Hypoxemia
Abnormal low amount of O2 in blood
Hypoxia
Decreased oxygen at the tissue level
Hypercapnia
Abnormal high amount of CO2 in the blood
Hypoventilation
Decreased rate and depth of respirations
Hyperventilation
Increased rate and depth of respirations
Labored Respirations
General term for slow, deliberate breathing associated with airway obstruction
Tachypnea
Fast respiratory rate
Bradypnea
Slow respiratory rate
Normal V/Q ratio
0.8
Shunting
Blood is flowing but there is no ventilation because alveoli is blocked by something like a mucous plug
Dead Space
Alveoli is getting ventilated but there is a blood clot that is blocking perfusion
No ventilation but positive perfusion
Shunting
Positive ventilation but no perfusion
Dead Space
Normal arterial blood pH range
7.35 - 7.45
What is pH?
Indirect measurement of hydrogen ion (H+) concentration (acid).
What is PaO2?
Refers to pressure of dissolved oxygen in the arterial blood.
Normal PaO2 arterial range
80 - 100mmHg
What is PaCO2?
Refers to the pressure of dissolved carbon dioxide gas.
Think Respiratory!
Normal PaCO2 arterial range
35 - 45mmHg
What is HCO3?
The body’s main bicarbonate.
Regulated by the kidneys.
Normal HCO3 arterial range
22 - 26mEq/L
What does the Oxyhemoglobin Dissociation Curve respresent?
Hemoglobin’s affinity for oxygen or how readily hemoglobin picks up oxygen in the lungs and releases it into the tissues.
Left shift in the Oxyhemoglobin Dissociation Curve
Oxygen does not readily dissociate into the tissues, oxygen likes to stay with hemoglobin.
At risk for tissue hypoxia which can then lead to tissue ischemia and tissue necrosis.
Right shift in the Oxyhemoglobin Dissociation Curve
Decreased hemoglobin affinity to oxygen. Bohr Effect makes it hard for oxygen to bind to hemoglobin in the lungs.
This is an association problem that can cause sickle cell anemia.
Patho of Respiratory Acidosis
Carbonic acid excess, increased retention of CO2
Etiologies of Respiratory Acidosis
Hypoventilation
Respiratory depression from diseases, poisons, anesthetics
Airway obstruction
Alveolar-capillary blockage
Inadequate mechanical ventilation
Inadequate chest expansion
Clinical Manifestations of Respiratory Acidosis
Respiratory: First increased then decreased
Neurological: Headaches, tremors, lethargy, disorientation, muscle twitching
Complications: Convulsions, arrhythmias, coma
How does the body try to compensate during Respiratory Acidosis?
Kidneys excrete H+ and reabsorb HCO3 to get pH up
Risk for hypokalemia
Patho of Respiratory Alkalosis
Carbonic acid effect
Etiologies of Respiratory Alkalosis
Hyperventilation
Hypoxemia
Fear
Pain
Anxiety
Exercise
Brain Injury
Clinical Manifestations of Respiratory Alkalosis
Respiratory: Hyperventilation/tachypnea (then decreased respirations to compensate)
Neurological: Dizziness, confusion, muscle cramps, tetany
Complications: Dysrhythmias, convulsions, coma
How does the body try to compensate during Respiratory Alkalosis?
Kidneys reabsorb H+ and excrete HCO3 to get pH down
Patho and Etiologies of Metabolic Acidosis
Increase in Acid: Inadequate elimination of H+ ions (Renal Disease), and excess production of H+ ions (DKA)
Decrease in Base: Inadequate production of HCO3 (Renal Disease), and excess elimination of HCO3 (diarrhea)
Clinical Manifestations of Metabolic Acidosis
Respiratory: Tachypnea
Neurological: Headache, confusion, lethargy (potassium shifts)
Complications: Coma, ventricular dysrhythmias, hyperkalemia
What does the body try to do to compensate during Metabolic Acidosis?
Lungs eliminate CO2 (Kussmaul)
Kidneys reabsorb HCO3 and excrete H+
Patho and Etiologies of Metabolic Alkalosis
Increase in Base: Ingesting bicarb
Decrease in Acid: NGT suctioning, vomiting
Clinical Manifestations of Metabolic Alkalosis
Respiratory: Hypoventilation to retain CO2
CNS: Skeletal muscle weakness, confusion, muscle cramps
Cardiac: Tachycardia
Complications: Dysrhythmias, convulsions, hypokalemia
What does the body try to do to compensate during Metabolic Alkalosis?
Lungs retain CO2 (slow breathing)
Kidneys reabsorb H+ and excrete HCO3
What is Asthma?
Chronic inflammatory disorder of the airways.
Patho of Asthma
Immune activation of IgE, mast cell degranulation, chemotactic mediators, leukotrienes and histamine, inflammatory response, vasodilation, increased capillary permeability, bronchospasm, vascular congestion, bronchial hyperresponsiveness
Etiologies of Asthma
Allergen
Irritant exposure
Risk Factors: Obesity, GERD, chronic viral infection
Clinical Manifestations of Asthma
Expiratory wheezing
Dyspnea
Chest tightness
Non-productive cough (the body’s way of trying to open up the airway)
Tachypnea
Tachycardia
Complications of Asthma
Hypoxemia
Status asthmaticus → severe bronchoconstriction
High risk for developing COPD
What is Chronic Bronchitis?
