Vocab quiz 4 (ch.15,16)

compliance

Ability of lungs to stretch and expand easily.

Compliance is about the flexibility of lung tissue + chest wall.

High compliance = easy to inflate, but may not recoil well

Emphysema (COPD)
→ lungs are floppy, over-expanded
→ air gets in easily but doesn’t come out well

Low compliance = stiff lungs that are hard to inflate

increased work of breathing

Pulmonary fibrosis
→ stiff, scarred lungs
→ hard to inhale → shallow breathing

expiration

Breathing air OUT of the lungs.

tidal volume

Amount of air inhaled/exhaled in a normal breath (~500 mL).
Low TV = shallow breathing → poor gas exchange

• Normal TV = effective ventilation

• High TV = deep breathing (often compensating for distress)

It directly affects CO₂ removal; If tidal volume drops, the body can’t get rid of CO₂ well → leads to: hypercapnia (↑ CO₂ in blood) & respiratory acidosis (↓ pH)

💡 Key idea:
“Shallow breaths = CO₂ retention”

Low tidal volume = hypoventilation → CO₂ builds up → respiratory acidosis risk
COPD → often shallow breathing + air trapping

Restrictive lung disease → low tidal volume (stiff lungs)

vital capacity

Low VC = reduced lung flexibility or incomplete expansion

_{Maximum air you can exhale after a deep breath (IRV + TV + ERV).}

_{“the most air you can use for breathing in and out”}

_{It reflects how well your lungs can expand and empty, so it’s often reduced in diseases that make lungs stiff or blocked.}

VC=IRV+TV+ERV

_{IRV (Inspiratory Reserve Volume) Extra air you can inhale after a normal breath in.}

_{TV (Tidal Volume) Normal resting breath.}

_{ERV (Expiratory Reserve Volume) Extra air you can force out after a normal breath out.}

residual volume

Air left in lungs after full exhale.

Your lungs never fully empty because residual volume is what:

keeps alveoli from collapsing, allows gas exchange to continue between breaths.

High residual volume happens in:

• COPD (especially emphysema) → air trapping

• Asthma → narrowed airways trap air

• Air trapping conditions in general

💡 Meaning:

You can breathe in, but you can’t fully breathe out → stale air builds up.

Low RV: restrictive lung diseases (lungs can’t fully expand, but RV usually doesn’t drop much compared to other volumes)
Atherosclerosis can worsen breathing problems because reduced blood flow lowers oxygen delivery, forcing the lungs to work harder and sometimes contributing to air trapping and increased residual volume in patients with combined heart and lung disease.

total lung capacity

Total air lungs can hold (everything combined).
TLC=IRV+TV+ERV+RV
TLC tells you the overall size and capacity of the lungs.

High TLC → often seen in COPD (lungs overinflated, air trapping)

Low TLC → restrictive diseases (fibrosis, stiff lungs, obesity)

Total lung capacity shows how much total air the lungs can physically hold, and changes in it reflect either lung overexpansion or restriction.

surfactant

Inside the alveoli, water creates surface tension that naturally tries to make them collapse. Surfactant acts like a slippery coating that prevents this collapse and makes it easier for lungs to expand.
Low surfactant → alveolar collapse → poor oxygen exchange

Surfactant lowers the effort needed to breathe and keeps alveoli open for gas exchange.

oxyhemoglobin

Hemoglobin bound to oxygen (Hb + O₂).

Oxygen from the lungs attaches to hemoglobin in red blood cells so it can be transported to tissues. This is the main way oxygen travels through the body.

• If oxyhemoglobin is low, tissues don’t get enough oxygen → hypoxia

• Even if lungs are working, low oxygen binding can still happen in:

  • lung disease (poor gas exchange)

  • anemia (not enough hemoglobin)

  • carbon monoxide poisoning (CO binds hemoglobin instead)

eupnea

Normal, effortless breathing. indicating adequate oxygen and CO₂ balance.

tachypnea

Abnormally fast breathing.

Happens when the body is trying to compensate for a problem like fever, anxiety, pain, or hypoxia.

