ASKEP EMBOLI PARU, EDEMA PARU, KOR PULMONAL

emboli paru
= Pulmonary emboli (PE) Sumbatan arteri pulmoner atau salah satu cabangnya oleh trombus atau benda asing Penyebab sumbatan gumpalan darah/trombus, droplet-droplet lemak, gelembung udara, tumor Berpotensi menimbulkan infark paru

FAKTOR PREDISPOSISI

mobilitas Bedah mayor Stroke !eganasan, kemoterapi "raktur tungkai atau pel#is $besitas !ateterisasi #ena sentral !ontrasepsi oral %uka bakar &riad #ircho'( hiperkoagulasi, perubahan hemodinamik, cedera /disfungsi endotel trombosis Predisposisi genetik untuk trombosis #ena

Perokok &erapi )ormon Sedang hamil )ipertensi Penyakit cardio#askuler *esistensi terhadap protein + (autoprothrombin , and blood coagulation factor - . pengaturan pembekuan darah, inflamasi, kematia sel, permeabilitas pembuluh darah) "aktor . leiden penyakit turunan hiperkoagulasi Stres

TANDA DAN GEJALA

Disp

eu N!eri "a"a Ba#u$ %emop#isis A sie#as Si $ope %ipo#e si Sia osis De !u# a"i lema& Kuli# "i 'i "a ber$eri 'a# Me 'i

PEMERIKSAAN FISIK
&akipnea )iperpnea &akikardi /istensi

#ena leher +rackles 0engi /emam minimal Pleural friction rub

PEMERIKSAAN PENUNJANG
1as darah arteri menurunnya kadar p$2 akibat #entilasi yang berkurang3 Plasma / dimer (u4i sampel darah utk diagnosa penyakit terkait hiperkoagulabilitas) meningkat (5677ng/ml) pada 89: pasien emboli pulmonal / dimer fragmen /-dimer/ fibrin degradation fragment E!1 biasanya minor, tidak spesifik, sifat sementara "oto thora; dpt memberi kesan normal atau minimal, bisa ditemukan pembesaran arteri pulmonal yang semakin bertambah Scan #entilasi/perfusi paru ,ngiografi pulmonar dapat menun4ukan diagnosa definitif bahkan pada emboli berukuran kecil (<-2 mm) +& scan angiografi sensiti#itas dan spesifitas tinggi untuk emboli paru di arteri besar dan arteri lobaris =S1 dopler non in#asif, trombosis #ena dalam

pa#&op&!siolo'!
&hree primary influences predispose a patient to thrombus formation .ircho' triad (Endothelial in4ury, Stasis or turbulence of blood flo', Blood hypercoagulability) Pulmonary emboli (PE) usually arise from thrombi originating in the deep #enous system of the lo'er e;tremities> ho'e#er, they may rarely originate in the pel#ic, renal, or upper e;tremity #eins or the right heart chambers3 ,fter tra#eling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise3 Smaller thrombi typically tra#el more distally, occluding smaller #essels in the lung periphery3 &hese are more likely to produce pleuritic chest pain by initiating an inflammatory response ad4acent to the parietal pleura3 0ost pulmonary emboli are multiple, and the lo'er lobes are in#ol#ed more commonly than the upper lobes3

&he risk of de#eloping a pulmonary embolism is increased in these indi#iduals( (e ous s#asis increased #iscosity may occur due to polycythemia and dehydration, immobility, raised #enous pressure in cardiac failure, or compression of a #ein by a tumor %!per)oa'ulable s#a#es +oncomitant hypercoagulability may be present in disease states 'here prolonged #enous stasis or in4ury to #eins occurs3 "actor . %eiden mutation causing resistance to acti#ated protein + is the most common risk factor3 Primary or ac?uired deficiencies in protein +, protein S, and antithrombin are other risk factors3 Immobili*a#io mmobili@ation leads to local #enous stasis by accumulation of clotting factors and fibrin, resulting in thrombus formation3 &he risk of pulmonary embolism increases 'ith prolonged bed rest or immobili@ation of a limb in a cast3 mmobili@ation (usually because of surgery) 'as the risk factor most commonly found in patients 'ith pulmonary embolism3

