Anatomy: Cardiovascular & Respiratory

Right atrium: receives deoxygenated blood from SVC, IVC, and coronary sinus. Right ventricle: pumps to pulmonary trunk → pulmonary arteries → lungs. Left atrium: receives oxygenated blood from 4 pulmonary veins. Left ventricle: pumps to aorta → systemic circulation. Left ventricle has the thickest wall.

Tricuspid (right AV valve): between right atrium and right ventricle. Pulmonary (semilunar): between right ventricle and pulmonary trunk. Mitral/Bicuspid (left AV valve): between left atrium and left ventricle. Aortic (semilunar): between left ventricle and aorta. AV valves have chordae tendineae and papillary muscles.

Venae cavae (SVC/IVC) → Right atrium → Tricuspid valve → Right ventricle → Pulmonary valve → Pulmonary trunk → Pulmonary arteries → Lungs (gas exchange) → Pulmonary veins → Left atrium → Mitral (bicuspid) valve → Left ventricle → Aortic valve → Aorta → Systemic circulation.

Left coronary artery (LCA) branches into Left Anterior Descending (LAD, supplies anterior interventricular septum and anterior LV wall) and Circumflex (supplies left atrium and posterior LV). Right coronary artery (RCA) supplies right atrium, right ventricle, SA node (in ~60%), AV node, and posterior interventricular septum. Blockage causes myocardial infarction (heart attack). LAD is called the 'widow maker.'

1) SA node (pacemaker, right atrium, ~60-100 bpm) → 2) Internodal pathways → 3) AV node (delays signal ~0.1 sec) → 4) Bundle of His (AV bundle, through interventricular septum) → 5) Right and Left bundle branches → 6) Purkinje fibers (distribute impulse to ventricular myocardium). This ensures atria contract before ventricles.

The sinoatrial (SA) node is located in the right atrium near the SVC. It has the fastest rate of spontaneous depolarization (~60-100 bpm), so it sets the pace for the entire heart. Its cells are autorhythmic (self-excitable) — they don't require neural input to fire, though ANS modulates rate. If SA node fails, AV node takes over (~40-60 bpm).

One complete heartbeat. Systole: ventricular contraction — ejects blood into pulmonary trunk and aorta; AV valves close (S1 'lub'). Diastole: ventricular relaxation — ventricles fill with blood; semilunar valves close (S2 'dub'). Atrial systole (atrial kick) contributes the final ~20% of ventricular filling at end of diastole.

S1 ('lub'): closure of AV valves (tricuspid and mitral) at the beginning of ventricular systole. S2 ('dub'): closure of semilunar valves (pulmonary and aortic) at the beginning of ventricular diastole. Murmurs = abnormal sounds caused by turbulent blood flow, often due to valve stenosis (narrowing) or regurgitation (incomplete closure).

CO = Heart Rate (HR) × Stroke Volume (SV). CO = volume of blood pumped by one ventricle per minute. Average resting CO ≈ 5 L/min (70 bpm × ~70 mL). Stroke volume is influenced by preload (Frank-Starling law), contractility (inotropy), and afterload (resistance ventricle must overcome).

The heart's stroke volume increases in response to increased venous return (preload). When cardiac muscle is stretched more (greater end-diastolic volume), it contracts with greater force — up to a physiological limit. This ensures that the heart pumps out whatever volume of blood it receives, matching left and right output.

Baroreceptors are pressure-sensitive stretch receptors in the carotid sinus and aortic arch. When BP rises → baroreceptors fire more → medulla decreases sympathetic and increases parasympathetic output → heart rate and vasoconstriction decrease → BP falls. When BP drops, opposite occurs. This is a rapid, short-term reflex mechanism (neural).

Low BP/low Na⁺ → kidneys release renin → renin converts angiotensinogen (from liver) to angiotensin I → ACE (in lungs) converts angiotensin I to angiotensin II → Ang II causes vasoconstriction (raises BP) and stimulates aldosterone release from adrenal cortex → aldosterone increases Na⁺/water reabsorption in kidneys → blood volume and BP increase. ACE inhibitors block this pathway.

ANP is released by atrial cardiomyocytes when atria are stretched (high blood volume/pressure). Effects: promotes Na⁺ and water excretion (natriuresis/diuresis), vasodilation, and inhibits renin and aldosterone release. Net effect: decreases blood volume and blood pressure. Opposes RAAS. BNP (from ventricles) has similar effects.

Arteries: thick walls (3 layers — tunica intima, media, externa), lots of smooth muscle and elastic tissue, carry blood AWAY from heart, high pressure. Capillaries: single layer of endothelium (tunica intima only), allows gas/nutrient exchange. Veins: thinner walls than arteries, larger lumen, have valves to prevent backflow, carry blood TOWARD heart, low pressure. ~60% of blood volume is in veins.

