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MedSurg I Unit 3 - Down & Dirty 2

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olanjones's version from 2016-12-12 06:09

Chronic Venous Insufficiency

Question Answer
CVI ManisRetrograde flow, persistent edema, ↑ pigmentation from hemosiderin deposition (leathery, brownish skin), varicosities, ulcers (usually above lateral/medial malleolus), & cyanosis in dependent position
CausesVein incompetence, DVT, valve incompetence (venous backs up --> ↑hydrostatic pressure --> fluid and blood cells “pushed” into the interstitial space --> edema)
TreatmentCompression (assess arterial circulation first), Biological dressings (Transparent film, hydro-colliods, impregnated gauze), Nutrition (adequate calories, proteins, Vit A, C, & Zinc - MUST CONTROL DM), Weight loss
Nursing ManagementAvoid limb trauma, Proper skin care & Compression (fit & replace Q 6 months), Proper foot & leg care (moisturizing), Appropriate activity & positioning (Avoid long periods of standing/sitting, Elevate legs above heart) **Teaching is key because recurrence is high
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Aortic Aneurysms

Question Answer
DistributionMost (75%) are in abdominal aorta below renal arteries; 25% in thoracic region (often asymptomatic, may have deep diffuse chest or interscapular pain)
Possibly s/s of ascending aortic aneurysmangina, hoarseness, JVD & head/arm edema, but usually asymptomatic
CausesAtherosclerosis (most common), but may be degenerative, congenital, mechanical, inflammatory, infectious, or from trauma
Two main classifications1. True aneurysm (entire wall of aneurysm, at least 1 vessel wall intact, can be fusiform or sacculated) 2. False aneurysm (rupture contained by surrounding tissue)
Since often asymptomatic, how are they dx?-During a physical as a pulsatile mass
-Imaging for unrelated problems (CT is most accurate to determine size)
-Auscuatated bruits; S/S of aortic compression
-"Blue-toe syndrome" (patchy mottling in feet & toes in the presence of palpable pedal pulses)
Treatment of small aneurysm (<4 cm)RF mods (↓BP), Monitor with US, MRI, CT q 6 months; threshold for repair 5.5 cm (<5.5 cm in women with AAA)
Surgical repair-required if ruptured (= EMERGENCY - btwn 33%-94% mortality w/ AAA)
-Pre-op reuirements: hydration, stabilize lytes, coag, & HCT
-may be done earlier in younger, low-risk patients or with rapidly expanding/symptomatic/high rupture risk
Risks associated with clamping?adequate perfusion (esp renal if clamped above renal arteries - ↑post-op risk), make sure good kidney perfusion before incision closure
Endovascular graft procedureInvolves placement of non sutured aortic graft into abdominal aorta inside aneurysm through femoral artery “cutdown”
Benefits of endovascular graft↓anesthesia & operative time, ↓blood loss; ↓morbidity and mortality & quicker recovery; shorter hospital stay & faster resumption of physical activity; higher patient satisfaction & reduction in overall costs
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Aortic Dissection

Question Answer
Is it a type of aneurysm?No!!! Often misnamed “dissecting aneurysm”
What is it?An acute & life threatening (90% mortality if not surgically tx) tear in the intimal lining of arterial wall (most commonly in thoracic aorta)
PathoTear in lining allows blood to “track” between intima and media, creating a false lumen of blood flow; As heart contracts, each systolic pulsation ↑ pressure on damaged area causing further ↑ dissection (May occlude major branches of aorta & blood supply to brain, abdominal organs, kidneys, spinal cord, and extremities)
Demographic affectedOlder people with chronic HTN; ↑ incidence in those w/ Marfan syndrome; Blunt trauma and/or pregnancy can precipitate
Manis (depend on location)Sudden, severe (ripping/tearing) pain in anterior chest (mimics MI) radiating down spine to abd or legs; May also have Cardio, neuro, & Respiratory signs; If Aortic Arch: ↓cerebral flow may cause neuro deficiencies
ComplicationsCardiac tamponade (blood escapes into pericardial sac); Aortic rupture (exsanguination and/or hemorrhage in mediastinal, plerual, or abd cavities); Occlusion of arterial supply to vital organs
What drugs may be used to ↓ BP and myocardial contractility?IV β-adrenergic blocker (esmolol); CCB, Sodium nitroprusside, ACE-I
When is conservative tx used?If no symptoms; success is judged by pain relief (but emergency sx required if involving ascending aorta)
Why is surgery delayed as long as possible?Give time for blood in false lumen to clot and for edema to decrease in the area of the dissection (even w/ surgery 30-day mortality is btwn 10%-28%)
AD Pre-op NIKeep in Semi-Fowler's, Maintain quiet environment, Manage meds (anxiety, pain, HTN), EKG & interarterial pressure monitoring, Monitor VS and changes in quality of peripheral pulses
AD Post-op & Home care NISame as AA repair (similar surgical procedure)
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Infective Endocarditis

