Pathophysiology - Exam 2

Varicose veins

A vein in which blood has pooled

Distended, tortuous, and palpable veins

Caused by trauma or gradual venous distention

Risk factors: Age, Female gender, Family history, Obesity, Pregnancy, Deep vein thrombosis, Prior leg injury

Stroke volume

(blood ejected by the left ventricle)

Amount of blood ejected with each heartbeat

Preload

Amount of stretch before contraction/ diastole

Decreased: Diuresis, Vasodilating agents (nitrates), Blood loss, Dehydration

Increased: IV fluids/ blood products, Control of blood loss

Afterload

Inverse relationship to stroke volume

Amount of resistance ventricle must overcome to eject blood

affected by systemic vascular resistance, pulmonary vascular resistance

Decreased: Mitral regurgitation, Vasodilation, Nitrates, ACE/ ARB inhibitors

Increased: HTN, Aortic stenosis, Aortic regurgitation, Systemic vascular resistance

Chronic Venous Insufficiency (CVI)

veins in the legs are not able to return blood to the heart leading to a buildup of blood and pressure

Symptoms: swelling, pain and skin changes in the lower extremities

Post thrombotic syndrome is a type that develops after a deep vein thrombosis (DVT)

Symptoms: Edema, skin changes, pain, stasis dermatitis

Stasis ulcers can be common

Lower extremity is a common place that ulcers are seen (area of medial malleolus)

Skin becomes dry, cracks and itches

Primary or essential HTN

Unknown cause

Secondary

Systemic disease process raises peripheral vascular resistance or cardiac output

Hypertension

Consistent elevation of systemic arterial blood pressure

Sustained systolic blood pressure of 130 mm Hg or greater or a diastolic pressure of 80 mm Hg or greater

Pathophysiology of HTN

1. Activation of RAAS

-Retention of sodium & water increases vascular resistance

2. Vascular remodeling

-Change in vessel walls permanently increases PVR

3. Kidneys activate SNS

-Increase in HR & systemic vasoconstriction increase in cardiac output & PVR

4. Inflammatory response

-Chronic inflammation damage to endothelial cells increase in SNS activation, vascular remodeling, smooth muscle contraction

5. Obesity & Insulin resistance

-Insulin resistance decrease in endothelial release of vasodilators & increase in retention of water and salt

Hypertension: Clinical Manifestations

“Silent killer”

Clinical manifestations are specific fir the organs/ tissues affected

Retinal damage, renal insufficiency/ failure, microalbuminuria

Microalbuminuria is an early stage of impending kidney damage

Complications of HTN untreated: CAD, chest pain, MI, stroke, HF

Treatment: Medications, Lifestyle modifications, Blood pressure control, diabetes control, lipid control

Masked hypertension

Blood pressure that is suggestive of hypertension that is paradoxically normal in health care settings

White coat hypertension

Hypertensive blood pressure readings in the health care setting that is paradoxically normal ranges in other settings

Hypertensive Urgency

Oral agents can be administered with the goal of normalizing blood pressure within 24 to 48 hours

Fast-acting oral agents: Beta-adrenergic blocker—labetalol, Angiotensin-converting enzyme inhibitor—captopril, Alpha2-agonist—clonidine

Patient requires close monitoring of blood pressure and cardiovascular status

Assess for potential evidence of target organ damage

Hypertensive Emergency

Caused by med non-compliance, stopping BB, adrenal glands, etc.

Caused Manifestations - >180/>120, HA, Blurry vision, confusion, nosebleed

Reduce blood pressure by no more than 25% in first hour

Reduce to 160/100 mm Hg within 2 to 6 hours, Then gradual reduction to normal 24 to 48 hours of treatment

Exceptions are ischemic stroke and aortic dissection

Medications - IV vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin

Need very frequent monitoring of BP and cardiovascular status

Orthostatic (postural) hypotension

Decrease in both systolic and diastolic blood pressure upon standing

Lack of normal blood pressure compensation in response to gravitational changes on the circulation

Atherosclerosis

Chronic, inflammatory disease of the arterial walls.

