Cardio Mod 4 Flashcards
Systemic Circulation Pathways
a. Arterial side
b. Venous side
c. Portal circulation pathways
Portal circulation pathways
• Two capillary beds before venous return
(i) GI/hepatic portal system
1. GI/spleen capillary bed sends blood to liver before blood empties into IVC
(ii) Renal system has two capillary beds within kidney to allow reabsorption
Venous Side of systemic circulation pathways
• Regions follow similar pathways until reach vena cava
(i) Superior vena cava
(ii) Inferior vena cava
Arterial side of systemic circulation pathways
• Aortic arch
(i) Head/neck via carotid and vertebral arteries
(ii) Upper extremities via subclavian arteries
(iii) Trunk via descending aorta
1. Thoracic and abdominal aortic branches
(iv) Pelvis via iliac arteries
(v) Lower extremities via external iliac/femoral arteries
Distribution of blood throughout each region
a. 70% of total blood volume via systemic circulation
(i) Arterial system = 16% of total blood volume
1. referred to as “stressed” volume
(ii) Venous system = 54% of total blood volume
1. Largest “reservoir” of blood volume in the body
2. referred to as “unstressed” volume
b. 18% of total blood volume in pulmonary circulation
c. 12% of total blood volume in coronary circulation
• “Small” organ but relatively large demand for blood supply for obvious reasons
Pressure gradients through heart chambers
• Starts at 0-4 mmHg and gradually increases to 100+ mmHg
(i) Myocardial contraction provides needed increase in pressure
(ii) NOTE: heart valves are open/closed via pressure gradients
Pressure gradients through systemic circulation
• Starts at 100+ mmHg and gradually decreases to 0-4 mmHg
(i) Cross sectional area and many other factors provide decrease in pressure
Pulmonary circulation pressures
a. Pulmonary trunk • Systolic 15-30 mmHg • Diastolic 3-12 mmHg b. Pulmonary capillaries • 10 mmHg c. Pulmonary veins • 4-12 mmHg
Heart/Systemic circulation pressures (7)
a. Left atria • 4-12 mmHg b. Left ventricle • Systolic 90 – 140 mmHg • End-Diastolic 4-12 mmHg c. Aorta • systolic 96-140 mmHg • diastolic 60-90 mmHg d. Capillaries • 20 – 40 mmHg • Except: Initial renal (glomerular) capillaries = 45 mmHg to encourage filtration e. Venous return to vena cava • 4 mmHg f. Right atria • 0 – 8 mmHg g. Right ventricle • Systolic 15-28 mmHg • End-Diastolic 0-8 mmHg
Most blood vessel walls are comprised of three layers
a. Tunica intima • Smooth frictionless inner layer • Endothelium, basement membrane and thin connective tissue layer b. Tunica media • Smooth muscle and elastic fibers c. Tunica externa (adventitia) • Thin layer of connective tissue
Arterial blood vessels—Elastic arteries
• Pulmonary trunk, aorta and major branches
• Thick tunica media - composition
(i) Elastin > Smooth muscle
(ii) Function: stretch to absorb systolic volume of blood and recoil to return to original diameter
Blood Flow Characteristics of Elastic Arteries
(i) High pressure
(ii) High velocity
(iii) Small total cross sectional area
1. large diameter vessel but not many in total thus small cross sectional area
Muscular arteries
• Medium and small size arteries
• Thinner tunica media - composition
(i) Transition to less elastin and more smooth muscle
(ii) Function: muscular control distributes blood flow to arterioles throughout the body
Arterioles/metarterioles
• Arterioles site of highest resistance in systemic circulation – acts as “controller” to direct blood to capillary beds at slow/low pressure flow
• Arterioles function is to slow the velocity, pressure and volume traveling into capillaries
(i) Change in pressure is small from aorta/major arteries to arterioles
1. Pressure entering arterioles ≈ 90-100 mmHg
(ii) Largest drop in arterial pressures occurs at arterioles
1. enter arterioles ≈ 90-100mmHg; leave arterioles ≈ 25-35 mmHg
• Arterioles major role in regulating resistance of systemic circulation
• Lumen < 0.5 mm in diameter
• Thin tunica media - composition
(i) Mostly smooth muscle and minimal amount of elastin
(ii) Function: regulate blood flow into capillary beds via precapillary sphincters
Blood Flow Characteristics of Arterioles
(i) Decreasing pressure
(ii) Decreasing velocity
(iii) Increasing total cross sectional area
Blood Flow Characteristics of Capillaries
• Low pressure
• Slow velocity
(i) Approximately 1.5 seconds for RBC to pass through capillary
(ii) Why? – allows ample time for gas exchange
• HUGE total cross sectional area (1,000x’s larger than aorta cross section)
(i) Individual cross section very narrow…”one cell at a time” but millions of capillaries to allow net total of large cross sectional area
Capillaries
• Single endothelial layer with basement membrane without tunica media and externa
c. Functional Role
• Site of respiration (gas exchange) as well as nutrient & water exchange
d. At any given moment only 5% of circulating blood is in capillary beds – not much but a very critical 5%!
