Cardiovascular III

Blood Vessels

• Arteries carry blood away from the heart.
• Veins carry blood toward the heart.
• The order of blood vessels is: arteries, arterioles, capillaries, venules, and veins.

Blood Pressure Changes

• Blood pressure (BP) represents the force exerted by blood on vessel walls, measured in mm Hg.
• As blood moves away from the ventricles (the heart's pumping chambers), blood pressure decreases.

Systemic Arterial Blood Pressure

• Systemic arterial blood pressure is measured in the largest arteries near the heart.
• Systolic pressure signifies the peak pressure in the aorta during ventricular contraction (systole).
• Diastolic pressure signifies the pressure in the aorta during ventricular relaxation (diastole).
• Pulse pressure is the difference between systolic and diastolic pressure.
• Mean arterial pressure (MAP) is the calculated average of systolic and diastolic pressures. Avoid just calculating the halfway point between the two values.

MAP Calculation

• MAP = diastolic pressure + (pulse pressure/3)
• Example: If systolic pressure is 120 mm Hg and diastolic pressure is 70 mm Hg, then MAP = 70 + ((120-70)/3) = 86.67 mm Hg.

Cardiac Output

• Cardiac output (CO) measures the amount of blood pumped by each ventricle in one minute, expressed in liters per minute (L/min).
• CO is calculated by multiplying heart rate (HR) by stroke volume (SV). CO = HR x SV
• Heart rate (HR) is the number of beats per minute.
• Stroke volume (SV) is the volume of blood pumped out by one ventricle with each beat and is calculated as the end-diastolic volume (EDV) minus the end-systolic volume (ESV).

Cardiac Output Calculations

• If average HR = 80 beats/min and average SV = 70 mL/beat, then CO = 80 x 70 = 5600 mL/min = 5.6 L/min.
• Normal adult blood volume is about 5L. This means that the entire blood volume passes through each side of the heart every minute.
• Increasing the stroke volume (SV) or heart rate (HR) will increase CO; increasing CO increases mean arterial pressure (MAP).

Frank-Starling’s Law (Starling’s Law)

• The greater the filling of the heart (EDV), the greater the amount pumped by the heart (SV).
• If EDV increases then SV increases.
• If EDV decreases then SV decreases.
• Increasing preload (EDV) increases stroke volume (SV); increasing SV increases cardiac output; increasing cardiac output increases MAP.

Factors Affecting Blood Pressure

• Cardiac output (CO) affects blood pressure. CO = HR x SV
• Total peripheral resistance (TPR) affects blood pressure.
  • TPR is affected by blood viscosity, blood vessel length and blood vessel diameter (vasoconstriction & vasodilation).
• Blood volume affects blood pressure.

Blood Pressure Regulation

• Short-term regulation influences BP by altering CO and/or TPR through neural and hormonal controls.
• Long-term regulation influences BP by altering blood volume through renal mechanisms (kidneys).

Short Term Neural Regulation of Blood Pressure

• Baroreceptors: Nerve endings detecting pressure and stretch, found in the aortic arch and carotid arteries
• Stretch information is relayed to the cardiovascular center in the medulla (brainstem).
• The cardiovascular center (medulla) consists of the cardioacceleratory center, the cardioinhibitory center and the vasomotor center.
  • The cardioacceleratory center has sympathetic output.
  • The cardioinhibitory center has parasympathetic output.
  • The vasomotor center controls sympathetic vasoconstriction.

Baroreceptor Reflex in Response to High BP

• High BP stimulates baroreceptors.
• Signals are sent to the cardiovascular center of the medulla:
  • Stimulates parasympathetic output
  • Inhibits sympathetic output
  • Inhibits vasomotor center
• Decreases heart rate (↓CO) and increases vasodilation (↓TPR).
• Blood pressure is lowered.

Baroreceptor Reflex in Response to Low BP

• Low BP inhibits baroreceptors.
• Signals are sent to the cardiovascular center of the medulla:
  • Inhibits parasympathetic output
  • Stimulates sympathetic output
  • Stimulates vasomotor center
• Increases heart rate (↑CO) and increases vasoconstriction (↑TPR).
• Blood pressure is raised.

Short term Hormonal Regulation of Blood Pressure

• Atrial natriuretic peptide (ANP) is a hormone produced by the atria of the heart.
• The stimulus for ANP release is an increase in BP.
• ANP's target is blood vessels, leading to vasodilation.
• ANP decreases TPR, which decreases BP.
• ANP helps with long-term regulation by targeting the kidneys to excrete more Na+ and H2O in the urine, decreasing blood volume and BP.

Long term Regulation Renal Mechanisms

• The renin – angiotensin – aldosterone system (RAAS) influences blood volume through effects on thirst, hormone release and can also influence TPR (short-term).
• Steps of the RAAS mechanism:
  • Low BP is detected.
  • The kidneys release renin.
  • Renin converts angiotensinogen (from the liver) to angiotensin I (inactive).
  • ACE (from the lungs) converts angiotensin I to angiotensin II.
  • Angiotensin II is active.
  • Angiotensin II triggers the sensation of thirst via the hypothalamus.
  • Angiotensin II stimulates the adrenal cortex to secrete aldosterone.
  • Aldosterone increases Na+ reabsorption and subsequent water reabsorption, which increases blood volume.
  • Angiotensin II stimulates the posterior pituitary to release ADH, increasing water reabsorption in the kidneys and increasing blood volume.
  • Angiotensin II elicits vasoconstriction (short term: increases TPR, increases BP).
• Decreases in arterial BP stimulates renin release to upregulate the RAAS and increase BP. High BP would inhibit renin release to downregulate the RAAS and decrease BP.

Pharmacological control of Blood Pressure

• In 2021, hypertension was a primary or contributing cause of 691,095 deaths in the United States.
• Nearly half of adults have hypertension (48.1%, 119.9 million) or are medicated for hypertension.
• The RAAS system is a primary target in the treatment of hypertension.
• ACE inhibitors and Renin inhibitors are used:
  • The first ACE inhibitor was approved in 1981.
  • The first renin inhibitor was approved in 2007.