Accumulation of cholesterol & immune cells build up and form plaques that narrow & harden the arteries

Risk factors: diabetes, smoking, hyperlipidemia/dyslipidemia, hypertension, autoimmunity

Causes: Endothelial injury, LDL oxidation & inflammation, Foam cell formation, Plaque formation, Plaque rupture & thrombosis

Atherosclerosis: Clinical Manifestations

Complete health history including risk factors and symptoms of ischemia

Arterial bruit

Lipids, blood glucose, high sensitivity CRP

ECG, CT, MRI angiogram

Management: Prevention, detection & treatment

Statins

If lesion obstructs blood flow, the goal is reperfusion

Results in—inadequate perfusion, ischemia, necrosis

Coronary Artery Disease (CAD)

Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia

Atherosclerosis is the most common cause

Primary cause of heart disease in U.S.

Risk factors:

Modifiable: Dyslipidemia, Hypertension, Cigarette smoking, Diabetes mellitus and insulin resistance, Obesity/sedentary lifestyle, Atherogenic diet

nonmodifiable: Advanced age, Male sex or female post-menopause, Family history

statins

a class of medications used to lower cholesterol levels in the blood. They work by blocking the production of cholesterol in the liver, which helps to reduce the risk of cardiovascular diseases such as heart attacks and strokes. Lower levels of LDL but do not raise HDL

Myocardial Infarction

Cell death/ necrosis

Same pathophysiology as unstable angina with the exception that the thrombus causes complete blockage of blood flow

Myocardial cells that are deprived of O2 lose contractility less pumping by the heart decrease cardiac perfusion

Characterized as STEMI & NSTEMI

CPK-MB & Troponin

Functional impairment depends on the size of the damage and site of infarction

Functional changes: Decreased cardiac contractility, altered left ventricle compliance, decrease stroke volume, ejection fraction, SA node malfunction, increased LVEDP

Clinical manifestations: Chest pain, Heavy, crushing, truck/ elephant sitting on my chest, Radiating pain, Neck, jaw, back, shoulder, left arm, Silent MI, Diabetics d/t microvascular changes d/t uncontrolled blood sugars, N/V/ GERD

Physical examination: Tachycardia, hypertension, murmurs, crackles, skin is cool and clammy

Initial Management: MONA

Morphine

Supplemental O2

Nitro

Aspirin

Cath lab for PCI

Thrombolytics

Pericarditis

Acute inflammation of the pericardium

Inflammation of the pericardium release of inflammatory cytokines

Causes: viral infections, MI, trauma, neoplasm, TB, SLE, RA, radiation, pacemaker insertion

Symptoms: fever, chest pain worsens with respirations, laying flat, radiating pain to the back, anxiety, weakness, fatigue

Physical evaluation: tachycardia, friction rub (cardiac apex & left sternal border)

Pericardial Effusion

Fluid in the pericardial space

Same causes as pericarditis

Pericardiocentesis

Complication: Cardiac tamponade

Cardiac Tamponade

Severe cardiac output loss

Pulsus Paradoxus: Arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10mmHg, Muffled heart sounds, Pericardiocentesis or pericardial window

Cardiomyopathies

Enlarged heart (myocardium)

Characterized by physiologic effects on the heart: dilated, hypertrophic, or restrictive

Dilated Cardiomyopathy

pumping problem

Most common

Left ventricle is dilated & dysfunctional (systolic dysfunction)

Causes: ischemic heart disease or valvular disease

Signs: dyspnea, fatigue, edema

Physical exam: displaced apical pulse, murmur, jugular vein distention, pulmonary congestion

Imaging: shows ventricular dilation

Management: Same as HF & prevent dysrhythmias

Hypertrophic Cardiomyopathy

Most common inherited cardiac disorder

Autosomal dominant

Left ventricle is hypertrophied with thickening of the septal wall

Cause of sudden death in athletes

Diagnosed after development of symptoms: Palpitations, exercise intolerance, syncope, heart murmur, abnormal ECG

Dx: echocardiogram, genetic testing

Avoid high- intensity sports; medications to decrease workload on the heart (calcium channel blockers, & beta blockers), cardioverter defibrillator

Restrictive Cardiomyopathy

Difficulty filling & increase in diastolic pressure

Normal pumping & normal ventricular wall thickness

Myocardium is rigid and non-compliant impairs ventricular filling diastolic dysfunction reduction in ejection fraction heart failure

