1. cardiac A & P 3/6 Flashcards
anatomy of heart:
1. how large is it?
- the size of your fist
2. the sternum and costal cartilages of 3rd, 4th, 5th ribs
- what is the Point of Maximal Impulse?
2. what may be palpated there?
- where the apex projects anteriorly and inferiorly
toward the left 5th intercostal space. - S1 may be palpated here.
the heart is rotated so that what ventricle makes up most of the anterior surface?
right ventricle
- what is the pericardium?
2. what are the 2 layers of the pericardium?
- A fibrous, double-walled sac that surrounds the heart and roots of the great vessels
- Composed of a visceral portion (contacts outer portion of heart) and an outer parietal portion (adheres to the fibrous pericardium)
- what is the paricardial sac?
- what is in it? How much? what does it do?
- what can happen to this “space”?
1.Pericardial sac -A thin potential space that separates the visceral and parietal pericardium
2• Contains 10-25 ml serous fluid that lubricates the heart allowing for free movement
3• In disease states, space can fill with blood and/or fluid, compress the heart, and decrease cardiac output. i.e. cardiac tamponade
- what does the right atrium do?
2. what vessel is located there?
- Right Atrium-Reservoir for the RV, receiving deoxy’d blood from SVC and IVC.
- Coronary sinus- largest venous channel
- what is job of right ventricle?
2. what vessel nourishes it?
- Right Ventricle: Ejects blood into pulmonary arteries for O2 and CO2 exchange.
- RCA
- what is the job of the left atrium?
2. what is the atrial contraction called & How much of output is it responsible for?
- Left Atrium-Reservoir for oxygenated blood
2. Responsible for 20-30% LVEDV via the “atrial kick”
- what is the left ventricle?
2. what is the thickness of the LV in comparison to the RV?
- Left Ventricle Receives oxygenated blood from LA and distributes to the body
2• 2-3x the thickness of the RV
- what is the myocardium?
- what type of muscle is in the myocardium?
- what are the three layers of the myocardium?
- Myocardium
Refers to the muscular cells of the heart that are arranged in 3 layers. - The myocardium has characteristics of both skeletal and smooth muscle.
- epicardium (outer) myocardium (middle) endocardium (inner)
- what part of the endocardium is most at risk for damage during MI?
- why?
- subendocardium
2. gets oxygen supply during diastole (diastole is most affected by rate changes, shorter diastole=less oxigenation).
Valves
- AV valves =name them, what sound does their closure make?
- where is the left valve located?
- where is the right valve located?
1• mitral and tricuspid; S1
2• Mitral- Left 5th interspace just medial to midclavicular line
3• Tricuspid -lateral to lower left edge of the sternum
Semilunar valves
- what are the Semilunar valves ? what sound does closure make?
- where is the left ventricles valve?
- where is the right ventiricles valve?
- aortic and pulmonic; S2
- Aortic- Right 2nd interspace close to sternum
- Pulmonic Left 2nd interspace close to sternum
valves:
- what is s1?
- what is s2?
- S1 = closure of antrioventricular valves (mitral and tricuspid)
- S2 = closure of semilunar valves (aortic and pulmonic)
atrial waveforms:
- what is an “a” wave?
- what is a “c” wave?
- what is a “v” wave?
1• a = contraction of the Right atrium
2• c = pressure of the ventricular isovolumetric contraction on the tricuspid valve
3• v = passive filling of the R atrium
- what are the only branches that come off the ascending aorta?
- Coronary blood flow through the coronary circulation is controlled by?
- The only way to increase oxygen delivery to the myocardium is to…?
1• Coronary Arteries
2• the factors that determine oxygen supply and demand
3• increase blood flow
VESSELS:
Left Main, what is another name for it?
Left Coronary Artery
VESSELS:
Left Anterior Descending (LAD):
1. what ekg leads show the areas it supplies?
2. what areas does it supply (4 areas)?
