Wk 1: Respiratory Flashcards
Define ventilation
the movement of air between the atmosphere and the lungs. Inspiration and expiration.
Define diffusion
the exchange of oxygen and carbon dioxide between the bloods red blood cells and the lungs.
Define perfusion
delivery of RBCs to the lungs
Define compliance
indication of how well the chest wall and lungs can expand and collapse. If the patient has decreased compliance, it is more difficult to inflate the lungs.
Define resistance in the context of airways
This relates to the size of the airway. The resistance of the airway increases when the diameter of the airway decreases.
Define V/Q mismatch
When there are issues with ventilation and perfusion, the diffusion of gases is altered. This is called a V/Q mismatch
(ventilation/perfusion)
What smaller systems become compromised in the context of APO?
Our lungs are kept dry by
- Lymphatic drainage
- Hydrostatic pressure (pressure exerted by fluid in vessel)
- Capillary oncotic pressure (pressure exerted by proteins, keeps fluid in the capillaries)
- Capillary permeability
- Presence of surfactant (repels water, stops fluid entering alveoli)
What does a disruption in the ‘drying’ system of the lungs cause in APO?
- abnormal accumulation of fluid on the lungs in the interstitial tissue and alveoli of the lungs.
What complication arrises from the build-up of fluid in APO?
- impaired gas exchange
- impaired lung expansion
What is the cause of cardiogenic APO?
- heart failure
Recall, what is heart failure?
Multiple processes that result from either;
- impaired left ventricular contraction (systolic heart failure)
- impaired left ventricular relaxation (Diastolic)
When it cant flow out into the body it backs up in the pulmonary veins and then into the lungs thus causing fluid not being able to move into the blood.
Explain the pathophysiology of cardiogenic APO
- When the heart is failing to meet the demands of the blood flow.
- as the pressures in the heart increase-> cardiac output (CO) is decreased, as the ventricle must pump against an increased systemic vascular resistance (SVR).
What pathophysiological processes are causes of cardiogenic APO?
- Blood returning to left atrium exceeds that leaving the left ventricle
- This results in an increased pulmonary venous pressure
- This then causes an increased pulmonary capillary hydrostatic pressure. As the hydrostatic pressure increases and exceeds the pulmonary oncotic pressure, there is a net filtration of protein-poor fluid out of the capillaries and into the interstitial spaces and alveoli.
What are some common cardiac-related causes of APO?
- heart disease/left ventricle dysfunction
- AMI
- acute dysrhythmia
- Valvular insuffucuency
- fluid overload
What are some common non-cardiac related causes of APO?
- capillary injury
- increased capillary pressure
- redistribution of blood volumes or flow to lungs as a result of patient positioning, administration of vasoactive drugs, cardiac shunts, anemia or exercise
- increased IV volume from over transfusion of fluids or renal failure - physical injury affecting pulmonary parenchyma (where gas exchange occurs)
- reduced drainage from interstitial space as a result of blood contents including electrolytes and plasma proteins creating an osmotic pressure that draws water from the IS to IV space.
- obstruction of the lymphatic system
- blood transfusion/fluid overload
- acute lung injury
- high altitude
- tissue injury due to toxicity
- tissue injury due to damaging pressure
- Common examples include pneumonia, aspiration of gastric contents, sepsis, thoracic surgery and large-volume blood transfusion.
- pulmonary contusion, inhalation of noxious substances and burns
- High-altitude pulmonary oedema is caused by cellular injury induced by pulmonary hypertension secondary to altitude-induced hypoxia.
- reduced drainage of the interstitial space
- neural and hormonal responses to cerebral lesions and head injuries
- left ventricular failure or mitral valve disease causing pulmonary venous pressure that increases pulmonary capillary pressure.
- In left ventricular failure, the ability of the heart to pump blood is impaired and this causes blood to back up into the pulmonary vasculature, leading to an increase in pulmonary capillary pressure. - inadequate CO results in peripgeral vaso constriction to bring blood bacll to the core orans which furthers the problem of pressures and furthers the leaking of fluid out of IV space due to the great hydrostatic pressure.
- Common causes of left ventricular failure include coronary artery disease, myocardial infarction, cardiomyopathies and excessive workload of the heart caused by hypertension, arrhythmias
(including atrial fibrillation) or valve disease
What are some clinical manifestations of APO?
- Sudden onset of extreme breathlessness/dysponoea
- particular dyspnoa when lying down.
- Tachypnoea
- Chest auscultation – crackles and rattles
- O2 desat
- Cough
- altered concious state
- Pink frothy sputum present if alveoli injured
- Cyanosis (late sign)
- Tachycardia
- Hypertension (because of hyper-adrenergic state)
- cardiac arrhythmias (e.g. A fib considering its high in heart failure)
- Hypotension = severe LVF and cardiogenic shock
- Diaphoresis
- Raised JVP
- Anxiety and agitation
- Confusion
- pink
(blood tinged) frothy sputum in late stages
What are some important considerations we must make when looking at one’s clinical manifestations in the context of APO?
= Think about why the pat would be experiencing these and link it to the pathophysiology.
For example, why would the patient develop tachycardia? Well, the patient who is experiencing cardiogenic APO has a failing left ventricle. The left ventricle is unable to pump effectively and eject blood forwards (into the aorta). This means that the patient has a reduction in their cardiac output (CO). If you think back to the equation cardiac output = stroke volume x heart rate (CO = SV x HR). So the patient will increase their HR as a way of increasing their cardiac output.
