Cardiovascular 36 questions 3 questions- atherosclerosis, arteriosclerosis, effect of LDLs & triglycerides, effect on BP (Melinda) McCance p.

. 115760; slides 2-8 Cardiovascular Fx. lecture. Arteriosclerosis - chronic; thickening & hardening of vessel wall d/t smooth muscle & collagen migration to tunica intima (innermost layer of endothelium; endo = inside). Atherosclerosis - Form of arteriosclerosis; progressive, inflammatory disease proces; thickening & hardening d/t accumulation of lipid-filled macrophages (foam cells) deposited in tunica intima of endothelium fatty streaks (accumulated foam cells) fibrous plaques VLDLs (triglycerides) & LDLs (cholesterol) role in atherosclerosis: Abnormal concentrations of serum lipoproteins associated with risk for atherosclerosis, especially LDLs Serum LDL controlled by liver; serum LDL levels w/ high fat diets and genetic factors Small dense LDLs = most atherogenic because they oxidize in endothelium Oxidized LDL endothelial injury, inflammation, immune response (key steps in atherosclerosis)

BP

HTN = 2 to 3-fold risk for atherosclerotic CVD BP due to forming plaques further endothelial injury & myocardial hypertrophy BP demands & overactivity of SNS & RAAS 1. Endothelial injury The usual suspects: release of

Atherosclerosis schematic:

Inflammation

proinflammatory cytokines: TNF, INF, IL-1, & heat shock proteins

Impaired ability to make a.) antithrombotic b.) vasodilating cytokines Oxidation

3. Macrophages (aka: pac-man)

Oxidized LDL penetrates the wall of tunica intima in endothelium Macros engulf oxidized LDL at tunica intima = foam cells (just as pac-man swallows the ghost) Accumulated foam cells = fatty streaks (these dont obstruct, smooth muscle + collagen build up on top - see bullet below) Fatty streaks produce more 02 radicalsinflammation + immune responsefurther damage to vessel wall Smooth muscle + collagen proliferation over fatty streak = fibrous plaque (this is atherosclerosis)

They go after (think: pac-man) and adhere to injured endothelium (thru adhesion molecules, like VCAM-1); Macros release enzymes & toxic 02 radicalsoxidative stress and oxidized LDLsmooth muscle proliferation and inflammation + immune response GF released: angiotensin II, Fibroblast GF, platelet-driven GFsmooth muscle proliferation

1 question aneurysm: dissecting vs fusiform vs saccular (Melinda) -please feel free to add; not a whole lot here

McCance p. 1146; slides 22 & 23 for Cardiovascular Fx. Fusiform

Circumferential and saccular True aneurysms: involve all 3 layers of arterial wall (from outside in: adventitia, tunica media, & tunica intima) vs. False aneurysm: there is previous damage to a vessel and the clot is formed outside of the vessel wall (same outline as a saccular aneurysm) Caused by weakened vessel wall

Dissecting Saccular Break in vessel wall, usually a result of trauma (most critical); as a result of damage in the vessel wall, blood enters into the damaged area --> bleeding in between layers of the vessel wall; as more blood is accumulated, more blood is being pushed through, leading to more tension in the balloon area

1 question angina (Victoria) (power point pg 9-10, book 1165-1167)

Angina Pectoris: chest pain (angina) occurs when there is deficient oxygen for the heart muscle. Often presents as: substernal chest discomfort, may radiate to lower neck/jaw, left arm/shoulder, commonly mistaken for indigestion. Supply and demand issue Angina Pectoris: 3 Types

Classic- exertional Variant- spasms of coronary arteries Unstable- due to plaque disruption (leads to MI and myocardial ischemia) Typically recurrent, intermittent, brief episodes of tightness in the chest Pain can radiate (not as severe as MI) Diaphoresis and nausea often present

S/S: (stops when exertion stops)

Angina: 3 Kinds (these are reversible)

Stable angina: pain when hearts oxygen demand increases (transient, lasts 3-5 minutes, can happen with stress, exercise d/t vessel narrowing, hardening wall = vessel cant dilate in response to increased myocardial demand.. Recurrent and predictable.) Variant angina or Prinzmetal: pain when coronary arteries spasm (unpredictable, transient, chest pain, almost always happens at rest/at night) Silent myocardial ischemia: myocardial ischemia without pain; no specific symptoms (can present as fatigue, dyspnea or feeling of unease).

1 question cardiomyopathy: dilated vs hypertrophic (Lindsay) (Slides p. 12) (McCance p. 1178-1180)

3 types of Cardiomyopathies, ALL caused by infection: Dilated (congestive) - ventricular dilation and grossly impaired systolic function --> dilated heart failure. Most commonly d/t ischemic heart disease or valvular heart disease. Diminished myocardial contractility --> diminished systolic function. All 4 chambers of heart are enlarged and weakened resulting in congestive heart failure and need for heart transplant. of cases are idiopathic. Most common symptoms are dyspnea and fatigue, initial elevated bp, but hypotension indicates progressive decrease in contractility. Tx includes salt restriction and meds.