• Often shallow and rapid

• Can be a sign the body is struggling to get enough oxygen or remove CO₂

apnea

Temporary or complete stopping of breathing.

Can occur in sleep apnea, drug overdose, or neurological issues

hypoxemia

Low oxygen in the blood.

Hypoxemia = decreased partial pressure of oxygen (PO₂) in arterial blood.

💡 Occurs when ventilation or diffusion is impaired, especially if gas exchange is disrupted between alveoli and blood (loss of normal steep gradients, surface area, or diffusion efficiency).
Mild hypoxemia → may have few or no symptoms

Severe or chronic hypoxemia → significant respiratory distress and systemic effects

Key clinical manifestation:

• Cyanosis = late sign of respiratory failure (blue discoloration due to low oxygen)

It may be caused by:

• Low oxygen in the air

• Nervous or circulatory system problems that affect breathing or blood flow

• Respiratory disorders, including:

  • hypoventilation (not breathing enough)

  • impaired gas diffusion (oxygen can’t pass well into blood)

  • poor blood flow through lung capillaries

  • ventilation/perfusion (V/Q) mismatch (air and blood are not properly matched)

hypoxia

Low oxygen in the TISSUES

It happens when cells are not getting enough oxygen to function properly, even if oxygen levels in the blood may or may not be normal.

Causes: High altitude, lung diseases, carbon monoxide poisoning .

• Hypoxemia (low oxygen in blood)

• Poor blood flow (circulatory problems)

• Problems with oxygen delivery or use at the tissue level

hypercapnia

increased CO₂ in blood.

It happens when the body is not ventilating well enough to remove CO₂, so it builds up in the bloodstream.

CO₂ builds up → blood becomes more acidic (respiratory acidosis) This condition can lead to symptoms such as headaches, dizziness, and confusion, and if severe, can cause respiratory failure.

aspiration

Food/liquid enters airways instead of esophagus.

It happens when the protective swallowing reflex fails and material goes into the trachea or lungs instead of the stomach.

Blocked airways → difficulty breathing

• Inflammation in the lungs

• Infection → can lead to aspiration pneumonia

• In severe cases → airway obstruction or respiratory failure

Causes;

• Impaired swallowing (stroke, neurologic disorders)

• Decreased consciousness (sedation, alcohol, anesthesia)

hemoptysis

Coughing up blood from lungs/airways.

It’s a symptom, not a disease, and it usually signals damage or irritation in the airways or lung tissue.

Common causes:

• Bronchitis or pneumonia (inflamed airways)

• Tuberculosis

• Lung cancer

• Pulmonary embolism (blood clot in lungs)

• Severe coughing that damages small vessels

dyspnea

Difficulty breathing / shortness of breath. often signaling impaired oxygen exchange or ventilation.

Causes;

Asthma or COPD (airflow obstruction)

Anxiety or panic attacks

• Increased work of breathing (use of accessory muscles)

• May be accompanied by tachypnea or low oxygen levels

orthopnea

Dyspnea when lying flat; shortness of breath that occurs when lying flat and improves when sitting or standing up.

Common causes:

• Left-sided heart failure (most common)

• Fluid buildup in the lungs (pulmonary congestion)

• Severe COPD in some cases

Physiologic explanation:

When lying flat:

• More blood returns to the heart

• A weak left ventricle can’t pump efficiently

• Fluid backs up into the lungs → makes breathing harder

When sitting up:

• Gravity reduces fluid in lungs

• Breathing becomes easier

retractions

visible pulling inward of the skin around the chest, ribs, neck, or sternum during breathing.

💡 It happens when a person has to use extra effort to breathe, and the chest wall gets “pulled in” because airflow into the lungs is difficult.

Common causes:

• Asthma (airway narrowing)

• Bronchiolitis or severe respiratory infections

• Upper airway obstruction (like croup)

• COPD exacerbations

Physiologic meaning:

• The body is trying harder to pull air into the lungs

• Negative pressure in the chest becomes stronger than normal

• Soft tissues get pulled inward during inspiration

auscultation

Listening to internal sounds with stethoscope, used to evaluate how well air is moving through the respiratory system.

adventitious

abnormal sounds heard during breathing when using a stethoscope.

