Objective 3Flow, Pressure and Resistance A.Definitions Blood Flow : the volume (quantity) of blood that flows through a vessel, an organ or entire circulation in a given period of time  usually measured in ml/min (What does this remind you of ?  for systemic circulation or pulmonary circulation, flow equals cardiac output  general flow equation: Pressure in arteries – Pressure in Veins Flow =Resistance Cardiac output!

Problem: For a patient with a pulmonary arterial pressure of 15 mmHg, a pulmonary venous pressure of 0 mmHg and a pulmonary vascular resistance of 3 mmHg  L/min, what is the pulmonary flow? Answer: 5 L/min

Blood Pressure: the force per unit area exerted on a vessel wall by the blood it contains  expressed in mmHg  pressure differences drive the flow of blood  blood flows from areas of pressure to areas of pressure high low

Because blood pressure changes during systole and diastole, mean arterial pressure is often calculated: Mean Arterial Pressure (MAP) MAP= diastolic pressure + pulse pressure/3 Pulse pressure (PP) PP= systolic pressure – diastolic pressure MAP is the pressure in arteries averaged over time; it is the pressure that propels blood to the tissues during the cardiac cycle

Problem: For a patient with a systolic arterial pressure of 136 mmHg, and a diastolic arterial pressure of 88 mmHg, what is the pulse pressure? What is the mean arterial pressure? PP = systolic pressure – diastolic pressure = 136 mmHg- 88mmHg = 48 mmHg MAP= diastolic pressure + pulse pressure/3 = 88mmHg + (48mmHg/3) = 104 mmHg

Pressure in arteries – Pressure in Veins Resistance Flow = Let’s review what we already know: If the pressure difference then flow What about the relationship between resistance and flow?

Resistance: opposition to or impedance of blood flow  resistance is encountered when blood experiences friction  for systemic resistance, the term peripheral resistance is used  The greater the resistance the slower the blood flow there are three factors that determine resistance and they are related by the following equation: vessel lengthX blood viscosity Resistance = (vessel radius) 4

Three factors affect resistance: 1.Blood viscosity – as viscosity increases, resistance ? What happens to flow? 2.Vessel length – as vessel length increases, resistance ? What happens to flow? 3.Vessel radius – as vessel radius increases, resistance? What happens to flow? * Vessel radius is the most important determinant of resistance* vessel lengthX blood viscosity Resistance = (vessel radius) 4 Pressure in arteries – Pressure in Veins Resistance Flow =

Question: A hypertensive patient is prescribed a vasodilator, and it was noted that the diameter of one of his blood vessels doubled. What is the change in the resistance? What is the change in flow? Resistance decreases by a factor of 16 Flow increases by a factor of 16 If vessel radius = 1, flow is 1ml/min If vessel radius = 2, flow is 16ml/min If vessel radius = 4, flow is 256ml/min

B.Putting It All Together  For systemic circulation: assume that: blood flow=cardiac output (CO) venous pressure=zero mmHg  then: Mean Arterial Pressure Cardiac Output= Resistance and: Cardiac Output X Resistance = Mean Arterial Pressure

Mean Arterial Pressure = Cardiac Output X Resistance Resistance is total peripheral resistance (TPR), the sum of resistances to flow by all systemic blood vessels To maintain blood flow MAP must be greater than resistance Changes in MAP is the result of changes in these two variables

Long term control Kidneys Short term control

Importance? This pressure is the driving force for blood flow through all organs except the lungs!

Summing up Flow, Pressure, and Resistance Flow = Pressure in arteries – pressure in veins resistance –To increase flow, decrease resistance, or increase pressure difference –An example: during rigorous exercise CO and SV increase, increasing pressure in the aorta Blood vessels in skeletal muscles dilate What happens to blood flow?

Predict the effect of the following on blood flow: Vasoconstriction of cutaneous blood vessels in response to cold temperatures? Vasodilation of cutaneous blood vessels in response to elevated body temperatures? Polycythemia?