- V3-V5
- (4 areas supplied by LAD):
• Right bundle branch
• Left bundle branch
• Anterior and posterior papillary muscles (mitral)
• Anterolateral left ventricle
VESSELS:
Circumflex:
1. what leads show the area the circ supplies?
2. what area does it supply?
- I and VL
2. Lateral left ventricle
VESSELS:
Right Coronary Artery:
1. what ecg leads show the area it supplies?
2. what does the RCA supply?
3. what does occlusion of the RCA cause (besides pain)?
- II, III, AVF
- Supplies the posterior heart (RV and RA) and part of the left ventricle.
• Supplies the AV and SA Nodes before terminating on the inferior surface of the heart as the Posterior Descending Artery.
• Will also see conduction changes with occlusion of the RCA.
VESSELS:
PDA:
1. what vessel supplies the PDA (most of the time)?
2. what is it called when the PDA is supplied by the RCA?
3. what is it called If the PDA is supplied by the circumflex?
4. what is it called If the PDA is supplied by the both the RCA and circ?
- In 70- 85% of people, the RCA gives rise to the posterior descending (PDA) which supplies the superior-posterior interventricular septum and inferior wall.
- -If the PDA is supplied by the RCA = “Right coronary dominant”
•If the PDA is supplied by the circumflex = “Left coronary dominant”
•If the PDA is supplied by the both the RCA and circ = “co-dominant”
VESSELS: Coronary sinus 1. what is it? 2. where is it located? 3. are coronary VEINS shunt flow?
- The largest venous channel
- Located between the AV orifice and the valve of the inferior vena cava.
- Coronary veins are not shunt flow
VESSELS:
- What are thebesian veins?
- what is special about them?
- what is “shunt blood”?
- thebesian veins- venous drainage from the heart, combined with
bronchial and pleural venous flows, contributes to the normal 1-3% of shunt, empty into coronary sinus. - only the thebesian veins are considered shunt flow because they have blood combined with pleural and bronchial flow.
- shunt blood is blood that HAS ALREADY HAD OXYGEN EXTRACTED from it.
- what is unique about coronary blood flow?
- what does the force of LV contraction do to blood flow?
- how is CPP (coronary perfusion pressure) calculated?
- when is the LV perfused? how much of it during this phase?
- when is the RV perfused?
- what part of the heart is most at risk for ischemia with decreased CPP?
- Coronary perfusion is unique because that it is intermittent, not continuous like other parts of the body.
- The force of LV contraction almost completely occludes the coronary arteries.
- CPP is determined by the difference between aortic diastolic pressure and ventricular pressure: DP-LVEDP= (50-120 usually)
- the LV is perfused almost entirely (75%) during diastole
- the RV is perfused during both systole and diastole.
- The endocardium is most at risk for ischemia when there are decreases in CPP
- blood flow to the heart is ___% of C.O.; what is (brain, liver, kidneys, muscles, skin & intestines)?
- what is a normal CBF (coronary blood flow) in cc/min?
- Blood flow to the heart is 5% of CO
(Brain 12% Liver 24% Kidney 20% Muscle 23% Skin 6% Intestines 8%) - CBF 225-250 cc/min
- Coronary blood flow normally parallels what?
- formula for CPP=
- how much is extracted during diastole?
- what factor regulates cpp at what range?
- myocardial metabolic demand.
- DP-LVEDP (diastolic pressure minus left ventric end diastolic pressure)• CPP=(50 or 60 mmHg-120mmHg)
- *75% occurs during diastole
- Autoregulation in the myocardium is regulated between 50/60-120mmHG.
- what is coronary MV02?
- how many mL/min/___ grams?
- what is the biggest determinant of myocardial blood flow?
- myocardial volume of oxygen (demand)
- Coronary MV02 8-10 ml/min/100 grams
- Myocardial oxygen demand is usually the most important determinant of myocardial blood flow.