Monitor for dysrhythmias

Valvular stenosis

Aortic stenosis

Mitral stenosis

valve orifices become constricted & narrowed → blood is unable to flow forward

Valvular regurgitation

Aortic regurgitation

Mitral regurgitation

Mitral valve prolapse (MVP)

Tricuspid regurgitation

valve leaflets do not close completely → blood leaks back → increases volume of blood → heart needs to pump harder, workload increases

Aortic Stenosis:

stenosis of the aortic valve (left ventricle to aorta)

Orifice of the valve narrows → causing resistance → to blood flow from LV to aorta

Most diagnosed valvular disease

Causes: congenital bicuspid valve

Rheumatic heart disease

Degeneration with age

Symptoms: angina, syncope, dyspnea

Mitral Stenosis

stenosis from the left atrium → left ventricle

Elevated atrial pressure

Symptoms: dyspnea, exercise intolerance, pulmonary hypertension, pulmonary edema &RHF

Aortic Regurgitation:

inability of the aortic valve to fully close during filling (diastole) → volume overload in the left ventricle → dilation of ventricle to compensate → ventricle dilates → HF

Symptoms: murmur, dysrhythmia

Mitral regurgitation

inability of the mitral valve to fully close causing backflow of blood from the left ventricle into the left atrium during ventricular systole (contraction) →dilation of left atrium & ventricle → HF

Symptoms: murmur

Mitral Valve Prolapse (MVP)

mitral valve cusps billow upward into left atrium during systole

most common valve disorder caused by degeneration of leaflets

symptoms: palpitation, tachycardia, chest pain, syncope, fatigue

may hear a murmur, many patients do not need an intervention

Rheumatic Fever

Systemic inflammatory disease caused by a delayed autoimmune response to infection by group A β-hemolytic streptococcus (GAS) that affects the joints, skin, nervous system & heart

It is a complication of untreated strep throat

Damages heart valves (most common is mitral valve)

Symptoms: fever, lymphadenopathy, N/V, abdominal pain & tachycardia

Hallmark diagnostic features: occur 1-5 weeks after GAS infection

Carditis: murmur, CP, pericardial friction rub, valvular dysfunction

Polyarthritis: affecting large joints. Heat, redness & swelling

Chorea: involuntary. Jerky movements of face/ limbs d/t CNS involvement

Erythema marginatum: rash on the trunk

Subcutaneous nodules: over bony prominences

Treatment: Antibiotics, NSAIDS, Steroids, Diuretics

Infective Endocarditis

Infection/ inflammation of the endocardium (cardiac valves)

Causes: bacteria

Streptococci, staphylococci, enterococci

Risk factors: trauma, congenital heart disease, valvular heart disease, prosthetic valve, dental procedures, IV drug users, poor oral hygiene

Patho: endocardial damage from risk factors → inflammatory reaction that exposes collagen & tissue factors underneath the endothelium → formation of small sterile clots (platelets + fibrin) → encounter with bacteria → bacteria adheres to the clot on the damaged endocardium → bacteria multiply & form vegetation

Findings: Fever, cardiac murmur, petechial lesions on skin, conjunctiva or oral mucos 

blood flow through the heart

(1) Deoxygenated blood enters the right atrium from the vena cava, (2) passes through the tricuspid valve, (3) into the right ventricle, (4) then through the pulmonary valve into the pulmonary artery to the lungs, (5) where it gets oxygenated, (6) and returns to the left atrium via the pulmonary veins, (7) through the mitral valve into the left ventricle, (8) which pumps it through the aortic valve into the aorta

Heart Failure

Inability to generate cardiac output causing inadequate perfusion of tissues

Causes:

Impaired contractility: MI, CAD ischemia, dilated cardiomyopathy

Increase afterload (pressure afterload): HTN, aortic stenosis

Increase in preload: aortic regurgitation, mitral regurgitation

Restricted filling: restrictive cardiomyopathy

Arrhythmias: tachycardia (reduced filling time) bradycardia (decreased CO)

Most often left ventricle dysfunction

HF can be classified in multiple ways:

Which side is affected? Right vs. left

Which part of the cardiac cycle is affected? Systolic vs. diastolic

Right Sided HF

Viscera and peripheral congestion, Jugular venous distention (JVD), Dependent edema, Hepatomegaly, Ascites, Weight gain

