Cardiovascular System Review PDF

WEEK 1 PART 1 Pericardial space – potential space in between DISTURBANCES IN OXYGENATION the pericardial space which contains pericardial...

WEEK 1 PART 1 Pericardial space – potential space in between DISTURBANCES IN OXYGENATION the pericardial space which contains pericardial fluid (amount is more or less about 20mL). This Components Involved in Oxygenation: will prevent friction between parietal and Heart – main pumping organ visceral pericardium during cardiac contractions. Lungs – responsible for gas exchange Pericarditis – inflammation of pericardium. If there’s Red Blood Cells – specifically, hemoglobin for inflammation, there will be fluid shifting from transportation of oxygen intravascular to interstitial space. Blood Vessels – pathway for passage of blood. - In short, pag namamaga pericardium, fluid will o Should be patent (walang bara), elastic accumulate pericardial space which is called pericardial effusion. If too much fluid Oxygenation – transportation of gases (O2 & CO2) to accumulated this space, there will be and from the cells. constriction affecting myocardial contraction. Hypoxia – decrease in oxygen Anoxia – total absence in oxygen = cells will die (first to 3 LAYERS OF CARDIAC MUSCLE TISSUE: die are brain cells) Epicardium: outermost layer Necrosis – death of cells Myocardium: middle layer responsible for contraction Anatomy and Physiology Review: Endocardium: innermost layer. Continuous with HEART the valves - cone-shaped hollow muscular organ located in *Inflammation of these layers: the mediastinum between the lungs ❖ Epicarditis - looks like an inverted cone with apex pointing ❖ Myocarditis downward and base pointing upward. ❖ Endocarditis (if there is endocarditis, there will - Stroke Volume – amount of blood pumped by be inflammation of the valves also which is called beat. (60mL/beat) valvulitis) - Cardiac Output – amount of blood pumped per *so, if there’s chronic inflammation of the valves minute. (5L/min) (valvulitis), wound healing will be by fibrous tissue o Formula: Cardiac output = Heart rate x formation. So, the valves will be thickened and unable to stroke volume open and close adequately. Kaya if there’s endocarditis, - pumps about 60ml/beat or 5L/min there will be valvulitis leading to narrowing or PERICARDIUM – protective covering of the inadequate OPENING of the valves which is called heart. A thin sac enclosing the heart. valvular stenosis. And it does not CLOSE adequately known as valvular regurgitation. *ex. There is mitral stenosis, meaning blood from LA find it difficult to enter LV. In the same way, tricuspid stenosis find it difficult to pump blood from RA to RV. LAYERS: Parietal pericardium – outermost layer Visceral pericardium – inner layer (color yellow sa pic) CHAMBERS: *there should be NO MIXING of blood. This is common in Right atrium (0-5 mmHg) children with congenital heart disease* o SVC, IVC, Coronary sinus Right Ventricle (25 mmHg) Left ventricular failure = Congestion in lungs Left atrium Right ventricular failure = Congestion in Left ventricle systemic circulation Receiving chambers: right and left atrium o Retention of blood in RV, unable to Distributing chambers: right and left ventricles accommodate blood coming from RA = blood will go back to SVC = distended VALVES: neck veins and high central nervous AV valves – atria-ventricular valves. Opening pressure. And there will be dump back between atria and ventricles. into the GIT evidenced by leg edema and o Right side: there will be organomegaly ▪ Tricuspid valve (hepatomegaly, splenomegaly) which o Left side: will lead to abdominal discomfort. ▪ Mitral valve 2 Semilunar valves CORONARY ARTERIES: o Pulmonic valve Left Coronary Artery o Aortic valve - will give rise to circumplex coronary artery which *These valves must open completely and close give primary blood supply to LA. Branching to completely to prevent backward flow of blood from one LADA (left anterior descending coronary artery) chamber to another. supplying primarily the LV o Left anterior descending: LV, Ventricular THE CARDIO-PULMONARY CIRCULATION septum, chordae tendineae, papillary muscle, RV (lesser extent) o Circumflex coronary artery: LA, lateral & posterior surfaces of LV, portion of interventricular septum, SA node, AV node Right Coronary Artery - will give rise to marginal artery which supplies primarily the RV and RA o RA, RV, inferior portion of LV *Branching pattern of the coronary arteries varies considerably among individuals. *colateral circulation that varies between individuals. Regular exercise promotes growth of colateral circulation *coronary artery arise from ASCENDING aorta* Unoxygenated blood → upper extremities thru SVC & Lower extremities thru IVC → coronary sinus → RA → Atherosclerosis – bara sa blood vessels like by deposition Tricuspid valve → RV → pulmonary valve → pulmonary of fats and lipids = decrease blood flow in the heart then artery → lungs → gas exchange → oxygenated blood → there will be imbalance in oxygen supply and oxygen pulmonary vein → LA → mitral/bicuspid valve → LV → demand which is known as Angina Pectoris. aortic valve → aorta → different parts of the body. In And kapag totally barado because of inadequate return, CO2 is being removed from the body opening. There is deposition of fats and lipids along the intima of the blood vessel, it is no longer elastic, may mga Rhythmicity: ability of heart to relax and pluck so masasabit ang blood cells and platelets and this contract in a definite pattern will initiate thrombus formation. Halimbawa may thrombus dito, so oxygen is not CONDUCTION SYSTEM: delivered to the heart so this part will be necrotic, known Sinoatrial node (SA node) (60-100 times/min) as Myocardial Infarction. o Main pacemaker because it is the fastest IN SHORTT: to fire impulse. As you can see its problem in cardio-pulmonary circulation = heart inherent impulse is 60-100 which is the failure. normal HR of a person. So sya ung basis Bara sa coronary artery = coronary artery kasi sya ung main pacemaker. diseases (angina pectoris and myocardial Atrioventricular node (AV node) (40-60 infarction.) beats/min) Bundle of His R & L bundle branches Purkinje fibers (20-40 beats/min) ELECTROPHYSIOLOGIC PROPERTIES OF THE HEART: Automaticity: initiate an impulse spontaneously & repetitively o Heart has its own pacemaker – the SA node (sinoatrial node) Impulse is initiated by the SA node → then impulse will Excitability (depolarization): respond to a quickly spread into the 2 atria through the internodal stimulus tracts (anterior, middle, posterior) → so there will be Conductivity: transmit electrical impulses atrial contraction which is seen in ECG thru P wave → Contractility: contract then, the impulse now go to the AV node where the o Ability of heart to shorten impulse