- how much of the oxygen delivered to the myocardium is extracted?
- if the heart needs more oxygen (increased metabolic demand), how does it get it?
- The myocardium extracts 65% of the oxygen in arterial blood that is delivered to it.
- If the heart needs more oxygen, it must be met by increasing coronary blood flow.
- What is the effect of volatile anesthetic agents on coronary blood flow?
- what is it rumored that VAs do to coronary blood flow?
- Direct vasodilators
- Reduce myocardial metabolic demands (mVO2)
- Reduce blood pressure (decrease both preload and afterload)
2. that volatile agents cause coronary steal HOWEVER, there is no proven evidence.
Cardiac Conduction System (Chronotropy):
- what conducts the cardiac rhythm?
- what is different morphologically between these cells and the other cardiac cells?
- within the myocardium lies a specialized conduction system comprised of special striated muscle cells that automatically initiate and coordinate the cardiac rhythm.
- These cells have fewer myofibrils than other cardiac muscle cells
SA node→
what is is? where is it?
Specialized pacemaker cells in the sulcus terminalis at the junction of the RA and the SVC.
what connects the SA node to the AV node?
internodal branches
AV node→(delay here to allow for filling)
- what prevents the ventricles from being stimulated when the atrium is stimulated?
- what keeps the impulse from going elsewhere?
- where is the AV node located?
- The Fibro-fatty atrioventricular groove insulates the ventricles from the atrial impulse.
- The AV node is the only normal gateway of conduction to the ventricles.
- Located in the septal wall of the RA.
what are the next conducting structures after AV node til conduction is done?
bundle of his→R and L bundle branches→Purkinje system
Structural and Regulatory Proteins:
- Myocardial cells are made of___?
- how does a cardiac muscle contract?
- what form of energy is needed for this process?
- sarcomeres, just like skeletal muscle cells.
- -calcium is released from the sarcoplasmic reticulum→
- binds to troponin/tropomyocin→
- sites on the myocin heads are uncovered→
- allows actin and myocin to bind - ATP is needed for this process
- what determines force of contraction of cardiac cells?
- what must cells do maintain in order to maintain optimal C.O.?
- what does that mean for the heart (in a nut shell)?
- what kind of patient would you see this in?
- what is this optimal length?
- Troponin C’s affinity for calcium determines the force of contraction of the cells
- Myocardial cells must maintain a length-force relationship in order to establish optimal CO.
- the more stretched out the myocardial tissue, the further apart the actin and myosin heads are (cant latch)
- CHF with boggy heart
- Optimal sarcomere length=2-2.4 um (micrometers)
- what is found in the heart in order to facilitate the propagation of action potentials?
- How does cardiac depolarization spread?
- what are Action potentials?
- Areas of low resistance are present between myocardial cells
- rapidly through the myocardium in syncitium.
- they are contractile responses to electrical impulses.
Ventricular Cells
- what is the normal resting membrane potential of a ventrical cell?
- what is the normal flow between sodium and potassium?
- what maintains this concentration?
- what is the permeability of K+ during resting phase?
- so what happens?
- The normal ventricular cell RMP is -80 to -90 mV.
- 3 Na+ out for every 2+ K+ in
- Atp pump maintains this concentration
gradient (ATPase) - During rmp, the cell is more permeable
to K+ (d/t leak channels)
-so more K+ moves outside of the cell and keeps the inside “more negative”
Phases of the Action Potential (part 1)
- what is the first phase ?
- what happens to sodium
- At what mV do Na+ gates open?
- Phase 0- depolarization
- Rapid Na+ influx
- Na+ gates open at -70/-65mV
Phases of the Action Potential (part 2)
- what is the second phase?
- what happens to change in voltage
- what happens to ion gates (sodium and calcium)
- Phase 1- initial repolarization
- Overshoot-change from +2-+30
- Na+ gates close, Ca++ entry begins
Phases of the Action Potential (part 3)
- what is the third phase?
