Cardiovascular System II: Blood Pressure, Cardiac Cycle, and Hemodynamics

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Blood Pressure and Heart Valves

Cardiac Mechanical Physiology

Cardiac mechanical physiology refers to the study of the physical processes that enable the heart to pump blood, including the generation of pressure, the movement of blood, and the function of heart valves.

Blood Pressure: The force exerted by circulating blood on the walls of blood vessels. It is typically measured in millimeters of mercury (mmHg).
Pressure Gradient: Blood flows from areas of higher pressure to areas of lower pressure. The pressure gradient is essential for blood movement throughout the cardiovascular system.
Heart Valves: Ensure unidirectional blood flow by opening and closing in response to pressure changes between heart chambers and vessels.
Valve Opening: Occurs when pressure behind the valve exceeds pressure in front of it.
Valve Closing: Occurs when pressure in front of the valve exceeds pressure behind it, preventing backflow.
Blood Volume and Pressure: An increase in blood volume within a chamber or vessel increases the pressure within it, and vice versa.

Diastole and Systole

Diastole: The phase of the cardiac cycle when the heart muscle relaxes and chambers fill with blood.
Systole: The phase when the heart muscle contracts and pumps blood out of the chambers.
Effects on Pressure: During systole, pressure in the contracting chamber rises; during diastole, pressure falls.
Sequence: The atria contract (systole) before the ventricles, ensuring efficient filling of the ventricles.
Importance: Atria and ventricles are not in systole simultaneously, preventing backflow and ensuring proper filling and ejection of blood.

Blood Flow Within and Out of the Heart

Interaction of Pressure Gradients and Valves

Atria to Ventricles: Blood flows when atrial pressure exceeds ventricular pressure and the atrioventricular (AV) valves are open.
Prevention of Backflow: When ventricular pressure exceeds atrial pressure, AV valves close, preventing blood from flowing backward.
Ventricles to Arteries: Blood is ejected when ventricular pressure exceeds arterial pressure, opening the semilunar valves.
Prevention of Arterial Backflow: When arterial pressure exceeds ventricular pressure, semilunar valves close.

Heart Sounds

Normal Heart Sounds and Murmurs

First Heart Sound (S1): "Lub"—caused by closure of AV valves at the beginning of ventricular systole.
Second Heart Sound (S2): "Dub"—caused by closure of semilunar valves at the beginning of ventricular diastole.
Heart Murmur: An abnormal sound indicating turbulent blood flow, often due to valve defects (e.g., stenosis or regurgitation).
Examples: Valve stenosis, valve insufficiency, septal defects.

Cardiac Cycle

Phases of the Cardiac Cycle

1. Ventricular Filling
2. Isovolumetric Contraction
3. Ventricular Ejection
4. Isovolumetric Relaxation

Ventricular Filling Phase

Pressures: Atrial pressure > ventricular pressure > arterial pressure.
Atria: Mostly in diastole; atrial systole occurs at the end to "top off" ventricular filling.
Ventricles: In diastole.
Blood Movement: Blood flows from atria to ventricles.
Volume Change: Ventricular volume increases.
End-Diastolic Volume (EDV): The volume of blood in the ventricles at the end of filling; average ~120 mL.
Valves: AV valves open; semilunar valves closed.
Heart Sounds: None typically produced.
Importance: Atrial contraction contributes a small amount to ventricular filling; ventricular contraction is more critical for blood ejection.

Isovolumetric Contraction Phase

Definition: "Isovolumetric" means volume does not change.
Pressures: Ventricular pressure rises rapidly, exceeding atrial pressure but not yet arterial pressure.
Atria: In diastole.
Ventricles: In systole.
Blood Movement: No movement; all valves are closed.
Volume: Remains at EDV.
Valves: Both AV and semilunar valves closed.
Heart Sounds: S1 (closure of AV valves).

