Chapter 4 & 5 Cardiovascular Function PDF

**Chapter 4 -Cardiovascular Function** **[Functions of the Cardiovascular System]** - Delivers vital oxygen and nutrients to cells - Removes waste products - Transports hormones **[Branches of the Cardiovascular System]** - Systemic - Carries blood throughout the body to meet th...

**Chapter 4 -Cardiovascular Function** **[Functions of the Cardiovascular System]** - Delivers vital oxygen and nutrients to cells - Removes waste products - Transports hormones **[Branches of the Cardiovascular System]** - Systemic - Carries blood throughout the body to meet the body's needs and removes waste products - Includes arteries, veins, and capillaries - Works with the lymphatic system - Pulmonary - Carries blood to and from the lungs for gas exchange - Get rid of co2 and back to the heart. **Notes:** **Perfusion=** is the body's ability to push fluids nutrient and oxygen out to tissues and filter through them ex: kidney. The more fluid you have in the cardiovascular system the higher the blood pressure. The cardiovascular is a closed circuit. Heart pumping to the lungs and back to the heart. Lymphastic system will help recup will help any fluid that doesn't get back from the erfused tissues into that cardiovascular circuit. **[Heart anatomy]**9781284121131\_CH04\_FIG01.jpg Anatomical position = RA, LA,RV, LV (largest and thickest) apex is where we hear the apical pulse when we do chest sound Top of the heart we have 2 atrium. \#1 and \#5. Return blood into RA from the supervior vena cava (top of the body). And inferior vena cava (bottom the bbody) Nutrients goes into liver from IVC goes into RA, pass through heart to get new Oxygen. Blood will go into RA, goes into lunges, goes through Pulmonary trunk/artery, Deoxygenated blood going into RV, going into pulmonary artery (away), goes into lungs and goes into Pulmonary veins. It goes into LA. LA will pump blood into LV into aorta to be pumped out to body..  Figure 04.F02: Pulmonary gas exchange 9781284121131\_CH04\_FIG03.jpg Figure 04.F03: A normal heart  Figure 04.F04: Heart valves 9781284121131\_CH04\_FIG05.jpg Figure 04.F05: Blood flowing through the heart **Deoxygenated blood enters** the heart from the body through two large veins, the **superior vena cava** (from the upper body) and the **inferior vena cava** (from the lower body). This blood enters the **right atrium**. From the **right atrium**, the blood flows through the **tricuspid valve** into the **right ventricle**. The **right ventricle** pumps the blood through the **pulmonary valve** into the **pulmonary artery**, which takes the blood to the lungs. In the lungs, the blood gets oxygenated (takes in oxygen and gets rid of carbon dioxide). Oxygen-rich blood returns to the heart through the **pulmonary veins** into the **left atrium**. From the **left atrium**, blood moves through the **bicuspid (mitral) valve** into the **left ventricle**. Finally, the **left ventricle** pumps the oxygen-rich blood through the **aortic valve** into the **aorta**, which distributes it to the rest of the body.  Figure 04.F06: Blood flow through the heart: (a) Blood enters both atria simultaneously from the systemic and pulmonary circuits. (b) When full, the atria pump their blood into the ventricles. (c) When the ventricles are full, they contract simultaneously, delivering the blood to the pulmonary and systemic circuits. **[Question Time]** The pulmonary trunk: - **A. Leaves the heart from the right ventricle** - B. Leaves the heart from the left ventricle - C. Leaves the heart from the right atrium - D. Leaves the heart from the left atrium The **pulmonary trunk** is a short, thick-walled blood vessel that carries **deoxygenated blood** from the **right ventricle** of the heart to the **lungs**. It's the main artery that branches into the **left** and **right pulmonary arteries**, which then take the blood to the respective lungs for oxygenation. So, to sum it up: the pulmonary trunk is like the highway that directs deoxygenated blood from the heart toward the lungs, where the blood will get oxygen before it heads back to the heart and out to the rest of the body. The **pulmonary trunk** is sometimes just referred to as the **pulmonary artery**, but specifically, it's the portion of the artery before it splits into the **left** and **right pulmonary arteries**. So, while \"pulmonary artery\" can refer to the whole structure (including its branches), the \"pulmonary trunk\" typically refers to the main, unbranched segment that connects the **right ventricle** to the lungs. **[Heart]** - Pericardium - Surrounds the heart to provide protection and support - Myocardium - Cardiac muscle - Endocardium - Inner structures, including the valves - Four chambers - Two atria: receiving chambers - Two ventricles: pumping chambers - Ventricular walls (esp. left ventricle)---thicker than atrial walls **[Blood Flow Through the Heart (1 of 2)]** - Deoxygenated blood from the systemic circulation enters from the superior vena cava and the inferior vena cava. - Blood empties directly into the right atrium. - From the right atrium, blood travels through the tricuspid valve to the right ventricle. - The right ventricle pumps blood through the pulmonic valve to the pulmonary arteries. - The pulmonary arteries carry blood to the lungs for gas exchange. - Oxygenated blood from the pulmonary circulation enters from the pulmonary veins. - Blood empties directly into the left atrium. - Blood leaves the left atrium through the mitral valve to the left ventricle. - The left ventricle then pumps blood through the aortic valve to the aorta. - From the aorta, the blood is carried the rest of the body. **[Question time]** - The left side of the heart has less oxygenated blood than the right. - True or **false** **False.** The left side of the heart actually has more oxygenated blood than the right. Here\'s why: - The **right side** of the heart pumps deoxygenated blood to the lungs via the **pulmonary artery** for oxygenation. - The **left side** of the heart pumps oxygenated blood to the rest of the body through the **aorta**. So, after the blood picks up oxygen in the lungs (via the right side of the heart), it travels to the left side of the heart, where it is then pumped out to the bod **[Chapter 4 part 2] ** **[Electrical Conduction of the heart]** **[Conduction System]** - Organizes electrical impulses in the cardiac cells - Controls - Excitability: ability of the cells to respond to electrical impulses - Conductivity: ability of the cells to conduct electrical impulses - Automaticity: ability to generate an impulse to contract with no external nerve stimulus Figure 04.F07: Electrical conduction through the heart **[Conduction Pathway]** (1 of 2) - Impulses originate in the **sinoatrial (SA) node** high in the right atrium at a rate of 60--100 bpm. - Impulses travel through the right and left atria, causing atrial contraction. - Impulses then travel to the **atrioventricular (AV) node**, in the right atrium adjacent to the septum. - The AV node can initiate impulses if the SA node fails (rate: 40--60 bpm). - Impulses are delayed in the AV node to allow for complete ventricular filling. - Impulses then