- what ion channel opens?
- what does this allow for?
- Phase 2-plateau
- Slow Ca++ channels open
- Allows for ventricular filling Lasts 0.2-0.3 seconds
Phases of the Action Potential (part 4)
- what is the 4 th phase? is it slow or fast?
- what is the ion movement?
- The cells are ____to __ ___ ___ until ___?
- what is the refractory period?
- Phase 3-repolarization (rapid)
- K+ leaves, Ca++ channel inactivated
- …refractory to subsequent depolarizing stimuli until phase 4.
- The refractory period is the minimum interval between two depolarizing impulses that are propogated.
Phases of the Action Potential (part 5)
- what is the 5th (last phase)
- what happens during this phase (regarding membrane potential)?
- what ion pump changes happen?
- what happens to the muscles?
- Phase 4-completion of repolarization
- Return to resting membrane potential—ready for the next action potential
- Na+/K+ pump reestablished
- Relaxation occurs as calcium is actively pumped back into the sarcoplasmic reticulum by Ca++-Mg++-ATPase
what is the difference between the 2 refractory periods?
- absolute refractory period?
- relative refractory period?
- Absolute refractory period-during this period, ABSOLUTELY NO STIMULATION can cause another action potential. This is the first part of the refractory period.
- Relative refractory period-during this portion, it is possible to cause another action potential, but the intensity of the contraction will be relative to the time in this period.
What is the diffeerence between Atrial& Ventricular action potentials and SA&AV node action potentials?
- Atrial & Ventricular
- SA & AV node action potentials
- Characteristics of Atrial and Ventricular Action Potentials
• Fast
• RMP= -80 to -90mV
• Bigger upstroke, faster conduction - SA and AV Node Action Potentials
• Slow
• RMP -55to-60mv(due to slow leak of Ca++/”leakiness”)
• No plateau, just phases 4,0,3 since no rapid
depolarization
• “ slow phase 4 depolarization”
•Note: inhalation agents depress SA node automaticity.
where does each antiarrhythmic affect the conduction phases (in myocardium & his-purkenjie only):
- class I antiarrhythmics? examples?
- class II antiarrhythmics? examples?
- class III antiarrhythmics? examples?
- classs IV antiarrhythmics? examples?
- class I; sodium channel blockers work on phase zero (in myocardium/ his-purkinjie); to prevent depolarization with sodium; procainamide, quinidine, lidocaine
- class II; beta blockers work on phase 2 (in myocardium/ his-purkinjie); prevent contraction
- classIII; potassium channel blockers; work on phase 3 in myocardium; prevent potassium from leaving to prolong repolarization;
- class IV; calcium channel blockers; work on phase 2 in myocardium/his/purkinjie; prevent calcium influx decreaseing strength of contraction; cardizem, nifedipine.
what antiarrhythmic affect the action potential cycle in the SA and AV node?
- phase zero:
- phaseIV:
- class II; class IV
2. class II; class IV
- Stroke volume is…?
- what is stroke volume? how do you calculate it?
- what is ejection fraction? how do you calculate it?
- SV is the area within the loop (the volume ejected with each beat)
- SV = EDV-ESV (stroke volume= end diastolic volume minus end systolic volume)
- EF = EDV-ESV / EDV (ejection fraction =end diastolic volume minus end systolic volume dividie by end diastolic volume)
- what is preload?
2. what is another way of experssing preload?
- Preload - ideally expressed as the wall tension at the end of diastole, often ventricular end-diastolic volume is used to reflect this.
- Preload is the end diastolic stress on the ventricle or the end diastolic fiber length just prior to contraction
The Pressure Volume Loops
what are they?
•They are tools to help us understand the relationship between LV filling/volume and LV pressure
- As preload increases…?
- Within a heartbeat, increased venous return to either ventricle is compensated for by…?
- This also serves to…?
