Exam 1 Content Flashcards
How does ADH affect free water clearance?
Renal Review
Clearance, Free Water Clearance
-Clearance: How much (volume) of plasma is cleared of a substance per unit/time
-Free water clearance: Refers to the volume of water being removed from the body per unit time.
If our ADH is high, free water clearance will be low
If ADH is low, free water clearance will be high
Free water clearance does not take into account electrolytes or any dissolved substances
Normal BP, MAP, MAP equation
Normal Pressure Values- Systemic Circuit
-Normal BP is SBP 120/80 DBP
-Estimate of normal MAP is 100mmHg
-MAP= DBP + 1/3 (SBP-DBP)
Gives us a MAP of 93mmHg w/ a normal BP
Vascular Resistance & Hydrostatic Pressure- Systemic Circuit
High resistance arterioles, pressures throughout the systemic circuit
-Arterioles are high resistance vessels
-Arteries upstream from the arterioles will be high
-Arteries downstream from the arterioles will be low
-Aorta is the source of the blood, the further we move away from the source, the lower the pressure becomes
-Capillary BP on arteriole end; 30mmHg
-Capillary BP on venous end; 10mmHg
-As we move closer to the R. Atrium (furthest point from Aorta, end of systemic circuit) pressure becomes 0mmHg
DeltaP of systemic circuit: 100mmHg-0mmHg
Vascular Resistance- Pulmonary Circuit
-Pulmonary arteriole pressure (PAP, MPAP): 16mmHg
-Reasonable BP for P.A 25/8 (does not calculate to 16mmHg)
-L. Atrium (end of pulmonary circuit) pressure should be 2mmHg
DeltaP of pulm circuit: 16mmHg- 2mmHg
How does compliance effect pulse pressure? & S.V?
Pulse Pressure- Systemic
Which type of artery has a higher pulse pressure than the aorta?
-PP is equal to the difference between SBP and DBP
-Pulse pressure near the aorta should be ~40mmHg
-Narrowing of pulse pressure: As blood is moving through an area of high resistance, pulse pressure is typically reduced (consequence of energy being used to move through the vasculature)
-Widening of pulse pressure: Typically happens in large arteries such as the femoral artery.
Why? Large arteries have less compliance; the more fluid that is pumped into this container, the higher the pressure will be
An increase in S.V should increase P.P.
Compliance and PP are inversely related
Pulse Pressure- Pulmonary Circuit
-PP is much less than in the systemic circuit
-Pulmonary vessels are 1. low resistance and 2. high compliance
How does blood get pumped through the systemic circulation during diastole?
What happens to the aorta’s ability to stretch as we age?
-The aorta has a high compliance; it’s job is to stretch to accomodate a large amount of volume being pumped from the heart during systole.
During diastole, the walls of the aorta come closer together, acting as a secondary heart pump, pushing the blood downstream
As we age, the aorta becomes less compliant causing a higher pulse pressure
Conductance, Diameter, & Resistance
-The single most important variable that controls conductane of blood flow is increases or decreases in resistance that occur due to vasoconstriction or relaxation
-A small change in diameter results in a huge change in resistance, and therefore, blood flow
-Resistance and flow are related to diameter to the 4th power
Equations
Vascular Compliance
Vascular Distensibility
Delta P/ Blood Flow/ Resistance
Conductance
Compliance: Delta V/ Delta P (mmHg in CV system, cmH2O in pulm)
Distensibility: Delta V/ (Delta P X Original Volume)
Distensibility = Expandibility
Delta P: F x R
F: Delta P/ R
R: Delta P/ F
Conductance: 1/Resistance
Conductance is inversely related to resistance
Pressure in the LA? The LV? LV pressure needs to be higher than what?
What about the RV?
-L.A pressure is ~2mmHg
-There is a wide range of pressures in the L. V. During diastole, pressure in the L.V should be pretty low because there is no squeeze.
During contraction, the pressure in the LV will rise significantly. The pressure in the LV needs to be higher than the pressure in the aorta during systole in order to eject blood into the aorta
-During diastole, the RV is going to have a low pressure.
During systole, the pressure can rise up to ~25mmHg
Velocity is dependent upon what?
Velocity & Blood Flow
the larger the cross-sectional area…
CO: 5l/min (HR x SV)
Velocity of blood flow is depended upon the cross-sectional diameter of the blood vessel
The larger the cross-sectional area, the slower the blood flow
Isogravometric point? Effect on measuring BP in upright position?
Gravity & It’s Effects on BP
Why is the pressure 0mmHg in the neck?
Pressure in the sinuses? What happens when exposed to air?
-Isogravometric point (phlebostatic axis): The point at which gravity has no effect on pressure because this point is located in the center of the pressure source (the tricuspid valve)
-As we move further below the isogravometric, the pressure will rise
-As we move further above the isogravometric point, the pressure will decrease
-The pressure in our neck is 0 because the veins are wide and thin-walled. These veins would collapse if there was a negative pressure
-The sinuses in the brain are very rigid, so when placed in an upright position, the pressure in these sinuses is subatmospheric. If this sinus is exposed to air, it will suck air in because of the negative pressure
How do we do this?
Measuring the effect of gravity on fluid
-Going 13.6mm below a source of pressure will give us a 1mmHg rise in pressure
The further below the source of pressure, the higher the pressure will be
-13.6mm = 1.36cm
Pressure changes in arteries w/ & w/o gravity
-Without the effect of gravity, pressure in the arteries should remain consistent until the arterioles (~100mmHg)
-With the effect of gravity, blood pressure is a combination of pressure generated by the heart plus the pressure that is a result of gravitational effects on the blood
Valves combat …? What happens as we age?
Take note of pressure differences in veins
-Veins have one-way valves that combat the effects of gravity. The valves prevent retrograde flow of blood, and promote blood return to the heart. Functioning valves also keep the pressure in the lower extremities from rising
-As we age, the valves begin to separate and do not prevent retrograde blood flow. This leads to higher pressures in the veins eventually causing varicose veins.
-Valves and veins rely on skeletal muscle contraction in order to effectively push blood back to the heart
Note what is happening w/ sympathetic inhibition & stimulation
Behavior of Vessel Walls
- ~700ml of fluid is found in our systemic arterial circulation at all times
- Arterial system operates at higher pressures with less volume (less compliant)
- Sympathetic Inhibition in arterial system w/ same amount of volume: blood pressure will decrease significantly
- ~2500ml of fluid is found in our systemic venous system at all times
- Venous system operates at a lower pressure with higher volume (more compliant)
Slope of the line is an estimate of compliance when the graph is set up with pressure on the side axis and volume on the bottom axis
What is it? Turbulent flow is associated with what?