Chronic inflammatory response from inspired irritants
Patho of Chronic Bronchitis
Chronic inflammation of airway, increase mucous production from goblet cell hyperplasia and hypertrophy, impaired ciliary function, hypertrophy and narrowing of airways, airway obstruction
Etiologies of Chronic Bronchitis
History of smoking
Occupation exposure to toxins
Disrupted lung growth
Clinical Manifestations of Chronic Bronchitis
Productive cough (smoker’s cough, wet sounding)
Dyspnea
Wheezing
Cyanosis
Polycythemia (increase in red blood cells)
Cor Pulmonale (can lead to right sided heart failure, right ventricular enlargement)
Complications of Chronic Bronchitis
Pulmonary Hypertension
Right sided heart failure
Cor Pulmonale
What is a Pulmonary Edema?
Excess fluid in the lungs
Patho of a Pulmonary Edema
Increased left atrial pressure, increased pulmonary hydrostatic capillary pressure → edema
Injury to capillary endothelium, increased capillary permeability → edema
Blockage of lymph vessels, inability to remove fluid from interstitial space → edema
Etiologies of a Pulmonary Edema
Left sided heart failure (MOST COMMON CAUSE)
Capillary endothelium injury, alveolar capillary membrane damage
Lymph vessel blockage (tumor or scar tissue)
Clinical Manifestations of a Pulmonary Edema
Dyspnea at rest
Anxiety
Inspiratory crackles
Tachycardia
Disorientation and confusion (from lack of oxygen to the brain and buildup of CO2)
Pink frothy sputum (from irritation)
Hypoxemia
What is a Pulmonary Embolism?
Occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or an air bubble.
Patho of a Pulmonary Embolism
Virchow triad, thrombus formation, embolus, occlusion, hypoxic vasoconstriction, pulmonary edema and atelectasis
Etiologies of a Pulmonary Embolism
DVT: Deep vein thrombosis
Virchow Triad: Venous stasis, hyper-coagulability, and injuries to the endothelial cells that line the vessels
Clinical Manifestations of a Pulmonary Embolism
Sudden onset of pleuritic pain
Dyspnea
Tachycardia
Tachypnea
Fever
Present grey in color
Most of the time, O2 stat is less than 90%
Complications of a Pulmonary Embolism
Cor Pulmonale
Pulmonary Infarction
What is Atelectasis?
Collapse of lung tissue
Patho of Atelectasis
Alveoli lack full inflation, buildup of secretions, collapse of alveoli, reduced gas exchange
Etiologies of Atelectasis
Obstruction of airway (by something like a mucous plug or food)
Hypoventilation from pain (inadequate surfactant production)
Compression of the lung or bronchi (by tumors, aneurysms, or enlarged lymph nodes)
Clinical Manifestations of Atelectasis
Dyspnea
Diminished breath sounds on that side
Productive cough (from secretions)
Fever (from inflammation and possible infections from the secretions)
Leukocytosis
Complications of Atelectasis
Can lead to pneumonia and hypoxemia
What is Emphysema?
Abnormal permanent enlargement of the gas-exchange airways after exposure to irritants.
Patho of Emphysema
Inflammation of airway epithelium (from smoking) or inherited alpha antitrypsin deficiency, bronchiole wall collapse, destruction of alveolar walls, loss of elastic recoil, air trapping, bullous bleb formation, decreased gas exchange
Etiologies of Emphysema
History of smoking
Alpha antitrypsin deficiency (inherited disorder)
Occupation exposure
Clinical Manifestations of Emphysema
Dyspnea
Wheezing
Barrel Chest
Club fingers
Use of accessory muscles
Complications of Emphysema
Cor pulmonale
Modifiable Risk Factors of Hypertension
High sodium diet
Glucose intolerance
Anemia
Obesity
Smoking
Heavy alcohol use
Non-modifiable Risk Factors of Hypertension
Family history
Advancing age
Gender: females over age 55 and males over age 74
Black Race
CAD Modifiable Risk Factors
Dyslipidemia
Hypertension
Cigarette smoking
Diabetes Mellitus
Obesity/sedentary lifestyle
Atherogenic diet (high fat and meat)
CAD Non-modifiable Risk Factors
Increased age
Family history
Gender
What is Myocardial Ischemia?
Local or temporary deprivation of the coronary blood supply
Patho of Myocardial Ischemia
Myocardial O2 deficit from decreased blood supply, impaired pumping, glucose deprivation = anaerobic takeover, decreased cardiac output, blood flow restored <20 minutes, contractility and aerobic metabolism return to normal
Etiologies of Myocardial Ischemia
Uncontrolled atherosclerosis
Coronary Spasm
Anemia
Clinical Manifestations of Myocardial Ischemia
Stable Angina: Chest pain with exercise or stress relieved by rest, uncontrolled atherosclerosis
Prinzmental Angina: Chest pain unpredictable, not related to exercise or stress, vasospasm of coronary artery.