move rapidly through the **bundle of His**, right and left **bundle branches**, and **Purkinje network** of fibers, causing ventricular contraction. - The ventricles can initiate impulses if the SA and AV nodes fail (rate: 20--40 bpm, which may be inadequate). **[Electrical Activity(1 of 2)]** - Depolarization = Ventricle Depolarization means they are contracting. - Increase in electrical charge - Accomplished through cellular ion exchange - Generates cardiac contraction - Repolarization = Atrium and ventricle are recovering and reseting their proper ion balance. - Cellular recovery - Ions returning to the cell membrane in preparation for depolarization - Can be read by an electrocardiogram - P wave: atrial depolarization - QRS complex: ventricular depolarization - T wave: ventricular repolarization - **Atrial Repolarization is in between Q and S** - Sinus rhythm - Electrical activity when impulses originate in the SA node - Dysrhythmias - Abnormal electrical activity - Can result from issues such as myocardial infarctions and electrolyte imbalances, especially sodium potassium and calcium are important for the heart to function properly. 9781284121131\_CH04\_FIG08.jpg Figure 04.F08: Characteristic features of a normal electrocardiogram **Atrial Repolarization is in between Q and S** **[Conduction Control]** - Electrolyte signals - **Sodium, potassium, and calcium** - Medulla monitoring - Autonomic nervous system, endocrine system, chemoreceptors =keep a balance of concentration of the blood. It keeps track to make sure there's enough co2 first and levels of oxygenation. - and baroreceptors= sense the pressure of blood in the cardiovascular circuit. It makes sure we have enough pressure to get up to the brain. **[Question time!]** - The qrs complex: - **A. Shows ventricular depolarization** - B. Shows atrial depolarization - C. Shows atrial repolarization - D. Shows ventricular repolarization - E. Two of the above The correct answer is **A. Shows ventricular depolarization**. The **QRS complex** on an ECG represents the depolarization of the ventricles, which leads to their contraction. - **Atrial depolarization** occurs just before the QRS complex, but it's not directly seen on the ECG because it's overshadowed by the larger electrical activity of the ventricles. - **Ventricular repolarization** is represented by the **T wave**, not the QRS complex. **[Blood pressure]** - Force that blood exerts on the walls of blood vessels - Reflects how hard the heart is working - Represented as a fraction - Systolic: top number; cardiac work phase (Contracting) - Diastolic: bottom number; cardiac rest phase (dying off or relaxing) - Normal BP according to AHA: 120/80 mmHg - Pulse pressure (\~40)---difference between the two numbers - Higher the pulse pressure the higher the pressure on the heart. - If it is higher the heart is pushing blood out harder **[Influences on Blood Pressure (1 of 2)]** - BP = CO × PVR - Cardiac output (CO) - CO = SV × HR - Stroke volume (SV) -- how much blood is pumped out of the heart (per pump) - Heart rate (HR) - Peripheral vascular resistance (PVR) - Sympathetic nervous system - Parasympathetic nervous system - Arterial elasticity Prefix- **[OGEN- inactive form of something in the body.]** **[Question time]** - Afterload is due to increase in pressure in the arterial system. - **True** or false. - **True.** - **Afterload** refers to the resistance the heart has to work against to pump blood out of the ventricles. It's primarily influenced by the pressure in the arterial system (especially in the aorta and pulmonary arteries). - When the pressure in these arteries increases, the heart has to exert more force to push blood into the circulation, increasing afterload. Conditions like high blood pressure (hypertension) can raise afterload, making the heart work harder. - Afterload: pressure needed to eject the blood - - - - - - - - Figure 04.F09: Role of kidneys in blood pressure The kidneys play a crucial role in regulating **blood pressure** through several mechanisms, largely centered around the **renin-angiotensin-aldosterone system (RAAS)**, **fluid balance**, and **sodium regulation**. Here\'s a breakdown of how the kidneys influence blood pressure: **1. Renin-Angiotensin-Aldosterone System (RAAS)** When blood pressure drops (such as from blood volume loss or dehydration), the kidneys sense this decrease through specialized cells called **juxtaglomerular cells** in the nephron. These cells release **renin**, an enzyme that triggers a cascade of reactions aimed at raising blood pressure. - **Renin** converts **angiotensinogen** (a protein produced by the liver) into **angiotensin I**. - **Angiotensin I** is then converted to **angiotensin II** by an enzyme called **ACE** (angiotensin-converting enzyme), primarily in the lungs. - **Angiotensin II** has several effects: - **Vasoconstriction**: It constricts blood vessels, increasing vascular resistance, which raises blood pressure. - **Aldosterone release**: Angiotensin II stimulates the adrenal glands to release **aldosterone**, a hormone that increases sodium and water retention by the kidneys. This increases blood volume, which in turn raises blood pressure. - **Antidiuretic hormone (ADH)** release: It also stimulates the pituitary gland to release **ADH** (also known as vasopressin), which promotes water retention in the kidneys, further contributing to increased blood volume and pressure. **2. Fluid and Sodium Balance** The kidneys regulate blood volume by controlling the amount of fluid and sodium in the body. When sodium is retained, water follows (due to osmosis), increasing the volume of blood circulating in the body. An increase in blood volume leads to an increase in **cardiac output**, which can raise blood pressure. - **Sodium reabsorption**: The kidneys can reabsorb sodium in various parts of the nephron (especially the proximal tubule, loop of Henle, and distal convoluted tubule). When sodium is reabsorbed, water follows, increasing blood volume. - **Diuresis**: Conversely, if blood pressure is high, the kidneys can increase urine output (diuresis) to reduce fluid volume and help lower blood pressure. **3. Autoregulation of Renal Blood Flow** The kidneys have an intrinsic ability to regulate their own blood flow, which helps to maintain a stable glomerular filtration rate (GFR) and normal kidney function even when systemic blood pressure fluctuates. This is done through mechanisms like: - **Myogenic response**: Blood vessels in the kidneys constrict or dilate in response to changes in blood pressure to keep renal blood flow stable. - **Tubuloglomerular feedback**: The macula densa (a group of specialized cells in the nephron) senses the flow of sodium chloride and adjusts the dilation or constriction of the afferent arteriole to maintain GFR. **4. Impact of Chronic Kidney Disease (CKD)** In cases of **chronic kidney disease**, the kidneys lose their ability to properly regulate fluid, sodium, and the RAAS system. This can lead to persistent high blood pressure (hypertension), which in turn can worsen kidney function, creating a vicious cycle. **5. Prostaglandins and Nitric Oxide** The kidneys also produce certain molecules like **prostaglandins** and **nitric oxide**, which help in regulating blood vessel tone and blood flow. These substances help to dilate blood vessels, which can lower blood pressure. In conditions like kidney disease, the production of these vasodilators may be impaired, contributing to higher blood pressure. In summary, the kidneys regulate blood pressure through: - **RAAS** activation to increase sodium and water retention, raise vascular resistance, and ultimately increase blood pressure. - **Fluid and sodium balance**, directly impacting blood volume. - **Autoregulation** to maintain stable kidney function despite changes in systemic pressure. Thus, the kidneys are essential in both the short-term and long-term regulation of blood pressure. When kidney function is compromised, blood pressure regulation can become dysregulated, often leading to **hypertension**. **[Blood vessels (1 of 2)]** - Arteries: carry oxygenated blood [away] from the heart, pulmonary arteries have deoxygenated blood. - Veins: carry deoxygenated blood [towards] to the heart, pulmonary veins have oxygenated blood. - Capillaries: site of exchange, one cell thick. 9781284121131\_CH04\_FIG10.jpg Figure 04.F10: The circulatory system **[Blood Vessels (2 of 2)]** - Three layers - Tunica intima: inner layer - Tunica media: middle muscular layer - Tunica adventitia: outer elastic layer - Exception - Pulmonary artery: carries deoxygenated blood away from the heart - Pulmonary vein: carries oxygenated blood to the heart Chap 4 part 3 -- 13:00  Figure 04.F11: The walls of the blood vessels are composed of three layers of tissue: the endothelium, elastic tissue, and the connective tissue. (a) Artery; (b) capillary; (c) vein. VEINS HAVE VALVES\*\*\*\* that helps return blood. **[Lymphatic System]** - Works to return excess interstitial fluid (lymph) to the circulation - Plays a role in immunity - Includes lymph nodes, the spleen, the thymus, and the tonsils 9781284121131\_CH04\_FIG12.jpg Figure 04.F12: The lymphatic system. (a) The lymphatic system consists of vessels that transport lymph\--that is, excess tissue fluid\--back to the circulatory system. (b) Lymph is picked up by lymphatic capillaries that drain into larger vessels. Like the veins, the lymphatic vessels contain valves that prohibit backflow. Lymph nodes are interspersed along the vessels and serve to filter the lymph. The **subclavian vein** is responsible for carrying deoxygenated blood from the arm and some parts of the chest back to the heart. It's located under the collarbone (clavicle) and serves as a major drainage point for the upper limbs and some regions of the head and neck. Specifically, it receives blood from the **axillary vein** (which drains the arm) and the **external jugular vein** (which drains blood from the neck). From there, it merges with the **internal jugular vein** to form the **brachiocephalic vein**, which then empties into the superior vena cava, bringing the blood back to the right atrium of the heart. In short, it's a key part of the venous system that helps return blood to the heart after it's circulated through the arms and upper regions. **[Question time!]** - Arteries always move away from the heart. - **True or** false **[Cardiovascular diseases]** **Understanding Cardiovascular Conditions** - Alterations resulting in decreased cardiac output: pericarditis, infective endocarditis, myocarditis, valvular disorders, cardiomyopathy, electrical alterations, heart failure, and congenital heart defects - Alterations resulting in altered tissue perfusion: aneurysm, dyslipidemia, atherosclerosis, peripheral vascular disease, coronary artery disease, thrombi and emboli, varicose veins, lymphedema, and myocardial infarction - Alterations resulting in both: hypertension and shock **[Pericarditis]** - Inflammation of the pericardium - Triggered by viral infection, thoracic trauma, myocardial infarction, tuberculosis, malignancy, and autoimmune conditions - Fluid accumulates in the space between pericardial sac and heart---pericardial effusion - Swollen tissue creates friction - Cardiac tamponade - Cardiac compression from excessive fluid accumulation - Life-threatening - Manifestations: falling arterial pressures, rising venous pressures, narrowing pulse pressure, and muffled heart sounds - Complications: heart failure, shock, and death - Constrictive pericarditis - Loss of elasticity (i.e., thick and fibrous pericardium) - Results from chronic inflammation - Manifestations: - Pericardial friction rub (grating sound heard when breath is held) - Sharp, sudden, severe chest pain that increases with deep inspiration and decreases when sitting up and leaning forward - Dyspnea - Tachycardia - Palpitations - Edema - Flulike symptoms **[Infective Endocarditis]** - Formally called bacterial endocarditis. - Infection of endocardium and heart valves. - Commonly caused by *Streptococcus* and *Staphylococcus* infections. - Vegetation forms on internal structures and creates small thrombi. - Thrombi can travel to other locations---embolism. - Embolism can create life-threatening complications like myocardial infarction, stroke, and pulmonary embolism. - Thrombus is attached to something but not traveling - Embolism is attached to something but its traveling, its bad and it will lodge into something cause MI, PE, stroke.. **[Myocarditis]** - Inflammation of the myocardium. - Uncommon; poorly understood. - Organisms, blood cells, toxins, and immune substances invade and damage the muscle. - Complications: heart failure, cardiomyopathy, dysrhythmias, and thrombus formation. **[Let's Practice!]**  =infective endocarditis 9781284121131\_CH04\_FIG13.jpg  Chap 4 part 4 **[Valvular Disorders]** - Disrupt blood flow through the heart - Stenosis: narrowing - Less blood can flow through the valve. - Causes decreased cardiac output, increased cardiac workload, and hypertrophy. - Regurgitation: insufficient closure - Blood flows in both directions through the valve. - Causes decreased cardiac output, increased cardiac workload, hypertrophy, and dilation. - Causes: congenital defects, infective endocarditis, rheumatic fever, myocardial infarction, cardiomyopathy, and heart failure - Manifestations: - Vary depending on valve involved - Reflect alteration in blood flow through the heart **[Cardiomyopathy]** - Conditions that weaken and enlarge the myocardium - Can be acquired or inherited - Classified into three groups: dilated, hypertrophic, and restrictive **[Dilated Cardiomyopathy]** - Most common type. - Cardiomegaly and ventricular dilation damage myocardium muscle fibers, resulting in decreased cardiac output and blood stagnation. Heart enlarges but is thin walled and flabby - Risk higher with advancing age and in African American men. - Causes: chemotherapy, alcoholism, cocaine abuse, pregnancy, infections, thyrotoxicosis, diabetes mellitus, neuromuscular diseases, hypertension, coronary artery disease, and hypersensitivity to medications **[Hypertrophic Cardiomyopathy]** - Thick walls of cardiac muscle. - More common in men and those who are sedentary. - Risk higher with hypertension, obstructive valvular disease, and thyroid disease. - May be autosomal dominant. - Ventricle wall becomes stiff and unable to relax. **[Restrictive Cardiomyopathy]** - Common in South and Central America, India, Asia, and Africa - Caused by rigidity of ventricles due to damage or scaring of the myocardium, leading to diastolic dysfunction - Causes: amyloidosis, hemochromatosis, radiation exposure to the chest, connective tissue diseases, myocardial infarction, sarcoidosis, and cardiac neoplasms **[Let's Practice!]