Hemodynamics: Blood Pressure, Flow, and Resistance

Detailed Notes

7.1 Blood Flow: Definition and Basic Principles

Blood flow is the volume of blood moving through a vessel, organ, or the entire circulation per unit of time, expressed in milliliters per minute (mL/min) or liters per minute (L/min). In a resting adult, total blood flow equals cardiac output (CO) — roughly 5 L/min.

The driving force for blood flow is a pressure gradient (ΔP) — blood moves from a region of higher pressure to one of lower pressure. In the systemic circuit, this gradient runs from the aorta (~100 mm Hg mean) down to the right atrium (~0 mm Hg). The relationship among flow, pressure, and resistance is captured by the fundamental hemodynamic equation:

Flow (F) ∝ ΔP / Resistance (R)

This is essentially an application of Ohm's law to fluid dynamics. When resistance rises, flow falls unless the pressure gradient increases to compensate. Conversely, vasodilation lowers resistance and boosts flow.

Poiseuille's law extends this relationship for laminar flow through a cylindrical tube:

F = (ΔP × π × r⁴) / (8 × η × L)

Where r = vessel radius, η (eta) = blood viscosity, and L = vessel length. The critical clinical takeaway is that flow is proportional to the fourth power of the radius (r⁴). This means a small change in vessel diameter produces a dramatic change in flow. Doubling the radius increases flow 16-fold; halving it reduces flow to 1/16 of its original value.

7.2 Peripheral Resistance

Peripheral resistance (also called total peripheral resistance, TPR) is the opposition to blood flow imposed by friction between blood and the vessel walls, primarily in the systemic arterioles. Three main factors determine resistance:

7.2.1 Vessel Radius (Most Important)

Vessel radius is the single most powerful determinant of resistance because of the r⁴ relationship in Poiseuille's law. Vasoconstriction (narrowing of the vessel lumen) dramatically increases resistance and decreases flow. Vasodilation (widening of the lumen) does the opposite. Arterioles — the "resistance vessels" of the circulation — are the primary site where the body adjusts radius to control resistance and thus blood flow to individual organs.

7.2.2 Vessel Length

Resistance is directly proportional to vessel length: a longer vessel offers more friction. In a healthy adult, vessel length is essentially constant, so this factor plays little role in moment-to-moment regulation. However, vessel length does matter clinically: as a person gains adipose tissue, new blood vessels elongate the vascular network, increasing total resistance and contributing to higher blood pressure in obesity.

7.2.3 Blood Viscosity

Blood viscosity is the thickness or "stickiness" of blood, determined mainly by the concentration of red blood cells (hematocrit) and, to a lesser extent, plasma proteins. Higher viscosity increases resistance. Conditions that alter hematocrit therefore alter resistance:

7.3 Laminar vs. Turbulent Flow

Under normal conditions, blood flows in a laminar (streamlined) pattern: concentric layers of fluid slide past one another, with the fastest flow at the center of the vessel and the slowest near the wall due to friction. This arrangement minimizes energy loss and is silent.

Turbulent flow occurs when blood moves in chaotic, swirling patterns that create eddies and increase resistance beyond what laminar equations predict. Turbulence is audible with a stethoscope as a bruit (a whooshing sound) or palpable as a thrill.

The Reynolds number (Re) predicts whether flow will be laminar or turbulent:

Re = (v × ρ × d) / η

Where v = velocity, ρ (rho) = fluid density, d = vessel diameter, and η = viscosity. A Reynolds number exceeding approximately 2,000–2,500 signals a transition to turbulence.

Clinically, turbulence occurs in several settings: narrowed heart valves (producing murmurs), atherosclerotic plaques (producing bruits in carotid or femoral arteries), anemia (lower viscosity raises Re), and high cardiac output states. Turbulence also underlies the Korotkoff sounds used during blood pressure measurement.

7.4 Blood Pressure: Definitions and Components

Blood pressure (BP) is the force per unit area exerted by blood against the vessel wall, measured in millimeters of mercury (mm Hg). In clinical practice, systemic arterial blood pressure is reported as two values:

• Systolic blood pressure (SBP): The peak pressure during ventricular systole, when the left ventricle ejects blood into the aorta. In a healthy young adult at rest, SBP is approximately 120 mm Hg. Systolic pressure reflects both the stroke volume ejected and the compliance (distensibility) of the aorta and large arteries.