Silent Ischemia: No chest pain but fatigue, dyspnea, uneasy feeling, slight disorientation, sometimes feel “butterfly in the chest”, left ventricular sympathetic intervention
What is Artherosclerosis?
A form of arteriosclerosis, tends to develop in medium and large sized arteries.
Patho of Artherosclerosis
Injury and inflammation of endothelium, cellular proliferation, macrophages migration, LDL oxidation, fatty streak, fibrous plaque, complicated plaque
Etiologies of Atherosclerosis
Smoking
Diabetes
Hypertension
Hyperlipidemia
Obesity
Clinical Manifestations of Atherosclerosis
Initially asymptomatic
Angina
TIA (transient ischemic attacks)
Intermittent claudication
Patho of Left Sided Heart Failure
Decreased contractility causes SV to fall and LVEDV increases → Dilation
Aortic pressure falls and systemic arterial pressure drops, baroreceptors sense a drop, activates SNS and ADH released, increase in preload and afterload
Kidneys sense a drop in blood flow, activation of RAAS, increase PVR, increase in preload and afterload
Elevated hydrostatic pressure into pulmonary system, pulmonary edema
Etiologies of Left Sided Heart Failure
CAD (coronary artery disease)
Myocardial infarction (remodeling)
HTN; Pulmonary HTN
Valve disease
CKD (chronic kidney disease)
Anemia
Hyperthyroidism
Clinical Manifestations of Left Sided Heart Failure
Dyspnea
Orthopnea
Frothy Sputum (pink tinged)
Fatigue
Decreased urinary output
Edema
Abnormal heart sounds (S3 gallop)
Pulmonary congestion (crackles)
Patho of Right Sided Heart Failure
Increased pulmonary vascular resistance, increased force of RV contraction, increased RV O2 demand and RV enlargement and increase in RV preload
Decrease O2 supply, RV hypoxia, decreased force of RV contraction, increased RV and RA preload, peripheral edema
Etiologies of Right Sided Heart Failure
Left sided heart failure
Increased pulmonary vascular resistance (cause RV to work against the resistance)
ARDS
COPD
Clinical Manifestations of Right Sided Heart Failure
Peripheral edema
Ascites
JVD
Hepatomegaly (enlargement of the liver)
Nocturia
Weight Gain
What is Pericarditis?
An acute inflammation of the pericardium after an MI.
Etiologies of Pericarditis
Idiopathic
Viral
Autoimmune
Post MI
Clinical Manifestations of Pericarditis
Fever
Tachycardia
Chest pain
Pericardial friction rub
Hypotension
ECG changes
What is HTN?
(Hypertension) Consistent elevation of systemic arterial blood pressure
Patho of HTN
Dysfunction of SNS, RAAS, or natriuretic hormones, vasoconstriction, renal Na+ and H2O retention, increased peripheral resistance, increased blood volume, sustained HTN
Risk Factors/Etiologies of HTN
Primary: 92% - 95% of cases, gradual development, idiopathic
Secondary: Underlying disorders like kidney disease, thyroid problems, and some endocrine problems
Clinical Manifestations of HTN
Headache (most common)
Fatigue
Impaired Vision
Decreased urine output
Dizziness
Epistaxis (nose bleeds)
Flushed Face
What is a Myocardial Infarction?
Death of cells in the myocardium, related to prolonged or severe ischemia lasting longer than 20 minutes.
Non-STEMI: Not full thickness, not as bad, easier to recover from
STEMI: Full thickness (transmural)
Patho of Myocardial Infarction
O2 deprivation for longer than 20 minutes from obstruction of a coronary artery, cellular loss of K+, Ca+, Mg+, decreased pumping ability, loss of contractility
Angiotensin 2 released, peripheral vasoconstriction fluid retention, increased myocardial work
Catecholamine release, coronary artery spasm
Etiologies of Myocardial Infarction
Uncontrolled atherosclerosis
CAD
Renal Disease
Uncontrolled type 2 diabetes
Clinical Manifestations of Myocardial Infarction
Sudden severe chest pain (for women it can radiate to the jaw and down the arm)
Nausea and vomiting
Diaphoresis
Cool clammy skin
Elevated troponins, CK - MB (creatine kinase, myocardial bands)
EKG changes
Complications of Myocardial Infarction
Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical instability
Cardiogenic shock
Pericarditis
Pericardial Tamponade
What is posturing
An abnormal motor response to a painful stimuli
Decorticate
Flexion of arm, wrists, and fingers with adduction in the upper extremity and extension, internal rotation, and plantar flexion of lower extremity.
Decerebrate
Indicative of a more severe brain injury.
Opisthotonos (hyperextension of vertebral column) with clenching of teeth, extension, abduction, and hyperpronation of arms with extension of lower extremities.