Objective 4 Mean Arterial Pressure A.Mean Arterial Pressure  is the average pressure exerted by the blood on the walls of arteries  is the driving force for the circulation of blood MAP=P D + PP/3

Mean Arterial Pressure (MAP) = diastolic pressure + pulse pressure/3 Given the following values calculate MAP –Systolic pressure = 135 mmHg –Diastolic pressure = 80 mmHg If person has a blood pressure of 128/92, what is their MAP?

Systolic Arterial Pressure (P s ):  is the pressure in an artery at the peak of ventricular systole  during ventricular systole, the artery receives the stroke volume  systolic pressure averages 120 mmHg

C.Diastolic Arterial Pressure (P D ):  is the pressure in an artery at the end of ventricular diastole  during ventricular diastole, blood is moving from the elastic arteries into smaller vessels  this is facilitated by the elastic recoil of the arterial wall  diastolic pressure averages 80 mmHg

D.Pulse Pressure:  pulse refers to the throbbing felt in arteries during the cycle of systole and diastole  Pulse Pressure: Pulse Pressure (PP) = Systolic Pressure (P s ) – Diastolic Pressure (P d )

Factors that influence pulse pressure:  Arterial distensibility (compliance*): how well the artery can expand to receive a stroke volume  Amount of stroke volume PsPdPsPd *Compliance = the ease with which a structure can be stretched

Question: What happens to pulse pressure when arteries become rigid? What happens to pulse pressure when blood volume decreases? increases decreases

Pulse can be felt in any elastic artery that lies close to the surface of the body and is positioned over firm tissue (muscle, bone) Common arteries used for evaluating pulse are:

E.Capillary Pressure and Venous Pressure Capillary pressure:normally low (averages 20 mmHg)  high capillary pressure would damage capillary walls  high capillary pressure would force excess fluids through capillary walls and create tissue edema

Venous Pressure: normally 0-20 mmHg  venous return is enhanced by respiratory pump and the skeletal muscle pump

Objective 5Cardiac Output, Resistance and MAP Mean Arterial Pressure = Cardiac Output X Resistance Mean Arterial Pressure = (SV X HR) X Resistance Factors Which Increase MAP Factors Which Decrease MAP Increased cardiac output Decreased cardiac output Increased blood volume Decreased blood volume Increased peripheral resistance Decreased peripheral resistance Regulation of MAP consists of: Short term controls (baroreceptor reflexes, chemoreceptor reflexes, chemical factors) Long term controls (kidney regulation via blood volume)

Long term control Kidneys Short term controls

Control of MAP via altering resistance vasoconstriction vs vasodilation Increased resistance Decreased resistance

A.Regulation of MAP by altering resistance (short term controls) The vasomotor center, baroreceptors and chemoreptors (short term) vasomotor center:sympathetic neurons in the medulla oblongata that control the resistance by stimulating vasoconstriction vasomotor tone:a state of partial arteriolar constriction that helps to maintain normal MAP baroreceptors:blood pressure receptors in the carotid sinuses and in the aortic arch; activated by increased MAP chemoreceptors:receptors (aortic and carotid bodies) in the aortic arch and carotid sinuses that monitor blood pH and plasma O 2 and CO 2 higher brain centers: the cerebral cortex and the hypothalamus can modify mean arterial pressure by acting through the medulla oblongata

The pathway for short term control of MAP 1. Receptors– baroreceptors, higher brain centers and chemoreceptors 2. Afferent nerves- CN IX and CN X 3. Control center- vasomotor center in medulla oblongata 4. Efferent nerves- sympathetic nerves 5. Effectors- smooth muscle in arteriolar wall Heart- SA node and myocardium

Now, before we start talking about mechanisms, a handy little reaction that you will come to know and love: 1.CO 2 + H 2 OH 2 CO 3 H + + HCO Increases in plasma H + cause decreases in plasma pH 3.Increases in metabolic rate are associated with - reduced plasma O 2, and -increased plasma CO 2 ( therefore, increased plasma H + and decreased plasma pH)

Adjustment to Increased MAP, Increased Plasma O 2 or Increased Plasma pH Increased MAP, Increased Plasma pH, Increased Plasma O 2, Decreased Plasma CO 2 Vagus (X) and glossopharyngeal (IX) nerves are activated The vasomotor center is inhibited SNS vasomotor nerves decrease their rate of firing Vasomotor tone is reduced Arterial pressure falls

