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NUR3310 > APO & PE > Flashcards

APO & PE Flashcards

1
Q

Define Acute Pulmonary Oedema (APO)

A

Normal lung processes to prevent fluid build-up are disrupted, causing accumulation of fluid in the interstitial tissues and alveoli of the lungs. This results in impaired gas exchange and lung expansion

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2
Q

What are the normal methods used to keep the lungs dry

A

lymphatic drainage, hydrostatic pressure, capillary oncotic pressure, capillary permeability, presence of surfactant

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3
Q

Outline how lymphatic drainage keeps the lungs dry

A

The lymphatic system drains fluid (called lymph) that has leaked from the blood vessels into the tissues and empties it back into the bloodstream via the lymph nodes

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4
Q

Outline how hydrostatic pressure keeps the lungs dry

A

Hydrostatic pressure is the pressure that any fluid in a confined space exerts. This pressure forces fluid out of the pulmonary capillaries into the interstitium

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5
Q

Outline how Capillary oncotic pressure keeps the lungs dry

A

Osmosis results in pressure exerted by proteins which keeps fluid in the capillaries

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6
Q

Outline how capillary permeability keeps the lungs dry

A

The ability of capillary walls to allow the selective flow of substances and cells in and out

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7
Q

Outline how the presence of surfactant keeps the lungs dry

A

Repels water, stops fluid entering alveoli

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8
Q

How can heart failure induce APO

A

> As pressure in the heart increases, cardiac output (CO) decreases
Blood return in left atrium exceeds blood leaving the left ventricle-> increased pulmonary venous pressure-> increased pulmonary capillary hydrostatic pressure->net filtration of protein-poor fluid out of capillaries and into the interstitial space + alveoli

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9
Q

What are common cardiac related causes of APO

A

Heart disease/LV dysfunction, AMI (heart attack), Acute dysrhythmia, valvular insufficiency

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10
Q

What are common non-cardiac related causes of APO

A

Capillary injury, lymphatic obstruction, blood transfusion/fluid overload, acute lung injury, high altitude

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11
Q

What are clinical manifestations of APO

A

Breathlessness, tachypnoea, chest auscultation (crackles), cough, pink frothy sputum (if alveoli are injured), cyanosis (Late term), tachycardia, HTN, Hypotension (due to cardiac shock), diaphoresis (excess sweat), raised JVP (elevated Jugular venous pressure, indicative of HF), anxiety, confusion

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12
Q

How is breathing regulated

A

Ventilation+RR is controlled by Autonomic Nervous System
Chemoreceptors detect high levels of CO2 in blood -> ventilation increase

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13
Q

outline the components of the Autonomic Respiratory system

A

Cerebral cortex: voluntary control over breathing
Hypothalamus: other receptors (ie pain) and emotional stimuli
Medulla & Pons: respiratory centre
Central+Peripheral chemoreceptors
Stretch receptors + irritant receptors in lungs
Receptors in muscles and joints

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14
Q

What effect does APO have on the brain

A

hypoxia can cause confusion and agitation

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15
Q

What effect does APO have on the heart

A

LV failure, ability to pump blood is impaired, backup of blood into vasculature, pulmonary capillary pressure increase -> vasoconstriction -> increase in pulmonary capillary pressure -> fluid leak into surrounding tissue

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16
Q

What effect does APO have on the lungs

A

alterations in capillary pressure, osmotic pressure and alveolar-capillary membrane integrity = increase of fluid in interstitial space + alveoli. Fluid in alveoli washes away surfactant -> alveolar collapse, reducing surface area for gas exchange -> hypoxia

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17
Q

What effect does APO have on blood pressure

A

usually HTN (can be Hypotensive when decompensating)

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18
Q

What effect does APO have on the liver

A

Hepatomegaly (enlarged liver) associated with HF. increased pressure on hepatic veins prevents adequate drainage of blood from the liver

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19
Q

What effect does APO have on the kidneys

A

RAAS (Renin-Angiotensin-Aldosterone System) system (hormone system or the regulation of blood pressure and fluid balance) simulated by sympathetic nervous system secondary to HF. results in vasoconstriction and fluid retention, which increases myocardial workload, which decreases heart function

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20
Q

What effect does APO have on the legs

A

pitting oedma may be present, associated with HF. activation of humoral & neuro-humoral mechanisms promotes sodium and water reabsorption

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21
Q

What effect does APO have on circulation

A

reduced cardiac output results in tachycardia. Peripheral shut down, skin cool and clammy

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22
Q

What is the assessment+ management for APO influenced airway

A

frothy sputum/cough/speech difficulty
= SUCTION

23
Q

What is the assessment+ management for APO influenced breathing

A

SOB/tachypnoea/increased WOB/hypoxia/crackles
= APPLY O2 and POSITION UPRIGHT

24
Q

What is the assessment+ management for APO influenced circulation

A

HTN/Hypotension (cardiogenic shock)/ tachycardia/ arrhythmia/pale+clammy
= REASSESS VITALS FREQUENTLY, assess PAIN & IVC, PATHOLOGY, ECG and CARDIAC MONITORING

25
Q

What is the assessment + management for APO influenced disability

A

altered consciousness/confusion/anxious
= GCS, BGL, IDC and REASSURANCE

26
Q

Outline Management of APO

A

> Continuous reassessment: ABCD
Respiratory: manage hypoxia
Oxygen: maintain sats 94%+ (88-92% COPD)
Ventilatory support: NIPPV
Cardiac: reduce preload & afterload
Pharmacology: Nitrates (GNT); sublingual or IV. Diuretics (Frusemide): IV not oral. Morphine: lack of good evidence for efficacy
Aetiology: treat underlying cause

27
Q

Outline NIPPV

A

Ventilatory support for a spontaneously breathing patient, improves lung compliance, reduces V/Q mismatch
Lowers intubation rates, less expensive, fewer complications

28
Q

What is NIPPV?