Blood Flow Characteristics of Veins
• Pressure continues to decrease…average vena cava pressure = 4 mmHg
• Velocity gradually increases
(i) By the time the blood gets back to the heart, velocity is traveling approximately 60% of original arterial velocity
Veins vs. Arteries
(i) veins have thinner and more fibrous walls
(ii) veins have less elastin vs arteries
(iii) veins have larger diameters when compared to it’s arterial blood vessel
Structure of Veins
• Compliance of venous system allows large blood volume fluctuations without dramatic blood pressure variations
(i) veins = “compliant” (distensibility – expand easily to accommodate volume increase)
(ii) arteries = “elastance” (elastin – more force required to stretch to accommodate volume increase)
• Veins have one-way valves to assist in directing blood flow back to the heart via the “muscle pump”
(i) Valves are formed by “in-folds” of tunica intima
DVT’s
• Stasis in veins prone to thrombus/clot formation
(i) Post surgical most common – meds and ankle pumps to prevent DVT’s,
(ii) Long plane flights – not as common but receives a lot of “media attention”
1. Prevention ankle pumps and frequent walking around flights
• Will discuss in later module
Mechanism to “pump” blood back to the heart through the venous system
• Heart pump itself…constantly forcing “new” blood into arterial system
• Elastic recoil of artery system
• Respiratory Pump
(i) Changes in intra-thoracic pressures influence venous return/atrial pressures
(ii) Inspiration – promotes venous return
1. transiently decreases right atrial pressure which allows increased filling
2. Ventilation compresses IVC which pushes more blood back to the heart
• “Muscular pump” during exercise
(i) Lower extremity valves “close” and the contracting leg muscles compress the blood toward the heart which “pushes open” the next set of valves
3 Factors affecting blood flow (volume per unit of time)
a. Velocity (distance per unit of time)
• Directly related to blood flow
• Inversely related to TPR
b. Pressure of fluid (blood)
• pressure gradients high to low
c. Laminar vs Turbulent flow
• Laminar = increased blood flow
• Turbulent (“funny flow”) = decreased blood flow
Most resistance in blood flow is due to:
Length and diameter of blood vessel
- Vasoconstriction/dilation provide increase/decrease resistance
(ii) Viscosity of blood itself will also increase vascular resistance - Increased hematocrit (RBC/whole blood volume) – acts like “sludge”
a. Ex: polycythemia and dehydration (↓ fluid volume)
Resistance is related to blood flow how?
• Resistance is inversely related to blood flow
i) Increased resistance = decreased blood flow (less volume per unit of time
Total Peripheral Resistance (TPR) is inversely related to blood flow (volume per unit of time)
(i) Sometimes referred to as systemic vascular resistance (SVR)
1. TPR (or SVR) = resistance to all systemic vasculature excluding pulmonary vasculature
2. Arterioles major role in regulating TPR (SVR)
a. Narrowed channel of arteriole provides most resistance – allows larger cross section of capillary bed to have slow low pressure flow for gas/nutrient exchange
(ii) Inverse relationship
1. ↓ TPR = ↑ arterial blood flow to tissues and ↑ blood flow to venous system.
2. ↑ TPR = ↓ arterial blood flow to tissues and ↓ blood flow to venous system.
