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Altered Perfusion.docx

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NURS 2090
Heather Helpard

Altered Perfusion Perfusion - Forcing blood or other fluid to flow through a vessel and into the vascular bed of tissue to provide oxygen *affects every system of the body Requirements for Effective Perfusion  Adequate ventilation and diffusion: ability to breathe in and transport O2  Intact pulmonary circulation: lower part of lung – low surface tension/max blood flow/O2  Perfusion cannot occur without inhalation/diffusion of O2.  O2 enters lungs – crosses alveolar cap junction – pulm circ  ∆ requires ventilation (intake of O2), Perfusion (movement of O2).  Ventilation-perfusion ratio (0.8:0.9) indicates that the rate of ventilation is slightly less than the rate of perfusion  The largest volume of ventilation- perfusion is the lower lungs where they are most easily inflated due to the low surface tension of the alveoli, which allows ventilation, and where the perfusion is best due to BP allowing max blood flow (also has gravity working for it!)  Adequate blood volume and components  Adequate cardiac output: optimal SV, HR, heart rhythm  Intact cardiac control center: needed to regulate HR and force of contractions  Intact receptors: for feedback  Intact parasympathetic and sympathetic nervous systems  Intact cardiac conduction  Intact coronary circulation: maintains perfusion to cardiac structures RCA  Intact systematic circulation  Adequate tissue uptake of oxygen Types of circulation: Circulation: effective circulation depends on patency (the condition of not being blocked or obstructed) of the blood vessels and on the adjustments of the microcirculation to meet the demands of the tissues. 1. Pulmonary- circulation through the lungs provides the ability to transfer O2 from the environment to the body  includes the right side of the heart and pulmonary arteries/capillaries and veins  pulmonary veins carry oxygenated blood to the left side of the heart  pulmonary artery carries deoxygenated blood to the lungs  Pulmonary circ works at a lower pressure than systemic b/c it moves blood slower through the lungs for maximal gas exchange 2. Systemic–distributed to body tissues  this system involves all of the arteries and veins except ones in the pulmonary circulation.  Functions at a higher pressure to work against resistance to get to peripheral tissues  Monitored by the left side of heart (esp. left ventricle which has strongest pumping) 3. Cardiac– this system includes the right coronary artery (RCA), the left coronary artery (LCA) and the left anterior descending coronary artery (LAD) which perfuse the right and left sides of the myocardium (muscle) of the heart. Coronary arteries: 1. RCA: supplies blood to the right ventricle  supplies 25-35% of blood to the left ventricle  supplies the SA node 2. LAD: branches off of the LCA  supplies 45-55% of blood to the left ventricle/provides much of the blood flow to the left ventricle which enables the propulsive force of ejection  known as the “widow-maker” because blockage of this artery is particularly associated with mortality 3. LCA: main coronary artery  feeds blood to the left side of the heart Pericardium: outer covering of the heart  holds heart in place/contains receptors that help regulate BP and HR  1 line of defense against infection and inflammation  contains pericardial fluid (lubrication) Myocardium: thick muscular layer  thickest at left ventricle (works the hardest – systemic circulation)  hypertrophy occurs here as workload increases Endocardium: inner lining of the heart, continuous layer of endothelium Cardiac Cycle – one contraction (systole: begins with closure of AV valve, ventricles have greater pressure and eject blood, lub) and one relaxation (diastole: ventricles relax, pressure greater in aorta/pulm artery, Aortic/pulm valves close and make the dub) AV Valves: bicuspid (mitral), tricuspid Contractions – rely on the passage of ions and electrical impulses from one myocardial cell to another. These are generated through action potentials. Two major types of action potentials; slow and fast, work in an organized manner Phases of action potential: 1. Rapid depolarization: fast Na