** 9781284121131\_CH04\_FIG15.jpg **[Electrical Alterations (1 of 2)]** - Dysrthymias classified by origin - Can affect cardiac output and blood pressure - Causes: acid--base imbalances, hypoxia, congenital heart defects, connective tissue disorders, degeneration of conductive tissues, drug toxicity, electrolyte imbalances, stress, myocardial hypertrophy, and myocardial ischemia or infarction - Manifestations - Vary depending on the specific dysrhythmia - May include palpitations, fluttering sensation, skipped beats, fatigue, confusion, syncope, dyspnea, and abnormal heart rate - Diagnosis: history, physical examination, electrocardiogram  9781284121131\_CH04\_FIG16B.jpg  **[Question time!]** - A patient with a dysrhythmia will always present with an increase in heart beats per minute. - True or false **False.** A **dysrhythmia** (or arrhythmia) refers to any abnormality in the heart\'s rhythm. While some arrhythmias can lead to an **increase** in heart rate (tachycardia), others can cause a **decrease** in heart rate (bradycardia), or even irregular rhythms without a change in the overall rate. For example: - **Tachycardia** (abnormally fast heart rate) can be caused by arrhythmias like **atrial fibrillation** or **supraventricular tachycardia**. - **Bradycardia** (abnormally slow heart rate) can be caused by arrhythmias such as **sinus bradycardia** or **heart block**. Some arrhythmias, like **atrial fibrillation**, can also result in an irregular heart rate, where the beats are uneven in terms of both timing and rate. So, not all dysrhythmias lead to an increased heart rate. **[Heart Failure (1 of 2)]** **[Types of Heart Failure (1 of 2)]** - Systolic dysfunction - Decreased contractility - Diastolic dysfunction - Decreased filling - Mixed dysfunction - Both - Left-sided failure - Cardiac output falls. - Blood backs up to the pulmonary circulation. - Causes: left ventricular infarction, hypertension, and aortic and mitral valve stenosis. - Manifestations: pulmonary congestion, dyspnea, and activity intolerance. - Right-sided failure - Blood backs up to the peripheral circulation. - Causes: pulmonary disease, left-sided failure, and pulmonic and tricuspid valve stenosis. - Manifestations: edema and weight gain. 9781284121131\_CH04\_TABLE02.jpg Table 4.02: Clinical Manifestations of Left- and Right-Sided Heart Failure  Chapter 4 part 5 **[https://www.youtube.com/watch?v=Pog1dWdQ4l4]** **[Congenital Heart Defects]** - Structural issues present at birth - Most common type of birth defect - Examples: - Septal defect -- holes in wall between - Atrial or ventricular -- foramen ovale - Patent ductus arteriosus -- ductus arteriosus between aorta and pulmonary trunk, doesn't close - Valve disorders - Tetralogy of Fallot- pulmonary valve stenosis, large ventricular septal defect, misplacement of aorta over the ventricular septal defect, right ventricular hypertrophy A diagram of the heart AI-generated content may be incorrect. **Lets Practice!** Ductos ateriousus in the circle.  https://www.epharmapedia.com/img/diseases/1300630039.jpg= Patent formen ovale **[Cardiac conditions leading to altered tissue perfusion]** **Aneurysms =**Weakening of an artery - Common in the abdominal aorta, thoracic aorta, and cerebral, femoral, and popliteal arteries - Can rupture: exsanguination - True aneurysms: affect all three vessel layers - Saccular aneurysm: bulge on the side - Fusiform aneurysm: affects the entire circumference - False aneurysms: do not affect all three layers of the vessel - For example: Dissecting aneurysms: occurs in the inner layers **[Dyslipidemia (1 of 4)]** - High levels of lipids in the blood. - Increases risk for many chronic diseases. - Lipids come from dietary sources and are produced by the liver. - Dietary sources - Cholesterol: animal products - Triglycerides: saturated fats - Classified based on density, which is based on the amount of lipids (low density) and protein (high density) - Very-low-density lipoproteins - Low-density lipoproteins---AKA "bad" cholesterol - High-density lipoproteins---AKA "good" cholesterol - Vldl - It begins as vldl in the liver, loses some triglycerides and is turned into ldl in the blood - Carries triglycerides into body - LdL - Most serum cholesterol is in LDL. - More invasive. - To decrease LDL level: lifestyle modification. - HDL - Helps remove cholesterol from bloodstream - To increase HDL level: lifestyle modification  Table 4.03: Adult Treatment Panel (ATP) III Classification of LDL, Total, and HDL holestorel (mg/dL) **[Atherosclerosis]** - Chronic inflammatory disease characterized by thickening and hardening of the arterial wall. The inflammation draws fat to it. Clots also like to adhere to it - Inflammatory process is triggered by a vessel wall injury. - Lesions develop on the vessel wall and calcify over time. - Leads to vessel obstruction, platelet aggregation, and vasoconstriction - Complications: peripheral vascular disease, coronary artery disease, thrombi, hypertension, and stroke **[Peripheral Vascular Disease (1 of 2)]** - Narrowing of the peripheral vessels - Causes: atherosclerosis, thrombus, inflammation, and vasospasms - Thromboangiitis obliterans: an inflammatory condition of the arteries which can lead to damaged tissue - Raynaud's disease: vasospasms of arteries, usually in the hands, because of sympathetic stimulation - Raynaud's phenomenon: associated with an autoimmune condition - Red white blue presentation in the patients hands **[Let's practice!]**  = aortic dissection False anusersym 9781284121131\_CH04\_FIG24.jpg = atherosclerosis = brain aneurysm 9781284121131\_CH04\_FIG27.jpg= raynauds phenomenon  = Thermonatrites obliterans 9781284121131\_CH04\_FIG20.jpg **[Chapter 5 part 6]** **[https://www.youtube.com/watch?v=1kSsugoVn9E]** **[Thrombus]** - Stationary blood clot consisting of platelets, fibrin, erythrocytes, and leukocytes - Due to inflammation on walls, increased turbulence (bifurcations), increased coagulation - Emboli: traveling body - May be a thrombus, air, fat, tissue, bacteria, amniotic fluid, tumor cells, or foreign substances - Can become lodged in places like the lungs, brain, and heart  **[Varicose Veins]** - Engorged veins resulting from valve incompetency. - Most common in the legs. - May also occur as esophageal varices and hemorrhoids. - Increased venous pressure and blood pooling lead to vein enlargement and valve stretching. - Valves become incompetent, leading to reversal of blood flow and increased distension. - Capillary pressure increases, which leads to fluid leak, resulting in edema and skin discoloration. **[Lymphedema]** - Swelling due to a lymph obstruction or removal lymphatics due to cancer or surgery. - Primary lymphedema - Rare, usually congenital- some malformation - Secondary lymphedema - Causes: surgery, radiation, cancer, infection, and injury **[Let's practice!]