~55% Plasma: water (90%), proteins (albumin, globulins, fibrinogen), electrolytes, nutrients, wastes, gases, hormones. ~45% Formed elements: RBCs/erythrocytes (~99% of formed elements), WBCs/leukocytes (neutrophils, lymphocytes, monocytes, eosinophils, basophils), Platelets/thrombocytes. Hematocrit = % of blood volume that is RBCs (~42-47%).

Hemoglobin (Hb) is a protein in RBCs with 4 subunits, each containing a heme group with an iron (Fe²⁺) atom. Each Hb can carry up to 4 O₂ molecules. Oxyhemoglobin = Hb bound to O₂ (bright red). Deoxyhemoglobin = Hb without O₂ (dark red). Also carries some CO₂ as carbaminohemoglobin. Carbon monoxide (CO) binds Hb with ~200x greater affinity than O₂ (poisoning).

Based on antigens on RBC surface and antibodies in plasma. Type A: A antigens, anti-B antibodies. Type B: B antigens, anti-A antibodies. Type AB: A and B antigens, NO antibodies (universal recipient). Type O: NO antigens, anti-A and anti-B antibodies (universal donor). Mismatched transfusion → agglutination (clumping) → hemolysis → potentially fatal.

Rh factor = presence (+) or absence (−) of the D antigen on RBCs. Rh− mother carrying Rh+ fetus can develop anti-Rh antibodies after exposure to fetal blood (usually at delivery). In subsequent Rh+ pregnancies, maternal antibodies cross placenta and attack fetal RBCs → hemolytic disease of the newborn (HDN/erythroblastosis fetalis). Prevented by RhoGAM injection (anti-D immunoglobulin).

1) Vascular spasm: damaged vessel constricts to reduce blood flow. 2) Platelet plug formation: platelets adhere to exposed collagen (via vWF), activate, and aggregate. 3) Coagulation cascade: intrinsic and extrinsic pathways converge at common pathway → prothrombin → thrombin → fibrinogen → fibrin mesh stabilizes the clot. 4) Fibrinolysis: plasmin eventually dissolves the clot during healing.

Extrinsic pathway: initiated by tissue factor (TF/factor III) from damaged tissue → activates factor VII → faster ('extrinsic' to blood). Intrinsic pathway: initiated by contact activation (factor XII contacts exposed collagen) → slower; all factors are 'intrinsic' to blood. Both converge at Factor X → common pathway → thrombin → fibrin. Measured by PT/INR (extrinsic) and PTT (intrinsic).

Nasal cavity (filters, warms, humidifies air; olfactory epithelium), Pharynx (nasopharynx — pharyngeal tonsil/adenoid; oropharynx — palatine tonsils; laryngopharynx — common passage for food and air). These structures conduct air and serve as the first line of defense (mucus, cilia, lymphoid tissue).

Cartilaginous structure connecting pharynx to trachea. Contains thyroid cartilage (Adam's apple), cricoid cartilage, and epiglottis (covers glottis during swallowing to prevent aspiration). Houses vocal cords (true vocal folds) for phonation. Glottis = vocal folds + the opening between them (rima glottidis).

Trachea: ~10-12 cm, C-shaped hyaline cartilage rings (open posteriorly for esophageal expansion), lined with pseudostratified ciliated columnar epithelium with goblet cells (mucociliary escalator). Bifurcates at carina into right and left main (primary) bronchi → lobar (secondary) bronchi → segmental (tertiary) bronchi → bronchioles → terminal bronchioles → respiratory bronchioles → alveolar ducts → alveoli.

Alveoli are thin-walled air sacs (~300 million in lungs) where gas exchange occurs. Type I alveolar cells: thin squamous cells forming the gas exchange surface. Type II alveolar cells: secrete surfactant (reduces surface tension, prevents alveolar collapse/atelectasis). Alveolar macrophages (dust cells): phagocytize pathogens and debris. Respiratory membrane = alveolar epithelium + fused basement membranes + capillary endothelium (~0.5 μm thick).

Active process. Diaphragm contracts and flattens (phrenic nerve C3-C5) + external intercostals elevate ribs → thoracic volume increases → intrapleural pressure becomes more negative → intrapulmonary pressure drops below atmospheric pressure → air flows IN (Boyle's Law: volume up → pressure down). Quiet inspiration uses only diaphragm and external intercostals. Forced inspiration adds SCM, scalenes, and pectoralis minor.

Quiet expiration is PASSIVE: diaphragm and external intercostals relax → elastic recoil of lungs and chest wall → thoracic volume decreases → intrapulmonary pressure rises above atmospheric pressure → air flows OUT. Forced expiration is ACTIVE: internal intercostals depress ribs + abdominal muscles (rectus abdominis, obliques) compress abdominal contents upward against diaphragm.