Hypertrophic - defects in contractile proteins make cells weak and unable to contract/relax in coordinated fashion --> cells hypertrophy (oblique and perpendicular orientation) to do same amount of work as normal cells --> cells need more oxygen and so perform less efficiently (vicious cycle) --> makes person prone to heart failure and may suffer sudden death during exertion. Always happens during exertion. Think of the bball player who drops dead. Often genetic (autosomal dominant inheritance). . Restrictive - heart chambers unable to fill w/ blood completely b/c of stiffness of heart and inability of heart muscle to relax during diastole. Most common manifestation is right-sided heart failure w/ systemic venous congestion.

3 questions hypertension/hypotension (Tracy C.) Definition of HTN according to American Heart Association (http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/AboutHighBloodPressure/Understanding-BloodPressure-Readings_UCM_301764_Article.jsp): Blood Pressure Category Normal Prehypertension Hypertension (Stage 1) Hypertension (Stage 2) Hypertensive Crisis (Emergency Care needed) Systolic (upper #) mm Hg < 120 120-139 140-159 160 or higher > 180 AND OR OR OR OR Diastolic (lower #) mm Hg < 80 80-89 90-99 100 or higher > 110

Etiologic Risk Factors (BBJ uses etiologic in the slides, but these are more like risk factors p.2 of cardio lecture): Family history Advancing age Race Increased salt intake Obesity Hyperinsulinemia High alcohol consumption DECREASED K, Ca, and Mg intake (slide is wrong in lecture) Use of oral contraceptives

TWO TYPES (p.2-3 of cardio lecture): 1) Primary HTN: Essential or idiopathic HTN (unknown cause) d/t: genetic and environmental factors (e.g. exercise, high fat diet, etc.)

Leads to increased peripheral resistance and/or increased blood volume sustained HTN (look at p.3 of cardio lecture for more detailed diagram)

Affects 90-95% of individuals with HTN

2) Secondary HTN:

Caused by systemic disease process that raises peripheral vascular resistance or cardiac output

Isolated Systolic HTN*: Elevated systolic pressure caused by increases in CO or total peripheral vascular resistance or BOTH. Complicated HTN*: chronic hypertensive damage to walls of systemic blood vessels hypertrophy and hyperplasia of smooth muscle cells w/ fibrosis of tunica intima and media aka vascular remodeling reduced blood flow and perfusion to organs Target organs: kidney, brain, heart, extremities, and eyes

Malignant HTN*: rapidly progressive HTN. Diastolic pressure usually > 140 mm Hg

Can increase capillary permeability edema (e.g. cerebral edema, papilledema)

*p.3 of cardio lecture - BBJ only said there were two types of HTN: primary and secondary, so Im thinking these 3 can fall under one of those types depending on the cause. Feel free to elaborate on this. Orthostatic (postural) Hypotension (p.3 of cardio lecture): Decrease in both systolic and diastolic BP upon standing. Lack of normal BP compensation in response to gravitational changes on circulation

Acute Orthostatic Hypotension (temporary type) Caused by sluggish regulatory mechanisms 2 forms: 1) Primary or idiopathic 2) Secondary to a disease (e.g. DM, metabolic disorders, or CNS or PNS diseases) Chronic Orthostatic Hypotension

8 questions & Case Study (for MI) -MI: relationship of CAD & MI and relationship of MI & HF, chronic ischemic heart disease, lab values, ECG changes, -types of MI Slides pg11, McCance pg 1171 ( SW ) Transmural: most common type, full thickness. If thrombus lodges permanently in the vessel, infarction will extend through the myocardium all the way from endocardium to epicardium (transmural), resulting in severe cardiac dysfunction. Clinically, individuals with transmural are at highest risk for serious complications, need intervention immediately. Individuals usually have marked elevations in the ST segments on ECG, categorized as STEMI. Subendocardial: inner half of heart wall. If the thrombus breaks up before complete distal tissue necrosis has occurred, infarction only involves myocardium directly beneath the endocardium. Usually presents with ST depression and T wave inversion without Q waves, clinically termed non-STEMI. -effects of angiotensin II, (SW) McCance 1126-1127. Powerful vasoconstrictor, considered a growth promoter in cardiovascular tissues. The resulting vascular hypertrophy is a significant factor in pathogenesis of hypertension. Chronically elevated Ang II in heart (like that seen in hypertension) contribute to myocardial hypertrophy and heart failure. Renin-angiotension-aldosterone system (RAAS): After hemorrhage or extracellular volume deficits (dehydration), there is a decrease in blood pressure or sodium delivery to kidneys, this stimulate secretion of renin, which forms Ang I, which is converted to Ang II which restores blood pressure. -SNS stimulation effects on heart (SW) Slides pg 15 (not much there), McCance 1150-1151. In healthy person, SNS helps maintain adequate blood pressure and tissue perfusion by promoting cardiac contractility and heart rate (maintains adequate cardiac output) and by inducing arteriolar vasoconstriction. In individuals with hypertension, overactivity (due to inc. production of catecholamines) of the SNS can result which causes increased heart rate and systemic vasoconstriction, results in raised blood pressure contributes to pathogenesis of HTN. SNS contributes to insulin resistance, which is associated with endothelial dysfunction and decreased production of vasodilators. SNS has procoagulant properties which make vascular spasm and thrombosis more likely. 3 questions-peripheral vascular disease: venous disease, arterial disease, Buerger disease/Raynauds disease (Moya) Peripheral Arterial Diseases Thromboangiitis Obliterans (Buerger Disease) -from slides & McCance pg. 1149 General: Occurs mainly in young men who smoke 95% cases: associated with smoking 5% cases: related to frostbite, trauma, or the use of