** A diagram of a human body AI-generated content may be incorrect. =  =embolismA close-up of a blood vessel AI-generated content may be incorrect. thrombus=  =lymhedmaA close-up of a leg AI-generated content may be incorrect. **[Coronary Artery Disease]** - Atherosclerotic changes of the coronary arteries - Impairs myocardial tissue perfusion - Angina: chest pain resulting from myocardium ischemia - Infarction: necrotic damage to the myocardium - Causes: atherosclerosis, vasospasms, thrombus, and cardiomyopathy **[Coronary Artery Disease]** - Angina: intermittent chest pain resulting from myocardium ischemia - Stable: goes away with demand reduction - Unstable: increased intensity or frequency, does not go away with demand reduction, or occurs at rest - Can occur due to coronary artery spasm - Infarction: permanent necrotic damage to the myocardium  Table 4.04: Risk Factors for Coronary Artery Disease **[Myocardial Infarction]** - Death of the myocardium. - Coronary artery blood flow is blocked due to atherosclerosis, thrombus, or vasospasms. - Risk factors are the same as for atherosclerosis. - Presents with chest and/or arm pain or tightness 9781284121131\_CH04\_TABLE06.jpg  Figure 04.F33: Myocardial infarction. (a) An overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. (b) A cross section of the coronary artery with plaque buildup and a blood clot. 9781284121131\_CH04\_FIG35.jpg Figure 04.F35: EKG ischemia and infarction patterns. (a) Normal EKG for comparison. (b) Mild ischemia demonstarted by inverted T wave. (c) Moderate ischemia demonstrated by slight ST-segment depression and inverted T wave. (d) and (e) ST-segment elevation myocardial infarction. (f) ST-segment myocardial infarction with prominent Q wave indicating more severe myocardial damage. **[Conditions resulting in decreased cardiac output and altered perfusion]** **Hypertension** - Most common form (essential, primary or idiopathic) - Develops gradually over time - Tends to be more sudden and severe - Causes: renal disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs - Malignant hypertension - Especially intense form - Does not respond well to treatment - Hypertension can be classified into systolic or diastolic based on which measure is elevated. **[Shock]** - Decreased blood volume or circulatory stagnation resulting in inadequate tissue and organ perfusion - Stages of Shock - Compensatory - Sympathetic nervous system and renin--angiotensin--aldosterone system are activated. - Progressive - Compensatory mechanisms fail. - Tissues become hypoxic, cells switch to anaerobic metabolism, lactic acid builds up, and metabolic acidosis develops. - Irreversible - Organ damage occurs. **[Types of Shock (1 of 2)]** - Neurogenic shock - Loss of vascular sympathetic tone and autonomic function lead to massive vasodilatation. - Septic shock - Bacterial endotoxins activate an immune reaction. - Anaphylactic shock - Excessive allergic reaction - **Cardiogenic shock** - Left ventricle cannot maintain adequate cardiac output. - Venous return reduces because of external blood volume losses or massive vasodilation. **Question time!** The correct answer is **A. They have decreased perfusion of their tissues.** When a patient is in **shock**, their body is not able to adequately supply oxygenated blood to the tissues and organs. This leads to **decreased tissue perfusion** and can result in organ failure if not addressed. Here\'s why the other options are incorrect: - **B. Stimulation of the parasympathetic nervous system**: During shock, the **sympathetic nervous system** is usually activated to try to compensate for the low blood pressure and poor tissue perfusion. This leads to increased heart rate and vasoconstriction. The parasympathetic nervous system, which generally works to slow heart rate and promote rest, is typically suppressed during shock. - **C. Inactivation of the renin-angiotensin system**: In shock, the **renin-angiotensin system (RAAS)** is actually **activated**, not inactivated. This helps to retain sodium and water, increase blood volume, and cause vasoconstriction to try to raise blood pressure and improve perfusion. - **D. Increase in blood volume**: In shock, blood volume is usually either **decreased** (e.g., hypovolemic shock due to blood loss or dehydration) or poorly distributed (e.g., in septic shock). The body may try to compensate by retaining fluid through mechanisms like RAAS, but overall blood volume is often insufficient to maintain adequate perfusion during shock. So, **A** is the best and most accurate description of what happens during shock. [**https://www.youtube.com/watch?v=YDxec\_PMwSQ**](https://www.youtube.com/watch?v=YDxec_PMwSQ) **[Chapter 5- Respiratory Function]** **Respiratory System (1 of 2)** - Two divisions - Air-conducting: delivers air in and out - Includes the nose, mouth, trachea, bronchi, and bronchioles - Gas exchange: swaps gases between air and blood - Includes alveoli and capillaries - Mucus, cilia, and immune cells protect the system from harmful inhaled particles. - Capillaries in the nose warm and humidify the air to protect the system from drying and damage from cold. \*CO2 is acidic, if you get rid of co2 is too alkaline\* **[Structures of the respiratory system]**  9781284121131\_CH05\_FIG01.jpg Figure 05.F01: The upper respiratory tract  Figure 05.F02: The respiratory system. (a) This illustration shows the air-conducting portion and the gas-exchange portion of the human respiratory system. The insert shows a higher magnification of the alveoli where oxygen and carbon dioxide exchange occurs. (b) A scanning electron micrograph of the alveoli, showing the rich capillary network surrounding them. BRONCHIOLE\* is where smooth muscle is , and in asthma it tightens down so air cant pass down. 9781284121131\_CH05\_FIG03.jpg Figure 05.F03: The vocal cords. (a) Uppermost portion of the respiratory system, showing the location of the vocal cords. (b) Longitudinal section of the larynx showing the location of the vocal cords. Note the presence of the false vocal cord, so named because it does not function in phonation. (c) View into the larynx of a patient showing the true vocal cords from above. Epigolltis is part of larynx,  Figure 05.F04: The bifurcation of the trachea at the carina into the right and left mainstem bronchi. 9781284121131\_CH05\_FIG05.jpg Figure 05.F05: Mucous trap. (a) Drawing of the lining of the trachea. Mucus produced by the mucous cells of the lining of much of the respiratory system traps organisms and other particulates in the air. The cilia transport the mucus toward the mouth. (b) Higher magnification of the lining showing a mucous cell and ciliated epithelial cells.  