Ventricular Ejection Phase

Pressures: Ventricular pressure > arterial pressure.
Atria: In diastole.
Ventricles: In systole.
Blood Movement: Blood is ejected from ventricles into arteries.
Volume: Decreases as blood is ejected.
End-Systolic Volume (ESV): Volume remaining in ventricles after ejection; average ~50 mL.
Valves: Semilunar valves open; AV valves closed.
Heart Sounds: None typically produced.

Isovolumetric Relaxation Phase

Pressures: Ventricular pressure falls below arterial pressure but is still higher than atrial pressure.
Atria: In diastole.
Ventricles: In diastole.
Blood Movement: No movement; all valves closed.
Volume: Remains at ESV.
Valves: Both AV and semilunar valves closed.
Heart Sounds: S2 (closure of semilunar valves).

Left vs. Right Heart

Blood Ejected: Both ventricles eject the same volume of blood per beat.
Maximum Pressures: Left ventricle generates higher pressures than the right ventricle.
Reason: The left ventricle pumps blood to the systemic circuit (higher resistance), while the right ventricle pumps to the pulmonary circuit (lower resistance).
Anatomical Difference: The left ventricular wall is thicker than the right.

Cardiac Output

Definitions and Calculations

Cardiac Output (CO): The volume of blood pumped by one ventricle per minute.
Heart Rate (HR): Number of heartbeats per minute.
Stroke Volume (SV): Volume of blood ejected by one ventricle per beat.
Equation:

Cardiac Output Equality: CO is the same for both sides of the heart under normal conditions.

Stroke Volume: Preload, Contractility, Afterload

Three Factors Affecting SV: Preload, contractility, afterload.
Pressure Gradient and Flow: Greater pressure gradient increases blood flow.

Preload

Definition: The degree of stretch of cardiac muscle fibers at the end of diastole (related to EDV).
Sarcomere Stretch: Increased stretch (within limits) increases force of contraction (Frank-Starling law).
Influences on EDV: Venous return and filling time.
Relationship: Increased preload increases SV and CO.

Contractility

Definition: The intrinsic ability of cardiac muscle to contract at a given fiber length, independent of preload.
Relationship: Increased contractility increases SV and CO.
Inotropic Agent: A substance that alters contractility (e.g., sympathetic stimulation, certain drugs).

Afterload

Definition: The force the ventricles must overcome to eject blood (primarily arterial blood pressure).
Relationship: Increased afterload decreases SV and CO.
Side Differences: Left ventricle faces higher afterload due to higher systemic arterial pressure.
Stroke Volume Equality: Both sides maintain equal SV by adjusting contractility and preload.
Ventricular Hypertrophy: Chronic high afterload leads to thickening of ventricular walls.

Putting It All Together

Changes in preload, contractility, and afterload interact to determine SV and CO.

Heart Rate

Chronotropic Agent: A factor that changes heart rate (e.g., hormones, autonomic input).
Factors Affecting HR: Autonomic nervous system, hormones, body temperature, electrolytes, fitness level, age.

Heart Failure

Definition: The inability of the heart to pump sufficient blood to meet the body's needs.
Effects: Decreased SV and CO.
Causes: Myocardial infarction, hypertension, valve disorders, cardiomyopathy.
Common Side Effect: Edema (fluid accumulation in tissues).

Hemodynamics and Blood Pressure

Definitions

Blood Pressure: The force per unit area exerted on a vessel wall by the contained blood.
Hemodynamics: The study of blood flow and the forces involved.
Driving Gradient: Blood flows from high to low pressure.
Resistance: Opposition to blood flow, mainly due to vessel diameter, length, and blood viscosity.
Relationship: Blood flow is directly proportional to the pressure gradient and inversely proportional to resistance.

Where is flow, is pressure gradient, and is resistance.

