Non-cardiovascular conditions (CMC) Flashcards
The respiratory system plays a crucial role in maintaining homeostasis by
facilitating gas exchange, delivering oxygen to the bloodstream and expelling carbon dioxide from the body
name the structures of the respiratory system
divided into upper and lower respiratory tracts, including nasal cavity, pharynx, larynx, trachea, bronchi, and lungs
(trachea is start of lower, or the area below the vocal cords so part of the larynx? but basically trachea)
what is an acute PE?
sudden blockage in one of the pulmonary arteries in the lunges, typically caused by blood clots that travel to the lungs from other parts of the body, a condition known as DVT. This blockage can cause significant impairment in pulmonary circulation, leading to respiratory distress and potencial CV compromise.
describe the pathophys of acute PE
involves obstruction of blood flow, which increases PVR. this increased resistance puts strain on the RV of the hart, which has to work harder to pump blood through the obstructed pulmonary circuit. If untreated, this can lead to RV failure and decreased CO, potentially resulting in hemodynamic instability and shock
s/s of PE
variety. sudden SOB, pleuritic chest pain (sharp pain that worsens with breathing), hemoptysis, signs of right heart strain (JVD)
if severe: syncope, sudden CV collapse
dx of PE
CTPA: computed tomography pulmonary angiography to visualize presence of clots in pulm arteries
additionally: D-dimer blood test, which can indicate clot formation
echo: to assess RV function
PE management
focus is on stabilizing patient and preventing further clot formation
AC therapy (heparin, DOAC)
if contraindicated or insufficient, thrombolytic therapy may be used.
if massive or hemodynaic instability: embolectomy or catheter-directed therapies may be necessary
PE prevention
prophlyactic AC for high risk patients
mechanical methods: compression stockings
lifestyle modifications to reduce risk factors for DVT
What is ARF (acute respiratory failure)?
life threatening condition characterized by the inability of the respiratory system to maintain adequate gas exchange, resulting in hypoxemia and/or hypercapnia.
In ARF, primary dysfunction involves either a failure in
oxygenation or ventilation
Describe Type 1 respiratory failure
aka oxygenation failure.
marked by a PaO2 less than 60 mmHg with normal or low PaCO2.
commonly due to conditions like pneumonia, pulmonary edema, or ARDS, where there is impaired gas exchange at the alveolar level.
Describe Type 2 respiratory failure
aka ventilatory failure
presents with PaCO2 greater than 50mmHg and often associated with hypoxemia
causes include COPD, neuromuscular disorders, or CNS depression affecting respiratory drive
clinical presentation of ARF
dyspnea, tachypnea, cyanosis, AMS, use of accessory muscles
abnormal ABGs: indicating hypoxemia and or hypercapnia
management of ARF
treat underlying cause, support oxygenation and ventilation
-supplemental oxygen. in cases of ventilatory failure or severe hypoxemia unresponsive to oxygen therapy alone, may need mechanical ventilation
NIPPV can be used sometimes to avoid intubation
Pharm interventions for ARF
bronchodilators for bronchospasm
corticosteroids for inflammation
abx for infection
diuretics for fluid overload
What is ARDS (acute respiratory distress syndrome)?
severe, life-threatening condition characterized by the acute onset of widespread inflammation in the lungs. It can result in impaired gas exchange and can lead to significant respiratory fialure. Often seen in critically ill pts and can be triggered by various direct or indirect insults to the lunge, such as pneumonia, sepsis, trauma, or inhalation injury
describe pathophys of ARDS
marked by increased permeability of the alveolar-capillary barrier, leading to pulmonary edema that is not caused by cardiac failure. This results in reduced lung compliance and impaired oxygenation. The hallmark of ARDS is the rapid onset of severe dyspnea, hypoxemia, and bilateral infiltrates on chest imaging that cannot be attributed to heart failure or fluid overload.
the categories of ARDS are based on
degree of hypoxemia: mild, moderate, severe
determined by the PaO2/ FiO2 ratio while on PEEP of at least 5cm H2O
mild vs mod vs severe ARDS
mild: PaO2/ FiO2 ratio between 200-300mmHg
mod: between 100-200mmHg
severe: less than 100 mmHg
management of ARDS
supportive care with mechnical ventilation using lung-protective strategies.
-includes low TV ventilation (6ml/kg of predicted body weight) and maintaining plateau pressures below 30cm of H2O to prevent ventilatory-induced lung injury
prone positioning has been show to improve oxygenation and outcomes in severe cases
other: conservative fluid management to minimize pulmonary edema
tx of underlying causes
prevention of complications (DVT, stress ulcers)
Pharm has limited roles. NMB in early severe ARDS to improve oxygenation
What is acute lung injury?
critical condition characterized by acute and persistent lung inflammation, leading to increased pulmonary vascular permeability and non-cardiogenic pulmonary edema.