sympathomimetic drugs

Inflammatory disease of peripheral arteries resulting in the formation of nonatherosclerotic lesions (non-plaques) inflammation, thrombus formation, and vasospasm obliterates the small and medium-sized arteries typical areas: digital, tibial and plantar arteries of the feet and the digital, palmar, and ulnar arteries of the hands pain, tenderness and hair loss in the affected area sluggish blood flow and include rubor (redness of the skin) due to dilated capillaries under skin, and cyanosis, which is caused by blood that remains in capillaries after its oxygen has diffused into the interstitium Chronic ischemia: skin thin & shinny; nails thicken & malformed Advance disease: ischemia can cause gangrene disease associated with cerebrovascular disease and rheumatic symptoms characterized by attacks of vasospasms in the small arteries and arterioles of the fingers and, less commonly, the toes secondary to systemic diseases (ie: scleroderma, chemotherapy, cocaine use, hypothyroidism, pulmonary hypertension, smoking, and environmental factors (cold and prolonged exposure to vibrating machinery)

S/S: Clinical Manifestations:

Raynaud Phenomenon -slides & McCance pg 1149-1150 General:

Clinical manifestations:

changes in skin color & sensation caused by ischemia vasospams: varying frequency and severity and causes pallor, numbness & the sensation of cold in the digits attacks: bilateral, begins distal at tips of digits and progress proximally sluggish blood flow, rubor w/ throbbing and paresthesisas can cause ulceration & gangrene (extremely rare) remove stimulus & treat the primary disease process associated with malignancy, surgal removal of the tumor may resolve the ischemia no malignancy: calcium channel blockers or other vasodilators

Tx:

Raynaud Disease

General:

characterized by attacks of vasospasms in the small arteries and arterioles of the fingers and, less commonly, the toes primary vasospatic disorder of unknown origin same as Raynaud Phenomenon Prevent stimuli that trigger attacks: emotional stress, cold, smoking pharmacological management: ie- calcium channel blockers, nitric oxide non-pharmacological manangement: EXERCISE - the cure to everything

Clinical Manifestations: Tx:

Peripheral Venous Diseases Varicose Vein (& valvular incompetence) -slides & McCance pgs 1142-1143 General: vein in which blood has pooled typically involves the saphenous veins of the legs distended, tortuous, and palpable trauma that damages one or more valves habitually standing for long periods, constricting garments, or cross the legs at the knees) Damaged valves cannot maintain normal venous pressure Tx: causes hydrostatic pressure in the vein to increase becomes tortuous and edema develops in the extremity Vein distends further

Causes: 1.

2. gradual venous distention caused by gravity on blood in legs (ie:

Non-invasive: leg elevation compression stockings EXERCISE endovascular ablation surgical ligation & vein stripping

invasive:

Chronic Venous Insufficiency (CVI) -slides & McCance pgs 1142-1143

General:

progresses from varicose veins and valvular incompetence inadequate venous return over a long period

S/S:

chronic pooling of blood in veins of lower extremeties hyperpigmentation of the skin of feet & ankles edema can extend to knees circulation becomes sluggish metabolic demands of cells for O2, nutrients, & waste are barely met causes cell death & necrosis (venous stasis ulcers)

Clinical manifestation:

any trauma or pressure can lower O2 supply

Deep Venous Thrombosis (DVT) -slides & McCance pgs 1143-1143

General:

formation of a thrombus in a deep vein

Causes:

Triad of Virchow:

1. venous stasis (ie: immobility, obesity, prolonged leg dependency,

age, CHF

2. venous endothelial damage (ie: trauma, medications) 3. hypercoaguable states (inherited disorders, malignancy,
pregnancy, oral contraceptives, hormon replacement, etc.) ------ hospitalized individuals: significant risk orthopedic trauma or surgery, spinal cord injury, and OB/GYN conditions associated w/ up to 100% likelihood of DVT

-------

genetic abnormalities, esp with hypercoagulability

Clinical manifestations

accumulation of clotting factors & platelets leads to thrombus formation in vein, often near venous value inflammation around thrombus further platelet aggregation & propagates or grows proximally increase pressure behind the clot causing edema of the extremity thromboembolization of a part of the clot from the leg to the lung (pulmonary embolism) post-thrombotic syndrome (PTS): frequent DVT complication -- chronic, persistent pain, swilling, and ulceration of the affected limb

can create venous flow obstruction

DVT can dissolve without treatment but untreated can cause:

