2.1 Cardiovascular & Respiratory Physiology

2.1 Cardiovascular & Respiratory Physiology

Quick Answer: For AFK biomedical items, treat the circulation and lungs as one delivery system: cardiac output (CO) = heart rate (HR) × stroke volume (SV) drives arterial pressure with systemic vascular resistance (SVR); lungs set PaO₂/PaCO₂ via ventilation and gas exchange. Oxygen rides mainly on hemoglobin; carbon dioxide is mostly converted to bicarbonate. Dental relevance is immediate—epinephrine, anxiety, hypoxia, and cardiovascular disease all change these numbers chairside.

Applied biomedical science is about 20 ± 5% of the AFK blueprint. Cardiovascular and respiratory physiology appear as stand-alone science stems and as the physiologic backbone of medical-emergency and local-anesthesia questions. Memorize equations, then practice translating them into patient scenarios (e.g., why a β-blocker patient may not mount a normal tachycardia response, or why a COPD patient retains CO₂).

Cardiac Output, Stroke Volume, and Blood Pressure

Cardiac output is the volume of blood the left ventricle ejects per minute:

CO = HR × SV

Typical resting adult values (order of magnitude for exam recall):

Stroke volume is end-diastolic volume (EDV) minus end-systolic volume (ESV). Three physiologic determinants matter:

1. Preload — wall stretch at end-diastole (roughly venous return / EDV). Frank–Starling: within physiologic range, greater stretch → stronger contraction → higher SV.
2. Afterload — impedance the ventricle faces during ejection (largely aortic pressure / SVR). Higher afterload tends to reduce SV if contractility is fixed.
3. Contractility — inotropic state independent of preload/afterload (sympathetic stimulation and catecholamines increase contractility; many anesthetics and ischemia decrease it).

Blood pressure relationships:

• Pulse pressure = SBP − DBP
• MAP ≈ DBP + ⅓(pulse pressure) (or CO × SVR, conceptually)
• Narrow pulse pressure can suggest low SV; wide pulse pressure appears with stiff arteries or high stroke volume states

Blood-Pressure Regulation (Short and Long Term)

Short-term (seconds to minutes): the baroreceptor reflex.

• Sensors: stretch receptors in the carotid sinus (CN IX) and aortic arch (CN X)
• High MAP → ↑ baroreceptor firing → ↑ parasympathetic / ↓ sympathetic outflow → ↓ HR, ↓ contractility, vasodilation → MAP falls
• Low MAP → opposite pattern: tachycardia, vasoconstriction, venoconstriction

Medium/long-term: renin–angiotensin–aldosterone system (RAAS) and renal fluid control.

• Low renal perfusion / sympathetic β₁ stimulation / low NaCl at macula densa → renin from juxtaglomerular cells
• Renin converts angiotensinogen → angiotensin I; ACE converts AI → angiotensin II
• Angiotensin II: potent vasoconstrictor; stimulates aldosterone and ADH pathways → Na⁺/water retention → expands blood volume and supports MAP

Dental chair links:

• White-coat and dental anxiety raise catecholamines → ↑ HR, SV, and often SBP
• Epinephrine in local anesthetic (and endogenous catecholamines) can raise HR and SBP; use lowest effective dose, aspirate, inject slowly, and heed cardiac disease limits taught in pharmacology chapters
• Orthostatic hypotension after long appointments: venous pooling + impaired baroreflex (elderly, antihypertensives) → stand patients slowly
• ACE inhibitors, ARBs, β-blockers, and diuretics reshape how patients respond to stress and volume change—know the physiology even when drug lists live elsewhere

The Cardiac Cycle

The cardiac cycle is the mechanical sequence of one heartbeat. AFK-level items focus on phases, valve events, and heart sounds—not catheter waveforms.

Phases (left heart focus)

1. Atrial systole — atrial contraction tops up ventricular filling ("atrial kick"); important when ventricular compliance is reduced
2. Isovolumetric contraction — AV valves closed, semilunar valves still closed; ventricular pressure rises with no volume change
3. Ejection — aortic (and pulmonic) valves open; SV is ejected; most stroke volume leaves early in systole
4. Isovolumetric relaxation — semilunar valves close; ventricular pressure falls with both sets of valves closed
5. Rapid and reduced filling — AV valves open; passive filling dominates, then slower filling until the next atrial systole

Valves and Heart Sounds

Coronary perfusion of the left ventricular myocardium occurs mainly in diastole—another reason severe tachycardia can impair myocardial O₂ supply even as demand rises.