Sur'er! a " #rauma Surgical and accidental traumas predispose patients to #enous thromboembolism by acti#ating clotting factors and causing immobility3 Mali' a )! Pulmonary emboli ha#e been reported to occur in association 'ith solid tumors, leukemias, and lymphomas3 Pre' a )! Oral )o #ra)ep#i+es a " es#ro'e repla)eme # %ere"i#ar! ,a)#ors antithrombin deficiency, protein + deficiency, Protein S deficiency, "actor . %eiden, Plasminogen abnormality, Plasminogen acti#ator abnormality, "ibrinogen abnormality, *esistance to acti#ated protein + A)u#e me"i)al ill ess , /S (lupus anticoagulant), +ongesti#e heart failure (+)"), 0yocardial infarction

Respira#or! )o se-ue )es

,cute respiratory conse?uences of pulmonary embolism include( increased al#eolar dead space, hypo;emia, hyper#entilation ,dditional conse?uences that may occur include regional loss of surfactant and pulmonary infarction3 ,rterial hypo;emia is a fre?uent, but not uni#ersal, finding in patients 'ith acute embolism3 &he mechanisms of hypo;emia include #entilation-perfusion mismatch, intrapulmonary shunts, reduced cardiac output, and intracardiac shunt #ia a patent foramen o#ale3 Pulmonary infarction is an uncommon conse?uence because of the bronchial arterial collateral circulation3

%emo"! ami) )o se-ue )es

Pulmonary embolism reduces the cross-sectional area of the pulmonary #ascular bed, resulting in an increment in pulmonary #ascular resistance, 'hich, in turn, increases the right #entricular afterload3 f the afterload is increased se#erely, right #entricular failure may ensue3 n addition, the humoral and refle; mechanisms contribute to the pulmonary arterial constriction3 +hronic pulmonary hypertension may occur 'ith failure of the initial embolus to undergo lyses or in the setting of recurrent thromboemboli3

PENATALAKSANAAN
trombolitik urokinase, streptokinase ,ntikoagulan heparin, 'arfarin, &erapi simptomatik petidin $ksigenasi Embolektomi pada pasien dgn kontraindikasi trombolisis
&erapi

PROGNOSIS
Berhubungan

dengan penyakit yang mendasari

PENCEGAHAN
Setelah pembedahan Stocking elastis mobilisasi

DIAGNOSA KEPERAWATAN
mpaired gas e;change related to decrease pulmonary perfusion associated 'ith obstruction of pulmonary arterial blood flo' by the embolus neffecti#e tissue perfusion related to impaired transport of o;ygen across al#eolar and/or capillary membrane /eficient kno'ledge (treatment regimen) related to comple; disorder and therapy *isk for in4ury related to thrombolytic or anticoagulant therapy $ther potential nursing diagnoses( ,n;iety related to change in health status

impaired gas e;change related to decrease pulmonary perfusion associated 'ith obstruction of pulmonary arterial blood flo' by the embolus
E;pected $utcome Patient maintains optimal gas e;change as e#idenced by( Aormal arterial blood gases (,B1s), Pulse o;imetry results 'ithin normal range, =sual mental status, Aormal respiration rate3 Suggested A$+ $utcomes Electrolyte B acid-base balance> *espiratory status( 1as e;change> *espiratory status( .entilation> &issue perfusion( Pulmonary> .ital signs Suggested A + %abels ,ir'ay 0anagement $;ygen &herapy *espiratory 0onitoring ,cid-Base 0anagement

i #er+e #io s
,ssess respirations( note ?uality, rate, pattern, depth, and breathing effort3 ,ssess lung sounds, noting areas of decreased #entilation and the presence of ad#entitious sounds3 ,ssess for signs and symptoms of hypo;emia( tachycardia, restlessness, diaphoresis, headache, lethargy, and confusion3 ,ssess for signs or symptoms of pulmonary infarction( cough, hemoptysis, pleuritic pain, consolidation, pleural effusion, bronchial breathing, pleural friction rub, fe#er3 0onitor #ital signs3 ,ssess for changes in orientation and beha#ior3 0onitor arterial blood gases (,B1s) and note changes3 =se pulse o;imetry to monitor $2 saturation and pulse rate continuously ,ssess skin color for de#elopment of cyanosis

