volume excess = hypervolumia hypertonic alterations — hypernatremia, hypercloremia, water deficit hypotonic alterations — hyponatremia (decreases ECF osmotic pressure & H2O moves into cell) HYPONATREMIA Na deficits cause plasma hypoosmolality & cellular swelling dilution hyponatremia — excess total body H2O (TBW) in relation to total body Na or shift of H2O from ICF to ECF = mannitol hypertonic hyponatremia — shift of H2O from ICF to ECF in hyperglycemia, hyperlipidemia, & hyperproteinemia hypotonic hyponatremia — TBW exceeds increase in Na although both are increased; severe CHF or ARF aldosterone, insulin, epi, & alkalosis facilitate K into cells; deficiency of these/ acidosis/strenuous exercise facilities it out hypokalemia causes — reduced K intake, increased K entry into cell, increased K loss, hyperaldosterone state, respiratory alkalosis hyperkalemia causes — increased intake, shift of K from ICF to ECF, decreased renal excretion, hypoaldosterone state, hypoxia, acidosis, insulin def., cell trauma HYPERKALEMIA mild attacks — tingling of lips & fingers, restlessness, intestinal cramping & diarrhea, peaked T waves severe attacks — muscle wkness, loss of muscle tone, flaccid paralysis, cardiac arrest renin is released by juxtaglomerular cells of kidney & stimulates release of angiotensin I (inactive) to angiotensin II (active) by ACE (angiotensin converting enzyme) in the pulmonary vessels which stimulates secretion of aldosterone HYPERPHOSPHATEMIA causes — exogenous or endogenous addition of P to ECF, long term use of P enemas or laxatives, renal failure high P levels related to low Ca levels manifestations — same as hypocalcemia with possible calcification of soft tissue HYPOPHOSPHATEMIA causes — intestinal malabsorption & renal excretion, vit D deficiency, antacid use, alcohol abuse manifestations — diminished release of O2, osteomalacia (soft bones), muscle wkness, bleeding disorders (plt impairment), leukocyte alterations if concentration of one increases the other decreases regulated by 3 hormones: parathyroid hormone (PTH) — increases plasma Ca levels via kidney reabsorption & is secreted in response to low serum Ca vit D — tat soluble steroid; increases Ca absorption from GI tract calcitonin — decreases plasma Ca levels HYPERCALCEMIA causes — hyperparathyroidism, bone metastasis, excess vit D, immobilization, acidosis manifestations — decreased neuromuscular excitability, muscle wkness, kidney stones, constipation, heart block HYPOCALCEMIA causes — inadequate intake or absorption, decreases in PTH & vit D, blood transfusion manifestations — increased neuromuscular excitability, muscle spasms, Chvostek & Trousseau signs, convulsions, tetany Causes: lactic acidosis, renal failure, DKA, starvation H+ ions move to intracellular space & K+ moves to extracellular space to maintain ion balance (both positive) pH drops below 7.35 HCO3 drops less than 24 mEg/L Manifestations: headache, lethargy, Kussmaul respirations Negative logarithm of H+ concentration. If H+ high in number, pH is low. If H+ low in number, pH is high. To maintain body's normal pH (7.35 - 7.45), H+ must be neutralized by retention of HCO3- or excreted. pH < 6.8 or > 7.8 = death pH = base/acid pH = renal regulation (slow)/ pulmonary regulation (fast) pH = metabolic acid-base function/respiratory acid-base function buffer = a chemical that can bind excessive H+ (acid) or OH- (base) without significant change in pH consists of buffering pair: weak acid & its conjugate base most important plasma buffering systems: carbonic acid-bicarbonate system & hemoglobin CARBONIC ACID—BICARBONATE BUFFERING operates in lungs & kidney must maintain ratio of bicarb & carbonic acid at 20:1 for pH to remain normal lungs can decrease carbonic acid kidneys can reabsorb or regenerate bicarb but don't act as fast as the lungs if bicarb decreases then pH decreases & can cause acidosis; pH can be returned to normal if carbonic acid also decreases — this is called compensation respiratory system compensates by increasing or decreasing ventilation; renal system compensates by producing acidic or alkaline urine RESPIRATORY & RENAL BUFFERING respiratory: acidemia causes increased ventilation; alkalosis slows respirations renal: secretion of H+ in urine & reabsorption of HCO3 normal arterial blood pH is 7.35—7.45 acidosis is pH 7.45; systemic decrease in H+ concentration or excess of base pH 7.35–7.45: based on H+ ions PaCO2 35–45mmHg: partial pressure of CO2 HCO3 (bicarb) 22–26mEq/L: calculated value of amount of bicarb in bloodstream base excess -2 to +2mEq/L: indicates amount of excess or insufficient level of bicarb SaO2 95–100%: arterial oxygen saturation 1. Respiratory acidosis — elevation of pCO2 as result of ventilation depression or alveolar hyperventilation; causes true hypercapnia 2. Respiratory alkalosis — depression of pCO2 as result of hyperventilation; causes hypocapnia 3. Metabolic acidosis — depression of HCO3 from ECF or an increase in non carbonic acids 4. Metabolic alkalosis — elevation of HCO3 usually as result of excessive loss of metabolic acids, like with vomiting, GI suctioning, excessive bicarb intake, hyperaldosterinism, & diuretic therapy Causes: prolonged vomiting, gastric suctioning, excessive bicarbonate intake, hyperaldosteronism with hypokalemia, diuretic therapy pH elevated above 7.45 HCO3 is elevated above 26mEq/L Compensation: hypoventilation (kidneys conserve H+ & eliminate bicarb) Manifestations: weakness, muscle cramps, & hyperactive reflexes with signs of hypocalcemia Causes: respiratory center depression (brainstem trauma/oversedation), respiratory muscle paralysis, disorders of chest wall (kyphoscoliosis, pickwickan syndrome, flail chest), disorders of lung parenchyma (pneumonitis, pulmonary edema, emphysemas asthmas bronchitis) pH is below 7.35 CO2 elevates (hypercapnia) >45mmhg Compensation: not as effective since kidneys take time but conserve bicarbonate & eliminate H+ Manifestations: headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma Must be careful when correcting because rapid reduction of PCO2 can cause respiratory alkalosis with seizures & death Causes: high altitudes, hypermetabolic states (fever, anemia, & thyrotoxicosis), early salicylate intoxication, anxiety or panic disorder, improper use of mechanical ventilators pH above 7.45 CO2 decreased through duct of Bellini —> intro into renal papillae (projections of ducts) —> into the calyces —> collected in renal pelvis inner layer — glomerular endothelium middle layer — glomerular basement membrane (GBM) outer layer — visceral epithelium that forms inner layer of Bowman capsule glomerular endothelial cells — synthesize nitric oxide la vasodilator), synthesize