Cardio Module 4 Flashcards
What are the 2 portal circulation pathways
1) GI/hepatic portal system - GI/spleen capillary beds sends blood to liver before blood empties into iVC
2) Renal system - has 2 capillary beds within kidney to allow reabsorption
What is the breakdown of blood volume in the body?
70% in the systemic circulation
- 16% in arteries (stressed volume)
- 54% in veins (unstressed volume)
18% in pulmonary circulation
12% in coronary circulationCirculation is _______ driven
Pressure
Pressure gradients in the systemic circulation stars at _____ mmHg and gradually decrease to _______ mmHg
100+
0-4
What is the circulation pressure in the left atria
4-12 mmHg
What is the circulation pressure in the right atria
0-8 mmHg
What is the circulation pressure in the left ventricle (Systolic and end-diastolic)
Systolic - 90-140 mmHg
Diastolic -4-12 mmHg
What is the circulation pressure in the right ventricle (Systolic and end-diastolic)
Systolic - 15-28 mmHg
Diastolic -0-8 mmHg
What is the circulation pressure in the 1) aorta, 2) capillaries and 3) venous return to Vena cava
1) 80-140 mmHg
2) 20-40 mmHg
3) 4 mmHg
Where would you find the largest functional change in arterial pressure
In the arterioles
As for pulmonary circulation, what is the circulation pressure in 1) Pulmonary trunk, 2) Pulmonary capillaries and 3) Pulmonary veins
1) 3-30 mmHg
2) 10 mmHg
3) 4-12 mmHg
Pressure gradients in the heart chambers start out at _______ and gradually increase to.______
0-4 mmHg
100+ mmHg
Pressure gradients thru the systemic circulation start out at _______ and gradually increase to.______
100+ mmHg
0-4 mmHg
What are the 3 layers of a blood vessel
1) Tunica intima - smooth frictionless inner layer
2) Tunica media - smooth muscle and elastic fibers
3) Tunica externa (adventitia) - Thin layer of connective tissue
What are the ‘elastic arteries’ and what are their function
Pulmonary trunk, aorta and major branches
- Elastin > smooth muscle
Function - To stretch to absorb systolic volume of blood and recoil to return to original diameter
What are the blood flow characteristics of elastic arteries
High pressure, High velocity, small tonal cross section area
What are the ‘muscular arteries’ and what are their function
Medium to small size arteries.
Have a thinner tunica media - transition to less elastin and more smooth muscle
Function: muscular control distributing blood flow to arterioles throughout body
What is the major role of arterioles?
They act as a controller to direct blood to the capillary bends at slow/low pressure flow. They slow the velocity, pressure and volume travelling into the capillaries.
What is change of pressure in the arterioles
The largest drop in arterial pressures happen here.
Enter arterioles - 90-100 mmHg
Leave arterioles - 25-35 mmHg
What’s the size and make up of arterioles
0.5 mm
Mostly smooth muscle and minimal elastin
what are the blood flow characteristics of the arterioles
1) Decrease pressure
2) Decrease velocity
3) Increase total cross section area
What controls the functions of arterioles
Intrinsic - Metabolic demands and conditions
Extrinsic - Autonomic nervous system
What is the physical make up of capillaries
A Single endothelial layer with a basement membrane without tunica media and externa
What are the blood flow characteristics of capillaries
LOW pressure
SLOW velocity (1.5 sec for RBC to pass thru capilaries0
HUGE total cross section area (1000 x larger than aorta)
Individual cross section very narrow (one cell at a time)
What is the cross section of capillaries
Individual cross section very narrow
Total cross section huge
What is the functional role of capillaries?
Its the site of respiration (gas exchange) as well as nutrient and H2O exchange
How much of the circulating blood is generally found in the capillaries?
About 5%
At any given moment, most capillaries are _____
closed
What are some differences between arteries and veins
1) Veins have thinner and more fibrous walls
2) Veins have less elastin than arteries
3) Veins have larger diameter
4) Greater compliance of venous system allows for larger blood volume fluctuations w/o dramatic BP variations
When it comes to blood vessels which are more related to ‘elastance”
Arteries - More force is required to stretch and accommodate volume increase
When it comes to blood vessels which are more related to ‘compliance”
Veins - They expand easily to accommodate volume increase
What assists veins to direct blood flow back to the heart
One way valves (formed by in-folds of tunica intima)
By the time that blood reaches the heart from the veins it has increased in velocity (for its original velocity by)
60%
Since the veins have lower pressure. What are two pumps that assist in bringing blood back to the heart?
Respiratory pump - Thru inspiration
Muscular pump - Lower extremity muscles contract pushing blood to the heart as valves behind it close
After surgery or during a long flight one should be instructed to do ________, This will help avoid_____?
Ankle pumps
DVT - Deep vein thrombosis
What are some factors that affect blood flow?
1) Velocity
2) Pressure of fluid
3) Laminar vs. Turbulent flow
4) Resistance
How does resistance affect blood flow?
