Chapter 10

What is the pacemaker of the heart?

The SA (sinoatrial) node.

What does the SA node do?

Starts electrical impulses that make the atria contract.

What slows down the heartbeat?

The vagus nerve.

What does the AV node do?

Sends the signal from the atria to the ventricles so they contract next.

What does the P wave represent?

Electrical signal spreading across the atria, causing atrial contraction.

What does the QRS complex represent?

Ventricular depolarization — the ventricles contracting to pump blood.

What does the T wave represent?

Repolarization — the ventricles relaxing and recharging.

Which pathway carries the signal to the ventricles?

The AV bundle and Purkinje fibers.

What neurotransmitters activate the sympathetic effect on the heart?

Epinephrine and norepinephrine.

How do epinephrine and norepinephrine increase heart rate?

By binding at the SA node, increasing cAMP, and opening Ca²⁺ and Na⁺ channels.

What neurotransmitter slows the heart rate?

Acetylcholine (ACh).

How does ACh affect cAMP and ion channels?

It decreases cAMP and opens K⁺ channels, leading to hyperpolarization.

Name the main types of cardiosensor receptors.

Baroreceptors (pressure) and chemoreceptors (blood gases).

Where are baroreceptors located?

Great vessels, atria, JG apparatus.

What do cardiosensors monitor?

Blood pressure and heart rate.

Which ion channel closes during low oxygen detection?

Potassium (K⁺) channels.

What happens after K⁺ channels close in oxygen sensing cells?

Calcium (Ca²⁺) enters the cell → neurotransmitter released.

What is the role of cAMP in CO₂ sensing?

Activates PKA, which opens L-type Ca²⁺ channels.

What is a main consequence of carotid body dysfunction?

Improper heart rate, blood pressure, and breathing responses to changes in O₂ or CO₂.

What is stroke volume?

The amount of blood ejected from the ventricle per heartbeat (EDV − ESV).

What is inotropy?

The contractile strength of the ventricle.

What does preload affect?

Venous return → filling of the heart before contraction.

What does afterload affect?

Resistance to ejection → how hard the heart must push blood out.

What is cardiac output?

The volume of blood pumped by the heart per minute.

How does cardiac output change if oxygen consumption increases but oxygen extraction stays the same?

Cardiac output increases to deliver more oxygen.

Cardiac output is directly proportional to which two variables?

Stroke volume (SV) and heart rate (HR).

What happens in valvular stenosis?

Valve doesn’t open properly → ↑ pressure upstream, ↓ forward flow

What happens in valvular regurgitation?

Valve doesn’t close → blood backflows → volume overload

Name four possible symptoms or complications from valve disease.

Lightheadedness, shortness of breath, chest pain, arrhythmias.

What is a myocardial infarction?

Death of heart muscle tissue due to local ischemia from blocked coronary arteries.

What is the functional consequence of MI?

Reduced heart pumping ability and potential arrhythmias.

What is cardiomyopathy?

Disease of the heart muscle causing thickened walls, enlarged chambers, or scarring.

Is cardiomyopathy a disease of the heart valves or the heart muscle?

Heart muscle.

Which proteins are typically defective in familial HCM?

Sarcomeric proteins (contractile proteins in heart muscle)

Can the heart try to compensate for familial HCM?

Yes, but compensatory responses may worsen stiffness or cause arrhythmias.

What is the main problem in Danon Disease?

Accumulation of cellular waste due to defective lysosomal degradation.

What protein is deficient in Danon Disease?

LAMP2 (lysosome-associated membrane protein 2).

What is Dilated Cardiomyopathy (DCM)?

Progressive enlargement and thinning of heart chambers, leading to impaired pumping.

Which chamber is typically affected first in DCM?

Left ventricle.

What are common causes of familial DCM?

Cytoskeletal defects (genetic).

What is Restrictive Cardiomyopathy (RCM)?

A condition where the heart walls become stiff, impairing ventricular filling without necessarily thickening.

What causes the stiffness in RCM?

Fibrotic lesions and myocyte hypertrophy, often secondary to amyloidosis.

Is RCM usually associated with thickened walls?

Not necessarily; stiffness is the main issue, not size.

What is a common systemic cause of RCM?

Amyloidosis (abnormal protein accumulation).

What is Peripheral Artery Disease (PAD)?

A condition where narrowed or stiffened arteries reduce blood flow to limbs.