channels open and the rapid influx of Na into the cell cause it to become positively charged 2. Early repolarization: fast Na channels close 3. Plateau – slow Na and Ca channels open and Na and Ca slowly enter the cell 4. Rapid repolarization: a regrouping phase in which the cell membrane becomes polarized with a positive charge on the outside of the cell and a negative charge inside the cell. The cell also becomes permeable to K and it exits the cell. 5. Resting phase PQRSTU Waves: electrical activity imposed by ions on cardiac cells can be measured using ECG/EKG P = depolarization of atria via SA node PQ interval = depolarization of AV nodes + bundle fibers QRS = depolarization of ventricles T = repolarization of ventricles U = repolarization of Purkinje fibers SA Node: pacemaker/ generates rhythmic impulses in atria/stimulated by slow response to NA and Ca channels opening AV Node: connects impulses between atria and ventricles/slow to allow atria to empty blood into ventricle/generates impulses that travel to bundle of His and culminate in Purkinje fibers Cardiac Output: depends on stroke volume (SV) and heart rate (HR)  CO = SV x HR  average CO is 3.5 – 8.0 L/min (can increase 4x during exercise) Stroke Volume: amount of blood pumped out of one ventricle in a single beat Heart Rate: number of beats per minute Major Factors affecting CO: 1. Preload: work imposed on heart just before contraction, depends on adequate venous return 2. Cardiac contractility: the ability of heart to ↑force of contraction without changing diastolic pressure, affected by Ca. 3. Afterload: amount of pressure in the ventricle toward the end of contraction, increases when valves are impaired. 4. Heart rate 5. Blood volume Blood Pressure: pressure or tension of blood in systemic arteries BP is maintained by: 1. Contraction of left ventricle 2. Peripheral vascular resistance 3. Elasticity of arterial walls 4. Viscosity and volume of blood *BP is a product of cardiac output and amount of resistance in the arteries Systolic BP: amount of pressure exerted during contraction of the left ventricle and ejection of blood into the aorta  affected by SV, HR and resistance  Exercise, smoking and CVD increase it Diastolic BP: amount of pressure remaining in the aorta during resting phase  Increase in diastolic may mean that the arteries are not allowed to rest between contractions.  Depressions can show lack of resistance in the aorta or backflow of blood Pulse pressure: difference between systolic and diastolic BP (a narrow pulse pressure indicates a loss of systolic pressure rather than in increase in diastolic) MAP: an adequate measure of systemic tissue perfusion is 1/3 pulse pressure + diastolic pressure Changes in BP occur as a response to: 1. Baroreceptors/chemoreceptors (detect changes in O2, CO2 and pH of blood) 2. RAAS (ANG II works to promote an increase in BP when acting as a vasoconstrictor on arteries and arterioles) 3. Kidneys (ANG II stimulates the adrenal cortex to increase aldosterone to increase Na/H2O retention by kidneys to expand BV) 4. Anti-diuretic Hormone (Vasopressin) secreted from posterior pituitary promotes retention of fluids by acting as a vasoconstrictor (enhances BV) 5. Epinephrine acts to promote BP by stimulating HR and contractility (promotes tension on vessels) Altered Perfusion- The inability to adequately oxygenate tissues at the capillary level **most common cause of hypoxia Cause: 1. Ventilation-perfusion mismatching: most common  Inadequate ventilation in well perfused areas of the lungs (asthma/edema)  Inadequate perfusion in well-ventilated areas of the lungs (embolus) 2. Impaired circulation: lead to inadequate or excessive blood flow to tissues and organs  Injury to vesselsdiabetes (build up of LDL + injury to vessel = inflammation)  Obstruction :  Virchow’s triad: vessel wall damage, excessive clotting, alterations of blood flow (thrombus formation).  