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83 Cards in this Set

  • Front
  • Back
Pressure in the right ventricle
25/0 mmHg
Pressure in the pulmonary artery
25/8 mmHg
Mean pulmonary artery pressure
15 mmHg
Pulmonary capillary pressure
7-9 mmHg
Pulmonary venous pressure
5 mmHg
Left atrium pressure
5-10 mmHg
Left ventricle pressure
120/0 mmHg
Aortic pressure
120/80 mmHg
Mean arterial blood pressure
(Systolic - diastolic / 3) + diastolic = 93 mmHg
Skeletal muscle capillary pressure
30 mmHg
Renal glomerular capillary pressure
45-50 mmHg
Peripheral vein pressure
15 mmHg
Right atrium pressure (central venous)
0 mmHg
Systemic circuit Vs. pulmonary system
Cardiac output and heart rate is the same as they're connected in series. The systemic circuit has higher resistance and lower compliance therefore work of the right ventricle is lower.
Highest resistance segment of the systemic circulation
Arterioles. Also responsible for greatest pressure drop.
Largest and smallest cross-sectional areas of the systemic circuit
Largest: capillaries; smallest: aorta
Fastest and slowest velocities in the systemic circuit
Velocity is inversely proportional to cross-sectional area. Aorta has fastest velocity; capillaries have slowest velocity.
Largest blood volumes in the cardiovascular system
Systemic veins then pulmonary system have the largest blood volume. Both represent reservoirs due to high compliance.
Poiseuille equation
Q = P1 - P2 / R;
Determinants of resistance
R ∝ vL / r4; if radius doubles, resistance decreses to 1/16; if radius decreases by half, resistance increases 16-fold
Reynolds number
RN = diameter x velocity x density / viscosity. If > 2,000 --> turbulent flow; if < 2,000 --> laminar flow
Vessel with the most turbulent flow
Aorta - has large diameter, high velocity. In anemia (↓ viscosity) --> aortic murmur
Features of a series circuit
Flow is the same at all points; the total resistance is the sum of all resistances; adding a resistor decreases flow at all points and vice versa;
↓ resistance, ↑ capillary flow, ↑ capillary pressure
Arteriole dilation - beta agonists, alpha blockers, ↓ sympathetic, metabolic dilation, ACEIs
↑ resistance, ↓ capillary flow, ↓ capillary pressure
Arteriole constriction - alpha agonists, beta blockers, ↑ sympathetic, angiotensin II
↓ resistance, ↑ capillary flow, ↓ capillary pressure
Venous dilation - ↑ metabolism
↑ resistance, ↓ capillary flow, ↑ capillary pressure
Venous constriction - physical compression, ↑ sympathetic
↑ capillary flow, ↑ capillary pressure, no change in resistance
↑ arterial pressure - ↑ CO, volume expansion
↓ capillary flow, ↓ capillary pressure, no change in resistance
↓ arterial pressure - ↓ CO, hemorrhage, dehydration
↓ capillary flow, ↑ capillary pressure, no change in resistance
↑ venous pressure - CHF, physical compression
↑ capillary flow, ↓ capillary pressure, no change in resistance
↓ venous pressure - hemorrhage, dehydration
Characteristics of parallel circuits
The reciprocal of the total resistance is the sum of the reciprocal of the individual resistances. Connecting a resistance in parallel lowers resistance, total resistance is always less than individual resistances.
Parallel circuits with greatest resistance
Coronary > cerebral > renal > pulmonary
What happens if a parallel circuit is added?
TPR decreases, pressure would decrease but a compensatory increases in CO maintains same pressure. Obesity.
What happens if a parallel circuit is removed?
TPR increases, blood pressure increases, CO might decrease to compensate increased blood pressure.
Wall tension
T ∝ Pr. In aneurysm, tension is high due to grater radius.
Factors that increase systolic pressure
↑ stroke volume, ↓ HR, ↓ compliance
Factors that decrease systolic pressure
↓ stroke volume, ↑ HR, ↑ compliance
Factors that decrease diastolic pressure
↓ TPR, ↓ HR, ↓ stroke volume, ↓ compliance
Factors that increase diastolic pressure
↑ TPR, ↑ HR, ↑ stroke volume, ↑ compliance
Factors that increase pulse pressure
↑ stroke volume (systolic > diastolic); ↓ compliance (systolic increases and diastolic decreases)
Determinants of mean arterial pressure
MAP = CO x TPR
What happens to cardiac output and mean arterial pressure if TPR increases?
MAP increases and CO decreases
What happens to cardiac output and TPR if mean arterial pressure decreases?
TPR decreases, CO decreases but then increases to compensate and maintain blood pressure
Hemodynamic changes in hemorrhage
Loss of circulating volume and CO --> less firing of carotid sinus (↓ BP) --> reflex sympathetic ↑ in TPR and CO --> ↓ venous compliance --> ↑ circulating volume --> compensated CO and BP
Hemodynamic changes during exercise
Dilation of arterioles --> ↓ TPR --> ↓ BP --> less firing of carotid sinus --> reflex sympathetic ↑ in CO --> ↑ BP
Hemodynamic changes due to gravity
↑ venous pressure, ↑ pooling of blood in veins, ↓ circulating blood volume (CO), ↓ BP --> compensation via carotid sinus --> ↑ TPR, ↑ HR
Effects of inspiration on blood flow
↓ intrapleural pressure --> ↑ venous return --> ↑ right ventricle output --> splitting of S2 --> blood in pulmonary circuit increases --> ↓ venous return to left heart --> ↓ systemic pressure --> reflex increase in HR
Effects of expiration on blood flow
↑ intrapleural pressure --> ↓ venous return --> ↓ pulmonary blood volume --> ↑ output of left ventricle --> ↑ systemic pressure --> reflex bradycardia
What factor controls blood flow to capillaries?