is a little bit delay because dadaan pa ung dugo Refractoriness: inability to respond until sa ventricles. Because the cardia conduction system is repolarization not just electrical activity but together with it is the o Meaning while the heart is in the state of mechanical activity wherein meron tayong cardiac contraction, no matter how strong the contraction. → then the impulse will spread to the stimulus is, it will not respond to another bundle of his, right and left branches → to the purkinje stimuli. If nagrespond sa another fibers → then there will be ventricular contractions stimulus, there will be abnormalities in which is makikita sa ECG as QRS complex. heart rate. Elasticity: ability to stretch *impulse from SA node should reach purkinje fibers may tachycardia and *if theres a problem with conduction or transportation palpitations and increase in BP. of electrical impulses, it is known as heart block. o Parasympathetic NS (vagus nerve), beta *Example: 50yr old male pt with RHD goes to the blockers, Ca++-channel blockers bathroom then suddenly biglang blackout (dumilim ▪ On the other hand, when we’re paligid nya) but there’s no chest pain but HR is 20bpm. asleep/resting, we conserve Cardiac output is 1200. Therefore, decrease cardiac energy so there’s predominant output kasi 1200 lang so decrease oxygen to the brain, function, the parasympathetic tissue perfusion. So, first drug to be given to stimulate system = slow HR. heart rate is atropine sulfate. So if nakailang ampule na ▪ Also, decrease in HR is nung drug tas di pa rin tumataas, need nya na ng secondary to effect of beta pacemaker insertion. blockers and calcium channel blockers SEQUENCE OF EVENTS DURING CARDIAC CYCLE: ▪ Beta blockers – it blocks Systole (contraction): emptying sympathetic activities of the Diastole (relaxation): filling heart. (E.g. -lol). Therefore, it Pulse pressure – difference between systolic and decreases heart rate and BP. diastolic pressure ▪ Calcium channel blockers – blocks inflacts? (TEH PIKON NA MECHANICAL PROPERTIES OF THE HEART: PIKON NA KO WTH) of calcium (Cardiac Output = HR x SV) ions into the myocardial cells, Heart Rate (HR) the smooth muscles. So also, it o Affected by stimulation of autonomic decreases heart rate and BP. (- nervous system dipine) o ANS, increase endogenous ▪ Digitalis – are inotropic. Anong catecholamines effect neto? Lanoxin, cedilanid, ▪ Catecholamines like anong effect? It strengthens the epinephrine and force of cardiac contraction but norepinephrine. It is produced slows down HR so it gives more by adrenal medulla. time for the heart to relax. ▪ So hormones secreted by the !!!before administering digitalis, adrenal medulla that of check HR 1 full min. 35 inches o Thru interview, physical examination by ▪ Men: abdominal circumference inspection, palpation, percussion, and = >40 inches auscultation Psychological variables o Demographic data – age, gender, ethnic o e.g. stress – increase HR and BP. If palagi origin ka stress, there is an increase of ▪ Age group – usually 40 and above catecholamines so it also raises the ▪ Gender – usually male probably glucose level = DM and chronic disease because of lifestyle (cigarette like hypertension smoker and alcohol drinker). But if o stress management female reach menopause period, Chronic diseases the incidence for both male and female are equal. Therefore, NON-MODIFIABLE RISK FACTORS: estrogen provides some degree of Age, Gender, Ethnic Background, Family History protection. o We can still prevent CDV by changing ▪ Ethnic origin – general population lifestyle like stop smoking, provide some affected form of mobility (e.g. exercise). For o Family history and genetic risk immobile, change position every 2hrs o Personal history  (turn to side, ROM, passive exercises of o Sudden loss of consciousness because of upper and lower extremities). decrease supply of oxygen in the brain. o Maintain ideal blood sugar, BP, have o Secondary to decreased cerebral healthy diet (low fat diet, low salt diet) perfusion Extremity pain: due to ischemia & venous ❖ PHYSICAL ASSESSMENT insufficiency - MAJOR symptoms of CVD: o Nagbabara peripheral blood vessels Pain/Discomfort supplying the leg o Chest pain is secondary to imbalance *presence of 1 of any of these, CONSULT YOUR oxygen supply and oxygen demand. DOCTOR! There is decrease supply of oxygen in the heart (angina pectoris). First drug to give - MINOR symptoms of CVD: is vasodilator (nitroglycerin). Skin color: o Acute chest pain secondary to total o pallor (anemia) (diagnosed thru CBC by absence of oxygen supply to the heart checking hemoglobin) (myocardial infarction). o cyanosis (late sign of decreased Dyspnea (DOE, Orthopnea, Paroxysmal perfusion) Nocturnal Dyspnea) o Conjunctiva & lips (normal should be o DOE – Dyspnea on Exertion pinkish) o Orthopnea – DOB in supine position and o Palm/Mucous membrane relieve when sitting up. Good question ↓/Cold Skin temperature: due to decrease to ask is how many pillows are you using blood flow (2 pillow orthopnea or 3 pillow Clubbing of fingers: chronic tissue hypoxia orthopnea) o secondary to chronic tissue hypoxia, o Paroxysmal Nocturnal Dyspnea – woke COPD, 7 congenital heart disease up in the middle of the night with DOB. (normal angle of nail should be less than Observe on pts with pulmonary 160 degrees) congestion and pulmonary edema. o Schamroth method: check for diamond Fatigue shape, if none then positive for early o Activity intolerance (madali mapagod) = clubbing DOB, chest pain. Or medical dx is CHF or Edema MI = CBR (complete bed rest w/ or w/o BP changes: Hypertension & Postural bathroom privilege) so ready bedside Hypotension commode o When assisting pt, allow pt to slowly sit Palpitations up on the bed and dangle legs. After a o Secondary to arrhythmias while, assist in standing up. This is to Weight gain: best indicator for fluid retention prevent dizziness secondary to Postural (edema) Hypotension o So pt kuware may heart failure then Pulse pressure (30-40mmHg) fluids accumulated the lungs or systemic circulation Precordium Assessment includes: o So in short, pt with heart disease also Inspection of apical impulse, skin color experiences weight gain, hindi lang ung ○ Apical impulse may be noted in mga pt with renal failure. thin patients but normally not in Syncope: transient loss of consciousness obese. If presence of impulse in (decrease cerebral perfusion) obese, could be a sign of RHD  Palpation chest pain & returns to normal 3-4 ○ If + thrills = sign of RHD days Percussion Myoglobin ( Fatty streak development (intimal layer) > Plaque (partial or complete occlusion of blood flow) > Complications COMPLICATIONS: *remember that atherosclerosis is a slow, progressive calcifications vascular (disease) that may start as early as childhood *hardening of tissues by the deposition of insoluble *vascular - meaning involved ang blood vessel/s. calcium compounds associated with arterial stiffness *However, the disease have the potential to progress ulceration rapidly or plaque formation may take place causing decreased amount of blood flow and oxygen supply to *formation of formation of a plaque (?) on the surface of the vital organs and extremities. the artery. ulcer forms when the cells die *heart attack may occur if the oxygenated blood supply thrombosis to the heart is reduced *local coagulation or clotting of blood. The clotting of *a stroke may also occur if the oxygen supply to the brain blood can add up to the blockage. is cut off *gangrene may occur if the oxygenated blood supply to the extremities, especially in the legs, is reduced. *if you will notice (sa photo above), there is a range of clinical symptoms in ages 35 to 70 and above. Ang problem ay the progress of the disease may increase during those ages.  