endothelium-1 (a vasoconstrictor), both which regulate glomerular blood flow visceral epithelium of bowman capsule & is composed of cells called podocytes; form elaborate network of clefts called filtration slits that modulate filtration plasma nitrate from glomerulus passes through glomerular membrane into the Bowman space to form primary urine JUXTAGLOMERULAR APPARATUS (JGA) juxtaglomerular cells — located around afferent arteriole macula densa — portion of distal convoluted tubule with specialized sodium & chloride-sensing cells control of renal blood flow (RBF), glomerular filtration, & renin secretion occurs at this site long intertwining smooth muscle bundles that pass through posterior aspect of bladder peristaltic activity moves urine to bladder & mictivition compresses lower end of water to avoid urine reflux glomerular filtration rate (GFR) — directly related to perfusion pressure in glomerular capillaries if mean arterial pressure decreases or vascular resistance increases, then the renal plasma flow (RPF) decreases & so does GFR myogenic mechanism (stretch) — as systemic pressure declines, glomerular perfusion increases an increase in systemic pressure decreases glomerular perfusion tubuloglomesular feedback (NaCl content) — when Na filtration increases then GFR decreases; macula densa cells stimulate efferent arteriolar vasoconstriction neural regulation — sympathetic nervous system (vasoconstriction diminishes GFR), baroreceptor reflex (vasoconstriction of afferent arterioles decreases perfusion & GFR), exercise & change of body position (mild vasoconstriction), severe hypoxia (decreases RBF) renin-angiotensin-aldosterone system (RAAS) — increases systemic arterial pressure & increases Na reabsorption BLADDER detrusor muscle — smooth muscle in bladder trigone — smooth triangular area lying between opening of the ureters & urethra URETHRA internal sphincters — smooth muscle at junction of bladder & urethra external sphincters — striated skeletal muscle under voluntary control females 3-4 cm long; males 18-20 cm long INNERVATION parasympathetic fibers (autonomic) — bladder & internal ureter sphincter that contracts detrusor muscle sympathetic (autonomic) — allows bladder to fill skeletal muscle neurons in pudendal nerve (somatic) — external urethral sphincter PROXIMAL TUBULE active reabsorption of Na (majority) LOOP OF HENLE concentration of urine descending loop — water reabsorption (Na diffuses in) ascending loop — Na reabsorbed by active transport) GLOMERULOTUBULAR BALANCE when GFR spontaneously decreases or increases — renal tubules & primarily the proximal tubules automatically adjust their rate of reabsorption of Na & water to balance the change in GFR compensatory hypertrophy & hyperfunction relief usually followed by post-obstructive dieresis — may cause fluid & electrolyte imbalance classified according to minerals that make up stone risk factors — male, most develop before age 50, inadequate fluid intake (most prevalent), geographic location 70-80% calcium oxalate & calcium phosphate (most common), 15% struvite (Mg, ammonium, P — forms during infection like klebsiella pseudomonas), 7% uric acid temperature & pH of urine influence risk of precipitation & calculus formation — pH more important renal colic is a manifestation that indicates obstruction of renal pelvis or proximal ureter renal adenoma — benign; located at cortex of kidney & can become malignant renal transitional cell carcinoma — rare renal cell carcinoma (RCC) — most common; adenocarcinomas that arise from tubular epithelium in renal cortex; clear cell has better prognosis & most common; papillary has worse prognosis classic clinical manifestations: hematuria, dull/aching flank pain, palpable flank mass in thin pts early stages often silent excretion of 3.0g or more of protein in urine caused by increased permeability of glomerular filtration membrane RIFLE — Risk, Injury, Failure, Loss, End-stage disease UREMIA syndrome of renal failure elevated blood urea & creatinine levels fatigue, anorexia, nausea, vomiting, pruritus, & near changes retention of toxic wastes, deficiency states, electrolyte disorders, & pro-inflammatory state patio manifestation to severe azotemia AZOTEMIA increased serum urea levels & frequently increased creatinine levels renal insufficiency or renal failure, causing azotemia measured clinically but no symptoms most common urological tumor; urothelial (transitional cell) carcinoma clinical manifestations: gross painless microscopic hematuria nonbacterial; thought to be result of autoimmune reaction responsible for inflammatory response that includes mast cell activation, altered epithelial permeability, & increased sensory nerve sensitivity infection of one or both upper urinary tracts (ureter, renal pelvis, & interstitum) acute pyleo — primarily affects tubules, glomeruli usually spared NEPHROTIC SEDIMENT massive amounts of protein & lipids microscopic amount to no blood NEPHRITIC SEDIMENT blood is present in urine with red cell casts & varying degrees of protein most common cause of internal renal failure occurs most often after surgery; also associated with sepsis, obstetric complications, & severe trauma/burns described as postischemic or nephrotoxic postischemic — involves persistent HTN, hypoperfusion, hypoxemia producing ischemia/reduced ATP, & generates toxic oxygen- free radicals with loss of antioxidant protection that causes cell swelling, injury, & necrosis nephrotoxic — produced by numerous antibiotics; neomycin, gentamicin, & torbramycin are major ones elastic arteries — absorb energy & stretch muscular arteries — can contract (vasoconstrict) & relax (vasodilate) veins — don't recall as quickly as arteries; muscle pump (pushes blood back to heart) capillaries — junctions between endothelial cells; blood flow into capillary beds controlled by contraction & relaxation of smooth muscle bands (precapillary sphincters) at the junctions between metarterioles & capillaries endothelium roles — transportation of substances, coagulation, antithrombogenesis & fibrinolysis, immune system function, tissue growth & wound healing, vasomotion (contraction & relaxation of vessels), performance of these vital functions through synthesis & release of vasoactive chemicals mediastinum — above diaphragm & lungs; where heart is located heart wall: epicardium — outer smooth layer myocardium — thickest layer of cardiac muscle endocardium — innermost layer pericardium — double-walled membranous sac parietal — surface layer visceral — inner layer; also called epicardium pericardial cavity — space between parietal & visceral layers; contains pericardial fluid (20ml) CHAMBERS OF THE HEART thickness of each