NSG 4330 Complex Midterm 1
COMPLEX MIDTERM 1
WEEK 1: CARING FOR CLIENTS REQUIRING COMPLEX RESPIRATORY CARE: LOWERING
RESPIRATORY DISORDERS & RESPIRATORY FAILURE Fourth Edition: -Ch30 (p. 623-638 -PDF: pg1846) -Ch40 (p. 930-937 – PDF: pg 2713*) -Ch70 (PDF: pg 5241) –Ch 68 (p.1742-1755 – PDF – 5128*) *Also need to read from Ch 19 about Acid/ Base RESPIRATORY FAILURE & COMPLEX RESPIRATORY CARE
Objective:
-hypoxemic vs hypercapnic -differentiate between hypoxia + hypoxemia -common pathologies and disorder that contribute to respiratory failure (venous thromboembolism + chest trauma) - differentiate between hypoxia + hypoxemia -ID the following V/G relationships: normal unit; V/Q mismatch; shunt; dead space -Describe ARDs -describe key concepts related to non-invasive + invasive resp support: (Peep, pressure support) + modes of ventilation ( volume, pressure ) -describe nursing interventions related to resp failure
Overview:
-primary fxn of lungs is gas exchange -process of effective gas exchange: ventilation, perfusion, diffusion: problems with any of the 3 can result in HYPOXEMIA or HYPERCARBIA
-Respiratory Assessment: inspection, ausc, palpation, percussion
-Ausc- AS fine crackles (hair rubbing), stridor (whitle), pleural friction rub (rubing together, coarse and rough) -Cheyne strokes – crescendo, goes up and then weans -Kussmul – deep and rapid resps -Palpation – sub cut emphysemia feels like rice krispies -Percussion- check for typamny, dullness etc Hypoxemia- low oxygen in BLOOD Hypoxia – low oxygen in TISSUES
Ventilation: air moving in and out
Perfusion: movement of blood capillaries
Diffusion: movement of gases between the alveoli and RBC
-think about: RBC - end organ perfusion, end organ oxygenation
-think about adventitious sounds: stridor, pleural friction rub, cheyne-stokes, breathing pattern, kussmal- Palpation: subcutaneous emphysema -tachypnea or bradypnea? 20-10 Lung Volume + Capacities:
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-know tidal volume
Tidal Volume: usually 500 ml – can measuer with ventilation – moves in and out normally – small bumps in normal breathing
Minute Ventilation: tidal volume * resp rate over a minute
Total Lung Capacity: almost like an impossible breath - 6 L
Vital Capacity: total amount that can be exhaled
Residual Volume: 1L that is in the lungs at all times
Respiratory Failure: - NOT disease – either hypoxemic or or hypercapnic
-state in which one or both gas exchanging fxns are inadequate: amount of 02 transferred to blood is insufficient *hypoxemia) or amount of c02 removed from lungs is inadequate (hypercapnia) – usually consequences of something else -Hypoxemia – amount of 02 transferred to blood is insufficient -Hypercapnia – amount of c02 removed from lungs is inadequate -Clinical states that interfere with 02 transfer result in HYPOXEMIA (low Pa02 tension in blood – Pa02 <60 mmHg) and a decreased in non specific arterial oxygen saturation Sa02 -insufficient C02 removal results in HYPERCAPNIA – presence of excessive amounts of C02 in the blood – also called hypercarbia – -when Sp02 is 90% - Pa02 is approx. 60 mm Hg – if PaC02 and pH are normal
HYPOXEMIC respiratory failure:
-Pa02 <60mmHg or 60% Oxygen (Fi02.60) (WHEN THEY ARE RECEIVING SUPPLEMENTAL OXYGEN) Pa02 of 60 mm Hg or less when pt receiving inspired 02 at a fraction concentration (Fi02) of 60% or greater – this def – two important conepts (1) the Pa03 lvl indicates inadequate 02 saturation of Hb (2) this Pa02 levels exists despite admin of supplemental 02 at percentage (60%) that is three times that in room air (21%) -what is Fi02 of room air? 21 – when you put patient on 1L of 02? is equivalent toa bout 6%.. so then that is 27 % - normal pressure of 02 ?-between 60-100% Sp02 – there is little change – but once below 60% - a lot of change -normal Pa02 is between 80-100 mmgHg; between 60-100mmHg wont see major differences between Sp02 – but under will see it – they are on 3x the oxygen in room air – so this is bad -often referred to as –oxygenation failure – prim program – inadequate 02 transfer between alveoli and pul capillary bed Resp cause: ARDS, pneumonia, toxic inhalation, hepatopulmonary syndrome, massive pulmonary embolism, smoke inhalation
Cardiac causes: anatomical shunt, cardiogenic pulmonary edema, shock
Clinical Manifestations: decreased 02 sats, increased WOB, intercostal retractions, tachypnea, accessory muscle use, - central cyanosis (very late sign) – changes in behaviour (restlessness, agitation), coma is a late sign – inability to speak without pausing to breath – cool, clammy and diaphoretic skin
HYPERCAPNIC Respiratory Failure:
-PaC02> 45mmHg in combination with acidemia (pH<7.35) -refered to as ventilator failure – prim problem – insufficient C02 removal -3 important concepts: (1) the PaC02 is higher than normal (2) there is evidence of the bodys inability to compensate for this increase (academia) (3) the pH is at a level at which a further decrease may lead to severe acid base imbalance -causes: condition that compromise lung ventilation and subsequent c02 removal – drug overdoses with CNS depressants, neuromusc diseases and trauma or diseases involving spinal cord