RISK FACTORS: MAJOR RISK FACTORS MINOR RISK FACTORS NON-MODIFIABLE: MODIFIABLE: - increasing age - obesity - male gender - physical activity - family history - stress ("type A" personality) -genetic abnormalities - post menopausal estrogen deficiency MODIFIABLE: - high carbs intake - hyperlipidemia - alcohol - hypertension *So ang pinakaneed sa kanila for a healthy heart ay - lipoprotein Lp(a) Vitamin B6, B9, and B12 - cigarette smoking - Hardened (trans)unsaturated - diabetes fat intake - Chlamydia pneumoniae *remember that although the etiology of atherosclerosis is unknown, there are still risk factors that may be associated with atherosclerosis. ASSESSMENT: BP (hypertension) Elevated cholesterol and triglycerides Presence of abdominal obesity Cholesterol is processed by the gastrointestinal tract into Elevated FBS lipoprotein globules called chylomicrons. These are Elevated homocysteine reprocessed by the liver as lipoproteins. This is a o blocks the production of nitric oxide on physiologic process necessary for the formation of the endothelium making cell wall less lipoprotein-based cell membranes and other important elastic and permitting plaque to build up metabolic processes. When an excess of LDL is produced, o test results are interpreted as: LDL particles adhere to vulnerable points in the arterial ▪ optimal: 12< µ mol/L endothelium. Here, macrophages ingest them, ▪ borderline: 12-15 µ mol/L contributing to plaque formation. ▪ high risk: 15> µ mol/L ❖ B-complex vitamin rich diet (folic acid) = ↓ homycysteine INTERVENTIONS: *homocysteine - is an amino acid that is linked to the Cholesterol screening development of atherosclerosis because it can damage the endothelial lining of arteries and promote thrombus formation. Therefore, an elevated blood level of homocysteine is ought (?) to indicate high risk for coronary artery disease, stroke, and PVT (?). Although it is not an independent mediator (?) of CAD, others may be genetic factors  *myopathy - muscle weakness *TG - triglycerides *Acute Coronary Syndrome ACUTE CORONARY SYNDROME (ACS) The American Heart Association (AHA) now suggest the term ACUTE CORONARY SYNDROME to describe any group of clinical symptoms compatible with acute myocardial ischemia - Atherosclerosis > ischemia > insufficient blood supply > ↓ oxygen, angina pectoris (pain), and/or myocardial *all adults 20 years of age or older should have a fasting infarction lipid profile, total cholesterol, LDL, HDL, and triglycerides performed once every 5 years and more often if the *myo means muscle profile is abnormal. *Patients who have had acute events, like MI, requires assessment of their low density lipoprotein (LDL) within a 2. ANGINA PECTORIS few months of the event, because LDL might be low after - "chest pain" of cardiac origin the event. Lipid should be monitored every 6 weeks until the desired level is achieved and 4 to 6 months. - most common clinical manifestation of myocardial ischemia Diet Smoking cessation - the cause is insufficient coronary blood flow, resulting Exercise in a decreased oxygen supply when there is increased Drug therapy myocardial demand for oxygen in response to physical o HMG-CoA reductase inhibitors "Statins" exertion or emotional stress. - 'the need for oxygen exceeds the supply' - a type of chest pain, pressure, or discomfort. - heart is not receiving enough oxygen due to narrowed coronary artery TYPES OF ANGINA PECTORIS: TYPES OF CAUSES SYMPTOMS ANGINA STABLE - 75% - Chest pain (15 mins or coronary less) and may radiate occlusion that *Remeber that HMG-CoA Reductase Inhibitors (statins) is accompanies - Similar pain severity, a substance that blocks an enzyme that is needed by the exertion frequency, and duration body to make cholesterol. It lowers the amount of with each episode. choelsterol in the blood. - elevated HR or BP *HDL - good cholesterol  - eating a An important characteristic of anginal pain is large meal that it subsides when the precipitating cause is removed or with nitroglycerin. UNSTABLE - progressive - Chest pain of increased worsening of frequency, severity, and stable angina duration poorly relieved with 90%> by rest or oral nitrates ASSESSMENT AND DIAGNOSTIC METHODS: coronary Evaluation of clinical manifestations of pain and occlusion patient history. VARIANT - arterial - Chest pain that occurs *patient will be interviewed about both patient and (Prinzmetal's) spasm in at rest (usually between family history. normal or 12am and 8am), sporadic *about din sa PQRST ng pain (??) nya diseased over 3-6 months, and coronary diminishes over time. Electrocardiogram changes (12-lead ECG), stress artery. (ECG: ST - elevation testing, blood tests. Echocardiogram, nuclear scan, or invasive procedures such as cardiac catheterization and coronary angiography. MEDICAL MANAGEMENT: The objectives of the medical management of angina are to decrease the oxygen demand of the myocardium and to increase the oxygen supply. Medically, these objectives are met through pharmacologic therapy and control risk factors. *Printzmetal - kulang ang supply kaya may ischemia Alternatively, reperfusion procedures may be *Chronic Stable - fixed na yung stenosis kaya may used to restore the blood supply to the myocardium. narrowing,, mas mataas ang demand These include PCI procedures (eg, percutaneous transluminal coronary angioplasty [PTCA], intracoronary *Unstable - clot stents, and atherectomy) and coronary artery bypass graft (CABG). CLINICAL MANIFESTATIONS: PHARMACOLOGIC THERAPY: Pain varies from a feeling of indigestion to a Nitrates, the mainstay of therapy (nitroglycerin) choking or heavy sensation in the upper chest Beta-adrenergic blockers (metoprolol and ranging from discomfort to agonizing pain. atenolol) Angina is accompanied by severe apprehension Calcium channel blockers/calcium ion and a feeling of impending death. protagonists (amlodipine and diltiazem) The pain is usually retrosternal, deep in the chest Antiplatelet and anticoagulant medications behind the upper or middle third of the sternum. (aspirin, clopidogrel, heparin, glycoprotein [GP]) Discomfort is poorly localized and may radiate to oxygen therapy the neck, jaw, shoulders, and inner aspect of the upper arms (usually the left arm). A feeling of weakness or numbness in the arms, wrists, and hands, as well as shortness of breath, SELF-ADMINISTRATION OF NITROGLYCERIN pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting, may accompany the pain. Anxiety may occur with angina.  