chamber depends on pressure or resistance it must overcome to eject blood atria separated by interatrial septum ventricles separated by interventricular septum GREAT VESSELS superior & inferior venae cavae — bring deoxygenated blood from the systemic circulation to right atrium R & L pulmonary arteries — transport unoxgynated blood from right heart to right & left lungs; branch into pulmonary capillaries pulmonary veins — carry oxygenated blood from lungs to left side of heart aorta — delivers oxygenated blood to systemic vessels that supply body one contraction & one relaxation; makes up one heartbeat diastole — relaxation/ventricles fill systole — contraction/blood leaves ventricles PHASES 1. Atrial systole /ventricular diastole 2. Isovolumetiric ventricular systole 3. Ventricular ejection (semilunar valves open) 4. Isovolumetric ventricular relaxation caortic valve closes) 5. Passive ventricular filling (mitral & tricuspid valves open) pumps blood thru lungs (pulm. circulation) delivers blood to lungs for oxygenation low pressure system pumps oxygenated blood to body (syst. circulation) delivers metabolic waste products to lungs, kidneys, & liver high pressure system ensure one way blood flow atrioventricular valves (AVs) atria to ventricles tricuspid valve — 3 leaflets or cusps bicuspid/mitral valve — 2 leaflets or cusps semilunar valves ventricles to either pulmonary artery or aorta pulmonic semilunar valve aortic semilunar value no sound when values open; heart sounds are result of value closure & vibration of surrounding fluids under certain pressure changes S1 — low pitch, long-lasting; closure of AV values S2 — rapid snap; closure of semilunar values S3 — low pitch; inrushing blood into ventricles S4 — hard to rear except in HTN pt with thick L ventricle; a triple contraction late in diastole Time between corresponds to diastole… AUTOMATICITY — property of generating spontaneous depolarization to threshold; all heart cells capable of spontaneous depolarization RHYTHMICITY — regular generation of action potential by heart's conduction system; SA node depolarizes spontaneously 60 - 100x/min AUTONOMIC NERVOUS SYSTEM — influences rate of impulse generation (tiring), depolarization, & depolarization; influences strength of atrial & ventricular contraction; produces changes in heart & circulatory system faster than metabolic or humoral agents sympathetic stim causes increased HR & increased contractility; norepinephrine & epinephrine parasympathetic (vagus) stim decreases HR markedly & decreases cardiac contractility slightly; acetylcholine increases electrical conductivity & strength of myocardial contraction; releases norepinephrine at sympathetic ending causes increase sinus node discharge; increases rate of conduction of impulse; increases force of contraction in atria & ventricles stimulation of both β1 & β2 — increases HR (chronotropy) & force myocardial contraction (inotropy) if HR is affected the effect is called chronotropy negative chronotropy — decreases HR positive chronotropy — increases HR if heart contraction is affected the effect is called inotropy negative inotropy — decreases force of contraction positive inotrophy — increases force of contraction β1 — normal heart activation leads to increases in contractile force & HR; located on pacemaker, myocardium, salivary gland ducts, scribe & apocrine sweat glands; norepinephrine & epinephrine β2 — vascular & nonvascular smooth muscle regulatory; inverse response ( stimulation = decreased activity or muscle tone); activation leads to vascular & nonvascular smooth muscle relaxation; located on smooth muscle (GI tract, bladder, some coronary arteries) causes hyperpolarization of cardiac pacemaker cells because of increased k+ permeability in response to acetylcholine; this causes decreased transmission of impulses reducing HR or temporarily stopping HR FACTORS AFFECTING CARDIAC OUTPUT Heart rate Average heart rate in healthy adults: ~70 beats/minute Cardiovascular control center Activation of sympathetic system: Increases heart rate Activation of parasympathetic system: Decreases heart rate; controls resting heart rate Neural reflexes Sinus arrhythmia Baroreceptor reflex: when blood pressure falls, heart rate increases and arterioles constrict Bainbridge reflex: changes in heart rate from IV infusions Atrial receptors Hormones and biochemicals Epinephrine, norepinephrine, thyroid hormone, GH Myocardial contractility Stroke volume — volume of blood ejected during systole Determinants of the force of contraction Changes in the stretching of the ventricular myocardium, caused by changes in ventricular volume (preload) Alterations in nervous system input to the ventricles Adequacy of myocardial oxygen supply Positive inotropic agents: Increase the force of contraction. Norepinephrine from the sympathetic nerves supplying the heart Epinephrine from the adrenal medulla. Thyroid hormone and dopamine Negative inotropic agents: Decrease the force of contraction. Acetylcholine released from the vagus nerve Hypoxia: Decreases contractility. degree of cardiac contractility heart rate venous return to the heart blood volume patency of venous system degree of arteriolar dilation differential pressure skeletal muscle pump respiratory pump Greater resistance, lower blood flow More stretch = force of contraction smaller chambers, and thicker chamber walls equal increased contraction force ventricular dilation the force needed to maintain ventricular pressure lessens available contractile force Excess K+ decreases contractility Cause heart to become dilated and flaccid, slows heart rate Rise to just 2-3 times normal (8-12mEq/L) can lead to death Excess Ca causes spastic contraction, and low Ca causes cardiac dilation. Arterial pressure — effects of cardiac output CO = MAP (when no decrease in peripheral resistance) CO = drop in MAP and flow rate Neural control of resistance Baroreceptors — reduce blood pressure to normal by decreasing cardiac output and peripheral resistance; also BP when needed. Arterial receptors: Chemoreceptors — sensitive to oxygen, carbon dioxide, or pH. Regulate blood pressure. Decrease in PaO2 or increase in PaCO2 causes increase in HR, SV, and BP LYMPHATIC SYSTEM special vascular system picks up excess fluid and returns it to the venous circulation moving lymphocytes & leukocytes between different components of the immune system is another important function has lymph nodes & vessels valves allow one way flow lymphatic fluid is made up of primarily water & small amounts of dissolved proteins, mostly albumin. cross-bridge cycling — attachment of acting into myosin at cross bridge; causes thin filaments to slide past thick filaments (contraction) calcium — enters myocardial cell from ISF after electrical excitation; diffuses towards myofibrils where it binds with troponin excitation contraction coupling — calcium-troponin complex facilitates contraction process myocardial relaxation — troponin release of calcium begins myocardial relaxation Cardiac Alterations Hypertension ○ Consistent elevation of systemic arterial blood pressure ○ JNC 8 Guidelines ○ < 150/90 is the goal; unless underlying comorbidities, DM, Renal disease then 140/90. Primary (essential) hypertension – no known cause; is 95% of those with hypertension. Secondary hypertension – caused by altered hemodynamics from an underlying primary disease or drugs. ○ Caused by systemic disease that raises peripheral vascular resistance and/or cardiac output ○ Renal artery stenosis, renal parenchymal disease, pheochromocytosis, and drugs are examples. Complicated hypertension – hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling Malignant hypertension ○ Rapidly progressive hypertension ○ Diastolic pressure is usually >140 mm Hg ○ Can lead to encephalopathy Aneurysm complication – aortic dissection ○ Tear in intima of aorta, into which blood flows furthering the tear. ○ Devastating complication that involves the aorta (ascending, arch, or descending); can disrupt the flow through the arterial branches. ○ Surgical emergency Deep venous thrombosis (DVT) ○ Thrombus: Clot ○ Detached thrombus: Thromboembolus; can lead to pulmonary emboli ○ Clot in a large vein ○ Obstruction of venous flow leading to increased venous pressure ○ Factors: Virchow triad Venous stasis Venous endothelial damage Hypercoagulable states ○ Postthrombotic syndrome Atherosclerosis – form of arteriosclerosis. Thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall; plaque development; leading cause of coronary artery and cerebrovascular disease. Coronary Artery Disease – any vascular disorder that narrows or occludes the coronary arteries. Results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients. Reversible myocardial ischemia or irreversible infarction may result. Most common cause: Atherosclerosis Dyslipidemia – an indicator of coronary risk. ○ Increased LDL: Play a role in endothelial injury, inflammation, and immune responses that are important in atherogenesis. ○ Low levels of HDL: Are responsible for “reverse cholesterol transport,” which returns excess cholesterol from the tissues to the liver. ○ Elevated serum VLDL (triglycerides) ○ Increased lipoprotein (a) Types of Myocardial Ischemia (coronary blood cannot meet the demand of the myocardium for oxygen and nutrients) ○ Stable angina: predictable chest pain. ○ Prinzmetal angina (variant): unpredictable chest pain. ○ Silent ischemia: no detectable symptoms. ○ Angina pectoris: transient substernal chest discomfort. Acute Coronary Syndromes – sudden coronary obstruction because of thrombosis formation over a ruptured atherosclerotic plaque ○ Examples: Unstable angina, MI ○ Most common complications: Dysrhythmias, congestive heart failure, and sudden death Myocardial Infarction – prolonged ischemia causes irreversible damage to the heart muscle (myocyte necrosis). ○ Myocardial stunning – temporary loss of contractile function that persists for hours to days after perfusion has been restored. ○ Hibernating myocardium – tissue that is persistently ischemic undergoes metabolic adaptation to prolong myocyte survival. ○ Remodeling – process that occurs in the myocardium after an MI. ○ Repair – consists of degradation of damaged cells, proliferation of fibroblasts, and synthesis of scar tissue Myocardial Infarction ○ Individuals experiencing MI at highest risk for complications are those with ST segment elevations (STEMI) on the ECG; this requires immediate intervention. ○ Smaller infarctions not associated with ST segment elevations (non-STEMI) suggest that additional myocardium is still at risk for recurrent ischemia and infarction. ○ Clinical manifestations: sudden severe chest pain, N/V, Diaphoresis, Dyspnea, ECG changes, Troponin I: Most specific (elevates in 2 to 4 hours), Creatine phosphokinase–MB (CPK-MB), LDH, Hyperglycemia ○ Complications: dysrhythmias, cardiogenic shock, pericarditis, Dressler (postinfarction) syndrome, organic brain syndrome Thromboangiitis obliterans (Buerger disease) ○ Occurs mainly in young men who smoke. ○ Is an inflammatory disease of the peripheral arteries. Digital, tibial, plantar, ulnar, and palmar arteries ○ Obliterates the small- and medium-sized arteries. Lesions accompanied by thrombi and vasospasm of arterial segments ○ Pain and tenderness develop in the affected part. Hair loss in affected area ○ Sluggish blood flow, rubor, and cyanosis result. ○ Can often lead to gangrenous lesions Raynaud phenomenon and Raynaud disease Episodic vasospasm (ischemia) in the arteries and arterioles of the fingers; less commonly in the toes Clinical manifestations: Changes in skin color and sensation caused by ischemia ○ Pallor, cyanosis, cold, and pain Raynaud phenomenon: Secondary to other systemic diseases or conditions Raynaud disease: Primary vasospastic disorder of unknown origin ○ Tends to affect young women ○ Vasospastic attacks triggered by brief exposure to cold or emotional stress Rheumatic fever ○ Abnormal immune response to the M proteins that cross react with normal tissues ○ Fibrinoid necrotic deposits: Aschoff bodies ○ Clinical manifestations Carditis: Murmur Polyarthritis: Large joints mainly affected Chorea: Sudden, aimless, irregular, involuntary movements Erythema marginatum: Truncal rash Valvular stenosis – valve orifice is constricted and narrowed ○ Forward blood flow impeded ○ Increased workload of chamber with affected valve ○ Intraventricular or atrial pressure increases ○ Leads to myocardial hypertrophy ○ Aortic & Mitral valves Valvular regurgitation ○ Also called insufficiency or incompetence ○ Valve leaflets, or cusps, fail to shut completely ○ Blood flow continues even when valve is closed ○ Increase volume of blood that heart must pump because of leaking back through valve ○ Increased volume lead to dilation ○ Increased workload leads to hypertrophy ○ Aortic, Mitral, & Tricuspid valves Aortic regurgitation ○ Inability of the aortic valve leaflets to close properly during diastole ○ Clinical manifestations: Widened pulse pressure as a result of increased stroke volume and diastolic backflow, diastolic murmur Mitral regurgitation ○ Most common causes: Mitral valve prolapse and rheumatic heart disease ○ Permits backflow of blood from the left ventricle into the left atrium ○ Results in LV hypertrophy because of increased volume in LA entering the ventricle. ○ Systolic murmur, pansystolic murmur ○ Presence