Reynold’s Number & Turbulent Flow
Arteries at risk for turbulent flow? Veins?
-Reynold’s number is a theoretical, unitless number that describes the chances of experiencing turbulent flow
-If the number is >2000, that means there will be turbulent flow
-Turbulent blood flow means there is blood flow moving in all different directions, wasting massive amounts of energy, and creating a high risk for blood clots. Turbulent flow is associated with volume, meaning you can hear the flow
V= Velocity
D= diameter
P= Density
N= Viscosity
An increase in V, D, or P will increase risk for turbulent flow
An increase in viscosity will decreased risk for turbulent flow
Aorta and large arteries closest to the heart are at the greatest risk for turbulent flow.
Venous system has a very low velocity, so there is hardly any risk for turbulent flow
Flowmeters & Pressure Transducers
Flowmeters:
-Electromagnetic probe that fits around a blood vessel. Measures the flow through the flowmeter in the probe by looking at the magnetic effect created by the iron in Hgb
-Ultrasonic flowmeter; has to be implanted & wrapped around a blood vessel
-Lasers; have imbedded senors that look at the light that’s being reflected from blood. Higher flow = different reflection
Pressure Tranducers:
- Blood flows through a needle/catheter connected to the CV system into the chamber tray. Within the chamber, there is a small electromagnetic probe that senses changes in pressure
Pressure Volume Loop- Period of Filling (I)
- Begins with the ESV (50mls) leftover from the previous cardiac cyle.
- Filling is primarily passive and dependent on preload. L. Atrial pressure is low (~2mmHg) until the ventricle reaches ~110ml.
- L. Atrium contracts –> remaining 10ml fills the ventricle –> EDV = ~120mls
-Atrial kick becomes very helpful when there is cardiac pathology. A sick heart may be dependant on the atria for atleast 25% of ventricular filling
Systole begins after the mitral valve closes
?
Pressure Volume Loop- Isovolumetric Contraction (II
-Very short in time
-Ventricle begins to contract –> left ventricular pressure becomes higher than left atrial pressure causing the mitral valve to close
-Aortic valve remains closed at this time
-Both valves are closed at this time, the volume remains the same; however pressure increases due to ventricular contraction. This causes the line on the graph to be straight up and down
-If there were valvular disease and valves could not close all of the way, that would change the slope of the line
-Pressure in the ventricle exceeds the pressure in the aorta, aortic valve opens
Pressure Volume Loop- Period of Ejection (III)
-Aortic valve opens; this is our DBP
-Blood is ejected from the ventricle into the aorta
-The difference in volume from the beginning of phase III to the end of phase III is our stroke volume (EDV - ESV =SV)
-Aortic pressure is at it’s highest, higher than the L. ventricular pressure –> aortic valve closes. SBP is measured here
Diastole begins here when the aortic valve closes
Pressure Volume Loop- Isovolumetric Relaxation (IV)
-Aortic and mitral valves are closed
-Intraventricular pressure begins to decrease
-Once intraventricular pressure is lower than L. atrial pressure, mitral valve opens and phase IV ends
-Volume remains the same
ECG: Depolarization happens first, then the physical force generated happens second
-QRS happens –> ventricular pressure increases
-Diastole begins when the aortic valve closes at the end of Phase III, and ends at the end of phase I
-Systole begins at the beginning of phase II, after the mitral valve has closed, and ends at the end of phase III
-The ventricle is filled during phase I, and blood is ejected in phase III.
-The vast majority of the filling is done in the first 1/3rd of ventricular filling
This graph is showing how the pressure volume loop can shift depending on stretch and volume of the heart
What is happening to CO in regards to normal heart, sympathetic/para?
Cardiac Output Curve
Normal Heart:
-Blue line shows us expected CO in a normal, healthy stimulated heart
-Once a R.AP reaches +4mmHg, CO plateaus at ~13L/min
Maximum sympathetic stimulation:
-Once R.AP reaches +4mmHg, CO plateaus at ~25L/min
-With the increase in the amount of work the heart is doing, the R.AP decreases –> increasin venous return
Parasympathetic stimulation:
-Once R. AP reachs +4mmHg, CO will plateau at ~7L/min
-When the heart is slowed down, R. AP begins to increase –> decreasing venous return
How does the body compensate? Acute vs Chronic hypoeffective heart?
Hypereffective vs Hypoeffective Heart
A hypereffective heart will begin to have a decrease in R. AP, creating a vacuum effect and increasing venous return.
A hypoeffective heart will have higher R. AP due to inability to pump. The body compensates by increasing PSF. If there is no compensation in the venous system, the heart will not be able to maintain a CO to sustain life.
Without compensation, R. AP will be slightly higher than normal. The compensation of increasing PSF leads to an even larger increase in R. AP (could be as high as 10+)
If this is an acute problem, the body increases circulating catecholamines to increase PSF
If this is chronic, the action of catecholamines is replaced by volume retention and blood expansion that happens at the kidneys
Frank Starling, Atrial Stretch, Bainbridge
CO Output Curve- The reasons for the steepness of the slope
Under normal circumstances, the heart is understretched. Providing the heart with more filling pressure will allow for more stretch:
Frank Starling Law: Increased venous return increases LVEDV/LVEDP –> increased stretch of the cardiac myocytes before contraction. This increases sarcomere length, which causes an increase in force generation allowing the heart to eject the additional venous return = increased SV
Direct Atrial Stretch: An increase in atrial stretch that results from an increase in filling pressures (under normal conditions) will cause an increase in HR by 10-15%
Bainbridge Reflex: An increase in HR by 40-50% in response to an increase in filling pressures.
-Afferent signal sent to brainstem, brainstem increases sympathetic outflow–> efferent signal sent via vagus nerve to decrease parasympathetic outflow
These mechanisms are the reason for the steep slope of the CO curve
What is PSF? How does it affect venous return?
Mean PSF
What two factors can alter mean PSF?
Mean systemic filling pressure: average of all pressures used to fill the heart including veins & arteries.
The number is 7mmHg and not closer to 100mmHg because of the high compliance of the venous system.
Two factors that can alter mean PSF:
Increase in blood volume or venous tone
-The most effective way to increase mean PSF is to constrict the large veins in the venous system
Normal R. AP? What happens w/ a low or high AP?