Angina pain occurs at rest or progresses rapidly over a short period of time. - supply ischemia, no infarct WHICH IS THE MOST SERIOUS ACS? - Subendocardial MI or Transmural *para malaman nyo ang sagot, let's continue the discussion. *Spoiler: Transmural MI ang more serious *hindi sya linalagay sa mga plastic pillboxes kasi nga inactivated by heat, moisture, air, light, and time ang 3. MYOCARDIAL INFARCTION nitroglycerin - an area of the myocardium is permanently destroyed, *pwede syang inumin before activities like exercising and typically because plaque rupture and subsequent the likes. thrombus formation result in complete occlusion of the artery. *hanggang 3 tablets ang pwedeng inumin at 5-min intervals ETIOLOGY AND GENETIC RISK: PRIMARY FACTOR: Atherosclerosis Nonmodifiable risk factors modifiable risk factors o Elevated serum cholesterol levels o CIGARETTE SMOKING!!! o Hypertension o Impaired glucose tolerance o Obesity o Physical inactivity o Stress ASSESSMENT: STABLE ANGINA Be alert for the following signs and symptoms: - pain develops when there is increased demand in the setting of a stable atherosclerotic plaque. The vessel is Cardiovascular unable to dilate enough to allow adequate blood flow to meet the myocardial demand. Chest pain or discomfort not relieved by rest or nitroglycerin. Heart sounds may include S3, S4, - demand ischemia, no infarct and new onset of a murmur. Increased jugular venous distention may be seen *meron na syang plaque, pero waley pang infarct if the MI has caused heart failure. Blood pressure may be elevated because of sympathetic stimulation or because of UNSTABLE ANGINA decereased contractility, impending cardiogenic shock, or medications. - The plaque ruptures and a thrombus forms around the Irregular pulse may indicate atrial fibrillation. ruptured plaque, causing partial occlusion of the vessel.  In addition to ST-segment and T-wave changes, *yellow area - area where pain can develop ECG may show tachycardia, bradycardia, or other dysrhythmias. PATHOPHYSIOLOGY: Sudden coronary obstruction caused by Respiratory thrombus formation over a ruptured or ulcerated plaque, the acute coronary syndrome Shortness of breath, dyspnea, tachypnea, and results. crackles, if MI has caused pulmonary congestion. Thus, MI occurs as a result of sustained ischemia, Pulmonary edema may be present. causing irreversible cellular damage, Gastrointestinal Unstable angina is associated with short-term occlusion, whereas MI results from significant or Nausea and vomiting complete occlusion that lasts more than 1 hour. Genitourinary Decreased urinary output may indicate RELATIONSHIP AMONG CAD, ACS, Stable/Unstable cardiogenic shock. Angina, and MI Skin Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation may indicate cardiogenic shock. Neurologic Anxiety, restlessness, and lightheadedness may indicate increased sympathetic stimulation or a decrease in contractility and cerebral oxygenation. The same symptoms may also herald cardiogenic shock. *Stable angina is under coronary artery disease, which Psychological can become unstable angina and can lead MI Fear with feeling of impending doom, or denial *ACS sakop agad both unstable angina and MI that anything is wrong. * ST-elevated MI - STEMI * Non-stemi-elevated MI - NSTEMI POSSIBLE PAIN PATTERNS: *red area - most common location of pain *orange areas - areas of referred pain and the location of pain in women. NSTEMI - During an NSTEMI, the plaque rupture and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium. - Subendocardial infarct *sa angina kanina diba wala pang infarct, dito meron na eyyyy *kapareho ni NSTEMI si unstable angina sa ECG reading STEMI *Q wave - zone of infarction - A STEMI is characterized by complete occlusion the Elevated serum creatine kinase isoenzyme (CK- blood vessel lumen, resulting in transmural injury and MB is primarily found in cardiac muscle - infarct to the myocardium, which is reflected byECG increase 3-6 hours after the onset of chest pain. changes and a rise in troponins. *eto na yung mga enzymes na pwedeng mag-elevate pag - Transmural Infarct may MI Elevated myoglobin LDH, AST, WBC, ESR. Elevated cardiac troponin T and I - identify very small amount of myocardial damage. Troponin T increases within 3-6 hrs after the onset of pain. Troponin I increases 7-14 hrs after the onset of pain. *so pinakauna ang troponin T, within 3 to 6 hrs lang Imaging studies identify presence and location of poor perfusion but do not indicate when. Tansmural MI INTERVENTIONS OF MI: - invovles the entire thickness of the myocardium Pain management: MONA Subendocardial MI *minsan raw OMNA,, inuuna yung oxygen - damage has not enetrated through the entire thickness o Morphine ▪ 2- to 10-mg IV q5-15 mins ▪ AE: respiratory depression, DIAGNOSIS OF MI: hypotension, bradycardia, ECG - Changes occur first in the ST segment hen severe vomiting the T-wave and finally the Q wave. As the ▪ Antidote: Naloxone (Narcan) 0.2 myocardium heals the ST and T waves return to - 0.8mg IV normal but the Q wave changes persist. o Oxygen: 2-4L/min by nasal cannula o Nitroglycerin *nagkakaron ng Q wave o Aspirin *aspirin is for the long term effect bc aspirin can make the blood thinner which prevents further formation of clots (it doesn't remove clots Coronary Bypass Grafting Positioning - semi-Fowler’s Provide a quiet and calm environment MEDICATIONS: Nitrates o Nitroglycerine, Isosorbide dinitrate (Isordil), Isosorbide mononitrate (Imdur) Beta blockers *yung mga '-lol' Calcium Channel Blockers Thrombolytics/Fibrinolytics *this can dissolve clots perooo dapat sure na may blood *para kang gagawa ng flyover clot bago iprescribe/administer *kukuha sila ng saphenous vein grafts (from the legs raw heolll), tapos yun yung ginagamit nila pang bypass from aorta (look nyo yung pic sa left) Percutaneous Transluminal Coronary Angioplasty *internal mammary artery graft naman yung nasa right para mas malaki *panglessen ng narrowing sa part ng artery *pwede rin maglagay ng stent para di na magsara [figure COMPLICATIONS OF MI: 41-6] *Dysrhythmias - most common - also called as arhythmias - present in 80-90% of MI clients - most common cause of death prior to hospital admission