Inadequate blood movement: common sites = bifurcations (regions where vessel branches), aneurysms (outpouches of weak wall), venous stasis (veins with reduced return)  Inadequate blood volume 3. Inadequate cardiac output: when heart is unable to successfully eject the necessary amount of blood to pulmonary/systemic circulation  Changes in blood viscosity (cancerhypercoagulationblood clots)  Impaired ventricular pumping : loss of muscle activity and ability to move blood forward. Leads to heart failure  Structural heart defects:ASD (opening in L/R atria), VSD (opening in L/R ventricle) and valve defects such as Stenosis (narrow valves) or Regurgitation (improper valve closure)  Conductions defects:  cardiac dysrhythmias (problems with SA, AV node or cardiac cells)  fibrillation: problems with ventricle vibrating instead of pumping  heart block: obstruction of cardiac conduction.  Changes in peripheral vascular resistance 4. Excessive perfusion demands : inability of heart to meet demands  Excessive demands extreme or prolonged exertion/metabolic alterations such as hyperthyroidism  Poor perfusion supply Atherosclerosis: 1. Injury to inner lining of vessel (HTN, smoking, environment 2. LDL filters and gets trapped, becomes oxidized and engulfed by macrophages, producing foam cells 3. Foam cells accumulate and combine with lipids to make fatty streaks, which become fibrous plaques 4. Plaques accumulate and get covered by platelets, which continue to expand. General Manifestations:  Variable depending upon source of altered perfusion  Cyanosis, pain, pallor, coolness, edema, shortness of breath, impaired growth, tachycardia, tachypnea,and fatigue  Hypotension or hypertension  Bleeding (petechiae, purpura, hematoma), bruising (ecchymoses)  Heart murmur Diagnostic Criteria:  Echocardiography or Doppler ultrasonography  ECG ultrasound of the heart – shows hypertrophy + ejection fraction (+ 55% = normal)  Chest x-ray  Cardiac catheterizationto diameters of LAD, LCA & RCA  Pressure measurements  Stress test Beta blockers: work by blocking B1 receptors to lower cardiac output Adrenergic receptors: control vasoconstriction via RAAS ACE inhibitors: too much blood volume requires a diuretic + 1-2 blockers + ACE inhibitor Atrial Fibrilation: shows up as a squiggly line on an ECG and heart will not contract properly indicating inefficient output – get out the paddles Shocking the heart stops and restarts it at a normal rhythm (can shock 3 times and then each subsequent shock should be followed by Epinephrine) Hypertension Pathophysiology: ↑ resistance = peripheral vascular, ↓ vessel diameter= atherosclerosis  A progressive cardiovascular syndrome detected by an elevation in blood pressure and/or the presence of organ damage due to persistent blood pressure elevations  Primary/ Esstential HTN: (90%-95%) Specific cause is unknown/multifactoral disease. Often asymptomatic/ when clinical manifestations do present; this indicates years of undetected HTN  Secondary: due to another cause (kidney/addisons)  ↑ BP results in heart attack, weakened blood vessels, ischemia, atropy  Rise in systolic pressure is the #1 predictor of coronary artery disease (CAD) Promotion of HTN: 1. Sympathetic Nervous System overstimulation (systemic vasoconstriction) 2. RAAS overstimulation (systemic vasoconstriction, Na and H2O retension by kidneys and increased blood volume) 3. Impaired Na excretion by kidneys (Na and H2o retention and increased blood volume) Systems Affected 1. CNS: elevated BP overwhelms cerebral blood flow causing intracranial pressure, O2 impairment and decreased brain function 2. Cardiovascular: HTN aids in development of atherosclerosis which contributes to obstruction in the arteries (pressure in the arterioles can lead to altered function of target organs especially kidneys, eyes, brain and heart)  Increased strain on the heart (left ventricle is most affected and becomes hypertrophic)  This impairs venous return and systemic perfusions and leads to pulmonary edema, myocardial ischemia and peripheral hypoxia 3. Kidneys: prolonged pressure on the kidney arterioles promotes chronic injury and inflammation which leads to nephrosclerosis (an overgrowth/hardening of tissues)  HTN is perpetuated b/c RAAS is stimulated by reduced blood flow to the kidneys, ∆ increased renin/ aldosterone  results in poor urinary output, hematuria, and proteinuria Risk factors:  Family history of hypertension  Excessive dietary sodium intake hypercholestrolemia  Smoking (same as diabetes)  Aging  Excessive alcohol intake  Diabetes mellit
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