💡 It means the normal airflow sounds are being replaced or mixed with extra, unwanted sounds, usually due to disease or obstruction. (wheezing, crackles).

Physiologic meaning:

• Air is not moving smoothly through the respiratory system

• Indicates fluid, mucus, narrowing, or airway obstruction

cyanosis

a bluish discoloration of the skin, lips, or nail beds caused by low oxygen levels in the blood.

💡 It becomes visible when there is an increased amount of deoxygenated hemoglobin in the blood.

Common causes:

• Hypoxemia (low oxygen in arterial blood)

• Severe lung disease (COPD, pneumonia, asthma exacerbation)

• Heart failure or poor circulation

• Airway obstruction or respiratory failure

Physiologic meaning:

• Not enough oxygen is being delivered to tissues

• More hemoglobin is carrying no oxygen (deoxyhemoglobin)

• Usually a late sign of respiratory or cardiac failure

clubbing

enlargement and rounding of the fingertips and nails due to long-term low oxygen levels (chronic hypoxia).

💡 It develops slowly and is a sign of chronic, not acute, disease.

Physiologic meaning:

• Chronic low oxygen changes blood flow to the fingertips

• Soft tissue under the nail bed increases

• Nail becomes curved and the fingertip becomes bulb-shaped

bronchiectasis

permanent widening (dilation) and damage of the bronchi due/lead to repeated infection or inflammation.

💡 Think of it as airways that are stretched out and no longer clear mucus properly.

What happens pathophysiologically:

• Damaged airway walls lose normal elasticity

• Mucus clearance is impaired

• Thick mucus builds up → bacteria grow easily → repeated infections

• Inflammation keeps worsening the damage (vicious cycle)

Common causes:

• Repeated lung infections (pneumonia)

• Cystic fibrosis

• Severe or chronic airway obstruction

• Tuberculosis or other chronic inflammatory lung diseases

air trapping

Air gets stuck in lungs (can’t fully exhale).

This leads to stale air staying in the lungs, increasing lung volume and making breathing less efficient.

Physiologic effects:

• Increased residual volume (more air left in lungs after exhale)

• Hyperinflation of lungs (lungs stay partially “stuck open”)

• Increased work of breathing

• Reduced ability to bring in fresh oxygen-rich air

Air trapping happens when exhalation is incomplete, causing excess air to remain in the lungs and reducing efficient gas exchange.

atopic

a genetic tendency to develop allergic hypersensitivity reactions.

💡 It means the immune system is overreactive to harmless substances (allergens) like pollen, dust, or pet dander.

What it involves:

• Overproduction of IgE antibodies

• Strong immune response to normal environmental triggers

Physiologic effect:

• Immune system releases histamine and inflammatory chemicals

• Causes airway inflammation, mucus production, and bronchoconstriction (in asthma cases)

pneumothorax

air leaking into the pleural space (between the lung and chest wall), causing partial or complete lung collapse.

💡 Normally, the pleural space is sealed and has negative pressure to keep the lungs expanded. When air enters, that pressure is lost and the lung can collapse.

Common causes:

• Chest trauma (stab wound, rib fracture)

• Spontaneous rupture of small air blisters (often in tall, thin individuals)

• Mechanical ventilation injury

• Lung disease (COPD, emphysema)

Physiologic effects:

• Loss of negative pressure → lung cannot stay inflated

• Reduced ventilation on affected side

• Decreased oxygenation (hypoxemia if severe)

atelectasis

collapse of alveoli (or part of the lung), leading to reduced or absent gas exchange in that area.

💡 Think of it as “air sacs that are not open anymore.”

Common causes:

• Airway obstruction (mucus plug, tumor, foreign body)

• Post-surgery shallow breathing (pain → not taking deep breaths)

• Lack of surfactant (especially in newborns)

• Compression from fluid, blood, or tumor outside the lung

Physiologic effects:

• Decreased ventilation in affected area

• Reduced oxygen exchange → can cause hypoxemia

• Blood may still flow to the area but without air → V/Q mismatch

• Increased work of breathing if large areas are involved

perfusion

The flow of blood through tissues or organs so they receive oxygen and nutrients.

blood flow through the pulmonary capillaries in the lungs for gas exchange.