Intrapleural pressure is the pressure in the pleural cavity (between visceral and parietal pleura). Normally subatmospheric (negative, ~-4 to -6 cmH₂O). This negative pressure keeps the lungs inflated by creating a transpulmonary pressure gradient. Pneumothorax: air enters pleural cavity → pressure equalizes → lung collapses (atelectasis).

O₂ diffuses from alveoli (high PO₂ ~104 mmHg) into pulmonary capillary blood (low PO₂ ~40 mmHg). CO₂ diffuses from blood (high PCO₂ ~45 mmHg) into alveoli (low PCO₂ ~40 mmHg). Driven by partial pressure gradients (Dalton's and Henry's Laws). The thin respiratory membrane (~0.5 μm) and large surface area (~70 m²) optimize diffusion.

S-shaped (sigmoidal) curve showing relationship between PO₂ and Hb saturation. Plateau at high PO₂ (lungs): Hb nearly 100% saturated. Steep portion at low PO₂ (tissues): small drops in PO₂ cause large O₂ unloading. Right shift (increased O₂ unloading): increased temp, increased PCO₂, decreased pH (Bohr effect), increased 2,3-BPG. Left shift: opposite conditions (Hb holds O₂ tighter — fetal Hb, CO poisoning).

The Bohr effect describes how increased CO₂ and decreased pH (more acidic blood, such as in exercising muscle) decrease hemoglobin's affinity for O₂, shifting the oxyhemoglobin dissociation curve to the RIGHT. This promotes O₂ unloading at active tissues where it is most needed. Conversely, in the lungs (low CO₂, high pH), Hb affinity for O₂ increases, promoting O₂ loading.

Tidal volume (TV): volume of air in one normal breath (~500 mL). Residual volume (RV): air remaining in lungs after maximal exhalation (~1200 mL, prevents lung collapse). Vital capacity (VC): maximum air exhaled after maximum inhalation (TV + IRV + ERV, ~4800 mL). Total lung capacity (TLC): total volume lungs can hold (VC + RV, ~6000 mL).

Anatomical dead space: volume of conducting airways where no gas exchange occurs (~150 mL; nose through terminal bronchioles). Physiological dead space: anatomical dead space + any non-functional alveoli (alveoli ventilated but not perfused). In healthy lungs, physiological ≈ anatomical dead space. Increased physiological dead space seen in pulmonary embolism (blocked perfusion).

Medulla oblongata: ventral respiratory group (VRG, generates rhythm for inspiration and forced expiration) and dorsal respiratory group (DRG, basic inspiratory rhythm). Pons: pneumotaxic center (inhibits DRG, limits inspiration, promotes smooth breathing) and apneustic center (stimulates DRG, prolongs inspiration). Higher cortical input allows voluntary control (singing, speaking, breath-holding).

Central chemoreceptors (medulla): respond to increased CO₂ (via H⁺ in CSF) — most important stimulus for increasing ventilation. Peripheral chemoreceptors (carotid and aortic bodies): respond to decreased PO₂ (below ~60 mmHg), increased PCO₂, and decreased pH. Hypercapnia (high CO₂) is the primary drive; hypoxemia is a secondary stimulus (important in COPD patients).

Three ways: 1) Dissolved in plasma (~7%). 2) Bound to hemoglobin as carbaminohemoglobin (~23%). 3) As bicarbonate ion (HCO₃⁻) in plasma (~70%) — formed by carbonic anhydrase in RBCs: CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻. HCO₃⁻ exits RBC via chloride shift (Cl⁻ enters). In lungs, reaction reverses to release CO₂ for exhalation.

Pulmonary: right ventricle → pulmonary trunk → pulmonary arteries → lung capillaries (gas exchange) → pulmonary veins → left atrium. Low pressure (~25/8 mmHg). Pulmonary arteries carry DEOXYGENATED blood. Systemic: left ventricle → aorta → systemic arteries → tissue capillaries → systemic veins → venae cavae → right atrium. High pressure (~120/80 mmHg). Systemic arteries carry OXYGENATED blood.

Blood pressure = force exerted by blood on vessel walls. Systolic (top number): peak pressure during ventricular contraction (~120 mmHg normal). Diastolic (bottom number): minimum pressure during ventricular relaxation (~80 mmHg normal). Pulse pressure = systolic − diastolic. Mean Arterial Pressure (MAP) ≈ diastolic + 1/3 pulse pressure. Hypertension: ≥130/80 mmHg (ACC/AHA 2017).