Figure 05.F06: The alveolar macrophages https://anatomywiki101.com/wp-content/uploads/2017/08/human-respiratory-system-diagram-unlabeled-simple-diagram-of-the-respiratory-system-unlabeled-tagged-human.jpg **[Chap5 part 2] ** [ ] If youre breathing deeply to calm down.. it calms your parasympathetic system **[The function of the respiratory system]** **Gas Exchange** - Requires adequate ventilation and perfusion - Ventilation/perfusion ratio (VQ ratio) - Normal ventilation = 4 L per minute - Normal perfusion = 5 L per minute - Dependent on alveolar and capillary surface area and thickness **Gas Transportation** - Carried by hemoglobin. - Once at the site, hemoglobin must be able to release the gases. - Affected by a variety of things such as pH and temperature  Figure 05.F07: Gas exchange in the lungs 9781284121131\_CH05\_FIG09.jpg Figure 05.F09: Oxyhemoglobin dissociation curve **[Question time!]** False. The membranes of the alveoli are actually thin, not thick. This thinness is crucial because it allows for efficient gas exchange between the air in the alveoli and the blood in the pulmonary capillaries. Oxygen passes through the alveolar membrane into the blood, and carbon dioxide moves from the blood into the alveoli to be exhaled. If the membranes were thick, it would impede this gas exchange process. **[Lung Compliance]** - Elasticity and recoil are vital. The lungs want to collapse but we have means to keep them open - Surfactant: lipoprotein - Has a detergent quality to break apart water in lungs - reduces alveoli surface tension to prevent collapse - pressure system in which the lungs have a change due to breathing - This pressure is always higher then intrapleural 1.Breathing is passive, it passively moving air into and out of the lungs 2\. Pressure in the lungs is higher than the pressure surrounding the lungs in the intrapleural space.  **[Pleural membranes]** **[Breathing]** - Largely involuntary - Controlled by the medulla oblongata + pons - Chemoreceptors - Stretch receptors - Inspiration: inhaling - Diaphragm lowers opening the space in the lungs - External intercostals contract in deep breathing. (inhalation) up and out. - Intercoastal will pull the ribs down and in and help with expiration (exhalation) , - Neck muscles contribute with labored breathing - Expiration: exhaling - Diaphragm relaxes into a curved position - Internal intercostals with deep breathing Breathing deep labored breathing uses neck muscles SCM and scalene. 9781284121131\_CH05\_FIG10.jpg Figure 05.F10: Breathing. The rising and falling of the chest wall through the contraction of the intercostal muscles (muscles between the ribs) is shown in the diagram, illustrating the bellows effect. Inspiration is assisted by the diaphragm, which lowers. Like pulling a plunger back onout on a syringe, the rising of the chest wall and the lowering of the diaphragm draw air into the lungs. Illustrations and X-rays showing the lungs in full exhalation (a) and full inspiration (b). **Question time!** The correct answer is **D. diaphragm**. The diaphragm is the primary muscle responsible for respiration. When it contracts, it moves downward, increasing the volume of the thoracic cavity and allowing air to be drawn into the lungs. The intercostal muscles (internal and external) also assist in breathing, but the diaphragm plays the central role. **Pulmonary Function Test (1 of 2)** - Tidal volume: amount of air moved in and out with a normal breath (\~500 mL) ( normal inhalation and exhalation) - Minute respiratory volume: amount of air moved in and out in one minute (\~6 L) - Inspiratory reserve volume: maximum amount of air that can be inhaled over tidal volume (2--3 L) ( if you decide to go excersie you need more air in and out) - Expiratory reserve volume: maximum amount of air that can be exhaled over tidal volume (1--1.5 L) **Lung volumes** - Vital capacity: sum of the tidal volumes and the reserves. - Residual volume: amount of air left in the lungs after forced expiration (1--1.5 L). - Forced expiratory volume in one second is compared to the forced vital capacity to diagnose pulmonary disease. - Normal fev1 should be 80 percent of lung volume or more  9781284121131\_CH05\_FIG11A.jpg Figure 05.F11A: Measuring air flow. (a) This machine allows healthcare workers to determine tidal volume, inspiratory reserve volume, and other lung-capacity measurements to determine the health of an individual's lung.  Figure 05.F11B: Measuring air flow. (b) This graph shows several common measurements. **[Role in pH Balance]** - Carbon dioxide is one of the body's acids. - Lungs alter the rate and depth of breathing to regulate pH. - Increased rate of breathing expels more carbon dioxide and raises pH. - Decreased rate of breathing retains more carbon dioxide and lowers pH. **[Question time]** The correct answer is **A. Systemic pH**. While systemic pH is important for overall body function, the **rate and rhythm of breathing** are more directly influenced by factors like **CO2 levels**, **COPD**, and other mechanisms that affect the respiratory centers in the brain. - **Increase in CO2**: This directly stimulates the respiratory centers in the brain (medulla and pons) to increase the rate and depth of breathing. - **COPD (Chronic Obstructive Pulmonary Disease)**: This condition can alter the normal regulation of breathing, often leading to a blunted response to CO2 and oxygen levels, affecting rate and rhythm. On the other hand, systemic pH (which is a reflection of overall acid-base balance) does not directly control breathing rate and rhythm, though pH changes can be a result of altered breathing. **[Chap 5 part 3] ** **[Respiratory diseases]** **[Infectious Rhinitis]** - Viral rhinitis and common cold - Usually caused by the rhinovirus - Highly contagious - May also see a secondary bacterial infection due to damaged membranes - Incubation period = 2--3 days - Manifestations: typical cold symptoms **[Rhinosinusitis]** - Inflammation of the sinus cavities. - Rhinosinusitis is the preferred term for sinusitis. - Causes: viruses, bacteria, and fungi. - Exudate collects and blocks the sinus cavities. - Manifestations: paranasal facial pain **[Epiglottitis]** - Inflammation of the epiglottis - Life-threatening - Causes: *Haemophilus influenzae* type B (Hib) - Manifestations: sore throat, difficulty swallowing **[Laryngitis]** - Inflammation of the larynx - Usually self-limiting - Causes: infection, increased upper respiratory exudate, and overuse - Manifestations: hoarseness, weak voice or voice loss, may show as a narrowing upon x-ray Let's practice- Upper respiratory diseases 9781284121131\_CH05\_FIG14.jpg=blocked sinus = steeple sign 9781284121131\_CH05\_FIG15.jpg  **[Laryngotracheobronchitis]** - Croup. - Common viral infection in children, usually parainfluenza viruses and adenoviruses. - Larynx and surrounding area swell, leading to airway narrowing, obstruction, and respiratory failure. - Manifestations: seal-like barking cough, hoarseness, inspiratory stridor, dyspnea **[Acute Bronchitis]** - Inflammation of the tracheobronchial tree or large bronchi - Causes: viruses, bacterial, irritant inhalation, and allergic reactions **[Influenza]** - Flu - Viral infection that may affect the upper and lower respiratory tract - Highly adaptive virus - Types - Type A: most severe and most common in US - Type B: less severe - Type C: usually causes small outbreaks - US flu season between October and March - Incubation period of 1--4 days - Can cause significant problems with children, elderly, and those who are immune compromised - Manifestations: fever, headache, chills, dry