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Cardiovascular Physiology: Cardiac Output, Stroke Volume, and Vascular Dynamics

Cardiac Output and Stroke Volume

  • Total blood volume in an average adult at rest is about ext{5 L}.
  • At rest, heart rate is around 75 \, ext{beats/min}; this means roughly the entire blood volume passes through the heart each minute, which is a respectable baseline.
  • Cardiac output (CO) is the product of stroke volume (SV) and heart rate (HR):
    CO = SV \times HR
  • Stroke volume is the amount of blood ejected by the ventricle per beat, and is given by the difference between end-diastolic volume (EDV) and end-systolic volume (ESV):
    SV = EDV - ESV
  • Maximal cardiac output (COmax) differs by fitness level:
    • In nonathletic people, COmax is typically 20\text{--}25\, \text{L/min} (four to five times through the heart per minute during maximal effort).
    • Trained athletes can reach COmax up to about 35\, \text{L/min}.
  • Cardiac reserve is the difference between maximal and resting cardiac output:
    \text{Cardiac reserve} = CO{\max} - CO{rest}
  • At rest, the CO (~5 L/min) versus during peak exercise shows large adaptive capacity of the heart.

Preload, Contractility, and Afterload (factors that regulate stroke volume)

  • Stroke volume is regulated by three major factors: preload, contractility, and afterload.
  • Preload
    • Definition: how much blood is in the ventricles before they contract (the amount of stretch on the ventricular walls).
    • The most important determinant of preload is venous return: more venous return stretches the ventricles more and increases the force of contraction (Frank-Starling mechanism).
    • Frank-Starling law: Increased venous return distends the ventricles and increases contraction force automatically.
    • Result: increased venous return → increased end-diastolic volume (EDV) → increased stroke volume (SV) → increased CO.
    • Relevance: exercising muscles help squeeze venous blood back to the heart, increasing venous return and EDV.
  • Contractility
    • Definition: the intrinsic strength of the cardiac muscle’s contraction, independent of preload.
    • Inotropic state: agents that change the strength of contraction are called inotropic agents.
    • Positive inotropic agents increase contractility; negative inotropic agents decrease it.
    • Positive inotropes examples: Epinephrine (adrenaline), thyroxine (T4), glucagon, Digitalis (digoxin), high extracellular calcium.
    • Other positive inotropes: Epinephrine again; Thyroxine; Digoxin increases force of contraction in heart failure.
    • Negative inotropes examples: Calcium channel blockers (used to treat chronic hypertension) reduce contraction force.
    • Effect on SV/CO: increased contractility lowers end-systolic volume (ESV) and raises SV and CO.
  • Afterload
    • Definition: the back pressure exerted by arterial blood that the ventricles must overcome to eject blood; primarily reflects systemic arterial pressure (and to some extent, pulmonary pressure for the right ventricle).
    • High afterload (e.g., chronic hypertension) makes the ventricles work harder to eject the same amount of blood, increasing ESV and reducing SV; this lowers cardiac efficiency.
    • Afterload is the problematic factor; reducing afterload improves cardiac performance.
  • Interrelations
    • EDV (preload) and afterload are linked to SV via the equation SV = EDV - ESV.
    • End-diastolic volume is more or less equivalent to preload, and systolic volume is related to afterload in the way SV is determined by the pressure the heart must overcome.
    • Increasing preload and contractility generally raise SV and CO; increasing afterload tends to reduce SV and CO.

Frank-Starling and Venous Return – Practical picture

  • Preload increases with venous return: more blood returning to the heart stretches ventricles more, increasing force of contraction.
  • Venous return increases EDV, which pushes the ventricle toward its maximum volume; as a result, SV and CO rise.
  • A simple visual (not shown) is a smiley face for the concept: greater preload leads to a stronger contraction and greater SV.
  • Exercise and activity increase venous return via skeletal muscle pump and changes in venous tone, contributing to higher preload during activity.
  • Preload optimization is beneficial for increasing cardiac output when needed.

Flow Charts and Study Strategy for Cardiac Output

  • Cardiac output is determined by stroke volume and heart rate: CO = SV \times HR
  • To study, start from the desired result (maximize CO) and trace back to the factors that influence SV and HR (preload, contractility, afterload; and heart rate regulation).
  • The flow charts can serve as a compact summary of how SV and HR contribute to CO and how various factors influence SV and HR.
  • Practice tip: create flashcards from the flowchart to test which factors affect SV and which influence HR.

