Path physio #2

hypoxemia v hypercapnia

1. hypoxemia is when there is low levels of oxygen and that means tissues can not undergo aerobic metabolism meaning there is no atp for the cells and the Na/K/atpase pump fails and the cells swell and die

2. Hypercapnia- elevated levels of CO2 in the blood means that the arterial blood is going to become more acidic and be acidosis

what three dysfunction can occur to cause hypoxia

problem in ventilation, diffusion, and perfusion

hypercapnia occurs with

decreased ventilation, co2 is more soluble as it diffuses 20 tx faster across the respiratory membrane- less affected by perfusion or diffusion of tissues and CO2 removal is more a matter of getting the CO2 out of the aveoli

overall disease that impair ventilation can cause hypercapnia

affects of hypercapnia and respiratory acidosis

• decrease contractability

• systemic vasodilation (decrease SVR)

• agitates nodal cells causing arrhyrhmias (means contractions are no longer efficient)

• in the CNS: edema which raised intracranial pressure can cause CNS depression, somnolence, coma

disease that disrupt ventilation

• extrapulmonary causes

• pnemothorax

• pleural effusions

• restrictive lungs disease (surfactant disorder and pulmonary fibrosis)

• obstructive (COPD, asthma)

inhalation relies on (how do we ventilate)

requires our skeletal muscle contraction (active process) on inhalation the diaphragm and intercostal muscles contract to increase cavity and that means the cavity pressure is less than atmospheric and air move into lungs

the negative intrapleural pressure keeps the lung expanded

the lung compliance meant that the elastin fibers with the help of surfactant allow for expansion

exhalation

passive process and the recoil from the elastic fibers will and relaxation from the diaphragm and intercoastal muscles cause the cavity volume to lower and the pressure becomes greater than atmospheric and cause air out of the lungs

what factors determine the alveolar ventilation rate

AVR= RR x (tidal volume-dead space) dead space is where no gas exchange occurs normally the only dead space is in the conductive pathways of our pulmonary tree

some diseases disrupt the ability of the alveoli to facilitate gas exchange, thus increase our dead space

How the CNS and neuromuscular disorders disrupts ventilation v. anatomic causes

• decreased respiration drive (brain does not tell muscle to inhale can be caused by drugs opiates or CNS trauma or infection

• disease of the NMJ or respiratory muscles (nerves can not communicate with muscle of inhalation) ex is myasthenia gravis

• Chest wall disorders: kyphoscoliosis, rib fractures-splitting due to pain

• obesity: causes hypoventilation syndrome

pneumothorax

air in pleural space and the Prescence of the air increase the intrapleural pressure (needs to be negative to adhere to the chest wall) the air makes the pressure positive and this means tidal volume will decrease (how it decrease ventilation)

how does air get into the pleural space

• primary spontaneous pneumothorax: occurs without underlaying lung disease most often tall young men. they grow to rapidly and the tissue is thin and they create bleb due to the shearing forces of inhalation and exhalation- blebs are weak and at risk for rupture under high

• secondary spontaneous pneumothorax: occurs in individuals due to underlaying lung disease- common in obstructive lung disease- hyperinflation cause bullae formation- at risk for rupture. Could also be due to lung cancer (destruction of tissue)

traumatic pneumothorax

•displaced rib fracture “pokes” hole in lung

•inspired air leaks into pleural space from the lung

why does pneumothorax cause pleurtic pain

because there is more air pleural space meaning there is more friction and that causes the pain when inhalation and the lungs are expanding

tension pneumothorax

occurs as a result of continuous rise of intrapleural pressure, leads to complete lung collapse the increase pressure pushes on structures in the thoracic cavity causes mediastinal shift and tracheal deviation and the heart and great vessels will become compressed and decrease venous return and stroke volume leading to hypotension

pleural effusion

fluid in the pleural space and inhibits the alveolar expansion to alveolar collapse (atelectasis)

2 major categories:  transudative and exudative 

• transudative: occur due to the imbalance of filtration and reabsorption in the pulmonary capillaries. fluid flows into the pleural space due to an imbalance of pressure in the capillary bed, favoring filtration so either:

  • increased hydrostatic pressure- acute pulmonary hypertension- CHF

  • decreased osmotic pressure: decrease albumin can be from kidney or liver disease (liver makes albumin or kidney loss in urine)

• Exudative: excess water, cells, and protein flowing OUT of the pulmonary capillaries. Increased capillary permeability due to inflammatory response: infections, lung cancer, and uremia (CKD)

disrupted ventilation: restrictive lung disease

characterized by decrease lung compliance and means it decrease the tidal volume two ways that the lung compliance can be reduced:

1. elastin- when it is replaced with stiff connective tissue- occurs with lung injury or scarring occurs with chronic inflammation of lung tissue (post ARDS, autoimmune, toxic)

2. surfactant- reduced alveolar surface tension to allow for expansion and prevent collapse- reduce surfactant production. surfactant production begins at 24 weeks so born premature= respiratory distress

obstructive lung disease

Characterized by airway obstruction, especially with exhalation.

•leads to common symptom of wheezing

•turbulent, obstructed air flow during exhalation

•leads to air trapping

•incomplete exhalation leaves CO2 rich air stuck in the alveoli, leading to:

•hyperinflation

•hypercapnia

how does obstructive lung disease cause a decrease in TV

continuous air trapping mean there is no room for subsequent breaths and you will see an inspiratory reserve volume

most common from chronic smoke inhalation:

2 types pf COPD: chronic bronchitis: bronchial inflammation and mucus production and emphysema- alveolar destruction

how does COPD lead to chronic bronchitis

a mucus problem

chronic inflammation and irritation of bronchioles- more bigger glands +ciliary damage- bronchial endothelial thickening+ excessive mucus production and retention- airway obstructive. Airway obstruction disrupts ventilation (tidal volume is reduced due to increase resistance to air flow in and out and air trapping leads to hyperinflation and reduced capacity for inhalation - hypercapnia. Damage to the mucociliary defense reduced clearance of pathogens increase risk of pulmonary infection

emphysema

a structural problem

normally resident alveolar macrophages phagocyte pathogens and irritant and release protease that help destroy pathogens but also break down collagen and elastin- in emphysema the chronic irritant exposure leads to increase protease production and results in destruction of alveolar tissue

alpha 1 antitrypsin deficiency

1. alpha 1 antitrypsin: protease inhibitor, synthesized by hepatocytes

2. alpha 1 antitrypsin deficiency: genetic disorder and deficiency in AAT= protease > antiprotease

results in a significant increase risk of emphysema, even with limited exposure to air pollutants

emphysema affects

destroy the septa of the alveoli and that reduces the surface area and increase the dead space. Also elastin destruction (protease) impairs ability to recoil and leads to air trapping, decrease tidal volume

why might a patient with COPD have polythemia

(increase in RBC) is a physiologic adaptation to chronic hypoxia