cough, body aches, nasal congestion, sore throat, sweating, and malaise **[Bronchiolitis]** - Common acute inflammation of the bronchioles, usually respiratory syncytial virus - More frequent in children under 1 year and during the winter months - Can lead to atelectasis and respiratory failure - Manifestations: cough, wheezing, rapid and shallow respirations, dyspnea **[Question time]** - Which of the following is the best description of respiratory diseases? A. Bronchiolitis is found in the main bronchi B. Flu is a bacterial infection **C. bronchitis is Inflammation of the tracheobronchial tree or large bronchi** D. Laryngotracheobronchitis never causes difficulty with breathing Let\'s break each option down: **A. Bronchiolitis is found in the main bronchi**\ This is **false**. Bronchiolitis typically affects the smaller bronchioles, not the main bronchi. It\'s most commonly seen in young children, often caused by viral infections like respiratory syncytial virus (RSV), and leads to inflammation and congestion in the smaller airways. **B. Flu is a bacterial infection**\ This is **false**. The flu (influenza) is caused by a virus, not a bacteria. It affects the upper and lower respiratory tract and can cause symptoms like fever, chills, and body aches. **C. Bronchitis is inflammation of the tracheobronchial tree or large bronchi**\ This is **true**. Bronchitis is the inflammation of the trachea and the larger bronchi. It can be acute (usually caused by viruses) or chronic (commonly related to smoking or long-term irritant exposure). In chronic cases, it can lead to persistent coughing and mucus production. **D. Laryngotracheobronchitis never causes difficulty with breathing**\ This is **false**. Laryngotracheobronchitis (commonly known as croup) can indeed cause difficulty with breathing, particularly due to the swelling of the upper airways. It often leads to a characteristic \"barking\" cough and can result in stridor (a high-pitched wheezing sound) and respiratory distress. So, the **correct answer** is **C**: Bronchitis is inflammation of the tracheobronchial tree or large bronchi. **[Pneumonia (1 of 3)]** - Infection that inflames alveoli - Causes: infectious agents, injurious agents or events, and pulmonary secretion stasis - Viral - Usually mild - Can lead to secondary bacterial pneumonia - Bacterial - More common than viral - Most often *Streptococcus pneumoniae* - Aspiration pneumonia - Causes: impaired gag reflex, improper lower esophageal sphincter closure, inappropriate gastric tube placement - Lobar pneumonia - Confined to a single lobe - Bronchopneumonia - Most frequent type - A patchy pneumonia throughout several lobes - Interstitial pneumonia or atypical - Occurs in the areas between the alveoli - Routinely caused by viruses or by uncommon bacteria - Nosocomial pneumonia - Develops more than 48 hours after a hospital admission - Community-acquired pneumonia - Acquired outside the hospital or healthcare setting 9781284121131\_CH05\_TABLE03.jpg Table 5.03: Comparison of Viral and Bacterial Pneumonia **[Legionnaires' Disease]** - Pneumonia caused by *Legionella pneumophila* - Thrives in warm, moist environments, particularly air-conditioning systems and spas - Not contagious---spread through aerosol droplets - Higher risk in the immune compromised - Can be life-threatening - Diagnosis: urine test for *Legionella* antigens ***Pneumocystic carinii* Pneumonia** - Caused by yeastlike fungus, *Pneumocystis jiroveci* - Opportunistic infection - Can be life-threatening - Diagnosis: sputum culture **[Pneumonia (1 of 2)]** - Complications: pulmonary edema, lung abscess, and acute respiratory distress syndrome - Manifestations: productive or nonproductive cough, fatigue, pleuritic pain, dyspnea, fever, chills, crackles or rales, pleural rub - Diagnosis: chest X-ray, sputum cultures - Prevention: hand washing, avoiding crowds, vaccinations, coughing, deep breathing, and smoking cessation **[Question time]** - Regardless of the cause, pneumonia causes fluid buildup in the lungs (both alveoli and the surrounding tissue) - **True** or false **True.** Pneumonia, regardless of its cause (bacterial, viral, fungal, etc.), typically leads to inflammation in the lungs. This inflammation causes fluid buildup in the alveoli (the small air sacs where gas exchange occurs) and sometimes in the surrounding lung tissue. The fluid may be made up of pus, mucus, or other inflammatory materials, depending on the cause of the infection. This fluid buildup interferes with the normal gas exchange, leading to symptoms like cough, fever, shortness of breath, and difficulty breathing. **[Tuberculosis (1 of 4)]** - Caused by the bacillus, *Mycobacterium tuberculosis* - Fairly controlled until recently - Resistant strains have developed in those immune compromised - Most frequently occurs in the lungs, but can spread to other organs - Carried by airborne droplets - Primary infection - When bacillus first enters the body. - Macrophages engulf the microbe, causing a local inflammatory response - Granuloma forms then tubercles form with calcium around them....they continue to form....until they get\> - Caseous necrosis and Ghon (calcified granuloma with caseous necrosis and surrounding tissue involvement) complexes develops. - Bacilli can remain dormant for years. - Usually asymptomatic. - Will test positive now. - Secondary infection - Reactivation of dormant bacilli - Can spread to other organs - Symptoms usually develop - Manifestations: productive cough, hemoptysis, night sweats, fever, chills, fatigue, unexplained weight loss, anorexia, and symptoms depending on other organ involvement - Diagnosis: skin test (Mantoux), chest X-ray, computed tomography, and sputum culture Let's practice!  9781284121131\_CH05\_FIG19.jpg = positive tb skin test  =ghon complex https://upload.wikimedia.org/wikipedia/commons/6/68/PulmonaryTBCXR.png=tubercles in lungs **[Asthma]** - Chronic disorder that results in intermittent, reversible airway obstruction - Characterized by acute airway inflammation, and spasms of the bronchioles, bronchoconstriction, bronchospasm, bronchiole edema, and mucus production - A variety of triggers from infections to smoke - Extremely common - Types - Intrinsic asthma - Not an allergic reaction due to smoke, infections, cold exposure. - Extrinsic asthma -- IGE synthesis releases inflammation, due to allergens - Nocturnal asthma - Usually occurs between 3:00 and 7:00 a.m. - May be related to circadian rhythms---histamine levels increase, leading to bronchoconstriction - Exercise-induced asthma - Usually occurs 10--15 minutes after activity. - Symptoms can linger for an hour. - Drug-induced asthma - Frequently caused by aspirin---which stimulate leukotriene release, a powerful bronchoconstrictor. - Manifestations: wheezing, shortness of breath, dyspnea, chest tightness, cough, and anxiety - Status asthmaticus - Life-threatening, prolonged asthma attack that does not respond to usual treatment - Can lead to respiratory alkalosis and respiratory failure quickly - Please watch Bronchial Thermoplasty for Asthma video. A very interesting approach to treatment  Figure 05.F20: Asthma. (a) Location of the lungs and airways in the body. (b) Cross section of a normal airway. (c) Cross section of an airway during asthma symptoms. **[https://www.youtube.com/watch?v=H8dYE6MSdHM]** **[Chapter 5 part 4]** **[Chronic Obstructive Pulmonary Disease (1 of 2)]** - Debilitating chronic disorders characterized by irreversible, progressive tissue degeneration and airway obstruction. - Severe hypoxia and hypercapnia can lead to respiratory failure. - Oxygen begins to drive breathing. CO2 should drive breathing - Can also lead to cor pulmonale. - Causes: smoking, pollution, chemical irritants, and genetic mutation - Often asymptomatic early or masked by smoking - Two main conditions: chronic bronchitis and emphysema **[Chronic Bronchitis(1 of 3) "Blue bloaters"]** - Characterized by inflammation of the bronchi, a productive cough, and excessive mucus production - Complications: frequent respiratory infections and respiratory failure - Manifestations: hypoxemia, cyanosis, hypercapnia, clubbing of fingers, dyspnea at rest, wheezing **[Emphysema (1 of 2) "Pink puffers."]