Key Concepts in Cardiovascular and Respiratory Physiology
Posted on May 8, 2025 in Biology
Fluid Dynamics and Capillary Exchange
Factors Affecting Capillary Fluid Shift
- Hemorrhage: Leads to a decrease in capillary hydrostatic pressure, causing a fluid shift towards absorption from the interstitium.
- Exercise: Increases capillary hydrostatic pressure, promoting a fluid shift towards filtration into the interstitium.
- Malnutrition: Results in decreased plasma protein concentration (and thus decreased plasma oncotic pressure), leading to a fluid shift towards filtration.
Pressure Gradients in Capillary Exchange
- ΔP (Net Hydrostatic Pressure Gradient): Favors filtration (movement of fluid out of capillaries).
- Δπ (Net Oncotic Pressure Gradient): Favors absorption (movement of fluid into capillaries).
- Capillary Fluid Exchange Summary: Bulk flow of fluid from capillaries to interstitial fluid (filtration) is favored by the net hydrostatic pressure gradient. Bulk flow from interstitial fluid to capillaries (absorption) is favored by the net oncotic pressure gradient.
Autotransfusion Mechanism
- Autotransfusion: Following hemorrhage, a drop in vascular pressure causes fluid to move from the interstitium into the capillaries to help restore blood volume.
Cardiac Physiology
Cardiac Cycle Phases and Valve States
- Isovolumetric Contraction/Relaxation: Both atrioventricular (AV) and semilunar (SL) valves are closed.
- Ejection Phase: AV valves are closed; SL valves are open.
- Ventricular Filling Phase: AV valves are open; SL valves are closed.
Heart Sounds and EKG Correlation
- S1 (First Heart Sound): Corresponds to the closure of AV valves, occurring around the end of the QRS complex on an EKG.
- S2 (Second Heart Sound): Corresponds to the closure of SL valves, occurring around the end of the T wave on an EKG.
- AV Valve State: Closed from S1 to S2 (during systole); Open from S2 to S1 (during diastole, for ventricular filling).
- SL Valve State: Closed from S2 to S1 (during diastole); Open from S1 to S2 (during systole, for ejection).
- Post-S2 Valve State: Immediately after the second heart sound (S2), both atrioventricular and semilunar valves are closed (isovolumetric relaxation).
Cardiac Contractility and Stroke Volume
- Increased Contractility: Leads to an increased ejection fraction (Stroke Volume / End-Diastolic Volume).
- Factor Increasing Stroke Volume: An increase in venous return is a key factor that increases stroke volume (Frank-Starling mechanism).
Heart Excitation Pathway
- Origin of Heart Excitation: The sinoatrial (SA) node.
- Depolarization Sequence: SA Node → (Gap junctions) → Atrial myocardium & Internodal pathways → (Gap junctions) → Atrioventricular (AV) Node → (Gap junctions) → Bundle of His → (Gap junctions) → Bundle branches → (Gap junctions) → Purkinje fibers → (Gap junctions) → Ventricular myocardium.
- Spread of Depolarization (Post-Atrial): Atrioventricular (AV) node → Bundle of His → Purkinje fibers → Ventricular myocytes.
Frank-Starling Law of the Heart
- Frank-Starling Law: States that an increase in stroke volume occurs with an increasing end-diastolic volume (EDV), meaning the heart pumps what it receives.
Autonomic Control of Cardiac Function
- Sympathetic Stimulation: Results in more forceful ventricular contraction (increased contractility) and an increased heart rate.
- Nervous System & Cardiac Contraction: The sympathetic nervous system enhances cardiac function by:
- Increasing ventricular contraction strength (contractility).
- Increasing the heart’s firing frequency (heart rate).
Respiratory Physiology
Ventilation Mechanics and Calculations
- Alveolar Ventilation Calculation: (Tidal Volume – Dead Space) × Breathing Frequency.
- Normal Ventilation Mechanics: During expiration, alveolar pressure is greater than atmospheric pressure, causing air to flow out. During inspiration, alveolar pressure is less than atmospheric pressure.
Gas Exchange and Transport
- Factors Decreasing Hemoglobin-Oxygen Affinity: Increased temperature, increased PCO₂, and decreased PO₂. These conditions (e.g., in working tissues) facilitate oxygen unloading to cells.
- PO₂ Gradient (Lowest to Highest): Working cells < Systemic veins < Alveoli < Atmosphere.
Lung Compliance and Airway Resistance
- Lung Compliance: Influenced by the elasticity of lung tissue and the surface tension of the fluid lining the alveoli (surfactant reduces this surface tension, increasing compliance).