Inability of right ventricle to provide adequate blood into the pulmonary circulation (Blood going to the heart to be oxygenated)

Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation

If left sided heart failure is not the culprit, it is then pulmonary disease: COPD, cystic fibrosis or ARDS

Pulmonary hypertension

Left Sided HF

Pulmonary congestion, crackles, S3 or “ventricular gallop”, Dyspnea on exertion (DOE), Low O2 sat, Dry, nonproductive cough initially, Oliguria

Left sided HF can cause Right sided HF

When left ventricle weakens, it cannot pump blood out of the body→ pressure builds up and forces blood and fluid back into the left atrium and into the lungs→ increase fluid in the lungs makes it more difficult for the right ventricle to pump blood into pulmonary arteries→right ventricle needs to work harder and over time, the right ventricle weakens and loses its ability to work effectively

Stable angina

a type of chest pain that occurs when the heart muscle does not receive enough oxygen. It is typically caused by a narrowing of the coronary arteries, the blood vessels that supply the heart with oxygen. 

• Occurs during physical activity or emotional stress

• Relieves with rest or nitroglycerin

• Is described as a tightness, squeezing, or pressure in the chest

• May spread to the left arm, shoulder, neck, or jaw

unstable angina

a type of chest pain that occurs when the heart muscle does not receive enough oxygen. It is a serious condition that can lead to a heart attack. Chest pain that is new, worsening, or occurs at rest

• Pain that may radiate to the arm, neck, jaw, or back

• Shortness of breath

• Nausea

• Sweating

• Palpitations

Hydrostatic pressure

“PUSHES” water and solutes out of the capillaries into interstital space

Promotes filtration

Oncotic pressure

“PULLING” pulls water into the capillaries from the interstitial space

Promotes reabsorption

Type of osmotic

Albumin

Osmotic pressure

“PULLING” of water between intracellular & extracellular based on solute concentration

Involves ALL solutes

HYPOVOLEMIA

Loss of extracellular fluid exceeds intake ratio of water

Electrolytes lost in same proportion as they exist in normal body fluids

Fluid Volume Deficit & Dehydration are different

Dehydration: Loss of H20 alone & increase in serum sodium levels because the ratio of sodium to water changes (higher)

Leads to hypernatremia

Increased serum osmolality

causes: Hemorrhage, GI loss (V/D/NG suction), Third spacing (burns), Excessive diuretics

Findings: Weight loss, Dry mucus and skin membranes, Decreased urine output, Rapid heart rate, Flattened neck veins, Normal or a decrease in blood pressure, tachycardia, low BP, dry, weight loss

Treatment: Fluid replacement c isotonic solution, 0.9%NS, Lactated Ringer, D5NS

Dehydration

A lack of fluid in the body, from insufficient intake or excessive loss

Causes: Hyperventilation or excessive perspiration without water treatment, Prolonged fever, Diabetic ketoacidosis & Diabetes insipidus, Insufficient water intake (enteral feeding without water administration, decreased thirst sensation, aphasia), Excessive intake of salt, salt tablets, or hypertonic IV fluids

Hypervolemia

involves an excess of water and electrolytes, so that the two are still in the right proportions. For example, excessive sodium intake causes the body to retain water

Clients who have fluid overload are at risk for developing pulmonary edema or congestive heart failure.

In older adult clients, the risk of fluid imbalance is greater due to changes in the body with age (such as reduced kidney function).

Causes of hypervolemia: Compromised regulatory systems (heart failure, kidney disease, cirrhosis), Overdose of fluids (oral, enteral, IV), Prolonged use of corticosteroids, Sodium retention with steroid use, Severe stress, Excessive cortisol, Hyperaldosteronism

Causes of overhydration: Water replacement without electrolyte replacement, excessive water intake (psychogenic polydipsia), Syndrome of inappropriate antidiuretic hormone (SIADH), Excessive administration of IV D5W; use of hypotonic solutions for irrigations

Fluid volume overload s/s

VITAL SIGNS: Tachycardia, bounding pulse, hypertension, tachypnea, increased central venous pressure

