Inflammatory & Structural

cdunbar4's version from 2016-12-07 06:26

Infective Endocarditis

Question Answer
Infective endocarditis (IE)infx of inner surface of heart (endocardial surface can also include the valves)
Subacute IEthose with pre-existing valve disease (months and months of tx)
Acute IEthose with pre-existing valve disease (months and months of tx)
Two examples of causesIV drug abuse and Prosthetic valve endocartitis
Organisms that cause IEmostly staph and strep: blood flow brings organisms to the endothelial surface or valve
Risk Factors IEprevious IE, prosthetic valves, cardiac lesions
Vegetations(bacteria, fungi, fibrin)-the primary lesions of IE; can embolize; L heart to heart, kidney, brain and R heart to lungs
Rheumatic heart disease is only 20% of cause, now...aging, prosthetic valves, intravascular devices, dialysis, IV drug abuse
Non-specific-multiple organ systems (vegetations or flow), look for?target organ changes like the kidney (↓UO), brain (altered LOC), gut (↓motility), etc.
How often do they have a low-grade fever with IE?90% of the time
Other non-specific manischills, weakness, malaise, fatigue, anorexia.
Sub acute non-specific manischills, weakness, malaise, fatigue, anorexia.
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 (arms & legs) manisgangrene from ↓ circulation
Brain-neurologic manishemiplegia, ataxia, aphasia, visual changes, changes in LOC
Lungs manisPE can occur in R-sided

Infective Endocarditis

Question Answer
Diagnostics1st get a good hx; blood cultures (**may be the most important intervention so you know which drugs to give)
How many blood cultures do you do?3, if negative, hold on to cultures as organism may be a slow grower
Other lab diagnositicsWBC & ESR & C-reactive protein for inflammation
Echocardiogrammay show vegetative masses (could be esophageal picture)
CXR can showcardiomegaly
EKGcan show dysrhythmias-esp. blocks
Cardiac cathterizationin order to assess valvular damage
Prophylactic Tx for those at risk & are about to undergo what types of procedures?dental, GI, GU, Respiratory
Drug Therapy-what must you do before?MUST ID cause 1st! BLOOD CULTURES ARE A PRIORITY
Long-term treatmentIV Abs in hospital & continue after d/c; TEACH pt. what to expect
Drug therapy, treat fever with?ASA, Tylenol, fluids, rest (do not need to be on complete bed rest though)
IE + _____ ______ = life-threateningHeart Failure

IE Nursing Process

Question Answer
Assessmentbaseline info.; heart sounds so you can not a change; arthralgia (muscle/jt. tenderness, ↓ROM); petichiae-oral, conjunctiva, upper chest and upper extremities
DiagnosesHyperthermia (infx & cardiac tissue); Activity Intolerance; Knowledge deficit (disease and tx)
Planningnormal cardiac function; tolerate ADLs; become knowledgable of therapeutic regimen
Implementation-Prevention via Health Promotion ID at-risk ppl & educate them, avoid those with infx, if have cold/flu get treated, avoid excessive fatigue, planned rest periods, good oral hygiene
Implementation-Ambulatory and home careantibiotics at least 4-6 wks (depends on culture); if HF pt., may need to learn about long-term IV line; teach early signs infx, emboli, prevention measures
Evaluationnormal temp., performs ADLs, adequate UO, verbalize understanding, verbalize willingness to comply

Acute Pericarditis

Question Answer
Acue Pericarditis definition & causeinflammation of the pericardial sac; often idiopathic, mostly viral
Other causesPost 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, pain, PAIN, PAIN 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
What is the "hallmark sign" of pericarditis?Friction rub; scratching, grating, high-pitched
2 complications of Acute PericarditisPericardial effusion; Cardiac Tampenode
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
Compensatory manifestation upon auscultation of heart?muffled heart sounds with normal BP, if not managed can lead to tamponade
Cardiac tampondaecompression on heart itself=inability for ventricles to relax and fill
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
CC CareID/treat underlying problem (KILL BUG!) antibiotics, steroids, pericardiocentesis
Nursing mgmt, what should you focus on? pain & anxiety; pain relief; monitor for tamponade

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
Clinical Manisevidence of GAS;
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
Nursing Goalsnormal or baseline cardiac function, daily activities w/o joint pain, pt. states: I can manage the disease
ImplementationHealth Promotion: It is preventable via detection & treat of GAS with penicillin
Acute interventionfull course of antibiotics, ASA, NSAIDs, corticosteroids, monitor fluid, rest (↓ workload), positioning joints for comfort, after acue is over, ambulate
Nursing mgmt Rheumatic Fever + Heart Diseasesecondary prevention is key: likely to get it again, monthly injectiion penicillin, more for dental surgery, nutrition, hygiene, adequate rest

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 clinical manisdyspnea, afib, chest pain, emboli, hemoptysis, pulm edema (red frothy sputum!)
MV regurgitationduring systole, MV should close, in regurg it stays open & backs up to LA
MV regurg, if chronic, could end up with?hypertrophy
If acute, what could happen?no time for structure to adapt and the increased pressure is felt back to the lungs and ends up with pulmonary edema, and possible, shock.
Clinical manis acute vs. chronicif acute, thready pulse, cool/clammy skin (↓ CO); if chronic weakness, fatigue, palpitations, orthopnea, paroxysmal nocturnal dyspnea)
Aortic Valve stenosis common cause in adultsrheumatic fever
Aortic Valve stenosis blood flow restricted leaving LV, similar sx to mitral valve stenosis
AV stenosis clinical manis↓CO, LVH→↑ myocardial O2 demand, eventually leads to pulm HTN & HF
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
Clinical Manis aortic valve regurgif acute: sever dyspnea, chest pain, hypoTN, possibly shock. If chronic: DOE, paroxysmal nocturnal dyspneaa
Diagnostics for valvular HDh&p, phsyical, echo, cardiac cath, CXR, EKG
conservative therapy percutaneous transluminal ballooon valvuloplasty: mitral, pulmonic & triscuspid stenosis (usually not aorta)
Surgical therapyvalve repair/valve replacement (prosthetic valve)

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