- …so does stroke volume.
- …increased output.
- …balance input to the two ventricles, preventing overloading of either the pulmonary or systemic circulation.
- The most important determinant of preload is___?
- preload is affected by:
- pre load is…
- venous return
- Blood volume
- Venous tone
- Ventricular compliance
- Ventricular afterload
- Contractility
- HR(↑ HR→↓ filling)(afib→no atrial contraction→↓ filling)
- 3. …the muscle length prior to contraction.
- Blood volume
- what is afterload?
- what is the measure of afterload (with a swan etc.)?
- what does vessel wall tension have to do with ventricles
- what happens to blood ejection as afterload (arterial wall tension) increases?
Afterload
- This should be seen as the sum of all forces opposing ventricular ejection (arterial wall tension-“the diameter of the hose”).
- SVR is used as the measure of afterload for the LV.( Right ventricular afterload is mainly dependent on pulmonary vascular resistance.)
- Wall tension is analogous to the pressure that the ventricle must overcome to reduce it’s cavity (pump out blood)
- As afterload increases, the ejection of blood slows and the volume ejected diminishes (for that beat).
- Myocyte stretching ___ sarcomere ___ which causes and____ in the force of contraction:
- This enables the heart to ___ additional venous return, thereby increasing ___ ____:
- The normal ventricle is capable of ____ its stroke volum to____ physiological increases in ____; this is called _____ autoregulation:
- ….increases the sarcomere length…increase
- ….eject the additional venous return, thereby increasing stroke volume
- …increasing its SV (stroke volume) to match the physiological increases in venous return (heterometric autoregulation)
- how does inotropy affect stroke volume?
- does inotropy depend on preload?
- what is going on inside the ventricle when inotropy increases?
- what must happen in order for inotropy to increase (think harder squeeze)?
- As inotropy increases, both stroke volume and velocity of ejection increase.
- Changes in inotropy result in changes in force generation that is NOT dependent on preload
- Changes in inotropy alter the force and pressure development in the ventricle → ↑’s the rate of ejection
- there must be an increase in calcium somewhere in the cycle
- what is chronotropy?
- what is dromotropy?
- what is inotropy?
- Chronotropy: Affecting a time or rate, as in heart rate.
- Dromotropy: Affecting conductivity of a nerve fiber;
- Inotropy: The force of muscle contraction.
- what happens during phase 2?
- what valves are open?
- what happens with the pressures?
- what happens to ventricular volume?
- Phase 2 = rapid ejection of blood
- Semilunar valves open
- Ventricular pressure is greater than aortic pressure
- Large decrease in volume
- what is the first cardiac phase?
a. what type of contraction
b. what valves open
c. what valves close (what does this cause?)?
d. what pressure changes occur? - this pressure does what to the valves?
- Phase 1 :
a. isovolumetric contraction from the beginning of ventricular systole
b. opening of the semilunar valve
c. AV valves close (1st sound)
d. Rapid increase in pressure (law of LaPlace) - The pressure generated in the ventricle is only enough to open the aortic and pulmonic valves
a. Volume is constant
b. C wave in atrial waveform-bulging of the mitral valve by increased ventricular pressure
Diastole:
- what is the first phase of diastole?
- what happens to valves?
- what heart sound is this?
- what happens to pressure?
- what is the change in ventricular volume?
- what wave will be seen ? why?
- what is seen on arterial line tracing?
Diastole: Ventricular relaxation
- Phase 1= isovolumetric relaxation
- Closure of the semilunar valves to the opening of the AV valves 3. S2
- Greatest decrease in pressure
- No change in ventricular volume
- V wave = atrial filling/increase in volume in atria
- Dichrotic notch on arterial tracing=retrograde blood flow back into the LV before AV valve closure
- What is phase 3?
- what happens with pressures?
- what happens to blood flow?
- what happens to ventricular volume?
- what does this represent on the EKG?