Hormonal, Ionic, Age, and Environmental Effects on Heart Rate

  • Hormones and autonomic inputs
    • Epinephrine (adrenaline) increases heart rate and contractility.
    • Thyroxine (thyroid hormone) increases heart rate and contractility.
    • Glucagon can increase heart rate and contractility.
  • Ions
    • Potassium balance is critical; imbalances can be dangerous to the heart and can be life-threatening.
    • Calcium balance influences contractility; high extracellular calcium can increase contractility; calcium channel blockers decrease it.
  • Other factors influencing heart rate
    • Age and body size: smaller bodies tend to have higher heart rates; fetal and newborn hearts have higher rates due to size and metabolic needs.
    • Gender: females tend to have smaller body size on average, often associated with higher heart rate.
    • Exercise: increases heart rate acutely.
    • Body temperature: higher temperature increases heart rate.
  • Practical takeaway: maintaining electrolyte balance and understanding autonomic control are essential for stable heart performance.

Congestive Heart Failure (CHF) – Overview and Progression

  • CHF is a progressive condition where cardiac output is insufficient to supply tissues with adequate oxygen.
  • Causes and progression
    • Coronary atherosclerosis leading to myocardial ischemia and infarctions reduces oxygen supply to the heart muscle, impairing contraction.
    • Persistent high blood pressure (afterload) increases the work the heart must do and contributes to hypertrophy and eventual failure.
    • Recurrent myocardial infarction and subsequent scar tissue reduce contractile function.
    • Hypertrophy initially compensates but can lead to dilatation and loss of contractile efficiency over time.
    • The heart may become dilated and functionally weaker, with visible scar tissue replacing dead myocardium after infarctions.
  • Left-sided vs right-sided failure
    • Left-sided failure → pulmonary congestion (blood backs up into the lungs); symptoms can include fluid buildup around the lungs and dyspnea.
    • Right-sided failure → peripheral congestion (edema in legs, hands, and other tissues); backup into systemic circulation.
    • In many cases, failure begins on one side and progresses to involve the other, leading to biventricular failure.
  • Clinical implications
    • Left-sided failure is often associated with pulmonary symptoms and edema; right-sided failure with peripheral edema.
    • Management aims to slow progression and reduce work on the heart (reducing afterload, supporting contractility, etc.).

Blood Vessels and the Direction of Blood Flow

  • Direction of flow, not oxygen content, defines arteries vs. veins
    • Arteries carry blood away from the heart; veins carry blood toward the heart.
    • The pulmonary circuit is an exception to the general oxygen-carrying rule (pulmonary arteries carry deoxygenated blood to the lungs; pulmonary veins carry oxygenated blood back to the heart).
  • Major vessel structure and layers
    • Tunica intima (innermost lining; endothelium)
    • Tunica media (muscle layer; thicker in arteries; smooth muscle abundant in muscular arteries)
    • Tunica externa (connective tissue outer layer)
  • Arteries vs. veins – key differences
    • Arteries: thicker walls, thicker tunica media, designed to withstand high pressure from the heart; smaller lumen relative to wall thickness;
    • Veins: thinner walls, larger lumens, lower pressure; serve as capacitance vessels and reservoirs; larger overall blood volume in veins at any given time.
  • vasa vasorum
    • Small vessels that supply the walls of large arteries and veins with blood; visible on cadavers in larger vessels.
  • Capillaries
    • Capillary beds: the site of exchange between blood and tissues; composed of endothelial cells and basement membrane.
    • Capillaries and their arrangement are critical for tissue perfusion and exchange.

Capillaries: Types, Permeability, and Locations

  • Continuous capillaries
    • Most common and least permeable; intact walls with tight junctions; found in skin, muscles, lungs, and CNS.
    • Permeability is limited; small molecules pass via clefts between endothelial cells.
  • Fenestrated capillaries
    • Have pores (fenestrations) that increase permeability; more open than continuous capillaries.
    • Locations: glands, kidneys (filtration), small intestine (absorption), endocrine organs where rapid exchange is needed.
  • Sinusoid capillaries (discontinuous)
    • Highly permeable, with incomplete basement membranes and large gaps; resemble almost-open channels.
    • Locations: liver, bone marrow, spleen, adrenal medulla; allow large molecules and even cells to pass; important for clearance, hormone release, and hematopoiesis.
  • Capillary beds and local control
    • Each capillary bed receives an arterial input, a capillary network, and a venule output.
    • Precapillary sphincters (bands of smooth muscle around entry to capillary beds) can relax or contract to regulate flow.
    • Thoroughfare channel provides a direct route when capillary beds are constricted, reducing perfusion to certain areas.
    • Local control of blood flow supports tissue needs (e.g., shunting to skin for temperature regulation in cold conditions).
  • Lymphatics
    • Lymphatic vessels run parallel to veins and assist in returning tissue fluid to the venous system.