Prevention:

due to being asymptomatic and difficult to detect clinically, prevention in at-risk individuals is CRUCIAL people should be mobilized ASAP after illness, injury or surgery prophylactic tx with anticoagulation meds anticoagulation contraindicated: inferior vena caval filter

8 questions & 1 case study -heart failure: right side vs left side failure, edema, clinical manifestations (Marcus) LEFT HF (aka, congestive heart failure): Think SYSTOLIC or DIASTOLIC HF (or both)

SYSTOLIC LHF (inability of ht to generate adequate CO to perfuse tissue)

(Remember: CO=HR x SV; and SV depends on contractility, preload, afterload - Starling forces) Contractility (Pathology: in general, disrupted MYOCYTE activity)

MI is most common cause of contractility (other causes: myocarditis, cardiomyopathies) SECONDARY causes of contractility (as seen in myocardial ischemia, myocardial workload) predispose to inflamm., immune, & neurohormonal changes that mediate VENTRICULAR remodeling.

Ventricular remodeling: where myocardial hypertrophy and dilation cause myocyte contractile dysfxn contractility SV, causing LVEDV dilation pre-load

Preload (essentially LVEDV, filling volume)

Remember: contractility results in LVEDV; up to a certain point, LVEDV can actually improve CO, but after a certain point, myocardium is too stretched out, dysfxn of sarcomeres, and ultimately contractility (think of a simple rubber band, and what overstretching can do) LVEDV often caused by: IV fl.administration, renal failure, MV dz

Afterload Most often a result of PVR (as seen in HTN) W/ PVR, LV has more emptying workload, resulting in myocardial hyperTROPHY

Vicious cycle

Hypertrophy is mediated by angiotensin 2 and catecholamines, to increase O2 and energy supply for thickened myocardium Myocardium depends on efficient ATP production and c-kinase system Energy-starved state contribs to ventricular remodeling, hence fxn Remodeling also results in COLLAGEN deposition b/w myocytes, which disrupt muscle integrity

CO and activation of RAAS leads to renal perfusion PVR and plasma vol. preload + afterload Central baroreceptors cause vasoconstr, hypothal.release of ADH pre-/after-load Sympathetics compensate by PVR + HR Cytotoxic to myocytes (apop, remodeling, dysrhythmias... good stuff!) preload + afterload

Catecholamine release

RAAS

Cytotoxic as well Ang2: contrib.to remodeling, sarcomere death, loss of collagen matrix, fibrosis Aldosterone: myocardial fibrosis, autonomic dysfxn, dysrhythmia

Arginine Vasopressin (ADH)

Peripheral vasoconstriction, renal fluid retention, exacerbatn of hyponatremia + edema Protective effect in preload, but not adequate in HF Endothelin (bad), TNF-a, IL-6 (both of which contrib.to remodeling)

ANP + BNP Inflammatory mediators

Myocyte calcium transport: decrease contractility Insulin resistance: causes abnormal myocyte FA metabolism and ATP genern, leading to contractility, remodeling

Chronic LHF DIASTOLIC LHF

In isolate: Pulmonary Congestion (despite noraml CO, SV) Causes 50% of all LHF cases, and is more common in WOMEN Causes

HTN-induced myocardial hypertrophy, myoc.ischemia w/ resultant remodeling Hypertrophy and ischemia: impair myocyte pumping of CALCIUM from cytosol, resulting in IMPAIRED RELAXATION Aortic valve dz, MV dz, pericardial dz Diabetes Alterations seen in collagen, resulting in altered myoc.structure Abnormality found in titin: intracellular protein component

Compliance

Abnormal lusitropy (relaxation) Abnormal relaxation caused by CA transport from myocyte, related to sarco.retic CA ATPase Result: poor acceptance of filling blood without resistance and wall tension LVEDP (LVEDV) causes backing up of fluid into pulm.circ, resulting in pulm.edema

CL.PRESENTATION of SYSTOLIC vs. DIASTOLIC HF Systolic

Diastolic

Result from pulm.vasc congestion and inadequate systemic circ.perfusion Dyspnea, orthopnea, frothy sputum, fatigue, urine output, CARDIOMEGALY S3 gallop Dyspnea on exertion w/ fatigue If severe, pulm.edema; S4 gallop LV hypertrophy Pulmonary congestion w/o cardiomegaly

 RIGHT HF

NORMAL ejection fractions, but poor ventricular filling

RV cannot provide adequate bl.flow to pulm.circ at normal central venous pressure (CVP) Most often SECONDARY to LHF w/ LV filling pressure, reflected into pulm.circ When pressure in pulm.circ rises, resistance to RV emptying increases RV generally cannot accommodate increased workload, leading to dilation and RV failure Result

pressure in systemic venous circ. Triad: JVD, peripheral edema, hepatosplenomegaly When RHF occurs in absence of LHF Results from diffuse hypoxic pulm.dz (COPD, CF, ARDS)

Cor pulmonale (ch.33)

4 questions-Valvular heart disease: stenosis vs regurgitation or incompetence, rheumatic heart disease (Dylan)