Resistance is inversely related to blood flow (increase resistance = decrease flow and volume per unit of time)
Describe Laminar flow
Perfect blood flow no resistance, RBC can ‘shoot’ thru system.
Describe turbulent flow
“Funny flow” something is getting in the way of the RBC making its way as fast as it can thru the system
Most resistance in blood flow is due to…(what else can?)
Length and diameter of blood vessels ( due to buildup or vasoconstriction and dilation)
Viscosity of blood - More ‘sludgy’ tougher time getting thru vessels
What is the most important determinant of blood viscosity
Hematocrit
What is the relation between hematocrit and blood viscosity.
As hematocrit increases, there is a DISPROPORTIONATE increase in viscosity.
Hematocrit increases from 40% to 60% viscosity doubles
Hematocrit = 40%, Relative viscosity = 4
Hematocrit = 60%, Relative viscosity = 8
What is Total Peripheral Resistance
Aka Systemic vascular resistance its the resistance to all systemic vasculature excluding pulmonary vasculature
What is the vessels play a major role in regulating TPR (total peripheral resistance)
Arterioles - The narrowed channel of arterioles provide the most resistance
What is the relationship between TPR (total peripheral resistance) and blood flow
Inverse: If you decrease resistance you are allowing for a larger diameter for blood to flow easier… It allows more arterial blood to reach the tissues and an increased blood flow to the venous system
What are things contribute to the Neural control of TPR?
1) Autonomic nervous system
- Sympathetic and Parasympathetic
2) Baroreceptors
3) Chemoreceptors
What are the sympathetic NS’s influence on TPR
1) Alpha and Beta receptors on BV
2) Epinephrine and norepinephrine
3) Nodal tissue and myocradium on the atria
4) Myocardium on ventricles
What are receptors on blood vessels that allow sympathetic influence on TPR
Alpha receptors (a1 and a2) - they CONSTRICT smooth muscles of BV - a1 - major constrictor - a2 - more inhibit relaxation (weaker constrictor) Beta receptors (B2) - they DIALATE (or inhibit contraction) of smooth muscle of BV
How does norepinephrine provide a sympathetic influence on TPR
NE has a strong affinity for alpha (both 1 and 2 but mostly a1) receptors that give a vasoconstriction response and they weakly bind to beta (B2) receptors which can help for vasodilation but it’s generally ‘overpowered’ by alpha receptor vasoconstriction
How does epinephrine provide a sympathetic influence on TPR
Epi has a strong affinity for beta (B2) receptors = vasodilation response in some organs
Epi’s response is ‘concentration dependent’ - High epi concentration will bind to alpha receptors and overpower beta and will vasoconstrict
What is the sympathetic NS role in the actual heart for TPR
In Atria - It acts on nodal tissue to increase HR and on the myocardium to increase the contractility of the atria
In Ventricles - It acts on the myocardium to increase contractility (strength) of the ventricles
What is the sympathetic NS role in the kidneys for TPR
It forces the kidneys to retain more fluid and up Blood volume
What is the parasympathetic NS influence on TPR
PS muscarinic (M3) receptors ‘indirectly’ promote vasodilation via a coupling reaction in BV wall. Acetylcholine binds to M3 recptors in BV that signals Nitric Oxide production. NO stimiulates vasodilation (counteracts a contraction that would have happened w/o NO.
How do conditions like HTN and Reynaud’s affect parasympathetic NS influence on TPR
They block NO and when Ach binds to M3 receptors they vasoconstrict and increase blood flow resistance
What is the parasympathetic NS role in the actual heart for TPR
Parasymp fibers innervate ATRIA ONLY.
Atria - Influence nodal tissue and decrease HR
Ventricles - NO INFLUENCE
Where are baroreceptors (stretch receptors) localted?
Located in the aorta and carotid sinus
How do baroreceptors (stretch receptors) affect HR
Pressure changes in the carotid flow will signal CV centers in the medulla to increase/decrease BV resistance and CO
If increase stretch (Simulated) (BP up) - Parasymp output up, Symp output down… CO/HR an contractility down. Systemic BV dilation up
If decrease stretch (BP down) - Parasymp output down and symp output up.
Where are Arterial chemoreceptors located
In aorta and carotid arteries. Central receptors located in the brainstem (medulla)
What is the major role of Arterial chemoreceptors
Respiratory rate but also has a smaller influence on resistance by vasodilating and constricting BV
What is compliance?
The ability for a BV to stretch per given increase in BP (veins more than arteries)
What is Elastance?
Ability for BV to return (Recoil) to original diameter. (arteries more than veins
Arteries will not accommodate______?
A large blood volume change (unless accompanied by a large pressure increase)
What is systolic pressure?
The highest atrial pressure during the cardiac cycle - It’s measured after the ventricular ejection
What is diastolic pressure?
The Lowest atrial pressure during the cardiac cycle. It’s measured during ventricular (passive) filling
What is pulse pressure
The difference btwen systolic and diastolic pressures (systolic - diastolic = PP).