Respiratory Volumes and Ventilation

Lung volumes are standard AFK physiology.

Minute ventilation (V̇E) = tidal volume × respiratory rate.

Alveolar ventilation is what actually participates in gas exchange: roughly (TV − dead space) × rate. Anatomic dead space is ~1 mL per pound ideal body weight (often taught ≈ 150 mL). Rapid shallow breathing wastes a larger fraction of each breath on dead space; slower deeper breaths improve alveolar ventilation for the same minute ventilation.

Control of Breathing

• Central chemoreceptors (medulla): respond primarily to brain PCO₂ / pH (CO₂ crosses BBB → carbonic acid → H⁺)
• Peripheral chemoreceptors (carotid and aortic bodies): sense PaO₂, PaCO₂, and arterial pH; become critical when PaO₂ falls substantially
• In many COPD patients, chronic hypercapnia blunts CO₂ drive; hypoxic drive can matter clinically—avoid indiscriminate high-flow O₂ without monitoring in susceptible patients (clinical judgment; know the physiology)

Oxygen and Carbon Dioxide Transport

Oxygen

• ~97–98% of arterial O₂ is bound to hemoglobin (Hb); only ~2% is dissolved (the dissolved fraction sets PaO₂)
• Content depends on Hb concentration × saturation + dissolved O₂
• The oxyhemoglobin dissociation curve is sigmoid: plateau at high PO₂ (arterial) protects content; steep portion at lower PO₂ (tissues) facilitates unloading

Right shift (easier unloading at tissues): ↑ temperature, ↑ 2,3-BPG, ↑ CO₂, ↓ pH (Bohr effect). Left shift (tighter binding): opposite changes, fetal Hb, carbon monoxide (CO also blocks O₂ binding sites and left-shifts remaining Hb).

Dental relevance of oxygenation:

• Pulse oximetry estimates SpO₂, not PaO₂ or total O₂ content—anemic patients can have normal SpO₂ with low O₂ content
• Sedation, airway obstruction, and syncope can drop SpO₂ rapidly; supplemental O₂ and airway maneuvers restore delivery
• Cyanosis is an unreliable late sign; monitor and act earlier

Carbon Dioxide

CO₂ is produced by aerobic metabolism and eliminated by ventilation.

Approximate transport fractions in venous blood (teachable numbers):

Key reaction (RBC, catalyzed by carbonic anhydrase):

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

HCO₃⁻ exits RBCs in exchange for Cl⁻ (chloride shift). In lungs the reactions reverse; CO₂ is exhaled. Hypoventilation raises PaCO₂ (respiratory acidosis risk); hyperventilation lowers PaCO₂ (respiratory alkalosis risk)—the bridge to the next section’s acid–base discussion.

Integrated Dental Scenarios

Use these patterns when AFK stems mix physiology with practice:

1. Anxious patient + epinephrine LA: expect ↑ HR and often ↑ SBP via β₁ (and some α) effects; limit cartridges, inject slowly, monitor, and avoid intravascular injection.
2. Heart failure history: limited SV reserve; tachycardia may cut diastolic coronary filling; minimize stress, consider medical consult, upright gradual positioning.
3. Asthma / COPD: reduced effective ventilation and gas exchange; keep appointments short, avoid respiratory depressant over-sedation, have rescue inhaler available for asthmatics.
4. Syncope (vasovagal): often ↑ parasympathetic tone → bradycardia and vasodilation → MAP falls → cerebral hypoperfusion; Trendelenburg/supine with legs elevated, airway, O₂, and monitoring per emergency protocol.
5. Pregnancy (third trimester supine hypotension): gravid uterus compresses IVC → ↓ venous return → ↓ preload → ↓ CO; left lateral tilt restores return.

AFK Study Checklist for This Section

• Write CO, SV, MAP, and minute-ventilation equations from memory
• List baroreceptor locations and the reflex response to ↑ and ↓ MAP
• Sketch the cardiac cycle phases and name what closes at S1 and S2
• Recite TV/IRV/ERV/RV/VC/TLC definitions
• State O₂ and CO₂ transport percentages and the carbonic anhydrase reaction
• Explain one right-shift and one left-shift of the O₂–Hb curve

Master these relationships now; later pharmacology and emergency chapters assume you can predict HR, BP, and ventilation responses without relearning the physiology.