Question Answer
How often do they have a low-grade fever with IE?90% of the time
Vascular manissplinter hemorrhage (black streaks in all nail beds); petechiae (embolizations)-conjunctiva, lips, buccal mucosa, palate, above ankles
Aside from low-grade fever, what is noted in most IE patients?onset of a NEW or CHANGING murmur can be auscultated in most pts. Most commonly aortic and mitral; usually regurgitant other than stenosed
Spleen manis from IEsharp LUQ pain, tenderness, rigidity
kidneys manis↓UO, flank pain, hematuria, & azotemia
periphery manisgangrene from ↓ circulation
Brain-neurologic manishemiplegia, ataxia, aphasia, visual changes, changes in LOC
Lungs manisPE can occur in R-sided
Lab diagnositicsBlood cultures (x2 or x3), WBC & ESR & C-reactive protein for inflammation
Echocardiogrammay show vegetative masses (could be esophageal picture)
CXR can showcardiomegaly
EKGcan show dysrhythmias-esp. blocks
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Acute Pericarditis

Question Answer
Acue Pericarditis definition & causeinflammation of the pericardial sac; often idiopathic, mostly viral (can also be Post MI, uremia, bacterial infection, TB)
Dressler Syndromeacute MI pt. has inital acute phase (2-3d) then late phase at 4-6 wks. where they are at ↑risk
Clinical ManisPAIN that is progressive, sharp, pleuritic, increases with inspiration, increases when supine
Pain sxmay radiate like angina to neck, arm, L shoulder
Dyspnea, why?Deep breaths hurt, so shallow ones, also have tachypnea
"hallmark sign" of pericarditis?Friction rub; scratching, grating, high-pitched
2 complications of Acute PericarditisPericardial effusion; Cardiac Tamponade
Pericardial effusionfluid accumulation in the pericardium; can be rapid (trauma) or slow (inflammation)
Manis due to pericardial effusion?COMPRESSION on pulmonary tissue=cough, dyspnea, tachypnea; on phrenic nerve=hiccups; on laryngeal nerve=hoarseness
New onset of these s/s are LIFE-THREATENINGC/O chest pain; confused, anxious, restless (hypoxia); BP muffled with increasingly NARROW pulse pressure; JVD to left side of jaw; pulsus paradoxus (sBP goes up 10 on inspiration)
Diagnostics EKG (may be normal; possible PR depression, ST elevation, T wave flat or inverted); CXR: posslble cardiomegaly but only later if ↑effusion
Nursing mgmt, what should you focus on? pain & anxiety; pain relief; monitor for tamponade
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Rheumatic Fever

Question Answer
Rheumatic FeverInflamm HD of all layers, scars and deforms valves, fibrous thickening of valves→↓ mobility
Aschoff's bodiesnodules from fibrous and scarring w/in the heart itself
Diagnosis is made with 2 major criteria, or 1 major & 2 minor criteria:Major: carditis, mono, chorea, erythemia marginatum, subq nodules Minor: fever, polyarthralgia, ↑ESR, ↑WBC, ↑CRP
Complicationschronic rheumatic carditis; mitral valve involvement; no definitive diagnostic tool
Drugs and supportantibiotics eliminates residual organisms, does not alter course of acute carditis, helps eliminate spread; Symptomatic Relief of fever and joint pain
nursing mgmtassessment of minor/major criteria, check past hx
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Valvular HD

Question Answer
Valvular HDcongenital or cardiac disease; one sign is a murmur, know effects of valvular heart disease on patient clinically.
Mitral Valve stenosisdoesn't open all the way, flow from LA to LV is restricted
Where does pressure build up in mitral valve stenosis?backward from LA & back to lungs, then eventually back to the R side of heart
MV regurgitationduring systole, MV should close, in regurg it stays open & backs up to LA
Aortic Valve stenosis blood flow restricted leaving LV, similar sx to mitral valve stenosis
Clinical mani triad AV stenosisangina, syncope, DOE
Why shouldn't you give Nitroglycerin for AV stenosis?it will reduce preload which you need, it will hide fluid, we need the fluid to keep moving
Aortic Valve regurg-what happens?retrograde flow from aorta back to LV, volume overload, short-term compensation via LVH, contracility declines, backflow to LV, LA, pulmonary bed and eventually to R side of heart
Diagnostics for valvular HDh&p, phsyical, echo, cardiac cath, CXR, EKG
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Stages of Shock (Remember - They are on a Continuum)

Question Answer
Initial Stage* Cellular metabolism changes from aerobic to anaerobic; Lactic acid accumulates requires unavailable O2 for removal = ↓ perfusion (not usually clinically apparent)
* Mean Arterial Pressure used to determine adequate perfusion (>60 organs are usually adequately perfused, below that may indicate ischemia)
Compensatory Stage: Body attempts to overcome consequences of anaerobic metabolism & tries to maintain homeostasis via SNS response, ADH release, RAAS activation
: Metabolic acidosis indicates compensatory --> progressive stage
S/S Compensatory Stage↓BP & ↓CO - 1st clinical signs
Progressive Stage* Proteins leak into interstitial space --> ↑ Systemic interstitial edema, May have anasarca (solid organs & peripheral tissue)
* VQ perfusion ration worsens from restricted blood flow, ↑ capillary permeability moves fluid into alveoli
* Aggressive interventions needed to prevent MODS
S/S Progressive Stagetachypnea, crackles; Changes in LOC; Weak, thready pulses & peripheral ischemia, ↑ likelihood of dysrhythmias, ischemia, & MI; Renal failure; GI ischemia; ↑ liver dysfunction
Irreversible StageExacerbation of anaerobic metabolism & Accumulation of lactic acid, ↑ Capillary permeability, Profound hypotension and hypoxemia, Tachycardia worsens, Decreased coronary blood flow, Cerebral ischemia --> Organ failure
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Low Blood Flow Shock