Venous Return
How does PSF affect venous return? Why does CO plateau @ 6L/min?
-Normal R. Atrial pressure of 0mmHg allows for 5ml/min of venous return
-Venous return is dependent on the DeltaP of the average filling pressure of the CV system (7mmHg) and the end of the circulatory system (R. Atrium)
-a higher R. AP, without any changes to PSF, will result in a lower venous return
-a lower R. AP, without any changes to PSF, will result in a higher venous return. The circulatory system has a plateau of ~6L/min. This limitation happens because if the R. AP is negative enough, the vena cavae will collapse
-The heart does not typically impact venous return as long as it maintains a CO of what is being returned to it
What is it? How does the slope on the graph change?
Resistance to Venous Return
Does RVR directly alter PSF?
-Describes how easy it is to get blood back to the heart. These changes do not directly affect PSF
-Low RVR (blue line): Means that it is easier for blood to return to the heart; therefore, resulting in a larger CO. Larger slope on the graph
-High RVR (pink line): Harder for blood to get back to the heart (obstructed in someway), resulting in a smaller CO. Smaller slope on the graph
What happens when there are changes to mean PSF?
Changes in Mean PSF
What does the body do when needing to enchance CO?
-Slope of the curve does not change.
Where the line intersects the x-axis will change based on what the mean PSF is
-A high PSF and normal R.AP will result in higher venous return, and higher CO
-A low PSF and normal R.AP will result in lower venous return and lower CO
When the body needs to enhance CO, it typically choses to increase the PSF by constricting arteries that are not needed, but also constricting veins. A minor constriction of the veins can cause a large change in PSF
CO depends on what 2 things
CO & Venous Return
CO depends on two things:
1. Conditions in the circulatory system
2. Conditions in the heart
CO needs to equal venous return.
The points where these two lines intersect on the graph should tell us our R. AP, CO, and venous return
Thorax & Barrier to Venous Return
How does phenylephrine help?
-Pressure in the thorax can be a barrier to venous return
-Primary obstacle for anesthesia will be PEEP –> high PEEP can impede blood flow back to the heart
-If this happens, the patient will either need more volume or phenylephrine
-Phenylephrine effectively constricts the veins, increasing PSF
How does the body increase CO in resoonse to metabolic rate?
Metabolic Rate, CO & O2 Consumption
-The body typically needs to increase CO to meet a high metabolic rate. It does so by dilating arteries to increase blood flow, and constricting the venous system to increase venous return
-If we have a low metabolic rate, we can get away with having a lower CO because our tissue needs are not as great
-CO is tightly linked to O2 consumption. For every increase in O2 consumption, we should see an equal increase in CO
What is going on in this graph?
Normal CO and venous return curve shown in black
The CO and venous return curves shown in red show that with a PSF of 20mmHg, R. AP will increase slightly in order to maintain a venous return and CO of ~22ish
CO & Vascular Resistance in r/t metabolic demand
How does a AV shunt decrease resistance?
This graph shows us the percentage of peripheral resistance on the x-axis and the percentage of CO on the y-axis
Conditions that decrease the body’s metabolic demands are to the right of normal, and conditions that increase the body’s metabolic demands are to the left of normal
Conditions that increase vascular resistance cause a decrease in CO (by decreasing metabolic demand)
1. Loss of organs, limbs
2. Hypothyroidism
Conditions that decrease vascular resistance will cause an increase in CO (because metabolic demand is increased)
An AV shunt decreases vascular resistance because it gives the blood another pathway, in parallel, to travel which inturn increases CO
What happens when a drug changes metabolic demand?
This graph shows what happens when a drug is given that alters metabolic demand, w/ and w/o nervous system control.
A drug like dinitrophenol needs to have cooperation from the nervous system. Without a normally functioning nervous system, arterial blood pressure will crash because vessels are all dilated, but the venous system is not able to increase PSF
With assistance from the SNS, CO will increase significantly
Cardiac Index
-CO/surface area
-L/min/m2
-Dependent on gender, sex, metabolism, size
-CI is at it’s highest when we are age 10 at 4L/min/m2
Normal 70kg adult has a surface area of 1.7m. Gives us a CI of about 3
How do they correlate? Measuring CVP? What happens as we age?
CVP & R. Atrial Pressure
Typically go hand in hand.
Normal R. AP is 0mmHg, CVP will be close to 0mmHg (we need a pressure gradient in order to promote venous return)
If something increases CVP, R. AP is likely to be increased as well
The further from the heart that you are measuring CVP, the higher it will be.
In a supine patient, the inferior vena cava is typically slightly lower than the heart so CVP will be increased
As we age, R. AP tends to increase and that is a function of CVP increasing
What happens to the heart as BP in the aorta declines?
Progressive Hemorrhagic Shock & CO
The heart relies on the blood pressure in the aorta to perfuse the coronary arteries
Progressive hemorrhage can cause the pressure in the aorta to decline, causing the heart to go into a death spiral because of lack of oxygen and nutrients
Inspiration? Expiration? Sustained positive pressure?
Thoracic Pressure & CO
Fluid surroundin the heart?
Intrapleural pressure= pressure in the thorax ( -4mmHg)
Pressure is typically negative here.
On inspiration, diaphragm contracts, shifts down, and the pressure in the thorax becomes more negative in order to suck air in. This also causes more blood to move into the heart by decreasing R. AP. This shifts the curve to the left
Expiration causes contraction of the abdomen, increasing pressure in the thorax (positive pressure).
Sustained positive pressure will shift the curve to the right
1. Mechanical ventilation
2. Opening the chest
The body compensates here by increasing PSF or we need to add volume
Fluid surrounding the heart- increases pressure around the heart, decreases the heart’s ability to pump effectively. This will decrease the slope of the CO curve
CO; Pump effectiveness & Thoracic Pressure Changes
Hypoeffective heart + reduced intrapleural pressure: Because the pump is not working well, our plateau phase remains at 6L/min. The reduction in intrapleural pressure causes a decrease in R. AP, shifting the curve to the left
Hypereffective heart + increased intrapleural pressure: A hypereffective heart will have a high CO, but because of the increased intrapleural pressure, the curve is shifted more to the right than normal
Simple CO Curve
Black line is normal
Enhanced= hypereffective, sympathetic stimulation
Depressed= hypoeffective, parasympathetic stimulation
Arterial -Specific Vasodilators
High venous return slope = decreased resistance to venous return. A decrease in venous return happens when arteries are dilated
Examples: Ace-inhibitors
hydralazine- primarily arterial; MOA unknown. Slow-ish onset
Venous-Specific Vasodilators
Nitroglycerin is an example
-Venous return curve is decreased (therefore, reducing preload) and filling pressure has changed; this indicates that it is a venous-specific drug
Mixed Vasodilators
Resistance to venous return is decreased due to a decrease in SVR. Systemic filling pressure is also decreased because venous compliance is increased
Nitric oxide donors do this- need to keep out of sunlight
Compliance, Volume, & Changes to PSF
Cv= Compliance
Increasing PSF:
-A decrease in compliance (the walls of the venous system are constricting)–> increasing PSF
-An increase in volume will also increase PSF
Decreasing PSF:
-An increase in compliance of the venous system
-A decrease in volume
SVR & Resistance to Venous Return
SVR is controlled by constricting or relaxing of the systemic arteries
-Relaxation of arterioles decreases SVR, causing a decrease in resistance to venous return
-Constriction of arterioles increases SVR, causing an increase in resistance to venous return
Filling pressure remains unchanged
Which drugs are in this category?