0aintain o;ygen administration de#ice as ordered, attempting to maintain $2 saturation at 87: or greater3 Position 'ith proper body alignment for optimal respiratory e;cursion Position patient to facilitate #entilation/perfusion matching3 =se upright, high "o'lerCs position 'hene#er possible3 Pace acti#ities and schedule rest periods to pre#ent fatigue Encourage deep breathing, using incenti#e spirometer as indicated3 ,dminister medications as prescribed3

Ineffective tissue perfusion

/ES *E/ $=&+$0ES &he client 'ill maintain ade?uate tissue perfusion as e#idenced by palpable peripheral pulses, 'arm and dry skin, ade?uate urinary output, and the absence of respiratory distress A$+ $=&+$0ES +irculation status> tissue perfusion( abdominal organs> tissue perfusion( cardiac> tissue perfusion( cerebral> tissue perfusion( peripheral> tissue perfusion( pulmonary A + A&E*.EA& $AS +irculatory care( arterial insufficiency> circulatory care( #enous insufficiency> cerebral perfusion promotion> cardiac care( acute, )emodynamic *egulation, Embolus care, Aeurological 0onitoring

i #er+e #io s

0onitior signs of tissue perfusion ade?uacy3 Aote skin color and feel temperature of the skin 0onitor peripheral pulses3 Aote the decrease in pulse +heck capillary refill3 0onitor neurological status

*isk for in4ury related to thrombolytic or anticoagulant therapy

E-PE+&E/ $=&+$0E &he patient 'ill remain free of unusual bleeding &he patient 'ill display no signs of recurrent emboly Suggested A$+ $utcomes 0edication response> *isk control

I #er+e #io s 0onitor for bleeding3 +heck color of urine, occult blood in stool, and/or changes in #ital signs3 (Patients 'ith history of peptic ulcer disease, alcoholism, kidney or li#er disease, and the elderly are at greatest risk for bleeding) 0onitor #ital signs3 ( ncrease in heart rate accompanied by lo' blood pressure or subnormal temperature may signal bleeding3 0onitor laboratory #alues( aP&& and P&& for therapeutic #alues3 0onitor +B+ in female patients 'ho are menstruating3 (,nticoagulation may cause e;cessi#e blood loss during menses3) E+alua#io E#aluate effecti#eness of drug therapy by confirming that the patient goals and e;pected outcomes ha#e been met3 &he clientDs laboratory #alues e;hibit a decrease in blood coagulation3

/eficient kno'ledge (treatment regimen) related to comple; disorder and therapy

E-PE+&E/ $=&+$0E &he patient and family 'ill describe the action, dosage, fre?uency, and ad#erse effects of the prescribed anticoagulant> acti#ities that can cause or pre#ent clot formation> and safety considerations 'hile the patient is on anticoagulant therapy3 Suggested A$+ $utcomes !no'ledge( &reatment regimen

EDEMA PULMONAL
Peningkatan 4umlah cairan yang berlebihan di al#eoli Pulmo ar! e"ema an accumulation of fluid in the al#eoli and interstitial spaces of the lungs 0engganggu difusi oksigen Bisa menyebabkan gagal nafas Edema paru kardiogenik disebabkan oleh peningkatan tekanan di dalam pembuluh darah paru akibat buruknya fungsi 4antung pada gagal 4antung kongestif, infark miokard, kelainan katup3 Edema paru non-kardiogenik disebabkan oleh faktor-faktor lain, seperti gagal gin4al, latihan fisik di ketinggian, trauma dada, kerusakan 4aringan paru &ekanan darah pulmonal 5 <6 mm)g edema pulmonal

.ar"io'e i) / +ongesti#e heart failure Pericardial effusion 'ith tamponade Se#ere arrhythmias (tachycardia/fast heartbeat or bradycardia/slo' heartbeat) Se#ere heart attack 'ith left #entricular failure

No 0)ar"io'e i)/ ,cute respiratory distress syndrome ,spirin o#erdose )igh altitude ntracranial hemorrhage !idney failure 0ethadone/heroin o#erdose Pleural effusion Pulmonary embolism Se#ere sei@ures/ ke4ang

TANDA DAN GEJALA

+oughing

and restlessness during sleep (premonitory symptoms)3 Sudden onset of dyspnea3 Se#ere an;iety, restlessness, irritability3 +ool, moist skin3 &achycardia $rthopnea Paro;ysmal nocturnal dyspnea /istended Eugular #eins Fhee@ing Aoisy, 'et respirations that do not clear 'ith coughing3 +ough 'ith "rothy, blood-tinged sputum3