It is an intermediary state between normal lung function and ARDS, with ALI being a less severe form.
defined by the acute onset of hypoxema, AEB PaO2/ FiO2 of less than 300mmHg, bilateral infiltrates, and absense of left atrial HTN (which differentiates it from cardiogenic pulmonary edema)
pathophys of ALI
direct or indirect lung insults
direct: pneumonia, aspiration, inhalation injury
indirect: systemic inflammatory responses such as sepsis or pancreatitis
the resultant damage to the alveolar-capillary membrane increases its permeability, allowing protein-rich fluid to leak into the alveoli, impairing gas exchange
clinical presentation of ALI
acute onset dypsniea, tachypnea, refractory hypoxemia
crackles due to alveolar flooding
ABG- hypoxemia and resp alkalosis initially
bilateral infiltrates without evidence of LA HTN or significant pleural effusions
management of ALI
supporitve care. underlying cause.
mechanical ventilation with low TV to prevent further lung injury
PEEP is used to maintain alveolar recruitment and improve oxygenation.
fluid management to maintain adequate perfusion while avoiding overload
what is the pleura/pleural cavity?
cavity: thin fluid-filled space between the two laters of the pleura surrounding the lungs.
pleura: consists of two layers. Visceral pleura covers the lungs. Parietal pleura lines the chest wall.
the pleural space contains a small amount of lubricating fluid to allow for smooth movement during respiration
what is a pleural effusion?
excessive accumulation of fluid within the pleural space.
what causes a pleural effusion?
can result from heart failure, infections (pneumona/tb), malignancies, or inflammatory diseases
s/s pleural effusion
dx/ tx
dyspnea, CP, reduced breath sounds
-CXR, US, thoracentesis
what is hemothorax?
accumulation of blood in pleural cavity, often due to trauma or surgical complications. presents with s/s of hypovolemic shock and respiratory distress.
management: volume resuscitation and evac of blood via thoracostomy
what is chylothorax?
accumulation of lymphatic fluid (chyle) due to thoracic duct injury or obstruction. presents with milky pleural fluid upon thoracentesis and requires dietary modifications and possibly surgical intervention.
what is pneumothorax?
accumulation of air in pleural space, area between the lung and the chest wall, which can lead to partial or complete collapse of the affected lung. disrupts normal negative pressure that keeps the lungs inflated, resulting in impaired respiratory function.
types of pneumothorax
spontaneous (primary or secondary), traumatic, iatrogenic
how does primary pneumothorax typically occur?
usually in young, healthy individuals without apparent lung disease, often due to the rupture of small air blisters (blebs) on the lung surface
how does tension pneumothorax develop?
trapped air progressively accumulates under pressure, leading to mediastinal shift and CV compromise.
how does secondary pneumothorax typically occur?
in patients with underlying lung pathology, such as COPD, cystic fibrosis, or TB
dx of pneumothorax
imaging
CXR to assess pleural space and lung collapse
sometimes CT for more info on the extent and underlying cause
management of pneumothorax
depends on size and severity.
some spontaneous
larger/ symptomatic: needle aspiration or CT insertion to evacuate air from pleural space and re expand lung.
Sx: video-assisted thoracoscopic surgery (VATS) for recurrent episodes.
what is pulmonary hypertension?
elevated blood pressure in pulmonary arteries, leading to increased resistance to blood flow through the lungs. defined by a mean PAP (mPAP) of 20mmHg or more at rest, measured by RHC.
causes of pHTN
genetic predisposition
connective tissue diseases
congenital heart defects
certain drugs or toxins
classes of pHTN
- pulmonary arterial hypertension
- PH due to left heart disease
- PH due to lung diseases and/or hypoxia
- chronic thromboembolic PH (CTEPH)
- PH with unclear multifactorial mechanisms
primary path of pHTN
vasoconstriction, vascular remodeling, thrombosis in situ within the small pulmonary arteries. leads to increases PVR and eventually right heart failure if left untreated
PH due to left heart disease is typically associated with conditions such as
heart failure with preserved or reduced EF, mitral valve disease, and other cardiac pathologies that increase left atrial pressure, subsequently elevated pressures in the pulmonary circulation
contributors of pHTN related to lung disease or hypoxia
and generally why these are problematic
COPD
interstitial lung disease
sleep apnea
living at high altitudes
-resulting hypoxic vasoconstriction and structural changes in the pulmonary vasculature lead to increases pressures
how does CTEPH occur?
from unresolved pulmonary emboli that cause mechanical obstruction of the pulmonary vasculature, necessitating surgical intervention or targeted medical therapy for management
s/s pHTN
DOE, fatigue, CP, syncope, edema
dx pHTN
echo
RHC
PFTs
CT or V/Q scans
management of pHTN
depend on underlying cause
endothelin receptor antagonist
phosphodiesterase-5 inhibitors
prostacyclin analogs
AC for CTEPH
address comorbidities
what is sleep apnea?
sleep disorder characterized by repeated interruptions in breathing during sleep. can last from a few seconds to minutes and may occur multiple times per hour.
excessive daytime sleepiness, loud snoring, observed apneas
most common form of sleep apnea
obstructive. occurs when muscles at back of throat relax excessively, causing airway blockage.
central sleep apnea
involves brain failing to send appropriate signals to muscles that control breathing.
why is sleep apnea significant in cardiac patients?
the repeated episodes of hypoxia and hypercapnia lead to SNS activation causing fluctuations in blood pressure and heart rate.
can exacerbate current cardiac conditions such as HTN, HF, afib, CAD
pathophysiology of OSA
collapse of pharyngeal muscles during sleep, leading to partial or complete airway obstruction. results in decreased airflow despite continued respiratory effort. resulting hypoxemia triggers arousal from sleep to restore normal breathing, fragmenting sleep architecture and reducing restorative sleep stages.
dx of sleep apnea
polysomnography (comprehensive recording of biophysiological changes during sleep)
measures parameters such as airflow, blood oxygen levels, heart rate, muscle activity
an apnea-hypopnea index (AHI) is calculated to determine the severity of the condition
management sleep apnea
lifestyle mod (weight loss, positional therapy)
CPAP (gold standard for OSA)
what is the endocrine system?
a complex network of glands and organs that produce, store, and secrete hormones. These hormones are chemical messengers that regulate various physiological processes, including metabolism, growth, development, tissue function, sexual function, reproduction, sleep, and mood.
hormones part of the stress response in the body
adrenaline (epinephrine)
noradrenaline (norepinephrine)
cortisol