Valve Defects

These can occur in any of the 4 heart valves However, more common in Mitral and Aortic Semilunar valves of Left Heart Stenosis Orifice is constricted and narrowed, impeding forward flow This makes chamber proximal to the stenosis work harder to eject blood hypertrophy of myocardium in chamber proximal to stenosed valve

Aortic Stenosis (stenosis of Aortic Semilunar valve) Most common valvular abnormality Impedes blood flow from LV to Aorta 3 major causes are 1) congenital bicuspid valve, 2) degeneration with aging, 3) inflammatory damage caused by rheumatic heart disease Linked with hyperlipidemia Chronic inflammation calcification of valve leaflets Causes hypertrophy of Left Ventricle Increased oxygen demand Angina MI Clinical manifestations: Angina, syncope, heart failure, weak pulses, decreased systolic BP Impedes blood flow from LA to LV

Mitral Stenosis

Most common cause is Acute Rheumatic Fever 2-3 times more common in women Leads to hypertrophy and dilation of LA Atrial Fibrillation thrombus formation Can cause blood to back up into lungs causing Pulmonary Edema and Right heart failure AKA insufficiency or incompetence Valvular leaflets fail to close completely blood leaks back into chamber proximal to valve This increases the volume of blood the heart must pump chamber dilation Increased workload of the chamber hypertrophy Aortic regurgitation (regurgitation of the Aortic semilunar valve) Causes: Congenital defect, rheumatic heart disease, bacterial endocarditis, syphillis, HTN, trauma, atherosclerosis, connective tissue disorders, idiopathic Leads to LV dilation and hypertrophy Heart failure Clinical Manifestations: Widened pulse pressure, dysrythmias Causes include mitral valve prolapse, Rheumatic heart disease Leads to dilation and hypertrophy of LA pulmonary edema Right heart failure Usually secondary to pulmonary HTN Leads to volume overload in RV increased systemic veinous BP

Regurgitation

Mitral regurgitation

Tricuspid regurgitation

Rheumatic Heart Disease Scarring and Deformity of Cardiac structures Caused by Rheumatic fever, a diffuse inflammatory disease caused by a delayed immune response to infection by Group A beta-hemolytic streptococci Usually occurs in children aged 5-15 Immune response causes inflammatory lesions to occur in connective tissue of the heart Clinical Manifestations

Stenosis/regurgitation of valves Pericarditis and pericardial effusions Heart murmur Enlarged heart

4 questions & (1 case study) -shock: septic, cardiogenic, circulatory shock (Yesol) Shock: Condition of acute and progressive circulatory dysfunction that results in inadequate delivery of oxygen and nutrients to tissues. Types:

cardiogenic: caused by heart failure hypovolemic: insufficient intravscular fluid volume obstructive: mechanical obstruction of blood flow through the central circulation distributive (vasodilatory): widespread dilation of small vessels -- effective blood volume. relative hypovolemia

septic: severe infection, endotoxins massive release of inflammatory mediators neurogenic (vasogenic): parasympathetic overstimulation or sympathetic understimulation d/t SCI, anesthesia, etc. anaphylactic: type I hypersensitivity

Septic shock: (will finish up tonight) Cardiogenic shock: heart failure of any cause (acute MI, valve failure, etc) -- impaired myocardial function compromises cardiac output unresponsive to treatment widespread impairment of cellular metabolism Compensatory mechanism:

Activation of renin-angiotensin, neuro-hormonal, sympathetic NS fluid retention, systemic vasoconstriction, tachycardia Catecholamine (epinephrine, NE, etc) release vasoconstrction, contractility, HR These responses normalize BP and increase cardiac performance, but increased myocardial demands for O2 and nutrients further strain the already failing heart.

It will be helpful to understand how an MI leads to left side heart failure and then leads to right side heart failure. (Note: I took a crack at this, please add accordingly if there are gaps (Marcus)) Apart from the relatively rare occurrence of cor pulmonale (pure RV dysfxn), myocyte necrosis as seen in MI is directly related to in CO, which is a key component of LHF (remember systolic HF, which is inability of heart to generate adequate CO to perfuse tissue), and less so RHF. Ischemic myocytes (MI) underlie systolic and diastolic dysfxn, which are sub-types of LHF. If the LHF is sufficiently severe, pulm.congestion and edema occur, resulting in RHF (direction of pathology is reverse; think UPSTREAM damage). Also, look at FUNCTIONAL changes seen in MI (McCance 1173): 1. contractility; 2. altered LV compliance; 3. SV; 4. EF; 5. LVEDP (LVEDV); 6. SA or AV node malfxn *** All these functional changes are characteristic of LHF pathophys; RHF is secondary to LHF...... usually. Pulmonary - 29 questions 4 general; types of respiratory patterns (Kussmauls vs Cheyne-stokes), effect of PNS stimulation on bronchioles, causes of chest wall restriction (NEH-DUH)

Kussmaul respirations, or Hyperpnea: Slightly increased Respiratory Rate, effortless tidal volumes and no expiratory pause. Cheyne-stokes respiration: Alternating periods of deep and shallow breathing with apnea (15-60sec) followed by increased respiration. Decreased Blood Flow to brain or respiratory center in brain stem.

