Clinical Pathophysiology Exam 2

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

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.