of S3 Tricuspid regurgitation ○ Leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure ○ Systolic murmur that increases with inspiration Tricuspid Stenosis ○ Patho essentially the same as MS, except that it occurs on the right side of the heart ○ Diastolic murmur Mitral valve prolapse syndrome ○ Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole ○ Clinical manifestations: Asymptomatic ○ Affected valves at greater risk of developing infective endocarditis Pulmonic Stenosis ○ Result of congenital anomaly ○ Systolic murmur Pulmonic Regurgitation ○ Seen with pulmonary hypertension ○ Diastolic murmur Infective Endocarditis – inflammation of the endocardium from infectious agents ○ Clinical manifestations: Osler nodes: Painful erythematous nodules on the pads of the fingers and toes Janeway lesions: Nonpainful hemorrhagic lesions on the palms and soles Constrictive pericarditis ○ Pericardium becomes rigid and impairs filling ○ Signs and symptoms similar to right and left sided heart failure. ○ Kussmaul’s sign Pericardial effusion ○ Accumulation of fluid in pericardial sac ○ Tamponade Severe restriction of cardiac motion Fatal if not resolved s/s hypotension, increased JVP, distant heart sounds Hypertrophic (asymmetric) cardiomyopathy ○ Hypertrophic obstructive cardiomyopathy ○ Common inherited heart defect of a thick septal wall ○ Clinical manifestations: Angina, syncope, palpitations, diastolic heart failure Hypertensive or valvular hypertrophic cardiomyopathy ○ Hypertrophy of the myocytes – attempts to compensate for increased myocardial workload. ○ Clinical manifestations: Asymptomatic or may complain of angina, syncope, dyspnea on exertion, and palpitations. Dilated (congestive) cardiomyopathy ○ Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure ○ Causes: MI; diabetes; alcohol; Valvular regurgitation ○ Clinical manifestations: Dyspnea and fatigue, systolic dysfunction Restrictive cardiomyopathy ○ Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole. ○ Clinical manifestations – right heart failure occurs with systemic venous congestion. Congestive (left) heart failure ○ Systolic heart failure or diastolic heart failure Cardiac output – depends on the heart rate and stroke volume ○ Stroke volume – contractility, preload, and afterload ○ MI – the most common cause of decreased contractility. ○ Preload – increased when decreased contractility or excess plasma volume is present. ○ Increased afterload: most commonly from increased peripheral vascular resistance. Systolic heart failure - ejection problem ○ Inability of the heart to generate adequate cardiac output to perfuse tissues ○ LVEF 40% Systolic heart failure ○ Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation ○ Dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema ○ Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop, and evidence of underlying CAD or hypertension Diastolic heart failure ○ Heart failure with preserved ejection fraction ○ Decreased compliance of the left ventricle and abnormal diastolic relaxation which leads to increased end diastolic pressure ○ Higher end diastolic left ventricular pressure transmitted to pulmonary circulation leads to pulmonary congestion ○ Causes: HTN, Ischemia, HR, Afib, ventricular hypertrophy, aging ○ Clinical manifestations non-specific; dyspnea, exercise intolerance, fatigue, weakness Clinical manifestations of R heart failure: ○ Pedal edema, ascites, enlarged liver, elevated JVP, sacral edema, nocturia, and even jaundice and coagulopathy. Staging Heart Failure A At high risk for heart failure but without structural heart disease without structural heart disease or symptoms of heart failure or symptoms of heart failure B Structural heart disease but without signs/symptoms of heart failure C Structural heart disease with current or past symptoms of heart failure D Refractory heart failure requiring specialized interventions High output failure ○ Occurs when CO is higher than normal ○ Underlying patho = reduced systemic vascular resistance ○ Is the inability of the heart to supply the body with bloodborne nutrients, despite adequate blood volume and normal or elevated myocardial contractility. ○ Common causes – Anemia, septicemia, hyperthyroidism, and beriberi Heart Blocks Multifocal atrial tachycardia (MAT) ○ Tachyarrhythmia starts at multiple sites ○ Occurs in pt’s with pulmonary disease ○ Multiple P wave morphologies Atrial flutter ○ Reentrant circuit in atrium; EKG with saw-tooth appearance of P waves Atrial fibrillation ○ Reentrant circuits ○ EKG wavy, chaotic, disorganized baseline without recongizable P waves ○ Rate >300 ○ Risk of thrombus, emboli, stroke, mesenteric ischemia Pre-excitation syndromes – Wolff-Parkinson-White and Lown-Ganong-Levine ○ Congenital presence of accessory pathways (bundle of Kent and Mahaim fibers) conducts very rapidly and bypasses the AV node. ○ Cause early ventricular depolarization in relation to atrial depolarization – PR shortened, Delta wave ○ Supraventricular tachycardia ○ Complications with AFib – sudden cardiac death Classifications of Pediatric Hypoxemia – based on blood flow ○ Lesions increasing pulmonary blood flow Defects that shunt from high-pressure left side to low-pressure right side with pulmonary congestion; acyanosis ○ Lesions decreasing pulmonary blood flow Generally complex with right-to-left shunt and cyanosis ○ Obstructive lesions Right- or left-sided outflow tract obstructions that curtail or prohibit blood flow out of the heart ○ Mixing lesions Desaturated blood and saturated blood mix in the chambers or great arteries of the heart Patent ductus arteriosus (PDA) ○ Vessel located between junction of main and left pulmonary arteries ○ Failure of the ductus arteriosus to close results in persistent patency of the ductus arterisus ○ PDA allows blood to shunt from the aorta to pulmonary artery causing left-to-right shunt ○ Hemodynamic effect is increased pulmonary blood flow, resulting in increased pulmonary venous return to the LA and LV with increased workload on the left side of the heart ○ Clinical manifestation Continuous, machinery-type murmur Risk for bacterial endocarditis Atrial septal defect ○ Abnormal opening between the atria; blood flows from left atria to right atria ○ Three major types: Ostium primum defect – opening found low in septum, may be associated with AV abnormalities, esp. mitral valve insufficiency Ostium secundum defect – opening in center of septum, most common Sinus venosus defect – opening is high in septum near superior vena cava and RA junction ○ Shunting from the left to right atrium because of higher pressure in left atrium and lower pulmonary vascular resistance – right atrial and ventricular enlargement ○ Clinical manifestations – often asymptomatic; diagnosed by murmur; pulmonary symptoms on exertion at later age Ventricular septal defect (VSD) ○ Abnormal communication between ventricles Shunting from the high-pressure left side to the low-pressure right side Amount of shunting dependent of size of defect and degree of pulmonary vascular resistance Small VSDs limit blood flow through defect therefore degree of pulmonary congestion is low, leading to minimal ventricular enlargement ○ Common congenital heart lesion (25% to 33%) ○ Pulmonary overcirculation accounts for symptoms associated with a large VSD ○ Clinical Manifestations – heart failure, poor weight gain, murmur and systolic thrill Tetralogy of Fallot ○ Syndrome represented by four defects 1. VSD 2. Overriding aorta straddles the VSD 3. Pulmonary valve stenosis 4. Right ventricle hypertrophy ○ Cyanosis and clubbing, feeding difficulty, squatting ○ Hypercyanotic spell or a “tet spell” that generally occurs with crying and exertion Coarctation of the aorta ○ Narrowing of the lumen of the aorta that impedes blood flow (8% to 10% of defects) ○ Is almost always found in the juxtaductal position, but it can occur anywhere between the origin of the aortic arch and the bifurcation of the aorta in the lower abdomen. ○ Directly at the insertion of the closed ductus arteriosus in the aortic arch ○ Causes condition in which there are higher pressures proximal to the site of stenosis and lower pressures distal ○ Direction of shunting depends on the pressure difference between PA and aorta and location of the ductus (always high to low pressure) ○ If blood pressure is greater in the aorta than PA = left to right shunting, resulting in increased pulmonary venous return to left side of heart, over time leading to hypertrophy of LV, and then HF ○ Clinical manifestations – newborns usually exhibit CHF. Once the ductus closes, rapid deterioration occurs from hypotension, acidosis, and shock. ○ Clinical manifestations – older children Hypertension in the upper extremities Decreased or absent pulses in the lower extremities Cool mottled skin Leg cramps during exercise Hypoplastic left heart syndrome ○ Left-sided cardiac structures develop abnormally. Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed. Obstruction to blood flow from the left ventricular outflow tract results in high pressure, leading to saturated blood entering the LA and then mixing with desaturated blood in the RA through atrial septal communication ○ As the ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock. ○ Fatal if left untreated Transposition of the great arteries ○ Aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. ○ Results in two separate, parallel circuits. ○ Unoxygenated blood continuously circulates through the systemic circulation. ○ Oxygenated blood continuously circulates through the pulmonary circulation. ○ Extrauterine survival requires communication between the two circuits. ○ Clinical manifestations – cyanosis may be mild shortly after birth and worsen during the first day. Pediatric systemic hypertension ○ Often have underlying renal disease or coarctation of the aorta. ○ Cause of hypertension is almost always found. ○ Commonly asymptomatic. ○ Clinical manifestations – systolic and diastolic blood pressure levels are greater than the 95th percentile for age and gender on at least three occasions. Kawasaki disease – mucocutaneous lymph node syndrome ○ Is an acute, self-limiting systemic vasculitis that may result in cardiac sequelae. ○ Approximately 80% of cases occur in children under the age of 5. ○ Cause – unknown ○ Theory – immunologic response to an infectious, toxic, or antigenic substance (including superantigen) VENTILATION — movement into & out of lungs DIFFUSION — movement of gases between air spaces in lungs & blood stream PERFUSION — movement up blood into & out of capillary beds of lungs to body organs & tissues upper airways (nasopharynx & oropharynx) — warms & humidifies air larynx — connects upper & lower airways lower airways (trachea, bronchi, terminal bronchioles) carina — ridge where trachea divides to R & L bronchi hila — where R & L bronchi enter lungs along with blood & lymph vessels goblet cells — produce mucus cilia — hairlike structures acinus — gas-exchange airways alveoli — primary was exchange units minute ventilation — total amount of air moved into and out of respiratory system per minute MV = TV x RR MV = 500 x 12 = 6000mL or 6L/min respiratory rate or frequency — number of breaths taken per minute anatomic dead space — part of respiratory system where gas exchange does not take place; normal 150mL alveolar ventilation — how much air per minute enters the parts of the respiratory system, in which gas exchange takes place AV = RR x (TV - dead space) AV = 12 x (500 - 150) = 4200mL or 4.2L/min determinants of arterial oxygenation — rate of O2 transport to tissues in blood; rate at which O2 is used by tissues retaining too much, CO2 will cause an increase in respiratory rate/ventilatory rate 60% venous CO2 is in bicarbonate form 90% arterial CO2 is in bicarbonate form TV — tidal volume: volume of air inspired or expired with each normal breath (~500mL) IRV — inspiratory reserve volume: extra volume of air that can be inspired, over and above the normal title volume when the person inspires with full force (~3000mL) ERV — expiratory reserve volume: max extra volume of air that can be expired by forceful expiration after end of normal title expiration (~1100mL) RV — residual volume: volume of air remaining in lungs after the most forceful expiration (~1200mL) FRC — functional residual capacity IC — inspiratory capacity VC — vital capacity: amount of air exchange from max inspiration to max expiration TLC — total lung capacity: total amount of air in lung after forced inspiration Pulmonary circulation has lower pressure (18 mmHg) than systemic circulation (90mmhg) high pressure = low flow = bronchial circulation low pressure = high flow = pulmonary circulation chest well includes the skin, ribs, and intercostal muscles pleura — serous membrane that adheres firmly to lungs pressure in pleural space — negative or subatomospheric (-4 to -10 mmHg); keeps lungs from collapsing perfuse lungs enabling the organs and tissues of the body to receive blood that is rich in oxygen and low in CO2 alveolar surface tension — attraction of water molecules at air dash water enter surface; trying to contract results in an attempt to force air out of Avola and them trying to collapse surfactant — detergent like substance secreted by type II alveolar epithelial cells in lungs that keep alveoli open and free of fluid and pathogens (collectins) dorsal respiratory