Question Answer
Cardiogenic Shock Structural problemsSystolic dysfunction (ineffective forward movement of blood --> ↓SV &↓CO); Diastolic dysfunction (ineffective filling --> ↑pulmonary pressure --> pulmonary edema --> ↓Oxygenation)
Causes of systolic dysfunctionMI, Cardiomyopathy (also diastolic), Blunt cardiac injury, Severe systemic/pulmonary HTN
Causes of diastolic dysfunctionCardiomyopathy (also systolic), Cardiac tamponade
Cardiogenic Manis (this +common)Tachycardia, Narrowed pulse pressure, Decreased cap refill time, Pallor (cool, clammy skin), ↑pulmonary artery wedge pressure, decreased renal perfusion & UO
Wedge Pressurepressure measured in pulmonary artery after occlusion of that artery; provides an indirect measure of the left atrial pressure
Tx Goal for CardiogenicRestore blood flow to the myocardium by restoring the balance between O2 supply and demand (↑coronary blood supply, pick drugs based on action, may need circulatory assist device)
Hypovolemic Shock - Two typesAbsolute hypovolemia (actual loss of fluid); Relative hypovolemia (3rd spacing)
Hypovolemic - Effects based on volume loss percentage15% ok; 15-30% compensation by SNS (↓EF & PAWP d/t decreased volume - may use volume expanders), >30% physiologic compensation begins to fail (need blood/blood products)
Tx Goal for HypovolemicPrimary Goal is to stop the loss of fluid and restore the circulating volume. Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)
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Maldistribution of Blood Shock

Question Answer
Neurogenic EtiologySNS is “turned off”; Results in massive vasodilation without SNS response leading to massive pooling of blood in arterial and venous vessels
Neurogenic Manis (this +common)Hypotension, Bradycardia, Temp dysregulation, Dry Skin, Hypothermia (poikilothermia = taking on temp of environment)
Tx Goal for NeurogenicTreatment of the hypotension & bradycardia with vasopressors (maintain BP) & atropine (bradycardia); Solumedrol for swelling --> prevent secondary damage to spinal cord; Monitor for hypothermia
*If spinal injury FIRST stabilize the spine
Anaphylactic Etiologyallergic response which results in massive vasodilation (same outcome as neurogenic) & capillary permeability
Anaphylactic Manis (this +common)Sudden anaphylactic rxn --> Respiratory distress --> laryngeal edema/bronchospasm --> circulatory failure
S/S of Anaphylactic RxnSense of impeding doom, Chest pain, Incontinence, Swelling of lips & tongue/angioedema, Wheezing/stridor, Flushing/pruritus/urticaria
Tx Goal for AnaphylacticControl histamine response: Epinephrine (vasoconstriction, bronchodilation & opposes histamine), Benadryl (blocks histamine), Maintain airway (risk for laryngeal edema/bronchoconstriction)
May need intravenous corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive therapy
Septic EtiologyStronger than usual immune response coupled with endotoxins from organisms stimulating additional immune response
Septic Patho* Normal immune response to damage but then --> vasodilation & increased capillary permeability third spaces fluid --> aggregations & fibrin occlude fluid movement = fluid loss
* ↑cytokines lead to myocardial depression
* Hypermetabolic state --> initial hyperventilation but then failure to compensate and respiratory acidosis occurs
Vascular damage immune responseDamaged epithelium, vasodilation, ↑capillary permeability, neutrophil & platelet aggregation/adhesion to epithelium
Septic Manis (this +common)Tachypnea/hyperventilation, temp dysregulation, ↓UO, GI dysfunction, Resp failure
Septic Shock Fun FactsMortality rate as high as 50%; Common organisms: gram - & + bacteria; Respiratory failure occurs in 85% of sepsis patients (ARDS accounts for 40%)
Tx Goal for SepticInitially --> *Aggressive fluid replacement to restore perfusion (6-10 L of isotonic crystalloids & 2-4 L of colloids)
*May need to add vasopressor drugs, corticosteroids to ↑BP and inotropic agent to ↑ contractility
*Antibiotics admin after cultures obtained; Monitor glucose levels (keep <150)
Obstructive ShockOccurs when blood flow is restricted by decreased CO (Restricted diastolic filling = Tamponade, Pneumothorax, abdominal compartment syndrome; Outflow obstruction = RV thrombi, PE) Result is JVD & Pulsus paradoxus
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