What’s happening in this graph?
-Venous constriction causes an increase in PSF
-Arterial constriction does not change PSF. Arteries constrict
–>SVR increases –> increased resistance to venous return –> decrease in venous return slope
Phenylephrine- venous constrictor, increasing preload
-With a damaged heart, we will see an increase in R.AP because the heart is not an effective pump.
Compensation mechanisms:
-Decrease in venous compliance (constricting the venous system), increasing PSF –> increasing R. AP
-Increase in SVR –> blood supply to non-essential organs is reduced. We can tell SVR is increased, resistance to venous return is increased, because of the dampened slope of the curve
Long-term compensation: - Kidneys expand blood volume in order to reduce arterial and venous vasoconstriction
-MI; “middle of the road”
-Point A: Normal CO and venous return lines are shown intersecting
-Point B: Patient then has an MI –> CO is reduced to ~2.5L
/min with a RAP of 4mmHg. No compensation is taking place
-Point C: Increase Venous Return
Short term compensation begin; sympathetic activity increases–> Two main effects:
1. Increase in venous tone–> increased PSF, RAP
2. SNS releases norepinephrine–> increased contractility, arterial vasoconstriction & CO
-Point D: Fluid Retention
In order to dial back the circulating catecholamines, the kidneys need to expand blood volume in order to achieve similar results. RAAS system is activated–> decrease in CO causes renin to be released. Renin combines with angiotensinogen to form ATI. ATI combines with ACE to form ATII –> leading to
1. Increase in SVR and arterial pressure
2. Na+ reabsorption and fluid retention
3. Release of vasopressin from posterior pituitary to increase water retention.
Because of the increase in volume, PSF is further increased –> RAP increased
-Point E:
Fluid retention has been increased enough that sympathetic activity has returned to normal
Preload, Afterload, Contractility
Preload- Pressure available to fill the heart. Measured at end of phase I/EDV (mmHg)
Afterload- Pressure in the aorta when the aortic valve opens. DBP
Contractility- A change in SV without change to preload or afterload
Changes to SV, ESV, EF, EDV?
Increased Preload:
Increased EDV
SV and ESV remains unchanged
EF increases slightly
The higher the preload, the more filling we have.
Changes to SV, ESV, EF, EDV?
Increased Contractility:
The lines at the top left corner are a measure of contractility
-Increased contractility is shown with a steeper line
SV increases
ESV decreases
EF increases
EDV remains the same
Increased contractility causes an increase in BP
Changes to SV, ESV, EF, EDV?
Decreased preload
SV decreases
EDV decreases
ESV remains the same
EF decreases slightly
Changes to SV, ESV, EF, EDV?
Increased Afterload
SV decreases
ESV increases
EDV remains the same
EF decreases
LV will need to come to a higher pressure in order to exceed pressure in the aorta. This will increase the amount of time spent in phase II–> decreasing the amount of time in phase III.
The high pressure during phase III causes the aortic valve to close prematurely.
The body’s compensation mechanism here may be to raise HR
Changes to SV, ESV, EF, EDV?
Decreased afterload
Reduction in pressure when the aortic valve opens and closes
SV increases as a function of ESV decreasing
EDV remains the same
Because the aortic valve opens at a lower pressure, there is more time spent in phase III
Changes to SV, ESV, EF, EDV?
Decreased contractility:
SV decreases
ESV increases
EDV remains the same
EF decreases
Decreased contractility causes a decrease in BP
Changes to SV, ESV, EF, EDV with treated vs untreated HF?
What happens after long-term compensation to the walls of the heart?
Decreased contractility will shift the pressure volume loop to the right due to the increase in ESV
Untreated HF significantly increases ESV. Passive filling pressure in the ventricle is also significantly increased (preload). Acutely, the increase in preload is helpful, but long-term, this will cause dilation of the heart walls
Afterload reducer decreases ESV, increases SV, and decreases work of the heart
Changes to SV, ESV, EDV, Preload? Pressure changes? Pulse Pressure?
Aortic Stenosis
-Most common valve dysfunction
-Can be treated the same as a high afterload issue. The pressure upstream from the valve/resistance will be high (LV pressure) and the pressure downstream from the resistance will be low or normal
-High resistance valve that occurs over time from age, infection, cholesterol. This impedes injection
-Increases the amount of time spent in phase II and significantly decreases the amount of time in phase III
-Compensation mechanism to have a normal CO is increase HR
-Increased outflow tract resistance causes an increase in delta p across valve during ejection
-LVEDP & LAP greatly increased. (LAP needs to increase to overcome LVEDP)
-LV concentric hypertrophy
-LA hypertrophy
Aortic valve will open at a lower DBP because the ventricle will high a much higher LVEDP
Shorter time spent in phase III, so aortic valve will close at a higher SBP
Very large increased in myocardial oxygen demand
-High risk for turbulent flow; when valve area is reduced, flow velocity increases 4-fold
Changes to SV, ESV, EDV, Preload? Pressure changes? Pulse Pressure?
Mitral Stenosis
-Increase in LAP and pressure gradient across the mitral valve during diastole
-Decrease in LVEDP & LVEDV
-SV greatly reduced
-LV will not contract as forcefully; therefore, peak SBP, SBP, and DBP will be slightly reduced
-LA hypertrophy
What is happening in each phase? PP, EDV, SV, LVEDP, Hypertrophy? PAP?
Aortic Regurgitation
Murmur
-Regurgitant/insufficient valves do not close well.