group — set, basic automatic rhythm; receives impulses from referral chemo, receptors in carotid & aortic bodies; detect the PaCO2 & amount of oxygen in arterial blood ventral respiratory group — contains inspiratory & expiratory neurons; active when increased ventilatory effort is required pneumotaxic & apeustic centers — located in the pons; modifiers of inspiratory depth & rate are established by medullary centers central chemoreceptors — reflex PaCO2, stimulated by H in cerebral spinal fluid (pH), increases respiratory depth & rate peripheral chemoreceptors — located in aorta & carotid bodies, stimulated by hypoxemia (Pa02), responsible for all of increase in ventilation that occurs in response to arterial hypoxia effective gas exchange needs approximately even distribution of gas/ventilation & blood/perfusion in all portions of lungs oxygen delivery — ventilation of lungs, diffusion of oxygen from alveoli to capillary blood, perfusion of systemic capillaries with oxygenated blood, diffusion of oxygen from systemic capillaries into cells carbon dioxide removal — diffusion of CO2 from cells into systemic capillaries, perfusion of pulmonary capillary bed by venous blood, diffusion of CO2 into alveoli, removal of CO2 from by ventilation diffusion depends on partial pressure of gas Haldane effect ventilation–perfusion ratio — normal 0.8 Lowering V/Q ratio = low PaO2 & high PaCO2; low ventilation, high perfusion Increasing V/Q ratio = higher Pa02 & lower PaCO2; high ventilation, low perfusion perfusion exceeds ventilation in the bases of the lungs because of gravity ventilation exceeds perfusion in the apices of the lungs NORMALIZING THE RATIO hypoxic vasoconstriction — when ratio is low this can occur & cause blood coming into area to be directed to other parts of lung decreasing perfusion of hypoxic region which raises ratio & brings ABG closer to what we expect; most important cause of pulmonary artery constriction is low PaO2 bronchoconstriction — high ratio bronchi will constrict slightly to increase resistance & decrease amount of ventilation coming into area that is not well perfused Measures lung & chest wall distensibility; represents relative ease with which the structures can be stretched. Reciprocal of elasticity. Low = increase work of inspiration (stiff lungs). High = increased work of expiration (easy to inflate; lost some elastic recoil) bronchoconstriction — increases airway resistance bronchodilation — decreases airway resistance tendency of lung in chest while to return to the resting state after inspiration; elastic recoil forces of the lungs & chest wall are in opposition and pull on each other creating the normally negative pressure of the plural space Pulmonary Alterations Dyspnea – subjective sensation of uncomfortable breathing Kussmaul respirations (hyperpnea) – slightly increased ventilatory rate, very large tidal volume, and no expiratory pause Cheyne-Stokes respirations – alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea Hypoventilation – leads to respiratory acidosis from hypercapnia Hyperventilation – leads to respiratory alkalosis from hypocapnia Peripheral cyanosis – most often caused by poor circulation ○ Best observed in the nail beds Central cyanosis – caused by decreased arterial oxygenation (low partial pressure of oxygen – PaO2) ○ Best observed in buccal mucous membranes and lips Pleural pain ○ Is the most common pain caused by pulmonary diseases ○ Is usually sharp or stabbing in character ○ Infection and inflammation of the parietal pleura (pleuritis or pleurisy) can cause pain when the pleura stretches during inspiration and is accompanied by a pleural friction rub. Chest wall pain ○ Might be from the airways. ○ Might be from muscle or rib pain. Hypercapnia – increased carbon dioxide (CO2) in the arterial blood ○ Occurs from decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation Hypoxemia (NOT hypoxia) ○ Ventilation-perfusion abnormalities – most common cause; shunting blood to areas that are better ventilated Acute respiratory failure ○ Gas exchange is inadequate (hypoxemia). ○ PaO2 is ≤50 mm Hg. ○ Hypercapnia occurs, during which partial pressure of carbon dioxide (PaCO2) is ≥50 mm Hg ○ pH is ≤7.25. ○ Important post op consideration or complication, smokers at increased risk. ○ Chronic disease patient also at increased risk Chest wall restriction ○ Chest wall is deformed, traumatized, immobilized, or made heavy by fat; work of breathing is increased, and ventilation may be compromised because of a decrease in tidal volume. ○ Impaired respiratory muscle function is caused by neuromuscular disease. Flail chest ○ Instability of a portion of the chest wall from rib or sternal fractures. ○ Causes paradoxical movement of the chest with breathing. ○ Causes pain, dyspnea, unequal chest expansion, hypoventilation and hyoxemia Pneumothorax ○ Presence of air or gas in the pleural space ○ primary (spontaneous) – occurs unexpectedly in healthy individuals. ○ secondary – caused by disease, trauma, injury, or condition. ○ iatrogenic – caused by medical treatments, especially transthoracic needle aspiration. ○ Open – air is NOT trapped ○ Tension – air is trapped; life-threatening Pleural effusion – presence of fluid in the pleural space ○ Transudative effusion – watery and diffuses out of the capillaries. ○ Exudative effusion – less watery and contains high concentrations of white blood cells and plasma proteins. ○ Chylothorax – chyle exudate ○ Hemothorax – blood exudate ○ Clinical manifestations – Dyspnea and pleural pain Empyema – infected pleural effusion; pus in the pleural space ○ Clinical manifestations – cyanosis, fever, tachycardia, cough, and pleural pain Restrictive lung disease – the compliance of the lung is reduced; increases the stiffness of the lung and limits expansion ○ In these cases, a greater pressure (P) than normal is required to give the same increase in volume (V) ○ Common causes of decreased lung compliance are pulmonary fibrosis, pneumonia and pulmonary edema ○ Difficult to get air in ○ FEV1/FVC ratio can be normal; or increased Restrictive Lung Disorders ○ Aspiration – passage of fluid and solid particles into the lungs Right lower lobe: Is the most frequent site. Clinical manifestations – both choking and intractable cough have a sudden onset. ○ Atelectasis – collapse of lung tissue Compression atelectasis – external compression on the lung Absorption atelectasis – gradual absorption of air from obstructed or hypo-ventilated alveoli Surfactant impairment – decreased production or inactivation of surfactant Clinical manifestations – dyspnea, cough, fever, and leukocytosis ○ Pulmonary fibrosis – excessive amount of fibrous or connective