Venous System and Capacitance Vessels

  • Veins hold most of the body's blood at any given time; they are capacitance vessels and reservoirs.
  • Structural features
    • Large lumens and thin walls overall favor storage and low-pressure flow.
    • Veins are more collapsible and are often larger in diameter than arteries of the same region.
  • Practical notes for lab observations
    • If a vessel is very round and snaps back after pinching, it is more likely an artery (thicker muscular wall).
    • Veins tend to be more collapsed and retain blood when cadaveric blood is present.

Blood Pressure and Systemic Circulation

  • Blood flow vs blood pressure
    • Blood flow is the volume of blood moving through a vessel or organ per unit time; historically and colloquially related to cardiac output.
    • Blood pressure is the force per unit area exerted on the walls of vessels by the circulating blood; expressed in millimeters of mercury (mmHg).
    • The driving force for blood flow is the pressure gradient from higher to lower pressure areas in the systemic circulation.
  • Flow and measurement notes
    • In systemic arteries near the heart, blood pressure is typically measured and discussed, whereas pulmonary pressures are not as readily measured noninvasively.
    • Flow is driven by the heart’s pumping action and maintained by the pressure gradient across the circulation.
  • Resistance to flow (three sources)
    • Viscosity: the internal friction of blood, influenced by the hematocrit and plasma proteins; higher viscosity increases resistance.
    • Total vessel length: longer distance from the heart increases resistance (the farther from the heart, the greater the cumulative resistance).
    • Vessel diameter (radius): the diameter is the primary modulator of resistance and can change quickly through vasoconstriction and vasodilation; small changes in radius lead to large changes in resistance (Lucas or Poiseuille considerations).
  • Practical notes on regulation
    • Vessel diameter changes rapidly via autonomic and local factors (vasoconstriction/vasodilation) to adjust blood pressure and flow as needed.
    • Blood viscosity and vessel length change more slowly (e.g., with hydration status, chronic growth, or body size).
  • Key clinical takeaway
    • Blood pressure must be maintained high enough to perfuse vital organs (kidneys, brain, heart) on a minute-to-minute basis, but excessive pressure is detrimental in the long term.

Capillary Exchange and Local Control of Blood Flow

  • Capillary exchange is essential for tissue perfusion and nutrient/waste exchange; different capillary types modulate what can pass between blood and tissue.
  • Local control mechanisms (neural and chemical) influence capillary bed perfusion.
  • Precapillary sphincters and thoroughfare channels create dynamic pathways for blood to reach tissues according to their needs (metabolic activity, oxygen demand, CO2 buildup).

Practical Contexts: Hemodynamics and Common Conditions

  • Hemodynamics involves balancing preload, contractility, afterload, and heart rate to optimize CO.
  • Common pathologies include shifts in afterload (hypertension), changes in contractility (myocardial infarction, cardiomyopathies), and edema from heart failure.
  • Understanding vessel structure helps predict responses to injury (e.g., arterial spurts vs. venous oozing) and informs interventions.

Quick Reference: Key Equations and Concepts

  • Cardiac output: CO = SV \times HR
  • Stroke volume: SV = EDV - ESV
  • Relationship overview:
    • Preload (EDV) ↑ → SV ↑ → CO ↑
    • Contractility ↑ → ESV ↓ → SV ↑ → CO ↑
    • Afterload ↑ → ESV ↑ → SV ↓ → CO ↓
  • Capillary types and permeability:
    • Continuous: least permeable; found in skin, muscle, CNS; small clefts allow limited exchange.
    • Fenestrated: more permeable; found in glands, kidneys, small intestine.
    • Sinusoid: highly permeable; found in liver, bone marrow, spleen, adrenal medulla.
  • Vessel layers:
    • Arteries: thick tunica media, thick walls, small lumen relative to wall.
    • Veins: thin tunica media, larger lumen, thinner walls, capacitance vessels.
  • Lymphatics: parallel to veins; assist in returning tissue fluid to the heart.
  • Key clinical concepts:
    • Left-sided heart failure → pulmonary congestion; Right-sided heart failure → peripheral edema.
    • Hypertension raises afterload and can drive hypertrophy and eventual failure.

Exam-oriented Notes (Recap)

  • Left vs Right CHF: identify which side is failing based on symptoms (pulmonary congestion vs peripheral edema).
  • Major regulators of CO: SV and HR; understand how preload, contractility, and afterload influence SV and thus CO.
  • Frank-Starling: more venous return increases ventricular stretch and contraction force.
  • Capillary permeability: continuous vs fenestrated vs sinusoid and where they are located.
  • Vascular regulation: diameter changes are the fastest way to adjust resistance and blood pressure.