Sympathetic influence on TPR–Blood vessel
sympathetic “fight or flight” stress role requires different responses of blood vessels depending on tissue
a. Vasoconstriction to preserve/increase systemic BP
i. peripheral and GI/GU blood vessels
b. Vasodilation to divert blood to tissues needed for “action/stress response”
i. skeletal muscle, heart and CNS blood vessels to promote action/stress response
c. Different sympathetic receptors allow dual response of blood vessels
i. Beta 2 (β2) - dilate smooth muscle of blood vessels
ii. Alpha 1 (α1) – constricts smooth muscle of blood vessels
Sympathetic influence on TPR– Heart
sympathetic increases heart rate (chronotropic)/contractility(inotropic)
a. Atria
i. Nodal tissue: increase HR (increase conduction rate)
ii. Myocardium (contractile tissue): increase contractility of atria
b. Ventricles
i. Myocardium (contractile tissue): increase contractility of ventricle
Parasympathetic influence on TPR– Blood Vessels
parasympathetic dilate GI/salivary gland blood vessels
a. Vasodilation to GI tract to promote energy uptake/conservation
b. Parasympathetic only innervate blood vessels of GI/salivary gland and erectile tissue
Parasympathetic influence on TPR– Heart
a. Atria:
i. Nodal tissue: decrease HR (decrease conduction rate)
ii. Myocardium (contractile tissue): decrease contractility of atria
b. Ventricles
i. No influence - parasympathetics DO NOT innervate ventricle
Baroreceptors (stretch receptors) influence on total peripheral resistance
(i) Located within aorta and carotid sinus
1. If increase stretch on baroreceptors (↑ BP) then receptors signal CV centers in medulla to ↑ parasympathetic output and ↓ sympathetic output
a. Net result = ↓cardiac output (↓HR, ↓contractility) and ↑ systemic blood vessel dilation
2. Or…if a decreased stretch on baroreceptors (↓ BP) then receptors signal CV centers in medulla to ↓ parasympathetic output and ↑ sympathetic output
Arterial chemoreceptors
(i) Located within aorta and carotid arteries
(ii) Central receptors located brainstem (medulla)
(iii) Major role in respiratory rate but also influence resistance by vasodilating and constricting blood vessels
Vascular compliance
a. Compliance – ability of blood vessel to stretch per given increase in blood pressure
• Compliance differences between blood vessel types
(i) veins more compliant than aorta
(ii) aorta more compliant than arterioles
Vascular elastance
b. Elastance – ability of blood vessel to return to original diameter
(i) Arterial vessels greater elastance than venous vessels
Arterial vs venous system
• Arterial system
(i) will not accommodate large blood volume change unless accompanied by large pressure increase
• Venous system
(i) will accommodate large blood volume change with only small increase of pressure (“reservoir system”)
Stiffness” (poor compliance/reduced elastance)
• Large increases in BP will correspond to increase blood volume in stiff blood vessels (arteriosclerosis, nicotine, etc…)
Systolic and Diastolic Pressures
a. Systolic pressure
• Highest arterial pressure during cardiac cycle - measured after ventricular ejection
• < 140 mmHg
b. Diastolic pressure
• Lowest arterial pressure during cardiac cycle - measured during ventricular filling (blood is “passively” filling ventricle)
• < 90 mmHg
Pulse Pressure
• Difference between systolic and diastolic pressures
(i) Systolic pressure – diastolic pressure = pulse pressure
• Pulse pressure is determined by stroke volume
• Clinical
(i) Any pathology that reduces contraction or filling of ventricle will reduce pulse pressure
(ii) Distal pulses “weak” vs “strong”
MAP (mean arteriole pressure)
• Average pressure of arterial system
• MAP = Diastolic pressure + 1/3 pulse pressure
• Values:
(i) Normal MAP values: 70 – 110 mmHg
(ii) Minimal MAP values: approximately 50-60 mmHg is threshold to sustain visceral organ health
(iii) Maximal MAP values: > 160 mmHg – may elevate CSF and intracranial pressures
• NOTE: at higher HR MAP becomes closer to actual average between systolic and diastolic pressure
• All changes in MAP are due to change in cardiac output or TPR (total peripheral resistance)
Central venous pressure (CVP)
• CVP catheter
(i) Assessment of right ventricular function and systemic fluid status
• Normal CVP values:
(i) 2-6 mm Hg – these are the values of the blood returning to the right atria
CVP is elevated by:
(i) “Over-hydration” which increases venous return
(ii) Heart failure causing congestion (“back-up”) within right heart chambers
(iii) Pulmonary trunk stenosis which limit venous outflow and lead to venous congestion
(iv) Positive pressure breathing (mechanical ventilator or bag mask – “pushes/forcing air into lungs”) or physiological straining
(v) Summary of ↑ CVP:
1. any pathology resulting in excessive ↑ venous return or ↑ right heart congestion/pressure
CVP decreased by:
(i) “Under-hydration” - hypovolemic shock from hemorrhage, fluid shift, dehydration
(ii) Transient: orthostatic – stand up and transient drop in venous return
(iii) Negative pressure breathing – mechanical ventilation that “sucks air into the lungs”
1. Patient who have lost motor control of muscles necessary for ventilation
2. Iron lung – polio epidemic in mid-1900’s
Normal CVP values
approximately 0-10 mmHg
- Decrease CVP: stand up and transient drop in venous return to the heart, drop in CO (and BP)
- Increase CVP: exercising muscle enhances venous return to heart which increases CO
Interpreting CPV Waves
- -A Wave
- C Wave
(i) Mean CVP: average the highpoint and low points of A wave
(ii) The A-wave
1. represents atrial contraction
2. High point of A wave represents right ventricular end diastolic pressure
a. Atria is contracted and tricuspid valve is open so pressures of atria and ventricles are equal.