tissue in the lung Idiopathic pulmonary fibrosis – no specific cause Clinical manifestations – increasing dyspnea on exertion Exposure to toxic gasses – ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide Clinical manifestations: Burning of the eyes, nose, and throat; coughing; chest tightness; dyspnea; hypoxemia ○ Oxygen toxicity – prolonged exposure to high concentrations of supplemental oxygen Severe inflammatory response mediated primarily by oxygen radicals Causes damage to alveolocapillary membranes, disruption of surfactant production, interstitial and alveolar edema, and decrease in compliance ○ Pneumoconiosis – any change in lung caused by the inhalation of inorganic dust particles; usually from the workplace Most common causes – silica, asbestos, and coal Clinical manifestations – cough, sputum production, dyspnea, decreased lung volumes, and hypoxemia ○ Systemic disorders and the lungs – several systemic diseases affect the airways, pleurae, or lung parenchyma. Granulomatous disorders, connective tissue diseases, Goodpasture syndrome Clinical manifestations of lung involvement – usually nonspecific and diagnosis is based on involvement of other organs. ○ Pulmonary edema – excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability Most common cause of pulmonary edema – left-sided heart disease Postobstructive pulmonary edema (POPE) – negative pressure pulmonary edema Rare life-threatening complication that can occur after relief of upper airway obstruction. Clinical manifestations – dyspnea, orthopnea, hypoxemia, and increased WOB ○ Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) – forms of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury Injury to the pulmonary capillary endothelium Increased capillary permeability Inflammation Surfactant inactivation Edema and atelectasis ARDS clinical manifestations in order: 1. Dyspnea and hypoxemia with poor response to oxygen supplementation 2. Hyperventilation and respiratory alkalosis 3. Decreased tissue perfusion, metabolic acidosis, and organ dysfunction 4. Increased work of breathing, decreased tidal volume, and hypoventilation 5. Hypercapnia, respiratory acidosis, and worsening hypoxemia 6. Decreased cardiac output, hypotension, death Obstructive lung disease – airway obstruction causes an increase in resistance ○ During normal breathing, the pressure volume relationship is no different from in a normal lung. However, when breathing rapidly, greater pressure is needed to overcome the resistance to flow, and the volume of each breath gets smaller ○ Common obstructive diseases include asthma, bronchitis, and emphysema. ○ Difficult to get air out ○ FEV1/FVC ratio decreased Obstructive Disease ○ Asthma – chronic inflammatory disorder of the bronchial mucosa. Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible. One half of all cases develop during childhood; a familial disorder – over 100 genes have been identified Reversible bronchoconstriction Leads to vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), and thick mucous secretions. ○ Chronic bronchitis – hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years ○ Emphysema – abnormal permanent enlargement of the gas-exchange airways accompanied by the destruction of the alveolar walls without obvious fibrosis Loss of elastic recoil Primary emphysema – inherited deficiency of the enzyme α1-antitrypsin Secondary emphysema – cigarette smoke Panacinar (Panlobular) – involves the entire acinus; damage is more randomly distributed Involves lower lobes of the lung ○ Cystic fibrosis – autosomal recessive multisystem disease Chloride transport is a fundamental abnormality Chronic inflammation leads to hyperplasia of goblet cells, bronchiectasis, pneumonia, hypoxia, and fibrosis, among other conditions Pneumococcal pneumonia – ALI, resulting in inflammatory cytokines and cells, causes alveolar edema. ○ Edema creates a medium for the multiplication of bacteria and aids in the spread of infection into adjacent portions of the lung ○ Involved lobe undergoes consolidation ○ Four phases: 1. Consolidation 2. Red hepatization 3. Gray hepatization 4. Resolution Viral pneumonia – seasonal; usually mild and self-limiting. ○ Can set the stage for a secondary bacterial infection. Provides an ideal environment for bacterial growth and by damaging ciliated epithelial cells, which normally prevent pathogens from reaching the lower airways. Most common form: Influenza ○ Clinical manifestations: preceded by an upper respiratory infection, ough, dyspnea, fever, chills, malaise, and pleuritic chest pain Abscess – circumscribed area of suppuration and destruction of lung parenchyma ○ Follows consolidation of lung tissue, in which inflammation causes alveoli to fill with fluid, pus, and microorganisms ○ Necrosis (death and decay) of consolidated tissue – abscess empties into the bronchus, leaving a cavity ○ Cavitation – process of abscess emptying and cavity formation ○ Most common cause – aspiration ○ Clinical manifestations – fever, cough, chills, sputum production, pleural pain, bronchus involvement (severe cough, copious amounts of often foul-smelling sputum, and occasionally hemoptysis) Pulmonary embolism – occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or air bubble ○ Pulmonary emboli commonly arise from the deep veins in the thigh ○ Virchow triad – venous stasis, hypercoagulability, and injuries to the endothelial cells that line the vessels ○ Clinical manifestations – sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety Pulmonary artery hypertension (PAH) – mean pulmonary artery pressure above 25 mm Hg at rest ○ Clinical manifestations – masked by primary pulmonary or cardiovascular disease First indication – chest radiograph (enlarged pulmonary arteries and right heart border) or an ECG that shows right ventricular hypertrophy Laryngeal cancer ○ Risk factors – tobacco smoke, heightened with smoking and alcohol consumption, GERD, HPV ○ Clinical manifestations – hoarseness, dyspnea, and cough Non-small-cell lung cancer ○ Squamous cell carcinoma – nonproductive cough or hemoptysis ○ Adenocarcinoma – tumor arising from glands; asymptomatic or pleuritic chest pain and shortness of breath ○ Large cell carcinoma (undifferentiated) – chest wall pain, pleural effusion, cough, sputum production, hemoptysis, airway obstruction resulting in pneumonia Neuroendocrine – small cell carcinoma (oat) ○ Worst prognosis – rapid growth, metastasize early ○ Arise from neuroendocrine tissue so there ectopic hormone secretion which results in paraneoplastic syndromes Hyponatremia (ADH), Cushing syndrome (ACTH), hypocalcemia (calcitonin), gynecomastia (gonadotropins) and carcinoid syndrome (serotonin)