- Phase 3=reduced ejection
- Aortic pressure is greater than ventricular pressure
- Slowing of aortic blood flow, blood moves to periphery
- Decrease in ventricular volume
- T wave in EKG
- what is the last phase of diastole?
- what is happening with blood flow?
- what happens to pressure in ventricles?
- what happens to volume?
- what is the A wave on the art wave form? what does it do?
- Phase 3 = reduced filling
- Blood returns from the periphery
- Gradual increase in pressure
- Slight increase in volume
- atrial systole (atrial kick) pushes last 20-30% of blood into ventricles
- what is the 2nd phase of of diastole
- what happens as far as filling
- what happens with valves? when?
- how much of the ventricle is filled?
- Phase 2
- rapid filling
- AV valves open when LVP≤LAP
- 80% of filling now
Cardiac Innervation:
- what “innervation” & “regulatory” mechanisms are involved?
- what nervous system controls strength and frequency of heart beat?
- what are the 2 parts of this system?
- Cardiac ANS Innervation/Neural Regulatory Mechanisms-
- The strength and frequency of the heart beat is controlled by the autonomic nervous system.
- Both parasympathetic and sympathetic parts of the autonomic nervous system are involved in the control of the heart.
what are the 3 factors that affect heart rate and contractility?
- cardiac innervation
- humoral control
- cardiac reflexes
- Parasympathetic fibers: what cranial nerve is the pathway?
- where is the center that controls parasympathetic?
- what is parasympathetics job on the heart?
- which innervation predominates on heart function?
- two branches of vagus, which goes to which node?
- Vagus
- originate in the medulla (dorsal nucleus)
- decreases the heart rate and contractility
- PNS tone/vagal tone predominates (normal resting heart rate is 72 bpm)
- R vagus innervates the SA node – L vagus innervates the AV node
Sympathetic fibers:
- where do sympathetic fibers originate?
- what is the path of these nerves into the heart
- what effect on heart do these fibers have rate and muscle?
- which has has greater effect on contractility SNS or PNS?
- Originate from T1-T4 of the spinal cord, then travel up the cervical thoracic (or stellate) ganglia to the heart
- pass into the -
a) cardiac plexus to the
b) SA node and the
c) cardiac muscle. - increases in heart rate; effect on the muscle is an increase in rise of pressure within the ventricle, thus increasing stroke volume. 4. SNS has a greater effect on contractility
Cardiac Reflexes: Reflexes involve three components:
- afferent nerves sense a change in the state of the system, and communicate this to the brain
- the brain process this information and implements an appropriate response
- this results in altering the activity of efferent nerves controlling cardiac and pulmonary function, thereby causing homeostatic response that reverse the change in state
- what is Humoral Control?
2. name the 5 major and some of the minor hormones that cause humoral control:
- Circulating substances that affect cardiac and vascular function.
- humoral controls:
• Circulating catecholamines from the adrenal medulla
• Renin-angiotensin-aldosterone system
• Atrial natriuretic peptid
• Antidiuretic hormone (vasopressin)
• Many others (ex. Insulin, thyroxin, growth hormone, estrogen)
- where are the baroreceptors located?
- which baroreceptors are dominant (aortic or carotid sinus)?
- which are the most sensitive?
- Located in the aortic arch and carotid sinus
- The carotid sinus baroreceptors are the dominant baroreceptors (the aortic arch arterial baroreceptors are secondary)
- The carotid sinus baroreceptors are also more sensitive than aortic arch.
What is the Baroreceptor Reflex?
“They are afferent (sensory) nerve endings in the walls of the carotid sinuses (thin walled dilatations at the origins of the internal carotid arteries) and the aortic arch. These mechanoreceptors sense alterations in wall stretch resulting from pressure changes, and respond by modifying the frequency at which they fire action potentials.”
aortic arch baroreceptors travel via…
Aortic arch baroreceptors travel by the aortic nerve, a branch of the CN X
how do carotid sinus receptors travel to the brain? (it is a branch of what cranial nerve)?