• Diastolic blood pressure (DBP): The minimum pressure during ventricular diastole, when the aortic valve is closed and the elastic recoil of the large arteries continues to push blood forward. Normal DBP is approximately 80 mm Hg. Diastolic pressure primarily reflects peripheral resistance — the state of the arterioles.

• Pulse pressure (PP) is the difference between systolic and diastolic pressure:

PP = SBP − DBP (normally ~40 mm Hg)

Pulse pressure reflects the stroke volume and the compliance of the large arteries. A widened pulse pressure (e.g., 160/70, PP = 90) can indicate increased stroke volume (as in anxiety, exercise, or aortic regurgitation) or stiffening of the aorta (as in aging and atherosclerosis). A narrowed pulse pressure (e.g., 90/80, PP = 10) can suggest reduced stroke volume (heart failure, hypovolemia) or increased peripheral resistance.

7.5 Mean Arterial Pressure

Mean arterial pressure (MAP) is the average pressure driving blood through the systemic circulation during a complete cardiac cycle. Because diastole lasts roughly twice as long as systole, MAP is weighted toward diastolic pressure:

MAP = DBP + ⅓ (SBP − DBP) — equivalently, MAP = DBP + ⅓ PP

For a typical BP of 120/80: MAP = 80 + ⅓(40) = 80 + 13.3 ≈ 93 mm Hg.

MAP is the pressure that organs "feel" — it is the driving force for tissue perfusion. A MAP below about 60 mm Hg is insufficient to perfuse vital organs (brain, kidneys, heart) for extended periods.

MAP can also be expressed in terms of cardiac output and total peripheral resistance:

MAP = CO × TPR

This equation reveals why blood pressure is regulated through two pathways: changing cardiac output (via heart rate or stroke volume) or changing peripheral resistance (via vasoconstriction/vasodilation). An increase in either CO or TPR will raise MAP unless the other factor decreases to compensate.

7.6 Blood Pressure Measurement

Blood pressure is measured indirectly using a sphygmomanometer (inflatable cuff) and a stethoscope — a technique called sphygmomanometry or the auscultatory method.

Procedure and mechanism:

1. The cuff is wrapped around the upper arm and inflated to a pressure above the anticipated systolic pressure (~160–180 mm Hg). This collapses the brachial artery completely, and no sound is heard because no blood flows.

1. As cuff pressure is slowly released, blood begins to spurt through the partially compressed artery only during systole (when arterial pressure momentarily exceeds cuff pressure). This turbulent, intermittent flow produces tapping sounds known as Korotkoff sounds, heard through the stethoscope placed over the brachial artery distal to the cuff.

1. The cuff pressure at which the first Korotkoff sound is heard marks systolic pressure (Phase I).

1. As cuff pressure continues to fall, the sounds change in quality — becoming softer, then muffled, then disappearing entirely. The pressure at which the sounds disappear (Phase V) marks diastolic pressure.

The five Korotkoff phases are:

7.7 Normal and Abnormal Blood Pressure Values

The American Heart Association (AHA) classifies blood pressure as follows:

Hypotension (low blood pressure) is generally defined as a systolic pressure below 90 mm Hg and/or a diastolic below 60 mm Hg. While chronic low pressure can be normal for some individuals (especially fit young people), acute hypotension is a medical emergency because it compromises organ perfusion.

Hypertension (high blood pressure) is a major risk factor for atherosclerosis, heart failure, stroke, myocardial infarction, kidney disease, and retinopathy. It is classified as primary (essential) hypertension when no identifiable cause exists (~90–95% of cases) or secondary hypertension when caused by an underlying condition such as renal artery stenosis, pheochromocytoma, Cushing's syndrome, or coarctation of the aorta.

7.8 Short-Term Neural Regulation of Blood Pressure

Rapid, moment-to-moment control of blood pressure is achieved by neural reflexes that adjust cardiac output and peripheral resistance within seconds. These reflexes are coordinated by the cardiovascular (CV) center in the medulla oblongata, which integrates sensory input and sends autonomic output to the heart and blood vessels.