Effect of PNS stimulation on bronchioles:: Restrictive diseases restrict lung or chest wall expansion. There are different types: Atelectasis: The collapse of previously expanded lung tissue which results in no alveolar gas exchange. Atelectasis is caused by airway obstruction and absorption of air from the involved lung area and by compression of lung tissue. Compression by external pressure. Absorption: Removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen.

Lung tissue is collapsed. This can be caused by physical blockage or surgery. Clinical manifestations increased secretions and decreased breath sounds.

Atelactasis can result from a tumor, fluid, or air in the pleural space OR Abdominal distention, bronchi obstruction

Pneumothorax: the presence of air or gas in the pleural cavity caused by rupture of the pleura. This destroys the negative pressure in the pleural space disrupting the recoil forces of the lung and chest wall. Air enters the pleural cavity, takes up space, restricting lung expansion. The affected lung can go through partial or complete collapse. The types are classified by cause

Spontaneous: an air-filled blister on the lung ruptures (bullae) Traumatic: air enters through injuries

Tension: air enters pleural cavity through wound on inhalation, cannot leave on exhalation. Clinical manifestations: Hypoxemia, dyspnea, hypotension, shock, bradychardia. When chest tube is placed, hear rush of air on insertion. Pleural pain, tachypnea, and mild dyspnea are experienced in Tension pneumothorax. Open: air enters pleural cavity through wound on inhalation, leaves on exhalation. Air pressure in the pleural space equals the barometric pressure because air that is drawn in during inspiration is forced back out during expiration. Pleural Effusion: Occurs when there is a collection of fluid in the pleural cavity, can collapse the lung partially or totally. This type is not a disease. Types of pneumothorax:

Primary- occurs spontaneously Secondary- secondary to complications of pulmonary disease. Tension- secondary to trauma, requires emergent care (you will see this in people who have been impaled).

1 influenza (Lindsay) (Slides p.2) In U.S., 36,000 die/year of flu-related illness (used to be the #1 killer) Transmitted by aerosol or direct contact --> RESP system affected first 3 types: A, B, C: We see Type A every year and epidemic form every 3-4 years; Type B epidemic every 4-6 years; Type C is endemic Leads to URI (rhinotracheitis) - like common cold w/ profound maliase Leads to Viral Pneumonia (lobar or bronchial)- fever, tachypnea, tachycardia, cyanosis, hypotenstion --> 2dary bacterial infection

3 pulmonary edema, paroxysmal nocturnal dyspnea, hypoxia (Julia Kwon) pulmonary edema (p. 1279) (Figure 33-7 on p. 1279 illustrates pathogenesis of pulmonary edema) (Julia Kwon) DEFINITION: excess water in the lung o Capillary fluid moves into alveoli and respiratory airways o When fluid flow out of capillaries > lymphatic systems removal of fluid (fluid builds up) o Can occur when circulatory system is overloaded with fluids Causes: MOST COMMON: Heart disease o Left ventricular failure/dysfunction o ARDS o Inhalation of toxic gases (i.e. ammonia) o Obstruction of lymphatic system Pathophysiology: Depends on cause o SEVERE pulmonary edema: capillary fluid moves into alveoli o Fluid accumulates in alveoli and respiratory airways o This causes lung stiffness o So, lung expansion is more difficult o Thus, gas exchange is impaired Clinical Manifestations: o Air hunger, dyspnea o Productive cough, often frothy, maybe blood tinged o Hypoxemia, in severe increase partial pressure of CO2 o Tachycardia o Skin: Moist and cool o Nail beds/Lips: Cyanotic o Confusion and stupor paroxysmal nocturnal dyspnea (p. 1267) o An alteration of pulmonary function o Dyspnea subjective sensation of being unable to get enough air o Air hungry, breathlessness o A positional dyspnea in which individuals with heart failure or lung disease wake up at night gasping for air and o must sit up or stand to relieve dyspnea hypoxia (p. 1269) Blood inadequately oxygenated. Reduced oxygenation of tissues, maybe caused by alterations of other systems o mistaken for hypoxemia o can result from other abnormalities o low cardiac output o cyanide poisoning o cant get patients to breathe o hypoxia can be caused by hypoxemia 2 TB (Victoria) power point pg. 5-6, book pg. 1293 - 1294 Worlds foremost cause of death from a single infectious agent Drug-resistant forms (require multiple therapies, very long duration: 6-12 mo. treatment) Myobacterium tuberculosis hominis (acid fast bacillus that affects lungs and may invade other systems) Airborne (droplets)--transmit person to person Protective waxy capsule (stays alive/protected) Can stay alive in suspended animation for years (latent)

More than half of new cases occur in foreign-born individuals Individuals with AIDS are highly susceptible Clinical Manifestations: Fatigue Weight loss Lethargy and anxiety Change in appetite Low grade fever Night sweats PPD (skin test, usually double test) CXR (chest x-ray to confirm) Sputum culture Macrophages begin a cell-mediated immune response Takes 3-6 weeks to develop positive TB test (need time to develop enough antibodies for + test) Results: granulomatous lesion or Ghon focus containing (triggered by immune response, walls off inactive TB bacteria) Macrophages T cells Inactive TB bacteria Central portion becomes caseous (cheese-like) and necrotic