The carotid sinus baroreceptors travel via the “nerve of Herring,” a branch of CN IX.
what factors decrease baroreceptor reflex sensitivity?
Aging, hypertension and athersclerosis decrease arterial wall compliance and thus baroreceptor reflex sensitivity.
- what part of the brain reacts to the changes in baroreceptor firing rate?
- according to marey’s law; baroceptors will __ firing rate and cause a ___ in the heart rate when stretch is increased by increased blood pressure?
- in other words someone dehydrated and hypotension will have a ___ heart rate d/t (increase or decrease) in firing of baroreceptors?
- medulla oblongata
- baroreceptors will increase firing causing a decrease in heart rate
- decreased firing of baroreceptors causes increased heart rate
Bainbridge reflex:
- where are the receptors found?
- how are they activated?
- what does increase filling of the heart cause?
- what happens if the heart is already high?
- is the bainbridge a real reflex or just a response?
1• Receptors are in the atria
2. An increase in preload directly stretches the SA node and causes an increase in SA node automaticity/↑HR
3• ↑filling of heart → ↑HR if the HR is low
4• If there already is a high HR, then additional fluid and stretch → ↓HR
5• a true reflex rather than a response to local stretch.
what is the Bainbridge Reflex?
Atrial Stretch Receptor Reflex
“a homeostatic reflex mechanism that causes acceleration of heartbeat following the stimulation of local muscle spindles when blood pressure in the venae cavae and right atrium is increased.”
chemoreceptor reflex
-
Respiratory Reflex
1.what are the receptors
1• Receptors are in the medulla
2• Inspiration→↑HR, Expiration→↓HR
- what does the frank starling curve tell you?
2. does frank starling curve show venous return: end diastolic volumes relationships? what does?
1•Frank-Starling curve looks at the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
2. F-S curves do not show how changes in venous return affect end- diastolic or end-systolic volume. You need to look at pressure- volume loops for this
frank starlings ventricular function curves:
- as inotropy decreses what increases
- what decreases with a decrease in inotropy?
- what kind of shift is this?
- left ventricular end diastolic volume (LVEDP)
- stroke volume
- shift to the right
Myocardial O2 Supply and Demand:
- what determines myocardial oxygen balance?
- what measures this?
- Myocardial oxygen balance is determined by the ratio of oxygen supply to oxygen demand. Increasing oxygen supply by increasing either arterial oxygen content or coronary blood flow leads to an increase in tissue oxygen levels
- measured as the partial pressure of oxygen,(pO2).
- what is ejection fraction?
- what is the normal EF?
- what does an increase in inotropy do for EF?
- what else can cause an increase in EF? what happens to the curve and what kind of shift is seen?
- EF is a way to evaluate the inotropic state of the heart; it is the fraction of the end-diastolic ventricular volume that is
ejected (measured of a percent of the total ventricular
blood volume). - Normal EF is 0.60
- An increase in inotropy leads to an increase in EF
- When there is a decrease in afterload or increased inotropy, there is a upward and to-the-left shift in the curve which reflects an increase in stroke volume/ejection fraction and a decrease in the size of the LV chamber (the opposite is also true).
What are the 6 Determinants of myocardial oxygen supply?
- Coronary artery anatomy
- Diastolic pressure
- Diastolic time
- Arterial Oxygen Content / Oxygen extraction
- Hgb
- SaO2
what percentage of delivered/ available oxygen is extracted by the myocardium?
The myocardium extracts 65-75% of the available oxygen that’s delivered to it.
1• VO2 = ?
- what is the formula for VO2?
- what is the normal VO2?
- cellular O2 consumption
- (CaO2 –CvO2) x CO
3• VO2 =8-10 ml/min/100g of heart
What are the 5 Determinants of myocardial oxygen demand?