NEUROMUSCULAR: Weakness, visual changes, paresthesias, altered level of consciousness, seizures (if severe, sudden hyponatremia/water excess)

GASTROINTESTINAL: Ascites, increased motility, liver enlargement

RESPIRATORY: Crackles, cough, dyspnea

OTHER SIGNS: Peripheral edema due to an excess of fluids within the body and lungs, resulting in weight gain, distended neck veins, and increased urine output, skin cool to touch with pallor, weight gain

HYPERnatremia

Serum sodium > 145 mEq/L

Increase in serum sodium= hypertonicity (solution with lots of solutes)

Will see central nervous system signs

Urine specific gravity is high

HYPOnatremia

Serum sodium is less than 135

Causes: loss of sodium, inadequate intake of sodium, dilutional d/t excess fluids

Loss of sodium= decrease in osmolality

Water moves into the cells because the cells have higher solute than ECF

Clinical manifestations:

severe deficit= 120 or less

Between 125-130 will see N/V

Below 125 will see severe neurologic symptoms: lethargy, headache, confusion, seizures & coma

Treatment: find underlying cause; treat with hypertonic solution

* Avoid giving it too fast as it can cause osmotic demyelination syndrome= brain cells shrink & myelin sheath is destroyed

Management of hypoNatremia

If the client can tolerate PO fluids, sodium can be easily replaced by intake of foods and fluids. Encourage foods and fluids high in sodium (beef broth, tomato juice).

Administer IV fluids

Severe NA < 120: treat with Hypertonic solution

Replacement of sodium should not occur rapidly because rapid rise in sodium level risks development of neurologic damage due to demyelination.

For fluid overload, restrict water intake as prescribed.

Monitor I&O and daily weight.

Monitor vital signs and level of consciousness. Report abnormal findings to the provider.

Weigh daily and notify the provider of a 1- to 2-lb gain in 24 hr, or 3-lb (1.4 kg) gain in 1 week.

Management of hyperNatremia

Monitor level of consciousness/ CNS changes and ensure safety.

Monitor vital signs and heart rhythm.

Fluids: Hypotonic solution

Auscultate lung sounds

Fluid overload

Provide oral hygiene and other comfort measures to decrease thirst.

Monitor I&O and alert the provider of inadequate urinary output.

Gradual lowering of serum sodium level via infusion of hypotonic electrolyte solution

Diuretics

Loop diuretics

Assessment for abnormal loss of water and low water intake

Assess for over-the-counter sources of sodium

HYPOkalemia

Serum potassium is less than 3.5

Causes: decrease in potassium intake, K moving into the cells, increase loss of potassium (e.g. hyperaldosteronism), GI upset (N/V/D), CKD, NG suction on continuous, Potassium- wasting diuretics (loop diuretics & thiazides), excessive aldosterone secretion, Low plasma magnesium

Clinical manifestations: neuromuscular excitability decreases– skeletal muscles become weaker, smooth muscles atony, cardiac dysrhythmias, glucose intolerance

Correct underlying issue, increase potassium in the diet, eat potassium rich foods

Hypokalemia concurrent with hypomagnesemia is refractory to treatment until magnesium levels are corrected because hypomagnesemia can enhance renal potassium excretion.

HYPERkalemia

K level over 5.5 mEq/L

Causes: Kidney unable to excrete K+, excess intake, Medications

Clinical manifestations: narrow & tall T waves, restlessness, cramping & diarrhea

Severe: muscle weakness, loss of muscle tone & paralysis

Treatment: treating the underlying cause & correcting potassium, calcium gluconate (decrease the threshold potential), administer glucose → insulin is secreted → pushes potassium back into the cell– (monitor for hypokalemia)

Administer kayexalate- which binds potassium & helps excrete it– will see diarrhea** or constipation

Clinical manifestations for hypokalemia

VITAL SIGNS: Decreased blood pressure, thready weak pulse, orthostatic hypotension

NEUROLOGIC: Altered mental status, anxiety, and lethargy that progresses to acute confusion and coma

ECG: Flattened T wave, prominent U waves, ST depression, prolonged PR interval

GASTROINTESTINAL: Hypoactive bowel sounds, nausea, vomiting, constipation, abdominal distention. Paralytic ileus can develop.