We will see a greatly enlarged, dilated LV. Typically a chronic condition, so the heart has remodeled to allow for a larger volume of blood.
Phase II: Mitral valve closes & LV begins to contract;
Under normal circumstances, this is where the LV would be at it’s highest volume; however, aortic pressure is greater than LV pressure and blood is flowing retrograde into the LV
Phase III: Aortic valve opens at a lower DBP. We will see higher than normal systolic pressures here because of the enhanced stroke volume & activation of the Frank Starling mechanism
Phase IV: Aortic valve closes at a higher SBP. Instead of an isovolumetric relaxation phase, the LV now begins to fill blood prior to the opening of the mitral valve
Summary:
-Widened Pulse Pressure
-Significantly increased LVEDV
-LVentricular and L. Atrial eccentric hypertrophy
-LVEDP and Pulm. Wedge pressure increased
-Increased SV, although net forward flow into aorta is reduced
-Diastolic murmur
-No isovolumetric relaxation or contraction
-Increased myocardial oxygen demand
Acute vs Chronic? What happens in each phase?
Mitral Regurg
Acute Mitral Regurg
-Occurs due to rupture of the chordae tendinae causing the mitral leaflets to bulge back into the LA during LV systole –> blood flow moves in the LA and out into the aorta
-L.AP and volume will be greatly increased, and acutely, this will cause pulmonary edema due to an increase in pulmonary wedge pressure
-LVEDP will also be elevated in response to the increase to the LAP
-Forward flow into aorta is decreased
-LV and L.A will be passively enlarged (no remodeling in acute)
Phase II: Not isovolumetric. LV begins to contract, and blood is ejected into the L.A
Phase III: Blood is ejected into both the aorta and the L.A
Phase IV: Aortic valve closes –> volume in the LV continues to decline because the pressure is higher than in the LA.
Mid-phase IV is when the LAP is higher than LVP (peak of V-wave)
SV Increased
EDV increased
ESV decreased
Forward flow into aorta is decreased
Chronic Mitral Regurg
More common
Volume overload of LV and LA causes remodeling –> eccentric hypertrophy
L.AP and LVEDP will be reduced due to cardiac remodeling
Pulmonary wedge pressure will be decreased
Forward flow into the aorta is decreased
Phase I: LVEDV is very high due to remodeling (190ml)
Phase II: Same as above
Phase III: SV is slightly higher than normal (90ml)
Phase IV: ESV is much higher (100ml)
Summary:
-Chronic:
-Increased EDV & eccentric hypertrophy
-Increased SV, decreased SV into the aorta (reduced forward flow)
-L. A eccentric hypertrophy, increased pulm wedge (but less than acute)
-Systolic murmur
-Tall v-wave
-Increased myocardial demand
-No isovolumetric relaxation or concentration
Vagus Nerve Input
-Right vagus nerve innervates SA node/R. Heart
-Left vagus nerve innervates AV node/L. Heart
-There is some sympathetic activity in the heart, w/o the SNS the HR would drop to about 60bpm
Pericardial Layers
-Fibrous Pericardium: External layer. Rigid, tough, inflexible
-Serous visceral percadrium. Stretches and allows the heart to move without any friction
-Serious parietal pericardium; Most inner layer of serious pericardium. Essentially glued to fibrous pericardium. Also helps the heart slide w/o friction
-Visceral serous pericardium is removed
-We can see the parietal layer of the serous pericardium inside, and the fibrous pericardium on the outside
Purpose of papillary muscles?
-View of the right ventricle. We can tell it’s the R. ventricle because the wall is thin
-Tricuspid valve –> chordae tendinae –> anterior papillar muscle –> posterior papillary muscle
-Papillary muscles are continous with the ventricular muscle fibers. Walls of the ventricles contract –> papillary muscles contract as well. These muscles reinforce the AV valves and help enforce them so they’re not “blown out” the back of the ventricle during contraction
-Can tell this is the left ventricle because the walls are much thicker
-Lateral view of mitral valve –> chordae tendinae–>
-Anterior & posterior papillary muscles
EF for our class?
SV/EDV
70/120
-View of the top of the heart after atria have been removed
-L heart: Biscupid/mitral valve.
-Posterior cusp
-Anterior cusp
-Pulmonary Valve:
-Right Cusp
-Anterior Cusp
-Left Cusp
-R. Heart: Tricuspid Valve
-Anterior cusp
-Septal cusp
-Posterior cusp
-Aortic Valve:
-Left Cusp
-Right Cusp
-Posterior Cusp
As we age, valves calcify or have cholesterol build up.
AV valves are open
Pulmonary & aortic valves are open
-Left & Right cusps of the aortic valve contain openings for the L & R coronary arteries
-The coronary arteries receive blood flow from this early part of the aorta
-Blood is ejected from the ventricle –> during diastole when the pressure in the aorta is really high, recoil of the aorta pushes blood forward and retrograde into the cusps. The cusps act as a bowl that can direct blood into the coronary arteries
Cardiac Cartilaginous Rings
Layer of insulation between the atria and ventricles
Cartiledge does not conduct electricity, so this serves to function as an electrical separation between the muscles of the atria & ventricles
Formed early in development and expands as the heart grows
Bundle of His pathway connects the atria & ventricles. If the heart is normal, this should be the only pathway connecting the top half of the heart to the bottom
Posterior, anterior, and septal cusps
three sets of papillary muscles connecting each cusp to the wall
Septal wall is thicker because it is continous with both ventricles
Comissural cusp is not large enough to be considered it’s own cusp. It is considered part of the posterior cusp
R. Coronary Artery
L. Coronary Artery
-Branches into the LAD and the circumflex artery
-LAD runs down the front
-Circumflex goes around to the back of the heart
Variations in circumflex anatomy, L vs R coronary dominance
R. Coronary Dominance; 75% of people
R. Coronary Artery –> feeds the posterior descending artery that runs along the posterior heart to the bottom of the heart (75% of people)
Circumflex Variation; L. Coronary Dominance; 15% of people
-PDA can branch off the circumflex –> L. CA –> PDA in some people
-This is bad. Most of the heart is dependent on a single artery. Mortality risk is increased in angioplasty & CABG procedures
In a very small percentage of people, the PDA branches off both the RCA and the L. circumflex
Great Cardiac Vein empties into the Coronary sinus –> dumps deoxygenated blood into the R. Atrium
Blood vessels in the heart are located where?
Vascular resistance of these vessels depends on what?