7.8.1 The Baroreceptor Reflex

The baroreceptor reflex is the primary short-term BP regulator. Baroreceptors are stretch-sensitive mechanoreceptors located in the walls of major arteries:

• Carotid sinus baroreceptors: Located at the bifurcation of the common carotid artery; their afferent signals travel via the glossopharyngeal nerve (CN IX) to the medulla.
• Aortic arch baroreceptors: Located in the wall of the aortic arch; their afferent signals travel via the vagus nerve (CN X).

Response to increased blood pressure:

1. Elevated BP stretches the arterial walls → baroreceptor firing rate increases.
2. Increased afferent signals reach the CV center in the medulla.
3. The CV center responds by:
   • Increasing parasympathetic (vagal) output to the SA node → decreased heart rate (bradycardia).
   • Decreasing sympathetic output to the SA node, ventricular myocardium, and arterioles → decreased heart rate, decreased contractility, and vasodilation.
4. Reduced CO and TPR bring blood pressure back down.

Response to decreased blood pressure:

1. Reduced BP → decreased baroreceptor stretch → baroreceptor firing rate drops.
2. The CV center responds by:
   • Decreasing parasympathetic output → heart rate increases.
   • Increasing sympathetic output → increased heart rate, increased contractility, and vasoconstriction (especially in skin, kidneys, and splanchnic organs — but NOT in the brain or heart, which need constant perfusion).
3. Elevated CO and TPR restore blood pressure.

The baroreceptor reflex is also responsible for preventing orthostatic hypotension — the drop in blood pressure upon standing. When a person stands, gravity pools blood in the lower extremities, reducing venous return and thus CO/BP. Baroreceptors detect the drop and trigger a sympathetic response that restores pressure within seconds. Failure of this reflex (as in autonomic neuropathy or prolonged bed rest) leads to dizziness or fainting upon standing.

7.8.2 The Chemoreceptor Reflex

Peripheral chemoreceptors are located in the carotid bodies (near the carotid sinus) and aortic bodies (in the aortic arch). These receptors are primarily sensitive to changes in blood chemistry:

• Hypoxia (low O₂) — strongest stimulus
• Hypercapnia (high CO₂)
• Acidosis (low pH)

Unlike baroreceptors, chemoreceptors play a minor role in normal BP regulation. They become important when MAP falls below about 60 mm Hg, at which point reduced blood flow causes local hypoxia and acid accumulation in the chemoreceptor tissues. Under these conditions, chemoreceptor firing triggers increased sympathetic output → vasoconstriction and increased heart rate. The chemoreceptor reflex is more crucial for respiratory regulation — increasing ventilation in response to hypercapnia and hypoxia.

7.8.3 The CNS Ischemic Response

The CNS ischemic response is an emergency mechanism activated when cerebral blood flow becomes critically low (MAP below ~50 mm Hg). Ischemia (inadequate blood supply) to the medullary CV center itself triggers a massive, last-resort sympathetic discharge — the most powerful vasoconstriction the body can generate. This response can raise MAP dramatically (to life-saving levels) but is not sustainable; it indicates severe circulatory failure and imminent cardiovascular collapse if perfusion is not restored.

7.9 Hormonal Regulation of Blood Pressure

Hormonal mechanisms act more slowly than neural reflexes (minutes to hours or days) but exert longer-lasting effects on blood pressure and blood volume.

7.9.1 Renin-Angiotensin-Aldosterone System (RAAS)

The RAAS is the most important long-term BP regulatory system. It is activated by:

• Decreased blood pressure (detected by reduced stretch of renal afferent arterioles)
• Decreased Na⁺ delivery to the macula densa of the distal tubule
• Increased renal sympathetic nerve activity

Step-by-step cascade:

1. Renin is released from juxtaglomerular (JG) cells of the kidney afferent arterioles.
2. Renin cleaves angiotensinogen (a plasma protein produced by the liver) into angiotensin I (a 10-amino-acid peptide, largely inactive).
3. Angiotensin-converting enzyme (ACE) — located primarily on the surface of pulmonary capillary endothelial cells — converts angiotensin I into angiotensin II (an 8-amino-acid peptide, the primary effector).
4. Angiotensin II has multiple potent actions:
   • Potent vasoconstriction of systemic arterioles → increases TPR → raises MAP (within seconds to minutes).
   • Stimulates aldosterone secretion from the adrenal cortex (zona glomerulosa).
   • Stimulates ADH release from the posterior pituitary.
   • Stimulates thirst at the hypothalamus → increases fluid intake.
   • Enhances renal Na⁺ reabsorption directly at the proximal tubule.
5. Aldosterone acts on the distal tubule and collecting duct of the kidney to increase Na⁺ reabsorption (and water follows osmotically) and K⁺ secretion. This expands blood volume, which increases venous return → CO → MAP.