** - Destruction of the alveolar walls leads to large, permanently inflated alveoli. - Enzyme necessary for lung remodeling is deficient. - Loss of elastic recoil and hyperinflation of the alveoli, leading to air trapping. - Causes: genetic predisposition and smoking. - Alpha 1 antitrypsin deficiency -- inherited disorder in which the alpha 1 antitrypsin is deficient. This is used to decrease overactive immune response in lungs. Without it, the lung tissue is destroyed just as in emphysema - Manifestations: dyspnea upon exertion, diminished breath sounds, wheezing, chest tightness, increased anterior--posterior thoracic diameter - When you exhale you have a collapse of bronchioles \* 9781284121131\_CH05\_FIG22.jpg Figure 05.F22: Chronic obstructive pulmonary disease (COPD) is often one disease or a mixture of two diseases---chronic bronchitis and emphysema  **QUESTION TIME!** WHICH IS EMPHYSEMA AND WHICH IS CHRONIC BRONCHITIS? **[Cystic Fibrosis]** - Life-threatening condition resulting in severe lung damage and nutrition deficits - Affects cells that produce mucus, sweat, saliva, and digestive secretions - Secretions become thick and tenacious. - Caused by mutation on seventh chromosome - Autosomal recessive - Complications: respiratory and malabsorption signs and symptoms - Manifestations: fatty stool, chronic cough, delayed growth and development, difficulty breathing overproduction of muscus, people with CF are thin, unable to digest food due to lack of digestive secretion - Treatment: cupping and enzymes for digestion **[Lung Cancer]** - Second most common cancer. - May occur as a primary or secondary tumor. - Deadliest of the cancers in men and women. - Smoking is the most significant risk factor, either first-hand or second-hand. - Types - Small cell carcinoma 10-15% - Also known as oat-cell carcinoma because the cells transform into oval shaped cells that look like grains of oats - Starts in bronchi - Occurs almost exclusively in heavy smokers - Less frequent but spreads quickly - May release hormones such as adh and acth (causing ectopic cushings) - Types - Non--small cell carcinoma 80% - Also known as bronchogenic carcinoma - Most common type of malignant lung cancer - Very aggressive lung cancer - May release hormones such at parathyroid hormone - Several subgroups--- - squamous cell carcinoma -- central lung. from squamous cells that line the airways - adenocarcinoma -- outer lung (adeno-glands) - Large cell -- larger cells located anywhere in the lungs. Grows and spreads quickly - Manifestations: persistent cough or a change in usual cough, dyspnea, hemoptysis, frequent respiratory infections, chest pain, hoarseness, weight loss, anemia, fatigue, and other symptoms specific to site of metastasis look for persistent signs that are new to that patient. - Lung cancer may also release hormones from the cancer itself  9781284121131\_CH05\_TABLE06.jpg Table 5.06: Staging and Treatment of Non-Small-Cell Lung Cancer **[Question Time]** **False.** A cough lasting for 7 days following a cold is generally considered a normal part of the recovery process. Post-viral coughs, which can linger after a cold or respiratory infection, are fairly common and usually resolve on their own. However, if the cough persists for **several weeks**, is **persistent and worsening**, or is accompanied by other concerning symptoms (like weight loss, coughing up blood, chest pain, or difficulty breathing), then further evaluation for lung cancer or other serious conditions might be warranted. In general, a cough lasting for just a week after a cold is not an immediate reason to screen for lung cancer. **[Pleural Effusion]** - Excess fluid in the pleural cavity. - Fluid may include exudates (more clear), transudate (colored), blood, and pus. - Can impair breathing. - May also see pleurisy---inflammation of the pleural membranes. - Manifestations: dyspnea, chest pain, tracheal deviation, and pleural friction rub. - thoracentesis  Figure 05.F26: Pleural effusion is a buildup of fluid in the lining of the lungs **[Pneumothorax]** - Air in the pleural cavity - Can cause lung to collapse - Risk factors: smoking, tall stature, and history of lung disease or previous pneumothorax **[Types of Pneumothorax (1 of 2)]** - Spontaneous pneumothorax - Air enters from an opening in the internal airways - Primary spontaneous pneumothorax - Occurs when a small air blister (bleb) on the top of the lung ruptures. - Blebs are caused by a weakness in the lung tissue. - Usually mild. - Secondary spontaneous pneumothorax - Develops in people with preexisting lung disease - Can be more severe and even life threatening - Traumatic pneumothorax - Result of a blunt or penetrating injury to the chest - Tension pneumothorax - Most serious type - Occurs when the lung has damage and air leaks out into the pleural space - Can cause the affected lung to collapse completely and shift the heart **[Pneumothorax (1 of 2)]** - Manifestations: sudden chest pain, chest tightness, dyspnea, **[Let's Practice!]** 9781284121131\_CH05\_FIG28.jpg = plerul effusion 9781284121131\_CH05\_FIG29.jpg = pneumothorax = Lung cancer **[Acute Respiratory Distress Syndrome]** - Rapidly developing respiratory failure - Results from fluid accumulation in the alveoli due to a systemic or pulmonary event that is not cardiac in origin. This decreases the transferring of gasses across membranes and decreases surfactant production - Causes: shock, burns, aspiration, and smoke inhalation - Complications: respiratory and metabolic acidosis; pulmonary fibrosis; pneumothorax; bacterial infections; decreased lung function, muscle wasting; memory, cognitive, and emotional issues; and death 9781284121131\_CH05\_FIG32.jpg Figure 05.F32: Acute respiratory distress syndrome **[Atelectasis (1 of 2)]** - Collapse of the alveoli - Causes: surfactant deficiencies, bronchus obstruction, lung tissue compression, increased surface tension, and lung fibrosis - Ventilation and perfusion problem - Manifestations: diminished breath sounds, asymmetrical lung movement, tracheal deviation - Must reinflate lungs  Figure 05.F33: X-ray of atelectasis (a) Normal lung. (b) Lung with atelectasis.