Diagnosis

Initial TB Infection/Pathophysiology

Ghon Complex Nodules in lung tissue and lymph nodes Caseous necrosis inside nodules Calcium may deposit in the fatty area of necrosis Visible on x-ray (why we confirm with CXR)

Primary TB (First exposure, if healthy --> wall off)

Usually isolated in Ghon foci --> bacteria are inactive AND not contagious OR If immune response is inadequate, bacteria multiply in lungs (immune suppressed cant wall off TB) --> progressive primary TB Reinfection from inhaled droplet nuclei OR Reactivation of previously healed primary lesion Immediate cell-mediated response walls off infection in airways Bacteria damages tissues in the airways, creating cavities Signs of chronic pneumonia: gradual destruction of lung tissue Consumption: eventually fatal if untreated

Secondary TB (Already exposed--see frequently with health care workers)

2 lung cancer (NERDA) The types of lung cancer:

Squamous cell: slow growth, late mets, cough, sputum.

Adenocarcinoma: Moderate growth, early mets, pleural effusion Large cell: Rapid growth, early wide mets, pain, pleural effusion, cough, sputum Small cell: Very rapid growth, very early to mediastinum, airway obstruction.

Bronchiogenic carcinoma: arises from epithelial cell lining. Small-cell lung cancer: have metastasized by the time of diagnosis. The prognosis is very poor in this type of cancer because it is not amenable to surgery. Strong association with smoking. Without treatment, half of those diagnosed die within 12-15 weeks.

Non-small-cell lung cancer Large cell carcinoma- poor prognosis, tend to spread to distant sites early in their course. Squamos cell: associated with smoking. This type is more amenable to early detection. Adenocarcinoma: most common type in North America. This type is more common in women and nonsmokers.

Manifestations of Lung Cancer Changes in organ function (damage, inflammation, and failure) Local effects of tumors (compression of nerves or veins, GI obstruction) Ectopic hormones secreted by tumor cells (paraneoplastic disorders). Such disorders include hypercalcemia, Cushing syndrome, SIADH, neuromuscular syndrome Nonspecific signs of tissue breakdown (protein wasting, bone breakdown)

Taken from McCance study guide: (Moya) Type/Frequency Adenocarcinoma; 35%40% Squamous cell; 30% Large cell undifferentiated carcinoma; 10%-15% small cell (oat cell) carcinoma Growth Rate Moderate Slow Rapid Metastasis Early Late Early and widespread very early to mediastinum or distally in lung Menifestations/Tx Pleural effusion; surgical tx/adjunctive chemotherapy Cough, sputum production, airway obstruction; surgical tx/adjunctive chemotherapy pain, pleural effusion, cough, sputum production, hemoptysis, airway obstruction results in pneumonitis or pleural effusion; treated surgically airway obstruction, excessive ACTH secretion with its signs and symptoms; chemotherapy and radiation

very rapid

3 asthma (Julia Kwon) (Pg. 1283-1286; slides 58-65 on Respiratory Pathology Powerpoint) Asthma is an obstructive pulmonary disease ASTHMA: lung disease characterized: o Airway obstruction, o Airway inflammation, o Airway hyperresponsiveness, o Episodes of bronchospasm Pathophys: GENETICS. Abnormality in IL4 gene - Increased IgE synthesis o Bronchial hyperresponsiveness= Exaggerated bronchospastic response,

Increased functions of inflammatory response, Degranulation of Eosinophils o Smooth muscle contraction o Microvascular leakage Clinical Manifestations: o Asymptomatic during full remission o ACUTE ATTACK: anxiety, cyanosis, chest constriction, inspiratory and expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, acidosis, tachycardia, tachypnea, with severe attacks on the accessory muscles of respiration TYPE I HYPERSENSITIVITY o ACUTE RESPONSE/Immediate or Early Phase Response Allergen Mast cells release inflammatory mediators Chemical mediators increased mucous production opening of mucosal intercellular junctions 10-20 minutes o LATE PHASE RESPONSE Airway inflammation Epithelial injury with decreased mucociliary function and accumulation of mucous. Release of inflammatory mediators Recruitment of Neutrophils, eosinophils, and basophils. Increased vascular permeability and edema Increased airway responsiveness and 4-8 hours 4 pleural effusion (types of exudates) & pneumothorax (understand the different types) (AK47) Note: pneumothorax is considered a restrictive disorder, which is why I listed the types of pneumothorax under that section. But for less confusion, I am pasting it under this section as well. Restrictive diseases restrict lung or chest wall expansion. There are different types: Atelectasis: The collapse of previously expanded lung tissue which results in no alveolar gas exchange. Atelectasis is caused by airway obstruction and absorption of air from the involved lung area and by compression of lung tissue. Compression by external pressure. Absorption: Removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen.