ADDITIONAL: *Troponin T - 84% sensitivity for MI 8 hrs after onset of ______ [di ko maintindihan guysss 58:10] *Troponin I - 90% sensitivity to MI 8 hrs after onset of _____  DISTURBANCES IN OXYGENATION AND UTILIZATION - Focuses on lungs Physiology of Respiration For respiration to occur: 1. There is adequate oxygen in the ambient air a. Air consists of nitrogen (78.6%), oxygen (20.8%), CO2 (0.04), other gases (0.05), total of 99.9%. b. Situations where this first criterion is not satisfied: victims of landslide (natabunan ng lupa so total absence of oxygen leading to sudden death), victims of smoke inhalation (na-inhale superheated smoke and particles of smoke, and carbon monoxide nagcocombine sa hemoglobin, di madeliver si oxygen) 2. Airway is patent a. Free from obstruction 3. Respiratory muscles and rib cage are functioning well a. Diaphragm innervated by phrenic nerve that arises from C3 to C5 b. If injury occurs to C3 to C5, one of the manifestations is severe respiratory difficulty, results to paralysis of respiratory muscle 4. There is negative intrapleural pressure a. There is small amount of fluid serving as lubricant to reduce friction between the pleura 5. Diffusion between alveoli and pulmonary capillary is effective a. Gas exchange happens between alveoli and Causes of Airway Obstruction: pulmonary capillary, there should be a matched 1. Accumulation of secretion ventilation perfusion ratio a. 100 ml of mucus – normal amount 6. Heart is an effective pump b. Coughing – clears up secretion a. Right ventricle pumps heart to the lung while left i. People with altered level of pumps to circulation consciousness are unable to cough, 7. Blood vessels are patent and elastic resulting to airway obstruction a. Can be obstructed by athero and arteriosclerosis, ii. Suction apparatus must be bedside for causing narrowing, reducing patency and this patient elasticity c. Infections or inflammation 8. There is adequate RBC and hemoglobin to carry i. Rhinitis, pharyngitis, bronchitis, oxygen tonsillitis a. Anemia ii. Vascular response results to secretion 9. Tissues utilize oxygen 2. Foreign body 3. Bronchospasm a. Allergy resulting to broncho-laryngospasm b. Hypocalcemia can cause laryngo-bronchospasm 4. Bronchial edema Intrapleural Pressure eme eme Normal atmospheric pressure at sea level – 760mmHg Intrapleural Pressure – 755mmHg Intrapulmonic Pressure – pressure sa loob ng lungs During inspiration, respi muscles contracts (bababa yung diaphragm) and thorax and lungs will increase in size, intrapleural and Intrapulmonic pressure will decrease, air then goes into the lungs During expiration, diaphragm goes up, thorax and lungs will decrease in size, intrapleural pressure goes up to 757mmHg and intrapulmonic pressure to 763mmHg, air then exits the lungs as it goes from higher to lower pressure Basta si air lagi siyang pupunta sa mas lower pressure, kaya pag inspiration yung intrapleural pressure yung lower, pero pag expiration yung normal atmospheric pressure yung mas lower Ventilation – movement of air during inhalation and exhalation Diffusion – movement of gas from higher to lower pressure External respiration – between alveoli and pulmonary capillaries Causes of Positive Intrapleural Pressure: Related ulit sa diffusion 1. Chest trauma resulting to blood or air accumulation in pleural cavity (hemo or pneumothorax) 763- Pulmonary capillary contains high levels of CO2 765mmHg Alveoli contains high levels of O2 CO2 from pulmonary capillary goes to alveoli while O2 Exchange of Gases: from alveoli goes to pulmonary capillary For diffusion to occur, there must be matched ventilation perfusion ratio Pulmonary perfusion – amount of blood flow to pulmonary artery Affects perfusion: Dead space unit – alveoli may problema 1. Pulmonary Embolism 2. Dislodged blood clot from deep vein thrombosis 3. Air embolism from IV or BT 4. Right ventricular failure Affects ventilation: Pag may airway obstruction, may increase of mucus secretion Shunted unit – paghinga problema, walang nakakarating Nagkakaron ng coughing, wheezing, crackles, DOB, na oxygen sa alveoli rapid breathing, altered breathing pattern 1. Plenty of secretions accumulated in airway Affects lower airway – asthma, chronic bronchitis, 2. Bronchial tumor/cancer, laryngeal cancer and bronchiectasis 3. Pneumo/hemothorax – positive intrapleural o Abnormal ABG resulting to respiratory acidosis pressure and hypoxemia 4. Atelectasis – collapsed lung Affects alveoli – emphysema o Abnormal hyperinflation of alveoli Silent unit – both perfusion and ventilation are abnormal o Only disease where there is normal ABG due to – silent kasi tahimik na yung pt kasi deads na hyperinflation Dead space unit – area of the lungs w/o gas exchange o Pero initially lang, pag tumagal yung hyperinflation magrurupture na yung alveoli and Shunted unit – called shunt because unoxygenated blood magddecrease yung area for gas exchange is being shunted back to the heart Management for these diseases: o Bronchodilators Walang gas exchange na mangyayare if kahit perfusion or o Mucolytic ventilation lang yung naapektuhan o Expectorant Kahit na okay yung isa pag yung isa naman hindi edi wala o Corticosteroids pa ring mangyayareng gas exchange o Nebulization o Suctioning Thrombolytics – dissolves blood clot o Chest physiotherapy Internal respiration – exchange of gases between cells and bloodstream BRONCHIAL ASTHMA Intermittent & reversible airflow obstruction CHRONIC AIRFLOW LIMITATIONS (CAL) (OR affecting the lower airway OBSTRUCTIVE DISORDERS) Allergic in nature, related to allergen A group of chronic lung diseases that includes: Obstruction is due to: o Asthma o Inflammation ▪ Chronic bronchial asthma can lead to o Airway hyper-responsiveness (bronchospasm chronic bronchitis, emphysema, and constriction) bronchiectasis ▪ Constriction of bronchia smooth muscle o Chronic Bronchitis due to stimulation of the nerve fibers o Emphysema Etiology: ▪ Can have emphysema even if pt is not o Allergens, cold air, dry air, airborne particles, smoker microorganism, aspirin -> inflammation ▪ Has genetic predisposition due to ▪ Pollen deficiency of alpha-1 antitrypsin ▪ Dust mites o Bronchiectasis ▪ Mold Or COPD ▪ Pet dander o Pag COPD, Chronic Bronchitis at Emphysema lang o Allergens – inhalants, ingestants, or contactants ▪ Because initially, bronchial asthma is o Airborne particles – dust reversible if naaddress yung cause o Exercise, upper respiratory illness (viruses), ▪ Pag di naaddress, chronic bronchial unknown reasons -> bronchospasm asthma na Most common cause is cigarette smoking Signs and symptoms overlap  (vasoconstriction to dilation -> tissue swelling -> increased secretions) Same process nangyayare kahit san ma-injure Leukotriene - primarily causes of bronchospasm Atopic or allergic asthma – cause is secondary to allergy – there is genetic tendency Atopy is associated with heightened response to allergens If di maidentify – simply bronchial asthma There is bronchial edema and buildup of mucus May chika si maam tungkol sa anak niyang mahilig sa 45- Upon exposure to allergens, it would cause injury to the day old chickens mast cells of the respiratory tract. The antibody responsible for hypersensitivity reaction is antibody E (IgE). Upon exposure, it would cause injury and the Nursing diagnosis applicable – ineffective airway injured cells would release chemical mediators, clearance related to bronchospasm, bronchial edema, histamine-like substances: - histamine, leukotriene, IL-4 increase of secretion (interleukin-4), eotaxin. Vasoactive-like substances, causing effect to blood vessels. Vascular response is Situation #2: Pt with DOB there is rapid breathing momentary vasoconstriction followed by vasodilation. Nursing diagnosis applicable – altered breathing pattern There is increase in blood flow and blood hydrostatic related to bronchospasm, bronchial edema, increase of pressure. There is also capillary permeability, resulting in secretion flow and shifting from intravascular to interstitial spaces, resulting to tissue swelling and bronchial edema, and Magagamit lang to pag di na normal yung respiration then increased secretions & mucus production. Situation #3: Poor gas exchange Nursing diagnosis – impaired gas exchange related to bronchospasm, bronchial edema, increase of secretion Magagamit lang pag may evidence like abnormal ABG Physical assessment findings: o Acute episode - audible wheezing & increased RR (acute episode) ▪ Wheezing is louder during expiration o Chronic severe asthma – dyspnea, cough, use of accessory muscle of respiration (intercostal retractions), barrel chest o Cyanosis, poor O2 saturation (pulse oximetry) Allergens -> damage mast cells -> release chemical o Change of LOC & tachycardia due to hypoxemia mediators (ex. histamine) -> cause inflammation ▪ Magalaw, disoriented, restlessness – panget ang oxygen to the brain  Laboratory assessment: o Relieve symptoms o ABG, elevated eosinophil count, elevated IgE o Prevent episodes levels ▪ Need maidentify allergens o Pulmonary Function Tests – most accurate Management plan includes: test for asthma (only needed for chronic o Client education asthma) o Drug therapy ▪ Determines lung volume and o Lifestyle management including exercise capacity Client Education Guide o Avoid factors that triggers asthma attack o Use bronchodilators 30 minutes before exercise to prevent or reduce exercise- induced asthma o Proper technique & correct use of metered dose inhalers o Adequate rest & sleep, reduce stress & anxiety; learn relaxation techniques ▪ Kasi merong stress-induced asthma o Failure of medications to control worsening symptoms, seek immediate emergency care Medications: Bronchodilators: o B2 agonist ▪ Albuterol (Ventolin), Bitolterol, Pirbuterol, Salmeterol, Formoterol ▪ Directly relaxes smooth muscle ▪ Thru inhaler, nebulizer o Methylxanthines o Eupnea – normal breathing ▪ Theophylline, Aminophylline, o Tidal volume (TV) – amount of air na Oxitriphylline lumalabas at pumapasok kada hinga – 500 ▪ Monitor for SE: excessive cardiac & CNS mL stimulation (check pulse & BP) o Total lung capacity (TLC) – maximum air na ▪ Due to sympathetic stimulation papasok, when doing deep breathing – up to o Cholinergic antagonist (anticholinergic) 6000 mL ▪ Ipatropium (Atrovent) o Vital capacity (VC) – from the point of ▪ Site specific, unlike B2 agonist maximum inhalation to how much can be Pag dinala sa hospital yung pt with severe attack, they are exhaled – 4800 mL given B2 agonist and cholinergic antagonist thru o Residual volume (RV) – the remaining air in nebulizer every 30 minutes, 1 hr, pag nag-improve na lungs after maximum exhalation – 1200 mL then 2 or 4 hrs. ▪ Pag may asthma, increased residual volume Kunware yung B2 agonist, 6 am tapos 10 am tapos 2 pm binigay Yung deep breathing yung malaking pagtaas nung wave sa picture, normal breathing yung iba na malilit lang Yung cholinergic antagonist naman, 8 am then 12 nn then 4 pm Nursing interventions: Para every 2 hrs, meron siyang dose of bronchodilators Goals: o To improve airflow Meron din daw combination of B2 agonist and Nagkwento si maam may faculty daw sila na nag-asthma cholinergic antagonist attack due to allergy nung kumakain sila Nung nagsabi na di na daw makahinga, sabi ni maam “nako lunch muna tayo” ee di na daw talaga makahinga kaya pumunta na sila FUMC Tinry pa talaga ni maam muna na maglunch muna Exercise/Activity o Aerobic exercise (recommended) ▪ Assist in maintaining cardiac health, enhancing skeletal muscle strength, and promoting ventilation and perfusion o Swimming Oxygen Therapy o Often used during an acute asthma attack Seritide – yung violet na iniinhale – combination of salmeterol and fluticasone Anti-inflammatory Agents: o Corticosteroids BRONCHITIS ▪ Oral – Prednisolone, Prednisone ▪ Inhaler – Budesonide, Fluticasone, Inflammation of bronchial mucosa which can be acute Beclomethasone, Triamcinolone, or chronic. Flunisolide o Mast cell stabilizer ACUTE BRONCHITIS ▪ Cromolyn sodium (Intal) – helps prevent atopic asthma attacks (prevent mast cell membranes from opening when an allergen binds to IgE but are not useful during an acute episode) o Monoclonal antibodies ▪ Omalizumab (Xolair) – approved in 2003 only – binds to IgE receptor sites on mast cells & basophils preventing the release of chemical mediators for inflammation  - Typically begins as an URTI (viruses, bacteria) - Auscultates breath sounds, monitors VS q 4 ➔ H. Influenzae hrs especially if client has fever. ➔ S. Pneumoniae - Encourage the client to cough & deep breath ➔ M. Pneumoniae q 2 hrs while awake & to expectorate rather - Chemical irritants (noxious fumes, gasses, air than swallow sputum. contaminants) - Provide humidification of the surrounding - TO PREVENT: Avoid smokey field (loosens bronchial secretions). environments and smoking. - Changes the bedding & client’s clothes if Assessment Findings: they become damp with perspiration. - Fever, chills, malaise, headache, dry - Offers fluid frequently (unless irritating nonproductive cough (initial) → contraindicated) mucopurulent sputum (mixed with pus, - Prevent infection (teach to wash hands color yellow or green) frequently). SIGN & SYMPTOMS: - Teach to cover the mouth when sneezing & coughing 1. Initial Response: Exposure to an agent (e.g., - Discard soiled tissues in a plastic bag; avoid pathogen, irritant) sharing of eating utensils & personal articles 2. Vascular Response: (to avoid cross contamination). - Initial Vasoconstriction - Vasodilation 3. Increased blood flow caused by the dilation of vessels CHRONIC BRONCHITIS (+ by an increase in hydrostatic pressure in the capillaries) 