Pulmonary Embolism Concept Map, Schemes and Mind Maps of Medical Sciences

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RISK FOR BLEEDING r/t anticoagulant or thrombolytlc reglmen therapy · Assess tor history of a high-risk bleeding condition

• Monitor IV dosage and delivery system · Assess tor signs and symptoms of bleeding; bleedJng from catheter insertion sites; GI or GU

bleeding; bleeding from the respiratory tract;

bleeding from mucus membranes: decreased hemoglobin and hematocrit

• Administer anticoagulant therapy as prescribed · Monitor platelet counts. coagulation test results (INR). PT. aPTT. and hemoglobin and hematocnt · Monitor platelets and the heparin-induced platelet aggregation (HIPA) status -Il the patient is HIPA positive, stop all heparin products and consult a hematologist

INEFFECTIVE BREATHING PATTERN r/t

acute chest paln

Assess the respiratory rate, rhythm, and depth.

Assess tor any increase in the work of

brealhing: shortness of breath and the use of accessory muscles. Assess characterlstics ol pain · Monitor ABG's Monitor oxygen saturation via pulse oxlmetry. · Position lhe patient in a sitting position, and change the position every 2 hours · Administer oxygen as prescribed Assist lhe patient with coughlng and deep breathing

Group 2

PRIORITY NURSING ACTIONS

Suspected Pu/monary Embolism

1. Notify the Rapid response team and heallh care provider (HCP)
2. Reassure the client and elevate the head ol the bed. 3. Prepare oxygen administrauon
3. Obtain Vital Signs and check tor lung sounds 5. Prepare to obtain artenal blood gas. 6. Prepare lor the administration of heparin therapy or other lherapies: embolectomy or placement of vena cava li Iter it necessary.
4. Document the event, interventions taken, and the dient's response to treatment.

DEFICIENT KNOWLEDGE rii activlties to

prevent embolism and setf-care alter diagnosis of embolism

• Ascertain level of knowledge, including anticipatory needs. · Determine chent's abilrty, readiness, and barriers to learning. (patient maybe physically weak and unable to participate) · Use short, simple sentences and concept. Repeat and summarize as needed. Previde mutuai goal setting and learning contracts.

PSYCHOSOCIAL ASPECTS

-Life-changing event -Shock/distress at uncertainty Il had happened lo me. Why me? Il was awful noi knowing whal had caused il. -Loss of self -Change in focus or direction

,----

IMPAIRED GAS EXHANGE r/t altered blood flow to alveoli secondary to embolus · Monitor vital signs, noting any changes

• Auscultate lung sounds · Assess skin color, nail beds, and mucus membranes lor color changes · Monitor ABGs
• Monitor oxygenation via pulse oxlmeter · Assess lor calf tenderness, swelling, redness, and/or hardened areas · Administer oxygen as needed
• Positton the pabent properly to facilitate ventilauon perlusion matching

ANXIETY rii fear of suffocation

• Review physiological factors, i.e. Post op pts.• Bed ridden pts., Pts with mobìhty problem, bone tractures (fat embolism)
• lf irrational thoughts are present previde patìent with accurate information on current disease condrt1on thai contribute pt's anxiety.
• Explain all activities. procedures, and issues that involve the client: use non-medicai terms and calm slow speech.

Pathophysiology of pul mona ry embolism

Sources: Circulation. 2003 Dee 2; 108(22):2726-9. I Hellenic J Cardiol. 2007 Mar-Apr;48(2):94-107.

Patients with risk factors (Virchow's triad) develop deep venous thrombosis (DVT), which ascends up the inferior vena cava to the right heart

and lodges in the pulmonary vasculature.

V:Q mismatch: Large emboli get stuck in the centrai vessels, which more likely leads to hemodynamic consequences. Small emboli clears the

large vessels and lodges in the peripheral vessels, leading to irritation of the pleura!. The primary defect in PE is V:Q mismatch because parts

of the lung are not perfused (distai to the emboli) and, as a result of vascular compromise (atelectasis) and inflammation

(bronchoconstriction), some parts are not ventilated. Arteria! hypoxemia follows, and is compensateci by increased minute ventilation. The

compensation often overshoots, blowing off more C02 than necessary, leading to hypocapnia.

Hemodynamic consequences: Mechanical occlusion of the

vessels and response vasoconstriction causes high pulmonary

resistance and subsequent right heart overload. lf the

occlusion is significant, forward flow to the left heart is

reduced, causing heart failure and shock.

Deep venous thrombosis

Pulmonary embolism

Large

'.

Small

Centrai PE

' in larger vessels

Peripheral PE near the pleura

_ -► Pleuritic chest pain

Parastemal heave

LDudP2 (^) ♦ lncreasedJVP

Tachycardia Hypotension Death

Shunting

No ventilation

Vascular compromise

leads to atelectasis in

parts of the lung.

I

More likely to

cause

I

Hemodynamic consequences

t

RV overload

lf severe

LV forward heart fai Iure

V:Q MISMATCH

t

V:Q = 1

Perfectly matched

Mechanical occlusion

Of blood vessels

Vascular compromise

.J.. surfactant

Atelectasis

Dead space

No perfusion

lnitially, the eia! blocks

perfusion, gjving rise to

dead space.

t dead space

Chemical mediators

Released by inflammation

Vasoconstriction

Hypoxemia

V:Q

'

t pulmonary resistance

Arterial lrritant

hypoxemia receptors

t minute ventilation

Tries to compensate

hypoxemia by t ventilation,

leading to J. CO

Hypocapnia

' � Dyspnea SYMPTOM Tachypnea SIGN

Secondary

bronchoconstriction

Bronchoconstriction

Alveolar hypoxia