Peripheral Resistance

Three Main Variables: Cardiac output, blood volume, peripheral resistance.
Peripheral Resistance: Resistance offered by the systemic blood vessels.
Relationship: Increased peripheral resistance increases blood pressure.
Determinants of Peripheral Resistance:
- Blood Vessel Length: Longer vessels increase resistance.
- Blood Viscosity: Higher viscosity increases resistance.
- Blood Vessel Radius: Smaller radius increases resistance dramatically (to the fourth power).
- Obstructions: Plaques or clots increase resistance.

Cardiac Output and Blood Pressure

Relationship: Increased CO increases blood pressure.
Equation: (where PR is peripheral resistance)

Blood Volume and Compliance

Blood Volume: Primarily determined by water content in plasma.
Processes Changing Volume: Fluid intake, urine output, sweating, bleeding.
Relationship: Increased blood volume increases blood pressure.
Compliance: The ability of a vessel to stretch in response to pressure.
Importance: High compliance prevents large changes in blood pressure.
Most Compliant Vessels: Veins.

Pressure Changes in Circuits

Variation Importance: Ensures proper flow and exchange in different vascular beds.
Pulmonary vs. Systemic Pressure: Pulmonary circuit has lower pressure than systemic circuit due to lower resistance.
Systemic Pressure Changes: Highest in aorta, drops through arteries, arterioles, capillaries, and is lowest in veins.
Arterioles: Major drop in pressure due to high resistance.

Systemic Arterial Pressure

Pressure Changes: Decreases from large arteries to arterioles due to resistance and branching.
Arterial Pressure Variability: Not constant due to cardiac cycle (systole and diastole).
Systolic Pressure: Peak pressure during ventricular contraction.
Diastolic Pressure: Lowest pressure during ventricular relaxation.
Pulse Pressure: Difference between systolic and diastolic pressures.
Mean Arterial Pressure (MAP): Average pressure in arteries during one cardiac cycle.

Where is diastolic pressure and is systolic pressure.

Systemic Venous Pressure and Venous Return

Capillary Pressure: Drops due to fluid exchange and resistance.
Venous Pressure: Low due to distance from heart and high compliance.
Pressure Changes in Veins: Increases from small to large veins due to merging vessels and proximity to heart.
Venous Return Difficulty: Low pressure and gravity hinder return to heart.
Mechanisms for Return: Skeletal muscle pump, respiratory pump, venous valves.

Regulation of Cardiac Output

Nervous System Regulation

Need for Regulation: To match tissue oxygen demand and maintain blood pressure.
Time Scale: Nervous system acts rapidly; endocrine system acts more slowly.
Sympathetic Division: Increases CO via norepinephrine (positive inotropic and chronotropic effects).
Parasympathetic Division: Decreases CO via acetylcholine (negative chronotropic effect, weak inotropic effect).
Main Parasympathetic Nerve: Vagus nerve (cranial nerve X).

Endocrine System Regulation

Three Categories of Hormones: Affect heart rate, contractility, or blood volume.
Examples: Epinephrine/norepinephrine (increase HR and contractility), thyroid hormone (increases HR), aldosterone/ADH (increase blood volume).
Time Scale: Slower than nervous system; some act quickly, others over hours to days.

Maintenance of Blood Pressure

Importance: Ensures adequate tissue perfusion and prevents organ damage.
Nervous System: Maintains BP short-term (seconds to minutes).
Endocrine System: Maintains BP both short- and long-term.
Three Targets: Peripheral resistance (short-term), cardiac output (short-term), blood volume (long-term).

Nervous System Mechanisms

Targets: Peripheral resistance and cardiac output.
Control Center: Medulla oblongata in the brainstem.
Receptors: Baroreceptors (detect pressure changes).
Feedback Loop: Negative feedback.
Sympathetic Activation: Increases BP.
Parasympathetic Activation: Decreases BP.

Endocrine System Mechanisms

Targets: Peripheral resistance, cardiac output, blood volume.
Hormones: Epinephrine/norepinephrine (increase PR and CO), angiotensin II (increase PR and blood volume), ANP (decreases PR and blood volume).