It depends on:

• Adequate cardiac output (heart pumping effectively)

• Open, unobstructed blood vessels

• Proper blood pressure and circulation

It matters in the lungs:

For oxygen to enter the blood, there must be:

• Ventilation (air in alveoli)

• Perfusion (blood in capillaries)

💡 If either one is off → gas exchange is impaired.

• Pulmonary embolism → blocks blood flow to lung area

• Heart failure → weak pumping reduces circulation

pericardium

Outer double-layered sac that surrounds and protects the heart.

Structure:

• Fibrous pericardium (outer layer): tough, anchors the heart in place

• Serous pericardium (inner layer):

  • parietal layer (lines sac)

  • visceral layer (directly covers heart, also called epicardium)

• Pericardial fluid sits between layers to reduce friction

myocardium

The muscular middle layer of the heart wall that actually contracts to pump blood.

• Contracts with each heartbeat to pump blood through the heart and into circulation

• Requires a constant supply of oxygen and nutrients through coronary arteries.

Ischemia → reduced oxygen to myocardium → chest pain (angina)

Damage to myocardium reduces pumping ability → can lead to heart failure

endocardium

the thin inner lining of the heart chambers and heart valves.

Thin layer of endothelial tissue

Lines the; atria and ventricles, heart valves

• Provides a smooth surface to help blood flow easily through the heart

• Helps prevent clot formation inside the heart

• Supports proper valve function

hemorrhage

Excessive bleeding. It occurs when a vessel is damaged and blood escapes into surrounding tissues or outside the body.

• External hemorrhage → blood leaves the body (wound, trauma)

• Internal hemorrhage → bleeding inside the body (organs, tissues)

Physiologic effects:

• Loss of blood volume → decreased oxygen delivery

• Can lead to hypotension (low blood pressure)

• If severe → shock (organ failure due to poor perfusion)

• Tissue hypoxia if oxygen supply drops

thrombosis

Blood clot formed in a vessel that stays in place and can partially or completely block blood flow.

Common causes (Virchow’s triad):

• Stasis of blood flow (slow circulation, immobility)

• Damage to vessel wall (injury, atherosclerosis)

• Hypercoagulability (blood clots too easily, e.g., thrombocythemia)

Physiologic effects:

• Blocks or reduces blood flow

• Decreases oxygen delivery to tissues (ischemia)

• If severe → tissue death (infarction)

• Can break off and become an embolus

atherosclerosis

buildup of fatty plaques (cholesterol, lipids, inflammatory cells) inside artery walls that causes narrowing and hardening of the arteries.

Physiologic effects:

• Decreased blood flow → reduced oxygen delivery (ischemia)

• Can lead to infarction (tissue death) if fully blocked

• Increases workload on the heart → higher risk of heart disease

Arteriosclerosis = general artery hardening;

atherosclerosis = plaque buildup causing that hardening.

aneurysms

a localized bulging or ballooning of a weakened blood vessel wall.

💡 Think of it as a “weak spot that stretches outward under pressure.”

pathophysiologically:

• Vessel wall becomes weak (often from atherosclerosis or hypertension)

• Blood pressure pushes against the weak area

• The vessel bulges outward

• Risk of rupture → life-threatening hemorrhage

venous stasis

slowed or stagnant blood flow in the veins.

💡 Think of it as “blood sitting still instead of moving.”

What happens pathophysiologically:

• Blood flow slows down → doesn’t return efficiently to the heart

• Blood begins to pool in veins (especially in the legs)

• Increased risk of clot formation (thrombosis)

Physiologic effects:

• Increased pressure in veins

• Fluid leaks into tissues → edema (swelling)

• Higher risk of deep vein thrombosis (DVT)

Common causes:

• Prolonged immobility (bed rest, long flights)

• Heart failure (poor circulation)

• Varicose veins

• Obesity or pregnancy (pressure on veins)

thrombocythemia

an abnormally high number of platelets in the blood.

💡 Platelets help with clotting, so too many makes the blood more likely to clot when it shouldn’t.