MUSCULAR: Weakness. Deep‑tendon reflexes can be reduced.

RESPIRATORY: Shallow breathing

Clinical manifestations for hyperkalemia

Vital signs: Slow irregular pulse, hypotension

Neuromusculoskeletal: Restlessness, irritability, weakness to the point of ascending flaccid paralysis, paresthesia

ECG: Premature ventricular contractions, ventricular fibrillation, peaked T waves, widened QRS

Gastrointestinal: Increased motility, diarrhea, hyperactive bowel sounds

Other manifestations: Oliguria

Management of hypokalemia

Replace lost potassium

Diet

Oral potassium supplements

IV potassium

Administer prescribed potassium replacement. Never give potassium via IM or subcutaneous route, which can cause necrosis of the tissues.

Monitor ECG changes

Monitor for digitalis toxicity

Fall precautions (muscle weakness)

Assess deep tendon reflexes d/t muscle contractility d/t K

management hyperkalemia

Urgency depends on EKG changes

Assess muscle weakness

Stop any potassium supplements

Restrict potassium in the diet

For severe Hyperkalemia: calcium gluconate

Monitor I & O

Fall precautions (muscle weakness)

Metabolic Acidosis

Characterized by pH <7.35 and a low bicarbonate concentration (<22 mEq/L).

Causes are often GI loss of bicarbonate or accumulation of acid (lactic acidosis, ketoacidosis, prolonged severe diarrhea, etc.).

Manifestations vary, but include:

warm and flushed skin

tachypnea (compensatory hyperventilation)

confusion

hypotension, and decreased cardiac output.

Treatment focuses on the underlying metabolic disorder.

Metabolic Alkalosis

pH > 7.45 and a high bicarbonate concentration (>26 mEq/L).

Can be produced by a gain of bicarbonate or a loss of H+ (usually by vomiting or suction).

Manifestations include: vomiting, hypoventilation (compensatory), muscle cramping, tremors, tingling extremities (similar to hypokalemia and hypocalcemia symptoms)

Treatment addresses underlying disorder as well as K+ replacement and fluid volume replacement.

Respiratory Acidosis

pH <7.35 and PaCO2 is >45 mm Hg.

Always due to inadequate excretion of CO2 with inadequate ventilation.

Manifestations vary, but include: hypoventilation, Hypoxia, Headache, cardiac dysrhythmias, disorientation

Treatment is directed at treating the cause of the hypoventilation.

Respiratory Alkalosis

pH >7.45 and PaCO2 is <35 mm Hg.

Always caused by hyperventilation (e.g., pain, anxiety)

Manifestation include: lightheadedness due to vasoconstriction and decreased cerebral blood flow, inability to concentrate, Hyperventilation, numbness and tingling of extremities (decreased calcium ionization)

Treatment depends on the underlying cause of respiratory alkalosis.

Alveolar surface tension and ventilation

Function of surfactant

Elastic recoil

ability of the lungs to return to resting state after inspiration

Compliance

ability to lungs to expand

Determined by alveolar surface tension & elastic recoil of the lungs

Airway resistance

PNS= constriction

SNS= bronchodilation

Ventilation

movement of air into and out of the lungs

Diffusion

movement of gases between air in the lungs & bloodstream

Perfusion

the delivery of oxygenated blood to the body's tissues and organs through the circulatory or lymphatic system

type 1 cells

alveolar structure

type 2 cells

production of surfactant

Signs and Symptoms of Pulmonary Disease

Dyspnea: Subjective sensation of uncomfortable breathing

Types: Dyspnea on exertion (DOE), Orthopnea, Paroxysmal nocturnal dyspnea (PND), Awaken at night gasping for air, Use of accessory muscles, Tripod position

Cough: Acute cough, Chronic cough, Cough hypersensitivity

Irritants

Abnormal sputum: Clear, foamy, purulent, bloody

Hemoptysis: Coughing up blood

Abnormal breathing patterns:

Kussmaul respirations (hyperpnea): deep, rapid & labored breaths

Cheyne-Stokes respirations: rapid, deep breathing, alternating with periods of apnea

Hypoventilation: CO2 removal less than CO2 production, Results in hypercapnia

Hyperventilation: CO2 removal greater than CO2 production, Results in hypocapnia respiratory alkalosis