Clinical Applications

Hypertension: Chronically elevated blood pressure; increases risk of heart disease and stroke.
Shock: Critically low blood pressure; leads to inadequate tissue perfusion.
Types of Shock:
- Hypovolemic: Low blood volume.
- Cardiogenic: Poor heart function.
- Vascular (Distributive): Excessive vasodilation.

Capillary Perfusion and Autoregulation

Capillary Beds and Perfusion

Function: Exchange of gases, nutrients, and wastes between blood and tissues.
Perfusion: The flow of blood through capillary beds.
Pathway: Arteriole → metarteriole → precapillary sphincter → capillary → thoroughfare channel → venule.
Sphincter Status: Open sphincters allow full perfusion; closed sphincters divert blood through thoroughfare channels.

Autoregulation of Perfusion

Type: Local regulation.
Importance: Matches blood flow to tissue needs.
Mechanisms: Myogenic and metabolic.
Main Change: Adjusting arteriole diameter.
Vasoconstriction: Decreases perfusion by increasing resistance.
Vasodilation: Increases perfusion by decreasing resistance.

Myogenic Mechanism

Goal: Maintain constant perfusion despite changes in systemic BP.
Stimulus: Stretch detected by mechanoreceptors.
Response: Increased pressure causes vasoconstriction; decreased pressure causes vasodilation.

Metabolic Mechanism

Goal: Match perfusion to metabolic activity.
Stimulus: Changes in local metabolites (e.g., O2, CO2, H+).
Response: Increased metabolic activity causes vasodilation; decreased activity causes vasoconstriction.

Capillary Water Exchange

Hydrostatic Pressure

Pathway: Water moves between blood and interstitial fluid across capillary walls.
Hydrostatic Pressure: The force exerted by fluid pressing against a wall; in capillaries, it is essentially blood pressure.
Gradient: Water moves from higher to lower hydrostatic pressure.
Arteriolar End: Higher hydrostatic pressure than venular end.
Interstitial Fluid Pressure: Effectively zero.
Direction: Hydrostatic pressure pushes water out of capillaries (filtration).
Filtration: Movement of water out of capillaries into tissues.

Osmotic Pressure

Osmotic Pressure: The force exerted by solutes drawing water across a membrane.
Relationship: Higher solute concentration increases osmotic pressure.
Gradient: Water moves toward higher osmotic pressure.
Capillary Osmotic Pressure: Relatively constant along capillary length.
Interstitial Fluid Osmotic Pressure: Relatively low.
Colloid Osmotic Pressure: Due to plasma proteins (mainly albumin).
Direction: Pulls water into capillaries (absorption).
Absorption: Movement of water into capillaries from tissues.

Net Filtration Pressure (NFP)

Filtration Favored By: Hydrostatic pressure.
Absorption Favored By: Colloid osmotic pressure.
Equation:

Where = capillary hydrostatic pressure, = interstitial fluid hydrostatic pressure, = capillary colloid osmotic pressure, = interstitial fluid colloid osmotic pressure.
Interpretation: Positive NFP = filtration; negative NFP = absorption.
Typical Locations:
- Arteriolar end: Net filtration.
- Venular end: Net absorption.
- Whole bed: Slight net filtration; excess fluid returned by lymphatics.
Edema: Excess fluid accumulation in tissues due to increased filtration or decreased absorption.
Causes of Edema: Hypertension (increased hydrostatic pressure), heart failure (increased venous pressure), liver failure (decreased plasma proteins, lowering colloid osmotic pressure).

Phase	Ventricular Pressure	Valve Status	Blood Movement	Heart Sound
Ventricular Filling	Low	AV open, SL closed	Atria → Ventricles	None
Isovolumetric Contraction	Rising	All closed	None	S1
Ventricular Ejection	High	AV closed, SL open	Ventricles → Arteries	None
Isovolumetric Relaxation	Falling	All closed	None	S2

Additional info: This table summarizes the main events of each cardiac cycle phase, including pressure changes, valve status, blood movement, and heart sounds.