Pathophysiologically:

• Excess platelets → increased clot formation

• Blood becomes more “sticky”

• Can lead to thrombosis (abnormal clots in vessels)

Causes:

• Primary (essential thrombocythemia): bone marrow disorder producing too many platelets

• Secondary (reactive): response to inflammation, infection, or other conditions

thromboembolus

a blood clot that forms in one place and then breaks off and travels through the bloodstream.

💡 It starts as a thrombus (stationary clot) and becomes an embolus (traveling clot).

embolus

any material traveling in the bloodstream that can lodge in a vessel and block blood flow.

💡 It does not have to be a clot

Types of emboli:

• Thromboembolus → blood clot (most common)

• Fat embolus → from bone fractures

• Air embolus → air bubbles in circulation

• Amniotic fluid embolus → during childbirth

infarction

tissue death caused by a lack of blood supply (and therefore lack of oxygen).

💡 Think: “no blood → no oxygen → tissue dies.”

What happens pathophysiologically:

• Blood flow is blocked (often by a thrombus or embolus)

• Oxygen and nutrients can’t reach the tissue

• Cells become ischemic → then die → necrosis (infarction)

Common causes:

• Thrombosis (clot in place)

• Embolus (traveling blockage)

• Severe atherosclerosis (narrowed arteries)

stenosis

abnormal narrowing of a blood vessel or valve.

💡 Think of it as “a tight or narrowed opening” that restricts flow.

What happens pathophysiologically:

• Lumen (opening) becomes smaller

• Blood flow is reduced or obstructed

• Pressure increases behind the narrowing

• The heart has to work harder to push blood through

Common causes:

• Atherosclerosis (plaque buildup)

• Congenital defects

• Scarring or inflammation

• Valve degeneration (like aortic stenosis)

Atherosclerosis causes plaque buildup, and that buildup can result in stenosis

regurgitation

backward flow of blood through a heart valve that does not close properly.

💡 Think of it as “leaky valve → blood goes the wrong way.”

What happens pathophysiologically:

• Valve fails to fully close

• Blood leaks backward instead of moving forward

• Reduces efficient blood flow through the heart

• Heart has to work harder to compensate

Physiologic effects:

• Decreased forward cardiac output

• Volume overload in the heart chamber

• Can lead to heart enlargement and heart failure over time

cardiac dysrhythmia

any abnormal heart rhythm (too fast, too slow, or irregular).

💡 It’s a problem with the heart’s electrical conduction system.

What happens pathophysiologically:

• Electrical signals in the heart are disrupted

• Heart may beat:

  • too fast (tachycardia)

  • too slow (bradycardia)

  • irregularly (uneven rhythm)

• This can reduce how effectively the heart pumps blood

Physiologic effects:

• Decreased cardiac output

• Poor perfusion to organs

• Can lead to dizziness, fainting, or even cardiac arrest

fibrillation

rapid, uncoordinated, and ineffective contractions of the heart muscle.

💡 Instead of a strong organized beat, the heart muscle quivers (shakes) irregularly, so it doesn’t pump blood well.

• Atrial fibrillation (AFib): atria quiver instead of fully contracting

• Ventricular fibrillation (V-fib): ventricles quiver → life-threatening emergency

Physiologic effects:

• Severe drop in cardiac output

• Poor perfusion to organs

• Can quickly lead to loss of consciousness or death (especially V-fib)

heart block

a delay or complete interruption of electrical signals as they move through the heart’s conduction system.

💡 Think: “the electrical signal gets slowed down or blocked.”

What happens pathophysiologically:

• Electrical impulses from the SA node don’t properly reach the ventricles

• This disrupts coordination between atria and ventricles

• The heart may beat too slowly or in an abnormal pattern

Physiologic effects:

• Reduced heart rate (bradycardia)

• Decreased cardiac output

• Poor perfusion to organs

ecchymoses

large areas of skin discoloration caused by bleeding under the skin (bruising).

💡 Think: “big bruise from blood leaking into tissue.”