Key clinical note: ACE inhibitors (e.g., lisinopril) and angiotensin II receptor blockers (ARBs, e.g., losartan) are first-line antihypertensive medications targeting this pathway.

7.9.2 Antidiuretic Hormone (ADH / Vasopressin)

ADH (also called vasopressin) is synthesized in the hypothalamus and released from the posterior pituitary in response to:

• Increased plasma osmolarity (detected by hypothalamic osmoreceptors)
• Decreased blood volume/pressure (via baroreceptor and atrial volume receptor input)

ADH has two major effects:

• Vasoconstriction (at higher concentrations) via V₁ receptors on vascular smooth muscle → raises TPR. This is where the name "vasopressin" comes from.
• Water reabsorption in the kidney collecting ducts via V₂ receptors → insertion of aquaporin-2 channels → increased water retention → expands blood volume → raises MAP.

7.9.3 Atrial Natriuretic Peptide (ANP) and B-Type Natriuretic Peptide (BNP)

ANP is released from atrial myocytes when the atria are stretched by increased blood volume. BNP is released from ventricular myocytes under similar stretch conditions.

Both hormones counterbalance the RAAS and sympathetic effects by promoting:

• Vasodilation → decreases TPR
• Increased natriuresis (Na⁺ excretion) and diuresis (water excretion) → reduces blood volume
• Inhibition of renin, aldosterone, and ADH release

In essence, ANP/BNP lower blood pressure by reducing both blood volume and peripheral resistance. Clinically, BNP levels are measured as a biomarker for heart failure — elevated BNP indicates ventricular wall stretch.

7.9.4 Epinephrine and Norepinephrine

Epinephrine (adrenaline) and norepinephrine (noradrenaline) are released from the adrenal medulla in response to sympathetic stimulation (fight-or-flight response). Both bind to adrenergic receptors:

• Norepinephrine primarily activates α₁-adrenergic receptors → widespread vasoconstriction → raises TPR and MAP.
• Epinephrine binds both α₁ and β₂-adrenergic receptors. At low concentrations, β₂ (vasodilatory in skeletal muscle and heart vessels) predominates, redistributing blood to active muscles. At high concentrations, α₁ (vasoconstrictor) effects dominate, raising TPR. Epinephrine also binds β₁-adrenergic receptors on the heart → increased heart rate and contractility → increased CO.

7.10 Comparative Summary of Regulatory Mechanisms

7.11 Clinical Applications

Orthostatic Hypotension

Orthostatic (postural) hypotension is a drop in systolic BP of ≥20 mm Hg or diastolic BP of ≥10 mm Hg within 3 minutes of standing. It occurs when the baroreceptor reflex fails to compensate for gravitational pooling of blood. Causes include autonomic neuropathy (diabetes, Parkinson's disease), hypovolemia (dehydration, blood loss), medications (vasodilators, diuretics, alpha-blockers), and prolonged bed rest. Symptoms include dizziness, lightheadedness, blurred vision, and syncope.

Primary vs. Secondary Hypertension

• Primary (essential) hypertension (~90–95% of cases) has no single identifiable cause. Risk factors include genetic predisposition, obesity, high sodium intake, sedentary lifestyle, alcohol, stress, and aging. It tends to develop gradually over many years.
• Secondary hypertension has an identifiable underlying cause: renal artery stenosis (reduced kidney perfusion activates RAAS), pheochromocytoma (excess catecholamines), primary hyperaldosteronism, Cushing's syndrome, coarctation of the aorta, thyroid disorders, and sleep apnea. Secondary hypertension often presents at a younger age, is more severe, and may be resistant to standard medications until the root cause is treated.

Shock Types

Shock is a life-threatening condition of inadequate tissue perfusion (MAP too low), leading to cellular hypoxia and organ dysfunction. The major types differ in their underlying hemodynamic disturbance:

In all shock types, compensatory mechanisms (baroreceptor reflex, RAAS, ADH, sympathetic activation) are triggered to restore MAP. However, if the underlying cause is not corrected, these compensations eventually fail, and multi-organ dysfunction ensues.