What is arteriosclerosis?

Stiffening and thickening of artery walls, often due to inflammation and damage.

What causes arteriosclerosis in PAD?

Chronic inflammation that damages the arterial lining and promotes hardening.

What causes contractile dysfunction?

Damage to the myocardium from infarction, hypertension, or cardiomyopathy.

What is the main endocrine system activated during heart failure?

The Renin-Angiotensin-Aldosterone System (RAAS).

How does RAAS activation affect the heart?

Causes vasoconstriction and fluid retention, which increase cardiac workload and worsen failure over time.

What hormone increases water retention in heart failure?

Antidiuretic hormone (ADH).

Name two resident immune cells found in alveoli.

Macrophages and dendritic cells.

What is ventilation?

Removal of waste CO2 from blood

What is oxygenation?

Transfer of O2 from air to blood

What do irritant receptors do?

They sense dust or smoke and make you breathe faster (and cause bronchoconstriction).

What do stretch receptors do?

They feel when your lungs are full and make you breathe slower.

What do J-receptors do?

They sense high pressure in the lungs and cause fast, shallow breathing.

What do chemoreceptors check?

They measure CO₂, O₂, and pH to control how fast you breathe.

What is the main role of CO₂ in blood pH?

CO₂ affects blood acidity; more CO₂ makes blood more acidic.

What happens if you breathe faster than normal?

You blow out CO₂ → blood becomes less acidic (more basic)

Why is bicarbonate (HCO₃⁻) important?

It acts like a sponge that soaks up extra H⁺ to keep blood pH balanced.

What are the two main sources of pH imbalance?

Metabolic (kidney/HCO₃⁻) and Respiratory (CO₂).

What does low HCO₃⁻ usually cause?

Acidosis (blood too sour).

What does low CO₂ usually cause?

Alkalosis (blood too soapy).

What does the V/Q ratio measure?

The efficiency of alveolar ventilation relative to blood perfusion.

What does a low V/Q ratio indicate?

Too much blood relative to air → poor oxygen transfer (like kids stuck waiting for slides).

What is bronchiolitis obliterans?

Fibrotic lesions in the small airways caused by toxins or injury.

What does diacetyl exposure do to lung cells?

Disrupts the electron transport chain → increases reactive oxygen species.

What happens if Trf1 is knocked out in the lung?

Telomeres degrade → DNA damage → lung scarring.

What happens if TERT is defective (TERTKO)?

Telomeres become abnormally short → lung cells lose protection → fibrosis.

What type of condition is asthma?

Chronic inflammatory condition of the airways.

What happens to the bronchi in bronchitis?

They become inflamed and swollen (edema).

How does bronchial muscle change over time in chronic bronchitis?

Muscles hypertrophy (get thicker), contributing to airway obstruction.

What happens to the mucus glands in bronchitis?

Goblet cells enlarge and increase mucus production.

What is the role of protease inhibitors in the lung?

Protect alveolar walls from destructive enzymes.

What happens when proteases outweigh inhibitors?

Alveolar walls are destroyed, leading to emphysema.

What is α1-antitrypsin’s role in the lungs?

It inhibits proteases to protect alveolar walls.

What happens if α1-antitrypsin is mutated?

Loss of anti-protease activity → uncontrolled alveolar destruction.

What is COPD?

A group of chronic respiratory disorders with progressive tissue degeneration and obstruction.

What happens to pulmonary blood vessels in COPD?

Vasoconstriction leads to chronic pulmonary hypoxia

How are alveoli affected in COPD?

Acinar enlargement and destruction → less surface area for gas exchange.

What is pulmonary hypertension?

High blood pressure in the pulmonary arteries due to narrowed/stiff vessels or heart dysfunction.

How does left heart failure cause pulmonary edema?

Blood backs up into the left atrium → increased pressure in pulmonary veins → fluid leaks into alveoli.

What is shock?

A state where oxygen delivery is inadequate to meet the body’s metabolic demands.

How does the body respond to shock?

Sympathetic nervous system activation → vasoconstriction, increased HR and CO; RAA system activation → water and solute retention to increase blood volume and pressure.

What causes cardiogenic shock?

Cardiac dysfunction → heart cannot pump enough blood

What happens in neurogenic shock?

Autonomic dysfunction → inability to maintain vascular tone → hypotension.