What happens pathophysiologically & Common causes: Ecchymoses are large areas of skin discoloration resulting from blood leakage to the tissues due to the rupture of small blood vessels. They commonly appear as bruising and are associated with trauma, aging, or blood disorders.

Physiologic meaning:

• Indicates bleeding under the skin from damaged vessels

• Larger than petechiae or purpura

petechiae

tiny pinpoint red spots on the skin caused by small areas of bleeding under the skin.

💡 Think: “micro-bruises from broken capillaries.”

pathophysiologically:

• Small capillaries break or leak

• A very small amount of blood escapes into the skin

• Blood stays trapped under the surface → visible dots

Common causes:

• Low platelet count (thrombocytopenia)

• Severe infection (like meningitis or sepsis)

• Excessive pressure (coughing, vomiting, straining)

• Blood clotting disorders

purpura

larger areas of purple or red discoloration on the skin caused by bleeding under the skin.

💡 Think: “bigger than petechiae, smaller than a ecchymoses. It can occur due to various conditions, including blood disorders or certain medications. .”

hematoma

a localized collection of blood outside of blood vessels that forms a raised, swollen “blood pocket.”

💡 Think: “a deeper, bigger bruise that forms a lump.”

What happens pathophysiologically:

• A blood vessel breaks (often from trauma)

• Blood leaks into surrounding tissue

• Instead of spreading flat like a bruise, it collects in a pocket

• This creates a swollen, raised mass

hypertension

persistently elevated blood pressure.
💡 Defined as systolic > 130 mmHg and/or diastolic > 80 mmHg.

Primary (essential) hypertension

• No clear cause (idiopathic)

• Related to genetics + lifestyle factors (diet, stress, obesity, etc.)

Secondary hypertension

• Caused by another disease or condition

• Examples: kidney disease, adrenal gland disorders, drugs (cocaine, amphetamines)

Blood pressure is controlled by:

• Neural system (cardiovascular + vasomotor centers)

• Hormones

  • ADH (raises water retention → ↑ blood volume)

  • Angiotensin (vasoconstriction → ↑ pressure)

  • Adrenal medulla hormones (increase heart rate/vasoconstriction)

  • Natriuretic peptides (lower BP by promoting sodium/water loss)

• Kidneys

  • Directly control fluid balance and sodium

  • Indirectly influence long-term blood pressure regulation

Pathophysiology (what high BP does):

• Thickens blood vessel walls (smooth muscle hypertrophy/hyperplasia) → narrows vessels

• Damages endothelium → promotes atherosclerosis and clot formation

• Increases workload on the left ventricle → can lead to heart disease and heart failure

Treatments & how they work:

• Lifestyle changes (weight loss, salt restriction)
  → reduces blood volume and vascular resistance

• Diuretics
  → remove excess water/sodium → ↓ blood volume → ↓ BP

• Beta-blockers
  → slow heart rate and reduce force of contraction → ↓ cardiac output

• ACE inhibitors
  → block angiotensin II formation → less vasoconstriction → lower BP

• ARBs (angiotensin receptor blockers)
  → block angiotensin II receptors → prevent vasoconstriction

• Calcium channel blockers
  → relax vascular smooth muscle → vasodilation → ↓ resistance

• Vasodilators
  → directly widen blood vessels → lower peripheral resistance

hypotension

abnormally low blood pressure.

💡 In general, it is when blood pressure is too low to adequately perfuse organs and tissues.

systolic < 90 mmHg

Common causes:

• Low blood volume (dehydration, hemorrhage)

• Heart problems (heart failure, slow heart rate, dysrhythmias)

• Vasodilation (sepsis, anaphylaxis, medications)

• Shock states (septic, neurogenic, anaphylactic, cardiogenic)

Physiologic effects:

• ↓ blood flow to organs (poor perfusion)

• ↓ oxygen delivery → tissue hypoxia

• Can lead to dizziness, fainting, organ failure if severe

septic shock

life-threatening drop in blood pressure caused by a widespread infection and overwhelming immune response.

💡 It is the most severe form of sepsis, where the body’s response to infection causes dangerous vasodilation and poor perfusion.