Granulocytes: Neutrophils (60-70%, first responders, phagocytize bacteria), Eosinophils (2-4%, fight parasites, modulate allergies), Basophils (<1%, release histamine and heparin). Agranulocytes: Lymphocytes (20-25%, T cells — cell-mediated immunity, B cells — antibodies, NK cells — kill abnormal cells), Monocytes (3-8%, become macrophages in tissues, phagocytize debris and pathogens). Mnemonic for most to least: Never Let Monkeys Eat Bananas.

Progressive inflammatory disease where plaques (fatty deposits of cholesterol, foam cells, smooth muscle, calcium) build up in the tunica intima of arteries. Narrows lumen → reduced blood flow (angina). Plaque rupture → thrombus formation → can completely occlude vessel → myocardial infarction (coronary artery) or stroke (cerebral artery). Risk factors: hyperlipidemia, hypertension, smoking, diabetes, obesity.

Thrombus: stationary blood clot formed within a vessel. Can partially or completely obstruct blood flow. Embolus: any intravascular mass (often a detached thrombus, but can be air, fat, or amniotic fluid) that travels through the bloodstream. Pulmonary embolism (PE): embolus lodges in pulmonary artery — often from DVT in leg veins; can be fatal.

The Haldane effect describes how the oxygenation state of hemoglobin influences its ability to carry CO₂. Deoxygenated hemoglobin (in tissues) binds MORE CO₂ and H⁺ than oxygenated hemoglobin. In the lungs, as Hb binds O₂, it releases CO₂ more readily — facilitating CO₂ elimination. The Haldane effect and Bohr effect work together to optimize gas exchange.

Surfactant is a phospholipoprotein mixture (mainly dipalmitoylphosphatidylcholine/DPPC) secreted by Type II alveolar cells. It reduces surface tension of the alveolar fluid, preventing alveolar collapse (atelectasis) during expiration. Without surfactant, small alveoli would collapse into larger ones (LaPlace's Law). Premature infants may lack surfactant → Infant Respiratory Distress Syndrome (IRDS/RDS). Treated with exogenous surfactant.

When CO₂ enters RBCs in systemic capillaries, carbonic anhydrase converts it to H₂CO₃, which dissociates into H⁺ and HCO₃⁻. HCO₃⁻ is transported out of the RBC into plasma via a Cl⁻/HCO₃⁻ antiporter (band 3 protein), and Cl⁻ moves in. This maintains electrical neutrality. In the lungs, the process reverses: HCO₃⁻ enters RBC, Cl⁻ exits, CO₂ is regenerated and exhaled.

Tunica intima (innermost): endothelium + basement membrane + subendothelial layer. Tunica media (middle): smooth muscle + elastic fibers; thickest in arteries; regulated by ANS. Tunica externa/adventitia (outermost): connective tissue with collagen fibers; anchors vessel; contains vasa vasorum (blood vessels of blood vessels) in large vessels and nervi vasorum (nerves).

Rings of smooth muscle at the junction where capillaries branch from metarterioles. They regulate blood flow into individual capillary beds. When contracted → blood bypasses capillaries through thoroughfare channel. When relaxed → blood flows into capillary bed for exchange. Controlled by local metabolic factors (O₂, CO₂, pH, histamine) rather than neural signals.

Ductus venosus: bypasses liver (umbilical vein → IVC); becomes ligamentum venosum. Foramen ovale: opening between right and left atria (bypasses pulmonary circulation); closes to become fossa ovalis. Ductus arteriosus: connects pulmonary trunk to aorta (bypasses lungs); becomes ligamentum arteriosum. At birth, first breath decreases pulmonary resistance → increased left atrial pressure closes foramen ovale; rising O₂ constricts ductus arteriosus.

Obstructive (COPD, asthma, bronchitis, emphysema): difficulty exhaling; air trapping; increased residual volume and TLC; decreased FEV₁/FVC ratio (<0.70). Restrictive (pulmonary fibrosis, scoliosis, obesity): difficulty expanding lungs; reduced compliance; decreased TLC, VC, and FVC; FEV₁/FVC ratio normal or increased (>0.70).

Venous return = volume of blood returning to the right atrium per minute. Assisted by: 1) Skeletal muscle pump (contractions compress veins), 2) Respiratory pump (breathing creates pressure changes), 3) Venous valves (prevent backflow), 4) Sympathetic venoconstriction (reduces venous capacitance). Venous return determines preload which determines stroke volume (Frank-Starling).

Absolute refractory period: cardiac muscle cannot be restimulated (~200 ms in ventricles) due to inactivated Na⁺ channels. Relative refractory period: a very strong stimulus could trigger a premature contraction. The long absolute refractory period prevents tetanus (sustained contraction) in cardiac muscle — unlike skeletal muscle — ensuring the heart relaxes and fills between beats.