↑ resistance of arterioles --> ↓ capillary flow and pressure; ↓ resistance of arterioles --> ↑ capillary flow and pressure
What factors affect capillary exchange?
Exchange is by simple diffusion only. Proteins do not cross the capillary membrane. Factors that affect diffusion rate are: surface area, membrane thickness, concentration gradient, solubility
When does the rate of uptake become perfusion-limited?
When concentration of the substance reaches equilibrium between capillary and tissue. ↑ blood flow converts perfusion-limited uptake to diffusion-limited again.
When does the rate of uptake become diffusion-limited?
When concentration between capillary and tissue are not in equilibrium.
What forces favor reabsorption?
Capillary oncotic pressure and interstitial hydrostatic pressure
What forces favor capillary filatration?
Capillary hydrostatic pressure and interstitial oncotic pressure
What happens to filtration in lung capillaries when intrathoracic pressure decreases?
↓ intrathoracic pressure promotes filtration. In ARDS --> ↓ intrathoracic pressure --> pulmonary edema
Conditions that affect capillary hydrostatic pressure
Essential hypertension increases resistance and decreases capillary hydrostatic pressure. Hemorrhage decreases capillary hydrostatic pressure and promotes reabsorption.
Conditions that affect capillary oncotic pressure
Increased by dehydration. Decreased by liver and renal disease and saline infusion
Conditions that affect interstitial oncotic pressure
Increased by lymphatic blockage and increased capillary permeability to proteins (burns)
Conditions that affect insterstitial hydrostatic pressure
Increased by negative intrathoracic pressure in ARDS
Fick principle
Measures cardiac output. Flow = O2 consumption / O2 concentration difference across the organ
Intrinsic autoregulation of blood flow
Resistance of arterioles is changed in order to regulate flow. No nerves or hormones involved. Independent of BP.
Metabolic hypothesis of autoregulation
Tissue can produce a vasodilatory metabolite that regulates blood flow. Example adenosine in coronaries.
Tissues that have autoregulation of blood flow
Cerebral, coronary and exercising skeletal muscle circulations
Extrinsic regulation of blood flow
Controlled by nervous and hormonal influences. NE via β2 vasodilates, via α1 constricts (dose dependant). Angiotensin II constricts.
Tissues that have extrinsic regulation of blood flow
Resting skeletal muscle, skin
Lowest venous PO2 in the body
Coronary circulation due to maximal extraction of O2. To increase delivery of oxygen, flow must increase.
Factors that control coronary circulation
Coronary circulation occurs in diastole and its determined by stroke work of the heart. Exercise increases volume work and coronary flow. Hypertension increases pressure work and coronary flow. Vasodilation is mediated by adenosine.
Factors that control cerebral blood flow
Flow is proportional to arterial PCO2. Hypoventilation increases PCO2 and flow. Hyperventilation decreases PCO2 and flow. PO2 determines flow only if theres a large decrease in PO2.
Factors that control cutaneous blood flow
↑ sympathetic tone --> constriction of arterioles --> ↓ blood flow, ↓ blood volume in veins --> ↑ velocity (↓ cross-sectional area). Increased skin temperature --> vasodilation --> heat loss
Highest venous PO2 in the body
Renal circulation
Factors that control renal circulation
Small changes in blood pressure invoke autoregulatory responses. Sympathetic may influence blood flow in extreme conditions (hemorrhage, hypotension)
Characteristics of pulmonary circuit
Low pressure, high flow, low resistance, very compliant, hypoxic vasoconstriction.
Pulmonary response to exercise
↑ CO --> ↑ pulmonary pressure --> pulmonary vessel dilation (due to high compliance) --> large ↓ resistance --> ↓ pulmonary pressure
Pulmonary response to hemorrhage
↓ CO --> ↓ pulmonary pressure --> pulmonary vessel constriction --> large ↑ resistance --> less blood volume
Fetal circulation: percent O2 saturation in umbilical vein
80% O2 saturation
Fetal circulation: percent O2 saturation in inferior vena cava
26% O2 saturation. Mixes with hepatic vein blood --> step up to 67%
Fetal circulation: percent O2 saturation from inferior vena cava into right atrium
67% O2 saturation. Blood from inferior vena cava enters right atrium and passes through foramen ovale
Fetal circulation: percent O2 saturation in superior vena cava
40% O2 saturation. Mixes with blood from inferior vena cava (67%) and passes to right ventricle at 50% saturation
Fetal circulation: percent O2 saturation in right ventricle
Contains blood from superior vena cava mixed with IVC --> 50% saturation. Passes through pulmonary artery and 90% is shunted through the ductus arteriosus into aorta
Fetal circulation: percent O2 saturation in ascending aorta
Contains blood from inferior vena cava --> 67%
Fetal circulation: percent O2 saturation in brachiocephalic trunk
Blood from left ventricle (67%) mixes with blood from ductus arteriousus (50%) --> yields 65%
Fetal circulation: percent O2 saturation in descending and abdominal aorta
Blood from left ventricle (67%) mixes with blood from ductus arteriousus (50%) --> yields 60%