-We need 70ml of blood per min for every 100gm of muscle
Avg heart needs 225ml/min
-Although blood vessels look superficial, they are imbedded in the walls of the heart because that’s where the oxygen and nutrients need to be carried.
-The vascular resistance of these vessels depends on the pressure of the surrounding heart wall; therefore, the vast majority of coronary blood flow occurs when the pressure in the heart is low.
LCA perfuses? RCA perfuses? When? Negative coronary flow?
-Left coronary artery provides blood flow to the more high pressure side of the heart
-Right coronary artery provides flow to the low pressure side of the heart
-There is cross-over between the two.
-RCA perfuses the low pressure side of the heart mostly during systole, but in a healthy person, perfusion is continouos throughout the cardiac cycle.
-LCA prefuses the high pressure side of the heart mostly during diastole.
Negative coronary bloow flow; there is retrograde blood flow from the walls of the heart –> LCA –> and then back out to the aorta during early systole
This happens because the epicardial and endocardial blood vessels were just heavily perfused during diastole. As the pressure in the left ventricle begins to skyrocket, the pressure in these coronary blood vessels also increases. This causes the blood vessels to squeeze blood in both directions
Coronary blood flow, delta P of aorta & wall pressure
Pressure & time?
Source pressure: Pressure that’s available to drive coronary blood flow = Aortic pressure
Delta P = Aortic pressure- wall pressure
-When aortic pressure is higher than wall pressure, there is a greater opportunity for blood flow
-When aortic pressure is lower than wall pressure, that will present an issue for coronary blood flow
Time is another factor in coronary blood flow. There is plenty of time for the coronary vessels to fill during diastole. Anything that reduces the time in diastole, reduces the amount of time that the coronary vessels have to fill.
Time x Delta P gives us how much time is available for coronary perfusion
How does the body compensate for less coronary filling time?
When HR increases, the heart skips the middle third of diastolic filling time, which decreases coronary filling time
In a healthy heart, this is not usually an issue.
If you have bad coronary arteries, you need that additional filling time for coronary perfusion, more so than diastole
A. Aortic stenosis:
Obstruction to outflow.
Pressure in LV will be much higher than the aorta.
Aortic valve will open at a lower DBP because the ventricle will high a much higher LVEDP
Shorter time spent in phase III, so aortic valve will close at a higher SBP
-How does this affect coronary perfusion? Wall pressure will be significantly higher than normal, decreasing the pressure gradient needed for coronary filling
B. Mitral Stenosis:
LV and Aortic pressure are relatively normal.
During ventricular diastole, LAP will be elevated and there will be a pressure gradient (rather than passive filling)
Diastolic murmur
What is happening in C?
C. Aortic Regurg:
We do not have major changes in early systole.
The LVEDV is higher, causing an increase in stroke volume.
This leads to a higher peak systolic pressure.
Once the aortic valve closes, the pressure in the aorta has a steep run off because blood is now flowing retrograde into the ventricle –> leading to a decrease in diastolic pressure and creating a widened pulse pressure.
The peak pressure gradient (highest difference between aorta and LV) is what drives the backward flow into the LV.
As we move further into diastole, pressures are reduced, and the velocity of the retrograde bloodflow is reduced
What is going on in D? Acute vs Chronic
Acute Mitral Regurgitation:
LV fills to a very high volume due to the increase in L.A filling, resulting in a very high LVEDP
LV pressure during systole should remain the same. L.AP during systole is very high–> receiving blood from the pulmonary circulation and the LV –> resulting in a prominent, tall V wave
Pressure falls as the mitral valve opens –> y-descent
Murmur begins at S1 (av valve closure) because once the ventricle begins to contract, even before the aortic valve opens, pressure begins to increase –> extends slightly beyond S2 when the pressures equilibrate
A Wave: When the atria contracts, blood moves both forward and backward. The a-wave is the retrograde blood flow during atrial contraction
C Wave: Beginning of systole. Function of AV valves from bulging backward
X Descent: Atria are empty, AV valves are no longer bulging backwards, pressure is significantly decreased. Mid systole
V Wave: Result of atrial filling while AV valves are closed (systole)
Y Descent: AV valves are open, blood leaves the atria, pressure is decreased
Normal values and equation for SVR/PVR
SVR:
-Avg; 1200 dynesXsec/cm5
-Range: 800-1600 dynes
PVR:
-Avg; 80 dynesXsec/cm5
-Range; 40-180 dynes
(Map-CVP (R.AP for our class)/ CO in L/min) x 80
-Normal SVR w/ this equation is 1600
(P.AP - L. Atrial (wedge)/ CO) x 80
Normal wedge = 8mmHg
mmHg/L/min
CGS units (dynesXsec/cm5)
How do we convert PRU to CGS?
PRU (SVR and PVR)
Peripheral Resistance Unit
Delta P / Flow
(Map - R. AP/ CO in L/min or ml/sec)
- 100mmHg-0mmHg/5L/min = 83.3ml/sec –> close enough to 100
- 100mmHg/100ml/sec = 1 PRU
Multiply PRU by 1333 in order to obtain SVR/PVR in CGS units
PVR:
16mmHg - 2mmHg (L. AP)/ 100ml/sec = 0.14mmHg/ml/sec
Approx 1/7th of SVR
CVP/PAP Changes w/ Breathing
-PAP & CVP tracings should follow a similar pattern
-Arrows indicate start of inspiration
-CVP is reduced significantly at the start of inspiration due to the negative pressure generated in the chest. Blood is brought into the veins in the chest during inspiration, but there is a slight delay in the blood moving from the chest to the heart. Preload is decreased quite a bit here
-CO can briefly drop during this time, causing a decrease in systemic blood pressure
-PAP pressure is reduced at the start of inspiration as a function of having very compliant blood vessels. Preload is reduced for the right side of the heart as well as afterload (PAP)
-Afterload is reduced at the start of inspiration for the right heart. Preload for the left side of the heart is decreased. Afterload does not change in the L. heart
How is CO affected initially? And after? How do we overcome this?
Positive Pressure Ventilation & It’s Effect on CVP/PAP
What happens to filling pressure?
Normal inspiration does not require positive pressure. Even at a low setting, the positive pressure is abnormal
-When initiating the first respiration using PPV, the positive pressure is pushing on a system that is currently full of blood. This increases preload on both sides of the heart –> increasing CO, initially.
-Once positive pressure has been used for awhile, preload will remain increased in both sides of the heart, but venous return is decreased because of the pressure being placed on the thorax
-Increasing pressure in the thorax causes an obstruction to venous return. Filling pressure will be increased, and we will need to overcome this by adding more volume or constricting the veins
How does that affect preload and EDV?