Cyanosis: Presentation → White/fair skin colors: bluish discoloration, Darker skin colors: grey or whitish

Causes: Peripheral vs. central cyanosis, Clubbing: Schamroth sign test

Pain: Pleurodynia, Pleural friction rub, Costochondritis, Costochondral junction

Hypoxemia

Reduced oxygenation of arterial blood (PaO2)

Hypoxemia vs. hypoxia

Ventilation-perfusion (V·/Q·) mismatch

Shunting

Hypoxic pulmonary vasoconstriction

Alveolar dead space

Acute respiratory failure

hypercapnia

Increased carbon dioxide concentration in arterial blood

Flail chest

Instability of a portion of the chest wall from rib fractures

Spontaneous pneumothorax

Primary: Unexpected, Bleb rupture

Secondary: Underlying respiratory disorder

Traumatic pneumothorax

Open vs. tension

Manifestations: Pain, tachypnea, dyspnea

Treatment: Chest tube

Pleural Effusion

Transudative (watery)

Exudative (WBCs and plasma proteins)

Hemothorax (blood)

Empyema (pus)

Compression atelectasis

When external pressure compresses the lung tissue, it forces air out of the alveoli (tiny air sacs). This causes the alveoli to collapse, leading to a decrease in lung volume. 

Obstructive (absorption) atelectasis

a condition where the alveoli (small air sacs in the lungs) collapse due to the absorption of gases into the bloodstream. 

Surfactant impairment (adhesive) atelectasis

a condition where the alveoli (tiny air sacs in the lungs) collapse and stick together, preventing oxygen from reaching the bloodstream. 

restrictive lung diseases

pulmonary fibrosis, NEUROMUSCULAR disorders, congestive cardiac failure, sarcoidosis, obesity

obstructive lung disease

copd, asthma, bronchiectasis, cystic fibrosis, bronchiolitis, antitrypsin deficiency

1. Exudative Phase (0-7 days) 

• Characterized by inflammation and fluid accumulation in the lungs.

• Alveolar epithelial cells are damaged, leading to increased permeability.

• Fluid leaks into the alveoli, causing hyaline membrane formation.

• Symptoms include shortness of breath, tachypnea, and hypoxemia.

2. Proliferative Phase (7-21 days) 

• Damaged cells are replaced with new ones, and fibroblasts produce collagen. 

• Alveolar walls thicken and become less elastic. 

• Oxygenation may improve slightly as the fluid is removed, but lung function remains impaired. 

• Symptoms may persist or worsen, and pulmonary hypertension can develop. 

3. Fibrotic Phase (21 days and beyond) 

• Chronic fibrosis develops, leading to permanent lung damage.

• Alveolar walls become permanently thickened, reducing gas exchange.

• Pulmonary hypertension and other complications may persist.

• Long-term lung function impairment and disability are common.

asthma

Chronic inflammation of the airways leading to bronchial hyperresponsiveness, constriction of airways, and reversible airflow obstruction

Flare-ups are common

Risk factors:

Hereditary, allergen exposure (IgE), environment, tobacco smoke, obesity

Pulsus paradoxus:

Decrease in SBP with inspiration

Status asthmaticus:

Bronchospasms that continue with treatment

Symptoms include expiratory wheezing, dyspnea, and tachypnea

Peak flow meters, corticosteroids, beta agonist inhalers, and anti-inflammatories used to treat

Chronic bronchitis

Hypersecretion of mucus and chronic productive cough that lasts for at least 3 months of the year and for at least 2 consecutive years

Inspired irritants increase mucus production and the size and number of mucous glands

The mucus is thicker than normal

Bronchodilators, expectorants, and chest physical therapy used to treat

Obstructive Lung Diseases: Emphysema

Abnormal permanent enlargement of the alveoli

Loss of elastic recoil collapse of airways during expiration

Air trapping - creates barrel chest

Renin-Angiotensin-Aldosterone System (RAAS)

a hormone system that regulates blood pressure and blood volume. It is activated by low blood pressure and works to increase blood pressure by causing vasoconstriction and increasing sodium and water retention. The process starts with the kidney releasing renin, which converts an angiotensinogen from the liver into angiotensin I, and then into the active angiotensin II with the help of ACE.