(iii) The c-wave
1. Occurs at closure of the tricuspid valve.
2. Peak of C-wave occurs from tricuspid valve bulging back into atrium.
(iv) X descent – represents atrial relaxation.
Interpreting CPV Waves
- -V wave
- -Z point
(v) V wave – represents the rise in atrial pressure before the tricuspid valve opens.
1. clinical: Enlarged in tricuspid regurgitation.
(vi) Y descent - represents atrial emptying as blood fills the ventricle.
(vii) The Z-point
1. Occurs just before the tricuspid valve closes (mid to end QRS)
2. Also can be used as good estimate of right ventricular end diastolic pressure if A-wave not visualized with pathology (A fib is an example).
How is PCWP measured?
(i) Balloon-tipped catheter (Swan-Ganz catheter) passed into peripheral vein – right atrium – right ventricle – pulmonary artery – branch of pulmonary artery
(ii) When balloon is inflated it is indirectly measure pressures within pulmonary veins and left atrium
Pulmonary capillary wedge pressure (PCWP)
• Pulmonary capillary wedge pressure (PCWP) provides an indirect estimate of left atrial pressure (LAP).
(i) Direct measurement of LAP isn’t practical:
1. Directly placing a catheter through artery – aorta – left ventricle - then into left atrium isn’t ideal
Why is PCWP measured?
(i) Evaluate severity of any pathology causing elevated LAP
1. left ventricular failure
2. mitral valve stenosis and regurgitation
3. Aortic valve stenosis and regurgitation
(ii) Evaluate pulmonary hypertension (which is really consequence of the above)
(iii) Monitor blood volume during hypotensive shock
(iv) Monitor and titrate diuretic meds
PCWP values
(i) Normal value of LAP = 8-10 mmHg
(ii) Abnormal elevation will cause congestion (“back-up”) into pulmonary system.
1. > 20 mmHg of LAP is threshold at which pulmonary edema may occur
Influences on MAP—Cardiac output
• Any increase in CO without a corresponding decrease in TPR will result in increase in MAP
(i) HR, SV, contractility, venous return, and systemic blood volume all influence MAP
Influences on MAP— Total peripheral resistance (TPR)
• TPR and MAP are directly related
(i) If TPR is decreased then MAP will decrease
ADH (antidiuretic hormone)—Hormonal control of MAP
stimulate retention of water
(i) Released from posterior pituitary gland
(ii) Triggers kidney to retain water which will increase blood volume and therefore increase MAP
Renin-angiotensin system— Hormonal control of MAP
(i) Renin released by kidney
(ii) Renin converts angiotensinogen to Angiotensin I
(iii) Angiotensin I is converted to Angiotensin II by the enzyme ACE (angitoensin converting enzyme produced in the lungs)
(iv) Angiotensin II stimulates the release of Aldosterone which signals the kidneys to retain sodium
1. water “follows” sodium which results in an increased blood volume and therefore increased MAP
(v) Clinical: ACE inhibitors to reduce BP
Atrial Natriuretic Peptide (ANP) – Hormonal control of MAP
stimulates excretion of sodium and water
- The right atria releases ANP in response to elevated atrial stretch
- ANP inhibits ADH thus encouraging excretion of sodium and water (thus decreasing blood volume and lowering MAP)
- NOTE: Natriuretic refers to sodium excretion (natriuresis)
Insulin and Adenomedullin— Hormonal control of MAP
• Adenomedullin
(i) Synthesized and secreted from endothelium and smooth muscle of BV
(ii) Vasodialtion effect on BV…thus decreasing MAP
• Insulin
(i) One role is to stimulate NO (nitric oxide) from endothelium to dilate blood vessel (thus attempting to lower MAP)
Venous regulation/influence on MAP
• Increased venous return increases preload-SV/CO and indirectly increases afterload
• Venous system can accommodate up to 60% blood volume and still maintain 10 mmHg pressure (thus very compliant blood vessel walls)
(i) as opposed to the arterial side which may contain 15% blood volume but have average pressure of 100 mmHg (MAP)
• Sympathetic nervous system will stimulate the venous system to contract (decreasing compliance) and thus increasing BP by “pushing more blood through the heart”
(i) increases preload which leads to increased SV/CO and afterload
• Muscular pump and respiratory pump do the same thing by “contracting” the venous return and “pushing more blood through the heart”