What happens pathophysiologically:

• Infection triggers massive immune response

• Inflammatory chemicals cause widespread vasodilation

• Blood vessels become “leaky” → fluid shifts out of circulation

• Blood pressure drops → organs don’t get enough blood

Physiologic effects:

• Severe hypotension

• Poor tissue perfusion → cellular hypoxia

neurogenic shock

a type of shock caused by sudden loss of nervous system control over blood vessel tone, leading to widespread vasodilation and low blood pressure.

💡 Think: “brain/spinal cord injury → vessels relax too much → blood pressure drops.”

What happens pathophysiologically:

• Damage to the spinal cord or nervous system (especially high spinal injury)

• Loss of sympathetic nervous system tone

• Blood vessels dilate widely (vasodilation)

• Blood pools in vessels → less blood returns to the heart

Physiologic effects:

• Low blood pressure (hypotension)

• Decreased cardiac output

• Poor tissue perfusion → cellular hypoxia

• Can lead to organ dysfunction if severe

anaphylactic shock

a severe, life-threatening allergic reaction that causes widespread vasodilation, airway constriction, and low blood pressure.

What happens pathophysiologically:

• Allergen triggers massive immune response (IgE-mediated)

• Release of histamine and inflammatory chemicals

• Blood vessels dilate and become leaky

• Airway smooth muscle constricts (bronchospasm)

• Fluid leaves bloodstream → drop in blood pressure

Physiologic effects:

• Severe hypotension (shock)

• Airway narrowing → breathing difficulty

• Decreased oxygen delivery → hypoxia

• Rapid progression to organ dysfunction if untreated

myocardial infarction

death of heart muscle tissue due to a sudden loss of blood flow (oxygen supply) to part of the heart.

What happens pathophysiologically:

• A coronary artery becomes blocked (usually by a thrombus from atherosclerosis)

• Blood flow to part of the myocardium stops

• Heart muscle becomes ischemic (low oxygen)

• If not restored quickly → tissue dies (infarction)

Physiologic effects:

• Damaged heart muscle cannot contract properly

• ↓ cardiac output → poor circulation to the body

• Can trigger dangerous arrhythmias (like fibrillation)

• Can lead to heart failure or sudden death

angina pectoris

chest pain or discomfort caused by reduced blood flow (oxygen supply) to the heart muscle, but without permanent damage.

💡 Think: “temporary heart ischemia → pain, but not cell death.”

Physiologic effects:

• Temporary oxygen shortage in myocardium

• No permanent tissue death (unlike myocardial infarction)

• Signals underlying coronary artery disease

systolic failure

the heart’s inability to contract strongly enough to pump blood out effectively.

💡 Think: Systolic failure = weak squeeze → poor pumping of blood.”

What happens pathophysiologically:

• The ventricles lose contractile strength (often the left ventricle)

• Heart cannot eject normal amount of blood

• Decreased stroke volume and cardiac output

• Blood begins to back up into the lungs or body

**Physiologic effects:

• Reduced forward blood flow → poor tissue perfusion

• Blood backs up into lungs → pulmonary congestion/edema

• Activation of compensatory systems (RAAS, sympathetic system) → can worsen condition over time

diastolic failure

the heart cannot relax and fill properly with blood between beats.

💡 Think: “stiff heart → can’t fill well.”

What happens pathophysiologically:

• The ventricles become stiff or noncompliant

• During diastole (relaxation phase), the heart doesn’t fill adequately

• Even though contraction may be normal, less blood enters the heart → reduced output

• loss of elasticity

Physiologic effects:

• Decreased ventricular filling → ↓ stroke volume

• Blood backs up into the lungs → pulmonary congestion

• Can still have normal ejection fraction early on, but overall output is reduced

congestive heart failure

a condition where the heart cannot pump blood effectively, leading to fluid backing up (“congestion”) in the lungs and/or body.

💡 It can involve systolic failure, diastolic failure, or both.