What are the common precipitating factors of APO?
- acute coronary syndrome
- new onset arrhythmia
- post surgery complications
Nursing management of APO
- multidisciplinary approach
- excellent communication
- pt and family reassurance in acute exacerbations as can be very frightening.
- accurate assessment, management and evaluation.
- continued evaluation post intervention
- continued assessment with acknowedgement of ow quickly deterioration can occur.
Explain the pathophysiology of general APO
- the amount of fluid in
the interstitial space increases, and the alveoli start to flood causing life-threatening impairment of gas exchange. - At its most extreme, the excess fluid causes ‘froth’ to form in the
lungs that blocks the airway
What are the four pathophysiological phases that occur in APO?
1: increase in interstitial fluid, but without fluid flooding the alveoli.
- The lymphatic system becomes distended as it fails to
completely drain excess fluid.
- Pressure on the capillaries can cause narrowing; however, overall alveolar function is maintained and the only clinical sign is mild dyspnoea.
- The lungs are distensible and are able to handle considerable volumes of fluid before gas exchange is affected.
- However, increasing pulmonary oedema reduces overall lung compliance.
2. fluid starts to infiltrate the alveoli, but gas exchange remains adequate.
- At this point, it is possible to detect clinical signs of oedema on chest radiography
3. clinical signs become more apparent where gas exchange becomes compromised further. Oxygenation is affected, though adequate removal of carbon dioxide may be maintained. On chest auscultation, rales are heard on inspiration and chest radiography shows opacity of the lungs.
4. flooding of the alveoli is extensive, pink frothy sputum is produced and this stage is likely to be fatal without treatment. The aetiology of pulmonary oedema is related to alterations in capillary pressure, osmotic pressure, airway pressure or alveolar-capillary membrane integrity.
What is the goal of treatment in APO?
- treat the underlying cause
- mitigate hypoxia
- mitiage fluid in lungs
What is the nursing management for APO: Airways?
- suctions
- focus on breathing management
What is the nursing management for APO: Breathing?
- consider position changes such as sitting up or standing (re-distribution of blood volume to peripheries takes load of heart)
- high flow via non-rebreather O2 (if below 90%)
*Oxygen is a powerful vasoconstrictor, and for patients for whom myocardial infarction is their primary event, this may worsen their prognosis. - NIPPV (CPAP or BiPAP)
What is included in your respiratory assessment?
Inspections
- peripheral and centeral cyanosis
- resp rate
- WOB
- O2 sats
Palpation
Auscultate
- note the presence of adverse noises and the level to which breath sounds extend.
- arterial blood gas (assess oxygenation and acid-base thus guide treatment)
- chest X-ray (show presence of pulmonary congestion)
Percussion
What focused assessments should be considered when suspected APO and why?
- Respiratory
- get a clearer picture of what is going on. - Cardiac
- as some symptoms including breathlessness are associated with MCI so must be counted out.
What does NIPT do for those with APO?
- reduce risk of endotrachael intubation
- improves gaseous exchange as increases O2 avalible
- optimises lung volumes
- reduces the WOB as reduces the force needed to initiate each breath.
- increases functional residual capacity and thus improves lung compliance
- positive intrathoracic pressure also decreases preload and left ventricular afterload as it is harder for blood to re-enter this area of the body.
- must consider hypotension as a side effect as low venous return to the heart.
What is the nursing management for APO: circulation?
- Manual pulse check to assess rhythm
- manage pain and recheck. often chest pain
- assess skin for cool clamy extremities indicating hypoperfusion
- 12 lead ECG may provide info on underlying cause
- IV pathology as per below
- take bloods for renal function (urea and creatinine), FBC, BGL and troponin.
- ?blood cultures if suspected infection
- FBC to monitor for renal perfusion
- ?need for catheter (consider insertion and how lying flat may impact them)
What are the two first-line medications for patients with APO?
- vasodilators e.g. GTN
* contraindicated in pts with aortic stenosis - diuretics e.g. fresuomide
What is the nursing management for APO: Disability?
- acute distress is common so reassurance
- check GCS frequently
- IDC
- BGL
- opioids can assist with this distress. Morphine for example is known as a mild vasodilator thus helping with pressure on heart.
- monitor AVPU in relation to hypoxic delirium
- check BGL (undiagnosed diabetes in common in heart failure patients)
What is the nursing management for APO: Exposure?
- check for signs of peripheral odema
- check core and peripheral temps
- Look out for a pattern of orthopnoea or a history of paroxysmal nocturnal dyspnoea where
a patient may describe waking suddenly feeling extremely breathless
Describe what the long term management of non-cardiogenic APO may be?
- discharging patients into a structured self-management plan is the best way to improve their long-term prognosis.
- GP check-up 1/52 post d/c
Describe what the long term management of cardiogenic APO may be?
- follow up with cardiologist or a specialist heart failure team within two weeks.
What dictates the autonomic nervous system’s control over our ventilation?
- Receptor in muscles and joints
- central chemoreceptors
- peripheral chemoreceptors in arteries
- other receptors (e.g. pain and emptional stimuli acting through the hypothalamus)
- higher brain centers (cerebral cortex-voluntary control over breathing)
These all impact the resp center (medulla and pons) and dictate stretch receptors in lungs and irritant receptors.
