Lesson 1 Part 1 The Cardiovascular System

Pulmonary Circulation

Low pressure circulation system that moves blood from the right ventricle through the lungs to the left atrium

Systemic Circulation

High pressure circulation system that moves oxygenated blood from the left ventricle to the body and returns deoxygenated blood to the right atrium

Aorta Pressure

120 mmHg

Large Arteries Pressure

110 mmHg

Arterioles Pressure

40 mmHg

Arteriolar Capillaries Pressure

30 mmHg

Venous Capillaries Pressure

18 mmHg

Central Veins Pressure

7 mmHg

Right Atrium Pressure

-5 mmHg

Arterial Flow Mechanism

Heart generates pressure; arteries contract or dilate to control flow and pressure; resistance to blood flow determined by diameter, length, and blood viscosity

Venous Return Mechanism

Blood flow mostly against gravity following pressure gradient; aided by constriction of venous smooth muscle cells, constriction of skeletal muscles, and one-way venous valves

Mean Arterial Pressure (MAP)

Cardiac Output (CO) × Systemic Vascular Resistance (SVR) = MAP

Cardiac Output (CO)

Heart Rate (HR) × Stroke Volume (SV) = CO; affected by preload, contractility, and afterload

Heart Rate Increase

Sympathetic stimulation via B1 adrenergic receptors innervating the SA node increases heart rate

Heart Rate Decrease

Parasympathetic stimulation via muscarinic receptors and vagus nerve innervating the SA node decreases heart rate

Parasympathetic NS Effects on Heart

Neurotransmitter is acetylcholine (Ach); decreases HR, lessens atrial and ventricular contractility, lessens atrial and ventricular conductivity; occurs when increased pressure is noted

Sympathetic NS Effects on Heart

Neurotransmitter is norepinephrine (NorEpi); increases HR, increases conduction through AV node, increases atrial and ventricular contractility, causes peripheral vasoconstriction; occurs when decreased pressure is noted

Stroke Volume (SV)

Amount of blood ejected by a ventricle with each heartbeat; normal volume is 60-100 ml/heartbeat; right and left ventricle volumes are the same

End-Diastolic Volume (EDV)

Amount of blood in the ventricle at the end of filling (relaxation phase)

End-Systolic Volume (ESV)

Amount of blood remaining in the ventricle after contraction (emptied state)

Stroke Volume Formula

SV = EDV - ESV (End-Diastolic Volume minus End-Systolic Volume)

Frank-Starling Law of the Heart

The more the heart muscle is stretched during filling, the more forcefully it contracts; increased ventricular filling stretches cardiac muscle fibers, which generate greater contractile force, resulting in larger stroke volume

Preload

Stretch applied to cardiac muscle prior to contraction; determined by amount of blood in the ventricle at the end of diastole (rest); affected by fluid volume (hypervolemia/hypovolemia) and venous tone

Frank-Starling Preload Relationship

The more you stretch the heart (increased preload), the greater the contraction and more blood ejected

Afterload

Pressure that the ventricle must overcome against the aortic/pulmonic valve to eject blood; operationally this is blood pressure; affected by vascular resistance

Right Ventricular Afterload

Resistance against pulmonary circulation (low pressure system)

Left Ventricular Afterload

Resistance against systemic circulation (high pressure system)

Factors Increasing Afterload

Hypertension, aortic stenosis, vasoconstriction

Blood Pressure Core Equation

Blood Pressure = Cardiac Output × Systemic Vascular Resistance

Cardiac Factors Affecting Cardiac Output

Heart rate, contractility (force of contraction), conductivity (electrical conduction)

RAAS Function

Renin-Angiotensin-Aldosterone System; increases blood volume and vasoconstriction to regulate fluid volume

Natriuretic Peptides Function

Promote fluid excretion and vasodilation to regulate fluid volume

Alpha Adrenergic Receptors (α₁ and α₂)

Sympathetic nervous system receptors that cause vasoconstriction

Beta-2 Adrenergic Receptors (β₂)

Sympathetic nervous system receptors that cause vasodilation

Neurohormonal Vasoconstrictors

Angiotensin II (from RAAS) and norepinephrine (from SNS)

Local Vasodilators

Prostaglandins and nitric oxide

Local Vasoconstrictors

Endothelin

ACE Inhibitors/ARBs Action

Target RAAS system to reduce blood pressure

Beta-Blockers Action

Reduce heart rate and contractility to lower blood pressure

Calcium Channel Blockers Action

Cause vasodilation to reduce blood pressure

Diuretics Action

Reduce fluid volume to lower blood pressure

Baroreceptors

Specialized nerve endings in aortic arch and carotid sinuses; sensitive to stretching and increases in arterial blood pressure; send impulses to sympathetic vasomotor center to constrict or dilate blood vessels

Vascular Endothelium Function

Essential to regulation of vasodilating and vasoconstricting substances

Renal System Blood Pressure Control

Controls sodium excretion and extracellular fluid volume through RAAS system and prostaglandins

Endocrine System Blood Pressure Control

Norepinephrine and epinephrine from adrenal medulla; aldosterone from adrenal cortex; ADH from posterior pituitary

Angiotensin II Effects Timeline

Constriction of arterioles (hours); stimulates aldosterone release

Aldosterone Effects Timeline

Retention of sodium and water (days)

RAAS Remodeling Effects

Remodeling of heart and vascular smooth muscle (weeks to months)

RAAS Ultimate Control

Ultimate control of blood pressure to maintain renal perfusionRetryClaude can make mistakes. Please double-check responses.