Pulse pressure is determined by….
Stroke volume
What are pathological effects of pulse pressure
Any pathology that reduces contraction or filling of ventricle will reduce PP.
What is Mean arteriole pressure (MAP) (how is it determined)
The average pressure of the arterial system. Measured by Diastolic pressure + 1/3 Pulse pressure
What are normal MAP values
70-110 mmHg
What are the Minimal and Maximal MAP values
Minimal - 50-60 mmHg (threshold to sustain visceral organ health
Maximal - > 160 mmHg (may elevate CSF and intracranial pressure.
All changes in MAP are due to
A change in CO or TPR
Why does a higher HR make MAP come closer to actual average btwn systolic and diastolic pressure (rather than diastolic + 1/3 PR
Because you’re eliminating or reducing the rest time in between heart beats when HR increases
What is CVP
Central venous pressure - the assessment of the right ventricular function and systematic fluid status
How is CVP measured
by a CVP catheter on the right side of the heart (on the SVC, IVC side to the right atria)
What are normal CVP values?
Btwn 2-6 mmHg (values of the blood returning to right atria)
What are factors that increase CVP?
1) Over hydration
2) CHF
3) Pulmonary trunk stenosis
4) Positive pressure breathing (like a ventilator or bag mask) or physiological straining
What are factors that decrease CVP?
1) Under hydration
2) Transient orthostatic (stand up)
3) Negative pressure breathing (Iron lung)
The mean CVP is determined by…
The High points and low points of the A wave
What is the A wave of an EKG
It represents atrial contraction (high point = right ventricular-end diastolic pressure). Atria is contracted and tricuspid valve is open so atrial and ventricle pressures are equal
What is the c wave of an EKG
Occurs at the closure of the tricuspid valve. Its peak occurs from the tricuspid valve bulging back into the atrium
What is the x decent of an EKG
Represents atrial relaxation
What is the V wave of an EKG
Represents the rise in atrial pressure before the tricuspid valve opens
What is the y decent of an EKG
Represents atrial emptying as blood fills the ventricle
What may tricuspid regurgitation show on an EKG
An enlarged V wave
What is the z-point in an EKG
It occurs just before the tricuspid valve closes (mid to end QRS)
What is Pulmonary Capillary wedge pressure (PCWP)?
Opposite of CVP it measures the back pressure of the left side of the heart
What is PCWP measured
A balloon tipped catheter (Swan-Ganz catheter) is passed into a peripheral vein and goes thru the right atrium, ventricle and into the pulmonary artery (and branch). When balloon is inflated it indirectly measures the pressures within the pulmonary veins and left atrium
What are the normal values of PCWP (or LAP Left Atrial PRessure)
8-10 mmHg
What will an abnormal elevation in PCWP cause
Congestion (back up) into the pulmonary system
What is the PCWP or LAP threshold (what happens then)
> 20mmHg, pulmonary edema may occur
Why is PCWP measured?
1) Evaluate severity of any pathology causing elevated LAP.
2) Left ventricular failure
3) Mitral or Aortic valve stenosis or regurgitation
4) Evaluated pulmonary HTN
5) Monitor blood volume during hypotensive shock
6) Monitor and titrate diuretic meds
What are some influences on MAP
1) CO
2) TPR
3) Hormonal control (endocrine system)
4) Venous compliance
What are the hormonal influences on MAP
1) ADH
2) Renin-angiotensin system
3) Natriuretic peptides (ANP)
4) Adenomedullin
5) Insulin
What is ADH’s influence on MAP
It stimulates the retention of water
What is the Renin-angiotensin’s influence on MAP
It stimulates the retention of sodium and constricts BV
What is Natriuretic peptides (ANP)’s influence on MAP
It stimulated excretion of sodium and water
What is Adenomedullin’s influence on MAP
From the endothelium and smooth muscle of BV. They have a vasodilation effect on BV and thus decreasing MAP
What is Insulin’s influence on MAP
Stimulates NO from endothelium to dilate BV
What is the net result of the renin-angiotensin-aldosterone system
1) Blood pressure down
2) Fluid volume down
3) B2 sympathetics up
What’s another role for Angiotensin II
It can be a direct vasoconstrictor
What is Natriuretic peptides (ANP)’s influence on MAP
It stimulated excretion of sodium and water. Opposite effect of Renin angiotensin and ADH.
What is Adenomedullin’s influence on MAP
From the endothelium and smooth muscle of BV. They have a vasodilation effect on BV and thus decreasing MAP
What is Insulin’s influence on MAP
Stimulates NO from endothelium to dilate BV
What is the net result of the renin-angiotensin-aldosterone system
1) Blood pressure down
2) Fluid volume down
3) B2 sympathetics up
What’s another role for Angiotensin II
It can be a direct vasoconstrictor
What is the venous return influence on MAP
Increase venous return increases preload SV/CO and indirectly increases afterload
How much blood volume can the venous system accommodate?
Up to 60% and still maintain a 10 mmHg pressure