- Airflow Rate Determinants: For a given pressure gradient (ΔP) between the atmosphere and alveoli, the rate of airflow is determined by airway resistance (R), which is primarily influenced by airway diameter. (Flow = ΔP/R).
- Asthma: A disease characterized by high airway resistance due to bronchoconstriction and inflammation.
Respiratory Cycle Events
- Diaphragm (and other inspiratory muscles) contract.
- Thoracic cavity volume increases, and lungs expand.
- Alveolar pressure drops below atmospheric pressure.
- Air flows into the lungs (inspiration).
- Diaphragm (and inspiratory muscles) relax.
- Thoracic cavity volume decreases, and lungs recoil (get smaller).
- Alveolar pressure rises above atmospheric pressure.
- Air flows out of the lungs (expiration).
Control of Ventilation
- Hyperventilation: Characterized by alveolar ventilation levels that exceed metabolic needs, leading to a decrease in arterial PCO₂.
- Primary Trigger for Increased Ventilation: A reflex increase in ventilation is primarily triggered by an increase in arterial PCO₂ (detected by central and peripheral chemoreceptors).
Pneumothorax Explained
- Pneumothorax: A condition where air enters the pleural space (due to a punctured chest wall or lung), causing the lung to collapse.
Blood and Circulation
Blood Composition and Hematocrit
- Formed Elements of Blood: Refers to suspended cells (red blood cells, white blood cells) and cell fragments (platelets). Red blood cells (erythrocytes) constitute most of the volume of formed elements.
- Hematocrit Misconception: A false statement about hematocrit is that it represents the percentage of hemoglobin saturated with oxygen. Hematocrit is actually the percentage of blood volume occupied by red blood cells.
Blood Flow Path and Oxygenation
- Deoxygenated Blood: Carried by the right side of the heart to the lungs.
- Oxygenated Blood: Carried by the left side of the heart to the systemic circulation. Found in the pulmonary veins (returning from lungs to left atrium).
- Left Ventricle Function: Pumps oxygenated blood to the aorta for systemic distribution.
- Capillary Function: Sites of nutrient and waste exchange between the vascular system and tissues.
- Airflow Sequence During Expiration: Alveolar ducts → Respiratory bronchioles → Bronchi → Trachea → Larynx → Pharynx → Nasal/Oral cavity.
- Path of a Red Blood Cell (Starting from Right Atrium): Right atrium → Tricuspid valve → Right ventricle → Pulmonary valve → Pulmonary arteries → Lungs (capillaries for gas exchange) → Pulmonary veins → Left atrium.
Regulation of Blood Pressure and Flow
- Flow Equation: Flow = ΔP / R (where ΔP is the pressure gradient and R is resistance).
- Increasing Mean Arterial Pressure (MAP): Arterioles need to vasoconstrict to increase total peripheral resistance (TPR).
- Venous Constriction Effect: An increase in venous constriction causes an increase in venous return to the heart.
- Local Blood Flow Regulation: If the pressure gradient (ΔP) is held constant, decreasing local resistance (e.g., vasodilation) will increase local blood flow.
- Metabolic Control of Blood Flow:
- Increased local metabolic activity (e.g., ↑CO₂, ↓O₂, ↑H⁺, ↑K⁺) causes vasodilation to increase blood flow.
- Decreased local metabolic activity causes vasoconstriction.
- Myogenic Response (Autoregulation):
- Decreased stretch of vascular smooth muscle (due to lower pressure) causes vasodilation.
- Increased stretch of vascular smooth muscle (due to higher pressure) causes vasoconstriction.
Responses to Positional Changes (Hypotension)
- Compensatory Response to Orthostatic Hypotension (Lying to Standing): The most immediate and significant response is increased arteriolar vasoconstriction to raise TPR.
- Detailed Response to Orthostatic Change:
- Moving from lying to standing causes gravity to pool blood in lower extremity veins, decreasing venous return.
- Decreased venous return reduces end-diastolic volume, leading to a decrease in stroke volume (Frank-Starling mechanism).
- Decreased stroke volume leads to a decrease in cardiac output (CO) and thus a decrease in mean arterial pressure (MAP).
- Baroreceptors (in carotid sinuses and aortic arch) detect the decreased MAP and reduce their firing rate.
- This signals the cardiovascular control center in the medulla, resulting in increased Sympathetic Nervous System (SNS) activation and decreased Parasympathetic Nervous System (PNS) activation.
- The reflex responses include:
- Increased Total Peripheral Resistance (TPR) due to arteriolar vasoconstriction.
- Increased stroke volume due to venoconstriction (enhancing venous return) and increased heart contractility.
- Increased Heart Rate (HR) due to increased SA node depolarization rate.
- Combined, these effects increase CO and TPR, helping to restore MAP towards normal.