/iagnostic $;ymetry or ,B1 .alues +hest --ray (may re#eal fluid in/around lung space or enlarged heart) Echocardiogram to detect #al#ular disease 0easurement of pulmonary artery 'edge pressure by s'an gan@ catheter Blood culture in suspected infection +ardiac markers in suspected 0

PENATALAKSANAAN
0eningkatkan

fungsi respirasi 0engatasi penyebab $ksigenasi 0edikasi

EDEMA PULMO 0 .ONGESTI(E %EART FAILURE #&erap!

/iuretics,

'hich remo#e e;cess fluids from the body 0edicines to strengthen the heart muscle, control the heartbeat, or relie#e pressure on the heart +ontractility enhancement therapy (digo;in G%ano;inH, dopamine G ntropinH, dobutamine G/obutre;H impro#es the ability of the heart muscle to pump more effecti#ely, allo'ing for complete emptying of blood from the #entricle and a subse?uent decrease in fluid backing up into the lungs3

complications of pulmonar !"!ma

/ysrhythmia *espiratory

failure

DIAGNOSA KEPERA1ATAN
<3 23

I3

J3

neffecti#e breathing pattern related to pulmonary edema3 mpaired gas e;change related to e;cess fluid in the lungs3 neffecti#e tissue perfusion related to decreased cardiac muscle contractility3 ,n;iety related to sensation of suffocation and fear3

I e,,e)#i+e brea#&i ' pa##er rela#e" #o pulmo ar! e"ema

Desire" Ou#)ome PatientCs breathing pattern is maintained as e#idenced by( eupnea, normal skin color, and regular respiratory rate/pattern Su''es#e" NO. Ou#)omes *espiratory Status( ,ir'ay Patency *espiratory Status( .entilation *espiratory Status( 1as E;change .ital Sign Status Su''es#e" NI. I #er+e #io s ,ir'ay 0anagement> $;ygen therapy> *espiratory 0onitoring Progressi#e 0uscle *ela;ation> ,n;iety *eduction>

I #er+e #io
,ssess

respiratory rate and depth ,ssess for dyspnea and ?uantify 0onitor breathing patterns Aote muscles used for breathing 0onitor for diaphragmatic muscle fatigue ,ssess position patient assumes for normal or easy breathing =se pulse o;imetry to monitor $2 saturation and pulse rate 0onitor ,B1s as appropriate> note changes 0onitor for changes in orientation, increased restlessness, an;iety, and air hunger

 Position

patient 'ith proper body alignment for optimal breathing pattern Encourage sustained deep breaths ,dminister o;ygen, as ordered, to maintain an acceptable le#el of o;ygen at the tissue le#el3 Suction air'ay as needed to maintain patent air'ays3 ,ssist patient to "o'lerDs position, 'hich 'ill promote e;pansion of lungs and pro#ide comfort3 ,ssist patient 'ith ,/%s as needed to conser#e energy and a#oid o#ere;ertion3

COR P#L$ONAL
+or Pulmonal (+P) hipertrofi dan atau dilatasi dari #entrikel kanan akibat hipertensi (arteri) pulmonal yang disebabkan oleh penyakit intrinsik dari parenkim paru, dinding thoraks, maupun #askuler paru3 Pulmo ar! &ear# "isease pelebaran #entrikel kanan sebagai respon terhadap peningkatan resistensi atau hipertensi pulmonal )arus dibedakan dengan penyebab lain dari hipertropi #entrikel kanan seperti stenosis mitral, kelainan 4antung ba'aan, gagal 4antung kiri3 +or pulmonal dapat bersifat akut akibat emboli paru yang pasif, dapat 4uga kronis

ETIOLOGI
Penyakit

parenkim paru, penyakit paru obstruktif menahun, bronkiektasis, fibrosis sistik, atelektasis, kelainan dinding thoraks dan otot pernapasan 0iastenia gra#is3 Penyakit #askuler paru, emboli paru

TANDA DAN GEJALA

Aafas pendek Fhee@ing Batuk berdahak kronik ,sites Edema kaki Peningktan E.P Pembesaran hati Sianosis Suara 4antung abnormal E!1