High compliance heart vs low compliance heart
-Normal compliance of the ventricle allows for filling at a relatively low preload
-Less compliant Heart:
Over time, with increased afterload or aortic stenosis, the pressure in the ventricle will be increased due to hypertrophy. A larger heart muscle means it will require a higher pressure to fill the ventricle
-Very Compliant Heart:
The amount of pressure required to fill the heart will be very low
Cardiac Pressure, Volume, and Kids
-Children have less compliant hearts and are very sensitive to fluid
-In order to compensate for a decrease in venous return, pediatric hearts will need to increase in HR because they do not have the ability to accept more volume
Heart sounds 1-4 and murmurs
-1st HS is AV valves closing at the start of systole
-2nd HS is Aortic valve closing at the start of diastole. The pulmonic valve closes slightly after the aortic on deep inspiration
-4th HS is the atrial kick and should not be audible in someone who is healthy. Happens with stenotic mitral valve- atria is contracting while it is fuller than it should be
-3rd HS is heard w/ peds or CHF due to low compliance ventricle
Aortic Stenosis- Systolic ejection murmur w/ possible 4th heart sound due to the increase in LAP
Mitral Regurg- Murmur begins at S1 (av valve closure) because once the ventricle begins to contract, even before the aortic valve opens, pressure begins to increase pushing blood into the LA –> extends slightly beyond S2 when the pressures in the LA and LV equilibrate
Aortic Regurg- Valve doesn’t close well during diastole. Diastolic murmur immediately after S2. The peak of the murmur is heard when the aortic pressure and LVP reach their peak pressure gradient different
Mitral Stenosis- Diastolic murmur. Murmur is greatest when the mitral valve opens because of the high pressure gradient. Murmur becomes less intense throughout diastole as the velocity of the blood slows
Where do you place your stethoscope to hear each valve/murmur
-Aortic; 2nd intercostal space, right sternal border
-Pulmonic; 2nd intercostal space, left sternal border
-Tricuspid; 5th intercostal space, left sternal border
-Mitral; 5th intercostal space, left mid-clavicular line
APTM- All physicians take money
What is a phonocardiogram used for?
-A healthy person cannot hear lower than 20hertz
-Some murmurs are inaudible to the healthy ear, so a phonocardiogram can be used to detect the sound
Mediastinum Sections & What is Contained in Them
- Superior Mediastinum:
- Inferior Mediastinum:
- Anterior Mediastinum: In front of the heart
- Middle Mediastinum: The heart, surrounding structures, ascending aorta, vena cavae, pulmonary trunk and arteries
- Posterior Mediastinum: Abdomen
Middle Mediastinum
- Vagus nerve
- L Vagus nerve
- Aorta
- Pericardiacophrenic nerve, aa, vv
- Superior vena cava
Posterior Mediastinum
- Cervical Esophagus
- Azygos vv
- Thoracic Esophagus
- Thoracic Aorta
Vagus nerves are also found here
Hemizygos vein not pictured, but found here
Overdamped vs Underdamped? How does it happen?
As blood generates more or less pressure on the sensor in the pressure transducer, an electrical signal is generated that creates the display we see on the monitor.
Art line needs to remain free of clots or air bubbles. The clot occludes the flow, and an air bubble acts as a spring. Any rapid changes will be overdamped
-The equipment is able to take the dicrotic notch and calculate BP, HR, some ECG tracings
- Overdamped: Air bubble or gain on amplifier not turned up. Underestimates SBP
- Normal
- Underdamped: Gain is turned up too high. Artifacts will be created. Overestimates SBP
Circumflex anastamosis, epicardial, endocardial, subendocardial
Circumflex anatomy is vastly different in everyone
In some cases, it’s an anastamosis between the RCA and LCA
-Whether this is a good or bad thing is still under review
-Allows for collateral circulation between the two arteries in case something goes wrong
-Epicardial: Large coronary vessels that can be seen on the surface of the heart (LAD, PDA). Lowest amount of pressure during cardiac cycle
-Endocardial: Deep portions of the heart wall
-Subendocardial: Below the endocardium
Both endocardial and subendocardial are subjected to high pressures; especially if they are located in the left ventricular wall
Reduced Ventricular Compliance
-Reduced ventricular compliance is going to require more work on the part of the atria to help with filling (increased contractility of atrial kick).
-CVP, PSF, and blood volume will increase as a compensatory mechanism
Conditions that increase atrial pressure cause…
Conditions that increase atrial pressure put the atria at risk of becoming stretched out
When the atria become stretched out, we are predisposed to atrial arryhthmias, decreasing the coordination between the atria and the ventricles
What can cause these?
Eccentric vs Concentric
-Eccentric LVH: Thin, dilated ventricular walls. Systolic dysfunction
-Congenital dilated cardiomyopathy; ace-i
-Aortic regurg
-MI
-Concentric LVH: Thick, hypertrophied walls. Diastolic dysfunction
-Aortic stenosis
-Chronic HTN
MI; Collateral flow, prolonged pathologies, remodeling?
If ischemia happens in a small artery of the heart, typically surrounding blood vessels can dilate and create collateral flow to the ischemic area.
If blood vessels cannot dilate, no collateral flow will be created. This happens when the blood vessels have been exposed to pathology for prolonged periods of time; high cholesterol x many years, smoking, ETOH, chronic HTN, diabetes
Dead tissues can be “remodeled” by using fibroblasts to create scar tissue in the area. This can be helpful, but what is problematic is that the heart doesn’t know when to stop creating scar tissue. This causes dilated cardiomyopathy or can cover functioning heart cells
-ACE-i slow this process
Fibrotic tissue causing an area of the heart to become dilated
In control conditions, flow through a blood vessel is 100 ml/min
under a pressure gradient of 50 mm Hg. What would be the
approximate flow through the vessel after increasing the vessel
diameter to four times normal, assuming that the pressure gradient
was maintained at 50 mm Hg?
If the diameter doubles (2×), flow increases by 16× (or 2 to the 4th power)
If the diameter triples (3×), flow increases by 81× ( 3 to the 4th power)
If the diameter quadruples (4×), flow increases by 256× (4 to the 4th power)
If diameter increases by 100%–> diameter is doubling
If diameter increases by 200% –> 4 to the fourth
Thyroid hormone is _____ - soluble? Where is it located?
Which other glands are located on the thyroid?