4. Increased permeability leads to swelling (edema) in the affected area. 5. Increased diastolic pressure that reflects the systemic effect of the increased blood flow. 6. Intravascular to Extravascular Shift: The increased permeability and hydrostatic pressure cause a shift of fluid and cells from the blood vessels (intravascular) into the surrounding tissue (extravascular), Prolonged inflammation of the bronchi accompanied contributing to edema and inflammation in the by a chronic cough & excessive production of mucus affected area. for at least 3 months each year for 2 consecutive Ps. Ayan ung sinabi niya, inayos ko lang para mas ma-gets niyo. years. Pa-list yan ha, like sunod sunod na process ng S/S. Kinakain ni Acute bronchitis can become chronic bronchitis. Ma’am ung words e. Gutom ata ^-^ Etiology: - Cigarette Smoking - Long history of bronchial asthma, RTI, air Medical Management: pollution - Usually self-limiting - Bedrest, antipyretics (reduce fever), expectorants (easier to cough up phlegm), antitussives (suppress cough for dry cough), ↑fluids, humidifiers, antibiotics - If the sputum is colored yellow, antibiotics are needed. - The best mucolytic is water.The best bronchodilator is a deep breath. (Bruners, old edition) Assessment Findings: - Chronic productive cough – thick white Nursing Management: mucus (earliest symptom) →yellow,  purulent, copious, blood streaked ➔ Preventing infection sputum ➔ Avoid other with RTI - Bronchospasm, Acute respiratory infections, ➔ Immunizations (flu & mucosal cyanosis, DOE, RSHF (cor pulmonale) vaccine) - Chronic Bronchitis + RSHF = cor pulmonale ➔ Monitors sputum for signs of infection ➔ Proper use of metered-dose inhaler (MDIs) EMPHYSEMA A chronic disease characterized by loss of lung elasticity & hyperinflation of the lung - Most common COPD Excessive mucus production clogs the airways leads to chronic cough → irritation causes inflammation → Chronic inflammation can cause structural changes in the airways, including fibrosis (thickening and scarring of connective tissue) → results in air trapping in the alveoli → Airway obstruction (narrowed airway) (sa pic ha) dahil prolonged air trapping causes the alveoli to sa chronic infection become overstretched and damaged → Kapag nag rupture ung alveoli dahil sa natrap na air, Emphysema ung lalabas don ang tawag is bullae. Emphysema Etiology: - destruction of alveolar walls reduces the - Major Cause: Smoking surface area available for gas exchange - Air pollution (minimal) - characterized by the destruction of alveolar walls and enlargement of air spaces - Both chronic bronchitis and chronic bronchial asthma can lead to emphysema. - CULPRIT IS CIGARETTE SMOKING. Medical Management: - Smoking Cessation - Bronchodilators, ↑fluid intake, well- balanced diet, postural drainage, steroid therapy, antibiotic therapy. - Alpha1-Antitrypsin Deficiency (AAT) ➔ AAT is made by the liver and is Nursing Management normally present in the lungs. - Focus: Educating clients in managing their ➔ Function: regulates proteases from disease working on lung structures. ➔ Smoking cessation ➔ If AAT is deficient, COPD develops ➔ Occupational counseling even if the person is not exposed to ➔ Monitoring air quality & pollution cigarette smoke or other irritants. levels ➔ Alpha1-Antitrypsin Deficiency (AAT ➔ Avoiding cold air & wind exposure deficiency) leads to reduced AAT (triggers bronchospasm) levels, which results in insufficient  inhibition of neutrophil elastase. “Each type can occur alone or in combination in the same This enzyme then breaks down lungs” elastin in the lungs, causing destruction of elastic fibers and lung tissue, leading to the Assessment Findings: enlargement of air sacs and the - Exertional dyspnea (1st symptom) development of emphysema. - Chronic productive cough with Pathophysiology: mucopurulent sputum - Decreased breath sound, wheezing, crackles - ‘Barrel shaped chest’ to accommodate the trap air in the alveoli. - Use of accessory muscle of respiration - Toxic CO2 levels → Lethargy, stupor, coma (carbon dioxide narcosis) Another term for Emphysema is PINK PUFFER, struggles. Other term for Bronchitis is BLUE BLOATER, don’t struggle. Medical Management: - Physical therapy Initially, pinkish in color, comfortable without dyspnea ang pt. - Deep breathing Kapag nag rupture na ung alveoli saka lang mag iiba ung - CPT wellbeing ng pt kahit atrest may dyspnea. - Postural Drainage - Medications: Classification: ❖ Panlobar or Panacinar ➔ Bronchodilators ➔ Destruction of the entire alveolus ➔ Mucolytics uniformly; diffuse & more severe in ➔ Antibiotics the lower lung areas ➔ Corticosteroids (limited basis to ❖ Centrilobular or centriacinar assist with bronchodilation & ➔ Openings occur in the bronchioles removal of secretions) and allow spaces to develop as Nursing Management: tissue walls breakdown; upper lung - Administer O2 via nasal cannula (2-3 L/min) sections ➔ High flow of O2 may lead to loss of ❖ Paraseptal or distal acinar hypoxic drive ➔ Only the alveolar ducts and alveolar ➔ Used na sa retention ng CO2 ang pt sacs are affected; the upper half of kasi laging mataas ang CO2 nila kaya the lungs. low level lang dapat na ibigay na O2  kasi un lang ung primary stimulus If may order na mouthwash, use plain water nila sa paghinga. only.) - Teach abdominal breathing (using - Hgb./Hct. diaphragm effectively), pursed-lip breathing - Serum electrolyte levels are examined because ↓phosphate, K+, Ca++ & Mg++ reduces muscle strength - CXR (Chest Xray, once or twice a year) to rule COPD out other chest diseases & to check the progress of clients with respiratory infections Clinical Manifestations: or chronic disease - General Appearance - Pulmonary Function Test - RR of 40-50 breaths/min ➔ Vital Capacity - maximum amount - Presence of Barrel chest of air a person can exhale after a - Cyanosis maximum inhalation. - Clubbing of fingers ➔ Residual Volume - amount of air - Manifestations of RSHF (dependent edema) remaining in the lungs after a full exhalation. ➔ Total Lung Capacity - total volume of air the lungs can hold, calculated as the sum of vital capacity and residual volume. Interventions: Mainstays of COPD management: - Airway maintenance ➔ Keep client’s head, neck & chest alignment (always support the HNC with pillow, vertical) ➔ Assist the client to liquefy secretions and clear the airway ➔ Breathing techniques Mas evident ang barrel chest if naka supine position ang client. Psychosocial Assessment - Socialization may be reduced when friend avoid the client with COPD because of annoying coughs, excessive sputum, dyspnea - So wear a facemask. Laboratory Assessment: - Abnormal ABG results (hypoxemia, hypercarbia) - Sputum C/S (morning dapat ang collection ng sputum dahil maraming naipon na sputum during the night. NO MOUTHWASH.  - Monitoring ➔ Assess COPD client at least q2. ➔ Assess VS, level of consciousness, character Mahaba dapat ang exhalation sa inhalation. and amount of sputum, lung sounds. - Drug therapy ➔ Involves the same inhales and systemic drugs for asthma - Mucolytics (acetylcysteine (mucomyst), Guaifenesin) ➔ Pneumonia - One of the most common complications of COPD; - Teach clients to avoid large crowds and stress the importance of receiving a pneumonia vaccination and a yearly influenza vaccine “flu shot” Percussion to para makahelp sa pagpapalabas ng sputum. - Kadalasan is matatanda ang may COPD. - O2 Therapy ➔ Need for O2 therapy & its effectiveness can be determined by ABG values & O2 saturation by pulse oximetry ➔ Usually 2-4 L/min or even 1-2 L/min via nasal cannula or up to 40% via venturi mask ➔ LOW-FLOW O2 because low arterial oxygen level is the COPD client’s primary drive for breathing. COMPLICATIONS (COPD) Postural drainage din to, 10-15 mins dapat sa position. Least ▪ Hypoxemia & acidosis - due to impaired desirable mag psotural drainage kapag after meal kasi baka exchange of gasses. masuka ang pt, magcause ng aspiration. ▪ Cardiac Dysrhythmias - results from ↓O2 supply to the heart, other cardiac disease, drug effects, or acidosis. ▪ Cor Pulmonale - RSHF caused by pulmonary disease.  ▪ Respiratory Infections - due to ↑mucus & - Kapag may affected na isang lobe, aalisin poor oxygenation (most common: S. isang lobe ng lungs (lobectomy) Pneumoniae, H. Influenzae, Moraxella - Right positioning ng pt after surgery para sa Catarrhalis) expansion ng affected lung. ➔ Due to infection, COPD - Turning sa side dapat sa unaffected lung. manifestations worsen due to Nursing Management: increasing inflammation & mucus - Instruct client in postural drainage production techniques DIET FOR COPD - Low Carb + High Protein + Low fat, small - CPT frequent meals (Mahirapan huminga kapag sobrang busog, - Oral hygiene (kasi magkakaroon sila halitosis hypoallergenic diet din dapat. or bad breathe kapag di maayos ang oral hygiene because of sputum.) BRONCHIECTASIS An abnormal and permanent dilatation of bronchi & bronchioles. It results from inflammation and destruction of the bronchial wall brought about by: - Chronic pulmonary infection (P. aeruginosa, H. influenzae) - Tumor or foreign body - Congenital abnormalities - Parating may plema kapag may bronchiectasis. The structure of the wall tissue changes, resulting in the formation of saccular dilatation which collects purulent materials causing more dilation, structural damage & more infection. Assessment Findings: - Chronic cough (copious, purulent, blood- streaked sputum) ➔ Coughing worsens when - Fatigue, weight loss, anorexia, dyspnea - CXR & bronchoscopy (procedure using a flexible tube with a camera to inspect the airways and lungs) – reveals increased size of bronchioles, atelectasis & changes in the pulmonary tissues. - During bronchoscopy need imonitor ang O2Sat. - Sputum C/S identify causative microorganism Medical Management: - Drainage of purulent material from the bronchi. - Antibiotics - Bronchodilators - Mucolytics - Humidification - Surgery removal of bronchiectasis if confined to a small area. NCMB312 ▪ Inhalation of foreign object or gastric contents during vomiting WEEK 4 PART 1 or regurgitation RESTRICTIVE DISEASES Ex. NGT tas napunta stomach acid sa lungs - Difficulty for air to enter the lungs as well as which is highly acidic = exhaling the CO2. irritation and trauma to lung structure Even if coma or PNEUMONIA unconscious pt, assume proper eating position - An inflammatory process affecting the (semi fowlers) then let bronchioles and alveoli stay in the position for - Can be called pneumonitis – inflammation of at least 30mins) lung parenchyma - Most common cause of death from an infection Another way of classifying pneumonia is according to the in the US (Smeltzer & Bare, 2004) lung part affected: - Usual cause is infection cause by microorganism - Causes: Bronchopneumonia o Usually infection - Infection is patchy, diffuse, and scattered ▪ Bacterial pneumonia “Typical throughout BOTH lungs Pneumonia” S. pneumoniae, P. carinii, S. aureus, K. pneumoniae, P. aeruginosa, H. influenzae ▪ Atypical Pneumonia Mycoplasma pneumonia, Chlamydia Lobar Pneumonia psittaci, Legionella - Inflammation is confined to one or more lobes of pnemophila, the lung mycobacterium tuberculosis, viruses, parasites, fungi o Radiation Therapy (Radiation pneumonia) ▪ Damage to the normal lung mucosa during radiation therapy for Breast CA, Lung CA o Chemical ingestion or inhalation (Chemical pneumonia) 4 General Categories of Pneumonia: ▪ Ingestion of kerosene, gasoline, or other chemical 1. CAP (Community-Acquired Pneumonia) ▪ Inhalation of volatile - Illness is contracted in a community setting or hydrocarbons within 48 hours of admission to a healthcare o Aspiration of foreign bodies or gastric facility contents (Aspiration pneumonia) 2. HAP (Hospital-Acquired Pneumonia)/Nosocomial Pneumonia  - Occurs in healthcare setting >48 hrs after inflammation and exudate formation. So diba admission may impaired gas exchange kaya magkakaron ng 3. Opportunistic Pneumonia hypoxemia (moderate to severe) and mid-low O2 (Immunocompromised Host) Sat and this is the reason why patient is - P. carinii pneumonia (Pneumocystis Jirovecii), submitted to the hospital. So, there could also be Fungal Pneumonia, pneumonia related to TB) bronchitis, CHF, empyema, pleurisy 4. Aspiration Pneumonia (inflammation of the pleura), septicemia (sepsis – may high grade fever na, chills, fatigue, high (guys panoorin nyo nalang if want nyo. Sample WBC (normal wbc is: 5000-1000) and if not situations lang naman sya abt dyan sa apat na yan. 7:04- managed promptly, patient could undergo septic 10:50) shock (-infection spread to the entire body, circulatory shock) then finally, death. PATHOPHYSIOLOGY: ❖ ASSESSMENT FINDINGS: ▪ Fever ▪ Chills ▪ Productive cough, sputum (rust colored) ▪ Discomfort in the chest wall muscles ▪ General malaise ▪ Pain during breathing (pt exhibits shallow breathing) - Cause is microorganism (could be bacteria or virus) which reach the lungs through inhalation of droplets, aspiration of organism from upper airways which means merong upper respiratory tract infection then ung microorganism is nakapasok sa lungs, or seeding from the bloodstream. In short, nakarating ung m.o. sa alveoli causing damage and injury to the lungs. So, magkakaron ng inflammation and infection, initially there will be redness or swelling, pain, and because of the vascular response and ❖ DIAGNOSTIC FINDINGS: cellular response there will be fluid exudation, ▪ Wheezing, crackles, decreased breath sounds wherein there will be shifting of fluid from (hypoxemia) intravascular to interstitial space. E diba nasa ▪ Cyanosis (nail beds, lips, oral mucosa) lungs tayo, so exudate