PEN2EBAB

,kut(

Emboli pulmonal !ambuhan kor pulmonal konik !ronik( +$P/ )ipertensi pulmonal primer ,sma )ilangnya 4aringan paru akibat trauma atau pembedahan Sickle cell anemia Sarcoidosis $bstructi#e sleep apnea ,ltitude sickness

PATOFISIOLOGI
.asokontriksi

pulmonal Perubahan anatomi #askuler Peningkatan #iskositas darah diopatik atau hipertensi pulmonal primer

pat%op% siolo&
%ung disorders cause pulmonary hypertension by se#eral mechanisms( K%oss of capillary beds (eg, due to bullous changes in +$P/ or thrombosis in pulmonary embolism K.asoconstriction caused by hypo;ia, hypercapnia, or both Pulmonary hypertension increases afterload on the *. (right #entricle) resulting ele#ated end-diastolic and central #enous pressure and #entricular hypertrophy and dilation3 /emands on the *. may be intensified by increased blood #iscosity due to hypo;ia-induced polycythemia3 *arely, *. failure affects the %. if a dysfunctional septum bulges into the %., interfering 'ith filling and thus causing diastolic dysfunction3

pa#&op&!siolo'! o, )or pulmo ale i )op"

PAH: pulmonal arterial h pertension

!IAGNOSIS
dada )ipertropi #entrikel kanan, dilatasi atrium kanan, paru perifer menun4ukan penurunan #askuler3 E!1 bisa didapatkan gambaran hipertropi #entrikel kanan-de#iasi aksis ke kanan, 1elombang * menon4ol di .< dan & in#ersi di lead precordial, S melebar di lead , L melebar di lead , P pulmonal lead , , a.", L lebar di lead Echocardiogram dilatasi #entrikel kanan, regurgitasi katup trikusidalis
*ontgen

PEA,&,%,!S,A,,A
0enghilangkan

penyebab yang mendasari Emboli pulmonal trombolisis, antikoagulan +$P/ terapi oksigen /iuretik notropik meningkatkan kontaktilitas 4antung $ksigenasi Bronkodilator ,gen mukolitik

NURSING DIAGNOSIS
/ecreased cardiac output related #entricular inefficiency mpaired 1as E;changed related to perfusion problem

/ecreased cardiac output related to an ineffecti#e #entricular pump Desire" Ou#)ome( patient demonstrates ade?uate cardiac output as e#idenced by blood pressure and pulse rate and rhythm 'ithin normal parameters> strong peripheral pulses> and an ability to tolerate acti#ity 'ithout symptoms of dyspnea, syncope, or chest pain Su''es#e" NO. OUT.OMES3 +ardiac pump( Effecti#eness> +irculation status> &issue perfusion( ,bdominal organs and peripheral> .ital sign status> Energy conser#ation> "luid balance INTER(ENTIONS3 +ardiac care> +irculatory care( 0echanical assist de#ice> "luid/electrolyte management> 0edication administration> 0edication management> $;ygen therapy> .ital signs monitoring

INTER(ENTIONS ,ssess restlessness ,ssess heart rate and blood pressure3 ,ssess skin color and temperature3 ,ssess peripheral pulses3 ,ssess fluid balance and 'eight gain3 ,ssess heart sounds, noting gallops, SI, SJ3 SI denotes reduced left #entricular e4ection and is a classic sign of left #entricular failure3 ,ssess lung sounds3 /etermine any occurrence of paro;ysmal nocturnal dyspnea (PA/) or orthopnea3 0onitor continuous E+1 as appropriate3 ,ssess response to increased acti#ity3 ,ssess for chest pain3 ,ssess urine output3

,dminister medication as prescribed, noting response and 'atching for side effects and to;icity3 0aintain optimal fluid balance3 0aintain hemodynamic parameters at prescribed le#els3 0aintain ade?uate #entilation and perfusion Place patient in semi- to high-"o'lerDs position3 ,dminister humidified o;ygen as ordered3 0aintain physical and emotional rest, as in the follo'ing( o *estrict acti#ity3 &his reduces o;ygen demands3 o Pro#ide ?uiet, rela;ed en#ironment3 Emotional stress increases cardiac demands3 o $rgani@e nursing and medical care3 &his allo's rest periods3 o 0onitor progressi#e acti#ity 'ithin limits of cardiac function3