A

Non-invasive positive pressure ventilation

29
Q

What are the three different types of NIPPV?

A

Continuous Positive Airway Pressure (CPAP)
Bi Level Positive Airway Pressure (BiPAP)
Positive End Expiratory Pressure (PEEP)

30
Q

What are indications for NIPPV?

A

APO, acute COPD, mod-severe respiratory distress, pneumonia, dyspnoea, SPO2 <90&, resp rate >24

31
Q

What are contraindications for NIPPV?

A

pt is uncooperative/anxious, impaired swallowing/cough (airway risk), poor respiratory drive, copious respiratory secretions, inability to seal mask

32
Q

What are some complications of NIPPV?

A

HTN (↑ intrathoracic pressure, ↓ venous return, ↓ CO) , altered conscious state, gastric distention (swallowing air), pressure sores

33
Q

Nursing management for NIPPV

A

monitor GCS, minitor aurway patency, minitor NIPPV settings, monitor breathing, 1:1 nurse ratio

34
Q

Define a pulmonary embolism (PE)

A

a partial or complete occlusion of a pulmonary artery, or one of its branches, by an embolism. The obstruction can be the result of a blood clot, air or fat. A PE prevents gas exchange, creates a V/Q mismatch, and an infarction of lung tissue

35
Q

What can result due to a PE?

A

vasocontriction of pulmonary capillaries, increased pulmonary artery pressure, increased dead space as perfusion decreases, decreased surfactant, hypoxaemia, arrhythmias, decreased cardiac output

36
Q

What are risk factors for PE?

A

Blood clotting from venous stasis
Hypercoagulability
Endothelial injury

37
Q

What are clinical manifestations of PE?

A

acute chest pain, dyspnoea, tachypnoea, tachycardia, acute anxiety, hypoxia

38
Q

Ways to investigate for PE

A

chest x-ray, ABG (arterial blood gas) , ECG, CTPA (CT pulmonary angiogram), CT

39
Q

What are the types/causes of a PE?

A

Thrombus: most commonly lower limbs
Fat: orthopaedic surgery/ long bone trauma
Air: CVC insertion, insufflation of air procedures
Amniotic fluid: birthing process
Septic: bacterial invasion of the thrombus

40
Q

Outline assessment/management of PE

A

O2 to maintain sats, limit activity, ensure airway patency, prioritise comfort, hypotension + pale, with tachycardia (compensatory)

41
Q

Outline anticoagulation treatment

A

Prevents the formation of new thrombi and allows
endogenous fibrinolysis to take effect on the embolus

42
Q

What are contraindications for anticoagulants?

A

Severe thrombocytopenia (low platelet count)
Active bleeding
History of haemorrhagic stroke
Severe hepatic disease (liver disease)
Bacterial endocarditis (infection caused by bacteria that enter the bloodstream)

43
Q

What are some anticoagulants that can be used to treat PE?

A

Heparin, exoxaparin, Warfarin, Rivaroxaban

44
Q

Outline Thrombolytics treatment

A

Accelerates clot lysis
use in massive PE, time critical, high risk of major haemorrhage/bleeding

45
Q

What are contraindications for thrombolytics?

A

active bleeding/bleed risk, recent stroke, recent surgery, recent head trauma, recent labour, severe HTN

46
Q

What is a thrombolytic?

A

Alteplase

47
Q

Outline an embolectomy

A

For life threatening PE, when thrombolytics are contraindicated
surgical embolectomy/transvenous catheter/inferior vena cava filter
high mortality rate

48
Q

What are risk factors for a VTE?

A

venous stasis, immobility, surgery, vessel damage

49
Q

Outline nasal prong therapy

A

1-4L, 22-35% oxygen delivery, risks include dry nasal mucosa and pressure injury

50
Q

Outline hudson mask therapy

A

5-10L, 35-60% oxygen delivery, risks include dry nasal mucosa, pressure injury, patient non-compliance, aspiration

51
Q

Outline non-rebreather facial mask therapy

A

10-15l, >60% oxygen delivery, risks include dry nasal mucosa, pressure injury, patient non-compliance, aspiration, and suffocation if oxygen in reservoir bag is insufficient

52
Q

Outline high flow nasal cannula oxygen delivery

A

10-60L, 21-80% oxygen delivery, an air/oxygen blender connected through a heated humidifier to the nasal cannula, allows adjustment of the Fio2 independently from the flow rate. Provides continuous, warmed and humidified oxygen, high oxygen flow can ‘force open’ respiratory passages and keep them open

53
Q

What are some clinical indications for High Flow nasal cannula oxygen?

A

Acute hypoxaemic respiratory failure
Cardiogenic pulmonary oedema
Prolonged use of oxygen therapy, for example in palliative care
Patients with either a tracheostomy or laryngectomy
Mask intolerance in traditional oxygen delivery systems
Supplemental oxygen delivery for longer than 12-24 hours

NUR3310 (9 decks)

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