What happens pathophysiologically:

• Heart pumps too weakly or doesn’t fill properly

• Blood backs up behind the failing side of the heart

• Fluid leaks out of vessels into tissues → congestion and edema

• Organs receive less oxygen-rich blood

Left-sided vs right-sided CHF:

• Left-sided failure → lungs

  • fluid in lungs (pulmonary edema)

  • shortness of breath, cough

• Right-sided failure → body

  • fluid backs up into systemic circulation

  • leg swelling, abdominal swelling (edema)

Physiologic effects:

• Reduced cardiac output → poor tissue perfusion

• Fluid buildup in tissues and organs

• Activation of compensatory systems (kidneys retain fluid, worsening swelling)

cor pulmonale

right-sided heart failure caused by chronic lung disease.

💡 Think: “lung disease makes the right side of the heart fail.”

What happens pathophysiologically:

• Chronic lung disease → low oxygen levels (hypoxia)

• Hypoxia causes pulmonary vasoconstriction (lung vessels tighten)

• This increases resistance in lung circulation (pulmonary hypertension)

• Right ventricle has to pump harder → becomes enlarged and fails

Physiologic effects:

• Right-sided heart strain and failure

• Blood backs up into systemic circulation

• Fluid accumulation in body tissues

Clinical manifestations:

• Swelling in legs (peripheral edema)

• Enlarged liver (hepatomegaly)

• Neck vein distention (JVD)

• Fatigue and shortness of breath

stroke

sudden loss of brain function caused by interruption of blood flow to the brain or bleeding in the brain.

💡 Think: “brain cells lose oxygen → they start dying fast.”
This can result in various symptoms depending on the area of the brain affected, including difficulty speaking, paralysis, or loss of coordination.

Ischemic stroke (most common):

• blockage of a brain artery (thrombus or embolus)

Hemorrhagic stroke:

• rupture of a blood vessel → bleeding into brain tissue

What happens pathophysiologically:

• Blood flow to part of the brain is cut off

• Neurons are extremely sensitive to oxygen loss

• Within minutes → cell injury and infarction (brain tissue death)

Physiologic effects:

• Loss of brain function in affected area

• Disruption of movement, speech, sensation, or cognition

• Can lead to permanent disability or death

transient ischemic attack (TIA)

a temporary blockage of blood flow to the brain that causes stroke-like symptoms but resolves quickly without permanent brain damage.

💡 Think: “mini stroke that goes away.”

What happens pathophysiologically:

• A brief interruption of blood flow to part of the brain (usually from a small clot or narrowing of a vessel)

• Brain tissue is temporarily ischemic (low oxygen)

• Blood flow restores on its own before permanent injury occurs

Physiologic significance:

• Warning sign of a future stroke

• Indicates underlying vascular disease (often atherosclerosis or emboli)

• Requires urgent evaluation even if symptoms disappear

DIC (disseminated intravascular coagulation)

a serious condition where the body forms widespread tiny blood clots throughout the bloodstream, then uses up clotting factors, leading to uncontrolled bleeding.

💡 Think: “clot everywhere → then no ability to clot when needed.”
What happens pathophysiologically:

• A major trigger (infection, trauma, cancer, obstetric complications) activates the clotting system

• Tiny clots form throughout small blood vessels

• This uses up platelets and clotting factors

• After depletion, the body cannot clot properly → bleeding begins

Physiologic effects:

• Blocked microcirculation → tissue ischemia and organ damage

• Simultaneous risk of severe bleeding

• Can lead to shock and multi-organ failure

Common causes:

• Severe infection (sepsis)

• Major trauma or burns

• Complications of pregnancy/childbirth

• Cancer (especially leukemias)

fibrinolysis

Fibrinolysis is the body’s system for breaking down and removing blood clots after they aren’t needed.

💡 Think: “clot cleanup system.”
What happens pathophysiologically:

• After a clot forms (to stop bleeding), the body activates enzymes

• Plasmin breaks down fibrin (the structural mesh of a clot)

• The clot dissolves and blood flow is restored

Physiologic purpose:

• Prevents clots from staying too long in vessels

• Helps maintain normal, open blood flow

• Works opposite of coagulation (clot formation)

Clinical relevance:

• Too little fibrinolysis → risk of thrombosis (dangerous clots)

• Too much fibrinolysis → risk of bleeding

• Used therapeutically in some cases (clot-busting drugs like tPA in stroke/MI)