•HR •Myocardial contractility -Myocardial wall tension •Preload •Afterload
how to shoot a cardiac output:
a) when in breathing phase do you inject saline? b) how many mLs? c) how many seconds should you wait between injections? d) Measured using the Fick principle; what is it?
a) • Shoot at the end of expiration
b) • Use 10ml over 4 seconds
c) • Wait 90 seconds between injections
d) • The Fick principle assumes that the rate at which oxygen is consumed is a function of the rate of blood flows and the rate of oxygen picked up by the red blood cells.
Cardiac Output:
- what does cardiac output measure?
- what is normal CO?
- what are determinants of CO?
- what is the normal C.I., and what does it measure?
1-measures rate of blood flow from the heart in liters per minute but also can be used to determine oxygen consmption based on fick principle 2•4-8 L/min 3• CO is determined by: – Preload/myocardial wall tension – Afterload/Mean arterial pressure – Heart rate – Contractility – Ventricular compliance 4• CI = 2.5-4 L/min Is cardiac output adjusted to the pt’s BSA
a) what is the calculation for Ejection Fraction (EF)?
b) what is the normal value
a) (SV / EDV) × 100%
b) .60 of LV function (60%)
a) what is the Calculation for Stroke Volume (SV)?
b) what is the normal value?
c) what is another way to calculate SV?
1a) EDV – ESV
1b) 60-80 ml/min or
c) SV= COx1000ml (per liter) divided by heart rate
ex: 4.8 x 1000= 4800 ml
4800 ml/80 bpm=60 ml/min
- what is end diastolic volume ?
2. is it higher or lower than end systolic volume?
- it is the amount of blood in the ventricle at the tail end of filling (which occurs during rest/diastole)
- end diastolic volume is high where as end systolic volume is low (because the heart has just ejected the blood).
a) what is the calculation for Cardiac Output (CO)?
b) what is the normal value for CO?
a) SV × HR
b) 4.0-8.0 L/min
a) what is the calculation for Cardiac Index (CI)(2 methods)?
b) what is the normal value
a. CO/BSA or (SV×HR)/BSA
b. 2.5-4.0 L/min/m2
c. (BSA=body surface area in Meters squared)
what is a normal CPP (coronary perfusion pressure)
60-80 mmhg
how to calculate SVR:
SVR = (MAP − RAP)x80 divided by CO
how to calculate MAP:
MAP = SBP + (DBPx2) divided by 3
what is a normal RVEDV (right ventricular end diastolic volume)?
100-160 ml
pressure loops 1:
- what is the left side variable (Y axis)? what is the range?
- what is the bottom variable (X axis)? what is the range?
- Left ventricular pressure; 0-120 mmHg
2. Left ventricular volume; 0-150 mL
pressure loops 2:
- what is the space between the Y axis and the pressure loop represent?
- what does it mean when the space is bigger?
- left end systolic volume (how much is left after systole)
2. the left ventricle is ineffecient and there are higher volumes left in the heart after systole
A=lower left corner; B=lower right corner; C=upper right corner;
D=highest peak of top curve; E=upper left corner
1. what happens at A?
2. what happens at B?
3. what happens at C?
4. what happens at D?
5. what happens at E?
- A= atrial systole; mitral and tricuspid valves open; ventricular volume and pressure begin to rise
- B=closure of mitral and tricuspids (S1); ventricular isovolumetric contraction begins to build pressure
- C=opening of aortic and pulmonic valves, blood ejection begins, volume begins to fall
- D=ejection pressure peaks, volume continues to fall
- E=blood continues to trickle out until valves close (S2); end systolic volume is measured here
if you cut the pressure volume loop in half diagonally from left upper to right lower corner …in regards to the cardiac cycle:
- what is the top right portion of the pressure loop?
- what is the bottom left portion of the pressure loop?
- systole
2. diastole
what does the space in the middle of the pressure/volume loop represent?
stroke volume