-Difficult to measure thyroid function accurately
-Thyroid hormone is fat-soluble and hangs out inside oily areas in our plasma bioproteins
-Unexplained increase in HR at rest–> giveaway for hyperthyroidism
-Thyroid gland is located next to the thyroid cartilege of the larynx (adam’s apple).
-Parathyroid glands are located on the thyroid
Large thyroid gland = goiter
Right, left recurrent nerve? Inferior?
What happens if we lose one recurrent nerve? Both?
-Thyroid Cartilage
-Thyroid gland is completely covered in blood vessels, this allows thyroid hormone to be carried into the CV system and distributed around the body very quickly. Massive bleeding hazard
-Left & Right reccurent laryngeal nerve: Motor neurons that control the skeletal muscles of the voicebox.
R. Reccurrent larygneal nerve: Branch of the vagus nerve runs inferior to the aortic trunk –> follows the trachea/splits into right reccurent nerve –> posterior thyroid –> voice box
L. Reccurent laryngeal nerve: Travels under the aortic arch before turning around and traveling up to the voicebox. Inferior to the R. reccurrent nerve Inferior Laryngeal Nerve: Part of the right reccurent nerve that travels down the trachea and to the aortic arch, just before turning around and becoming the left recurrent
We can still speak if there is loss of one recurrent nerve. If we lose both, we cannot.
How are t3 & t4 made? How much iodide do we need per year?
Tyrosine- limiting factor in making T3, T4.
Tyrosine + 1 Iodide = Monoiodotyrosine; one benzene ring
Tyrosine + 2 Iodide= Diiodotyrosine; one benzene ring
Monoiiodotyrosine + Diiodotyrosine = Triiodothyronine (T3)
-two benzene rings
T2 +T2 = Thyroxine (T4)
-two benzene rings
T4 is predominantly produced here, some T3
Need 50mg of iodide per year
-
Hypothalamus controls the pituitary gland with TRH (thyrotropin releasing hormone)
–> TRH is released in response to metabolic stimulus
–> travels to adenohypophysis/anterior pituitary gland to release TSH (thyrotropin)
—> Increase in TSH –> Increase in T3 and T4.
T3/T4 are carried through the blood by carrier proteins:
1. Thyroxine binding globulins; TBG
2. Thyroxine binding prealbumin
3. Albumin
All three are produced in the liver
Where is T3 predominantly produced?
-Thyroid hormone is transported to the CV system via carrier proteins. (Mostly T4, but T3 is also transported)
-lipid soluble, so has no problem crossing cell membrane
-Iodinase cleaves on iodide from T4 to make T3 –> this is where T3 is predominantly produced
-Once in the cell wall, another carrier protein will carry the thyroid hormone into the nucleus where the thyroid hormone receptors are located
-T3 binds to receptor –> causes gene transcription and:
Metabolism increases: Increases in O2 consumption, glucose absorption, gluconeogenesis, glycogenolysis, lipolysis, protein synthesis, and BMR
Will need more mitochondria, atp
CV effects: Increase in CO, tissue blood flow, HR, contractility, and RR/depth. BP does not increase, SVR is reduced
Proper CNS development is dependent on appropriate amounts of thyroid hormone
Conditions that cause hyperthyroidism? What happens to cholesterol?
Hyperthyroidism
-In hyperthyroidism, cholesterol is being used at an increased rate at the cellular level, decreasing overall cholesterol levels
-Pituitary Tumor secreting TSH –> hypothalamus will stop producing TRH.
-Labs will show high TSH, high T3/T4, high metabolic rate, absence of TRH
Thyroid tumor secreting T3/T4 –> hypothalamus will stop reducing TRH, pituitary gland will stop producing TSH
-High T3/T4, low TRH, low TSH
Hypothalamic tumor secreting TRH–> High TSH production by pituitary –> increase T3/T4 released by thyroid gland
-TRH, TSH, T3/T4 are all elevated
-Grave’s Disease: Body produces antibodies that interact with TSH receptors on the thyroid gland –> Increased T3/T4 but TSH, TRH will be low.
-plasmapheresis to remove antibodies
Thyroid hormone and thyroxine take how long to take effect?
Hypothyroidism
Hasimoto’s: Antibodies that destroy the thyroid gland.
-TRH will be high, TSH and T3/T4 will be low
Lack of iodine–> increased release of TRH and TSH, T3/T4 will be low. Enlarged thyroid gland
Thyroid cancer- I 131; radioactive iodine to treat
Thyroxine injection takes ~10days to take effect
Thyroid hormone takes 6-8hours to take effect
People don’t like to take synthroid
What happens when a massive amount of iodide is introduced to the body?
Interferes with the thyroid’s ability to form T3/T4
Can help thyroid storm
Can happen with amiodarone administration (too fast, too much, too long duration)
Shock Classifications
Problem getting require nutrients to tissues
Hypovolemic
Cardiogenic- MI
Neurogenic: Volatiles, high spinal
Anaphylactic: Histamine and mast cells
Septic: Gram (+)
Venous return pathologies: Obstruction
Neurovascular Compensation to Hypovolemia
-Removing 10% of blood volume; arterial pressure and CO are relatively normal
-20%; arterial pressure may remain normal (compensation), but CO will be reduced
-SVR is increased to maintain BP, but CO is reduced because venous return is reduced
Difference between first three animals and last three?
When fluid shifts, where does it come from?
In the first three animals, they are bled out until for a brief period of time but are able to recover because the pressure never dropped below 50% of normal
-fluid shifts and other compensation mechanisms take place here.
Where does the fluid come from? Blood storage pools; the spleen, the pulmonary circulation, and the GI system can shunt blood to the systemic circulation
If blood pressure is reduced to <45% of normal MAP due to bleeding, the animal most likely will not survived. They make a brief recovery and then progress to death
-BP was most likely low enough to prevent coronary arteries from being perfused as well as other vital organs
Compensation:
-Increased SNS activity to increase venous return, CO, and PSF
-Kidneys: Increase blood volume
A severely failing heart (massive MI) where the SNS and kidneys are still unable to meet the critical CO level, the person is going to die without medication.
Cardiac glycosides (dig) can be helpful- but last resort
Milrinone/dobutamine
The kidney’s help is useful in heart failure until about point C.
The kidneys will continue to retain volume until there is a normal BP; however, in this case, there will never be a normal BP
Because of the continued increase in volume, the PSF has been high enough to stretch the heart past the point of it being useful –> CO is then decreased again
-Need to give diuretics here