Lung tissue is collapsed. This can be caused by physical blockage or surgery. Clinical manifestations increased secretions and decreased breath sounds.

Atelactasis can result from a tumor, fluid, or air in the pleural space OR Abdominal distention, bronchi obstruction

Pneumothorax: the presence of air or gas in the pleural cavity caused by rupture of the pleura. This destroys the negative pressure in the pleural space disrupting the recoil forces of the lung and chest wall. Air enters the pleural cavity, takes up space, restricting lung expansion. The affected lung can go through partial or complete collapse. The types are classified by cause

Spontaneous: an air-filled blister on the lung ruptures (bullae) Traumatic: air enters through injuries

Tension: air enters pleural cavity through wound on inhalation, cannot leave on exhalation. Clinical manifestations: Hypoxemia, dyspnea, hypotension, shock, bradychardia. When chest tube is placed, hear rush of air on insertion. Pleural pain, tachypnea, and mild dyspnea are experienced in Tension pneumothorax. Open: air enters pleural cavity through wound on inhalation, leaves on exhalation. Air pressure in the pleural space equals the barometric pressure because air that is drawn in during inspiration is forced back out during expiration. Pleural Effusion: Occurs when there is a collection of fluid in the pleural cavity, can collapse the lung partially or totally. This type is not a disease. Types of pneumothorax:

Primary- occurs spontaneously

Secondary- secondary to complications of pulmonary disease, mechanical ventilation, or chest trauma. Tension- secondary to trauma, requires emergent care (you will see this in people who have been impaled).

Pleural Effusion

Presence of fluid in pleural space, causes compression atelectasis (from pressure) and mediastenal displacement. Clinical manifestations-dyspnea (most common symptom), compression atelectasis, impaired ventilations, mediastenal shift, pleural friction rub.

The 5 types of Pleural Effusion - great chart on table 33-2, pg 1274

Transudates- water diffuses out of capillaries- CV, HTN, hypoproteinemia Exudates- Protein rich fluid- infection, inflammation, malignancy Empyema- Pus--infection Hemothorax or hemmorhagic pleural effusion- blood present- this means trauma to blood vessels. Chylothorax- milky fluid with lymph and fat dumped by lymph vessels.

5 ARDS: pathophysiology and clinical manifestations (Marcus)

Fulminant resp failure char.by: Acute lung inflammation Diffuse alveolocapillary injury

Results often from injury to lung by numerous unrelated causes Predisposing factors:

MOST COMMON: Sepsis, multiple trauma (transfusions esp); Other: burns, pneumo, aspiration, pancreatitis, drug OD, smoke, DIC Cause massive pulm.inflamm injuring alveolocapillary membrane, producing severe pulm.edema Alveolocapillary damage can be direct (aspiration) or indirect (chem. mediators released in response to systemic disorders, eg, sepsis) Initial injury

Pathophys

Complement activn: lung capillary damage Platelet aggregn Intravascular thrombus formation Inflammy cascade by macrophages (MOs): TNF, IL-1, alpha-, beta-chemokines Attracted/activated by substances released by platelets Release inflamm.mediators: proteolytic enzymes, oxygen free radicals, PAF Result in: damage to alveolocapillary membrane and capillary permeability ***Hallmark feature of ARDS*** Allows fluid, protein, blood cells to leak from cap.bed into pulm.interstitium & alveoli Result in: pulm.edema & hemorrhage, resulting in lung compliance Caused by mediators released by PMNs (and in part by MOs)

Neutrophils

Capillary permeability

Vasoconstriction

Causes secondary pulm.HTN Uneven distribution of vasoconstriction underlies V/Q mismatch in some areas of lung Produced by type 2 alveolor cells, Inactivated by inflammn lung compliance Result in: work of breathing, minute ventilation, hypercapnia W/in 24-48 hrs: hyaline membrane formation W/in 7 days: fibrosis obliterates alveoli, resp.bronchioles, interstitium Leading to functional residual capacity (FRC), V/Q mismatch, R-to-L shunt

Surfactant

After 24 hours...

ARDS can lead to MODS: MODS often is cause of death, not necess the initial ARDS Primary symptom: Progressive dyspnea 24-48 hrs: CxR reveals interstitial and alveolar infiltrate; HYPOXEMIA and resp ALK As pulm.edema worsens Hypoxemia becomes refractory to O2 therapy Hypoventilation develops ( PaCO2)

Clinical Presentation

Worsening hypoxemia and hypercapnia Resp.failure O2 delivery: met.ACIDOSIS, organ dysfxn CO, hypotension: death ***7 steps***: Dyspnea + Hypoxemia Hypervent + Resp.ALK Tissue perfusion + Organ dysfxn + Met.ACID TV + Hypoventilation Resp.ACID + Hypoxemia CO + Hypotension DEATH

5 & 1 case study: COPD, emphysema, chronic bronchitis: be able to differentiate pathophysiology and clinical manifestations (Carla) Ill be posting this tonight*** It will be very helpful to be able to differentiate between emphysema and chronic bronchitis (Sakhiba)