Adjustment to Decreased MAP, Decreased Plasma O 2 or Decreased Plasma pH Decreased MAP, Decreased Plasma O 2, Decreased Plasma pH, Increased Plasma CO 2 Vagus (X) and glossopharyngeal (IX) nerves are not activated The vasomotor center is “disinhibited” SNS vasomotor nerves increase their rate of firing Vasomotor tone is increased Arterial pressure rises

Remember: MAP = CO X R MAP = (SV X HR) X R Follow pathway for adjusting MAP through changing CO Then follow pathway for adjusting MAP through changing peripheral resistance (vasomotor) Make a flow chart!

2.Chemical Controls: Norepinephrine (NE) and Epinephrine (E) Source: Mechanism: NE and E (generally) vasoconstrict and increase CO Effect: increased resistance, increased CO and increased MAP Adrenal medulla Remember: MAP = CO X R

Diuresis Atrial Natriuretic Peptide (ANP ) Source: Released by atrial cardiac muscle cells Mechanism: ANP causes increased loss of Na + and water in urine (targets the kidneys) and causes generalized vasodilation Effects are decreased blood volume decreased resistance and decreased MAP Remember: MAP = CO X R

Antidiuretic Hormone (ADH) Source: Manufactured by the hypothalamus and secreted from the posterior pituitary gland Mechanism: ADH increases the retention of water by the kidneys and in high amounts can cause vasoconstriction Effects are increased blood volume and in high amounts, increased resistance; increases MAP Remember: MAP = CO X R

Angiotensin II Source:see below Mechanism:A strong vasoconstrictor that also stimulates the release of aldosterone from the adrenal cortex Effects: increases resistance and increases MAP Endothelin: Source:Secreted by vascular endotheliuum MechanismIs a vasoconstrictor Effects:increases resistance and increases MAP Nitric Oxide (NO) Source:Secreted by vascular endothelium MechanismIs a vasodilator Effects:decreases resistance and decreases MAP Remember: MAP = CO X R

Inflammatory Chemicals (kinins, histamine, prostacyclin) Source:secreted by damaged tissue cells Mechanism are vasodilators Effects:decrease resistance and decrease MAP Alcohol: Source:ingestion Mechanisminhibits ADH secretion, depresses the vasomotor center and acts as a vasodilator Effects: decreased blood volume and decreased resistance; decreased MAP Remember: MAP = CO X R Using the space at the bottom of page 3.27 make a table listing the chemicals this way: Vasodilators ( resistance) vs Vasoconstrictors ( resistance)

Long term control of MAP: mediated by renal mechanisms via changes in blood volume Direct renal mechanisms Indirect renal mechanisms Keep this in mind: Increasing blood volume will increase MAP Decreasing blood volume will decrease MAP

1. Direct renal mechanism: changing blood volume by changing water output (independent of hormones, alteration via GFR) If MAP increases Increased urine output Decreased blood volume Decreased MAP If MAP decreases Increased MAP Decreased urine output Increased blood volume

Indirect renal mechanism: the renin angiotensin pathway decreased renal blood pressure kidneys secrete renin angiotensinogenangiotensin I angiotensin converting enzyme (ACE) angiotensin Iangiotensin II Effects of angiotensin II:  is a strong vasoconstrictor  stimulates the release of aldosterone from the adrenal cortex  stimulates thirst and stimulates the release of ADH

Objective 6 Hypertension/Hypotension DisorderCause(s)Characteristics Hypotensionlow blood volume,reduced MAP (P s <100 mmHg) orthostatic, hypothyroidism,can lead to dizziness, fainting, Addison’s disease,blurred vision, inadequate protein malnutritionorgan perfusion HypertensionPrimary (essential)elevated MAP (> 140/90) no underlying cause is evident, but riskprolonged hypertension can factors include poorlead to vascular damage, diet, obesity,heart failure, renal disease alcohol/cigarettes,and stroke family history Secondary cause is identifiable, such as excess renin, pregnancy, septal defects, hyperthyroidism, atherosclerosis, etc