Resp Causes: asthma, COPD, CF
CNS: brainstem, infarction, sedative and opioid OD, SCI, severe head injury
Chest wall: Thoracic trauma, Kyphoscoliosis, pain (often with fractured ribs), morbid obesity Neuromuscular system: myasthesnia gravis, critical illness polyneuropathy, acute myopathy, toxic ingestion, amyotrophic lateral sclerosis, phrenic nerve injury, Guillain-Barre syndrome, poliomyelitis, muscular dystrophy, MS
Clinical Manifestations: 2 / 4
-increased C02 and already compensated, will become more tired and lethargic; late sign would be unconscious – behaviour signs are big deal – continue to do CAMs to assess for delirum and rule it out -reduce tidal volume, minute ventilation, and resp rate – sometimes high resp rate – with shallow resp – reduce DTR, muscle weakness and tremors and seizures
Etiology and Patho: from text
HYPOXEMIC RESP FAILIRE: text
-four mech may cause hypoxemia and subsequent hypo resp failure -most common VS mismatch and shunting (1) Ventilation-Perfusion Mismatch -in normal lung - blood perfusion lungs – 4-5 L per min (amt of fresh gas that reaches alveoli each min) -in perfect match system each portion of lung would reeive approx. 1 ml of air for each 1 ml of BF VQ ratio of 1:1
- ml of air per 1 ml of blood VQ =1
-at lung apex VQ ratios are greater than 1 (more ventilation than perfusion) -at lung base VQ ratios are less tan 1 (less ventilation than perfusion) -common: increased sescretions in airways (COPD) or alveoli (pneuo) and when bronchospasm (asthma) – also in atelectasis or from pain -increase in 02 consumption and c02 production – increased metabolic demands (02) and ven demands – and airflow (ven) and alveoli is limited – no effect on BF (perfusion) is exerted to balance equation VQ MISMATCH Tx: 02!!(2) Diffusion Limitation: decrease in gas exchange across alveolar-cap membrane by processes that thicken or destroy the membrane - condition that affect the pulmonary vascular bed – severe emphysema or recurrent pul emboli can worsen DL -DL is more likely to cause hypoxemia during exercise – blood moves faster through lungs – has shorter time for diffusion of 02 across alveolar capillary membrane -classic sign of DL is hypoxemia during exercise but not at rest (3) Alveolar Hypoventilation: decrease in ven that results in an increase in PaC02 and consequence decrease in Pa02 -alveolar hypoven may result from restrictive lung disease, CNS, disease, chest wall dysfunction, neuro musc disease - primary mechanism of HYPERCAPNIC RF but also hypoxemia
(4) Interrelationship of Mechanisms:
-often caused by combo of all above 4 – Ex: combo of VQ mismatch and shunting because of inflame edema and hypersec -hypoxemia results from shunting does not respond to increases in supplemental 02
HYPERCAPNIC Respiratory Failure: text
-imbalance between ven SUPPLY and ven DEMAND
- Ven supply: max ventilation (gas flow in and out of the lungs) that pt can sustain without developing resp muscle
fatigue
-Ven demand: is the amount of ven is needed to keep the PaC02 normal
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-normally ven supply far exceeds ven demand so when exercising there is increase in C02 but no increase in PaC02 - in lung disease – cannot effectively increase lung ventilation -often accompanies resp acodisis Disease involved resp failure can be grouped in four cats: (1) abnormalities of airways and alveoli (2) abnormalities of CNS (3) abnorm of chest wall (4) neuro-musc conditions -more in textbook about clinical manifestations, specific clinical manifestations, consequences of hypoxemia and hypoxia
Ventilation-Perfusion Relationships:
-want good ven + per – 02 comes into alveoli and deoxy blood passes from vein into alveoli
Normal Unit:
VQ Mismatch: may have great ventilation at top of lungs but poor perfusion in the bases – it is hard to get air in there can have a partially compromised situation where there are secretions in alveoli but good perfusion – could have normal alveoli and asymtomic PE that is in the capillary resulting in mismatch
Absolute Shunt:
Dead Space: alveoli is fine – but message PE – good ventilation, no perfusion – fully blocking – so good V and bad P due to dead space -Diffusion Limitation: fibrotic lung tissue – capillary membrane is bad - still oxygenation but perfusion is limited
Alveolar Hypoventilation: CNS difficulty – chest wall dysfunction
-1 ml of 1 ml of gas – is equal – functioning well but can have mismatching that are normal and are expected -we could have some secretions – but still good secretions - dead space block – no perfusion -first line of tx for VQ mismatch – give 02 ( supplemental )
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