CV1-CM Flashcards
what is the number one cause of death for males and females?
cardiovascular disease
what are the most cardiovascular deaths caused by?
42% from coronary artery disease
how many times a day does the heart beat?
100,000 times a day
how much does the heart weigh?
9-12 oz
what is the purpose of the structure of the heart?
maintain pressure differences
the chest cavity is ______ the sternal boarder?
2/3 the sternal border
where is the myocardium most vulnerable to external forces?
the ventricle lays right along the rib cage along the left border of the sternum, if you got hit directly here it can put you into a dangerous rythmn and kill you
you want to protect this area
how many times does your heart beat a per day and per year?
100,000 per day
- 35 million per year
what is the function of the coronary arteries?
where do they originate from?
provide the heart with its blood supply
they originate from the base of the ascending aorta
does the heart recieve blood during systole or diastole?
during diastole!!!
what four arteries does the right coronary artery (RCA) feed into? why is this so important?
- SA NODE artery
- AV NODE artery
- acute marginal artery
- posterior descending artery
**this is important because it controls the electrophysiology of the heart, if there isn’t any blood getting to the SA and AV nodes, then the heart won’t function**
what are the two main branches the left coronary artery branches into?
what are the two subbranches of each of these?
1. left anterior descending artery
a. 1st septal artery
b. anterior diagonal
2. circumflex artery
a. oblique marginal
b. posterior lateral circumflex
which is the worst artery to get an occlusion in?
left main coronary artery
because it brances into the left circumflex artery and left anterior descending artery basicaly knocks out the entire left side of the heart and the left side of the heart is most important!!
***the left anterior descending is know as the widow maker because it is the most important and basicallly feeds the wole left ventricle, if this ventricle doens’t work, your body doesn’t get blood!!!**
how does high intensity cardio workouts effect the coronary arterys?
it doesn’t make more of them like it would by making collateral arteries….
….it just makes them LARGER!!!
Explain what the areas of the heart are?
- lateral
- inferior
- apex
- anterior
- posterior
where is the worst place for you to get a MI?
the left coronary artery is the worse place for you to get a MI because it feeds the entire left side of the heart! so if you block this it will likely cut off most of the blood supply
this is known as the widow maker!
what is a threshold?
the minimal chance in polarity to produce a AP
what is the primary ion repsonsible for depolarization at the SA and AV node?
CALCIUM
the massive influx of calcium causes the SA and AV nodes to depolarize!
**keep in mind this is opposit of the perkinje fibers which depolarization is caused by Na***
absolute refractory period
for myocardial cell
no stimulus no matter how strong will depolarize the myocardial cell
**see area in yellow**
this is the time that the myocardial cell is contracting
relative refractor period
of myocardial cell
a sufficiently strong stimulus will depolarize the myocardial cell
this signal must be recieved before it has depolarized or after it has repolarized
see green areas in the picture, this is at the resting membrane potential
how many times longer is the cardiac action potentential than the muscle action potential?
why is this a good thing?
cardiac AP is 10x longer than skeletal muscle potentential
think about when you flex your bicep to show off your muscle, it stays flexed because the AP for skeletal muscles are really short, so they keep firing quickly to keep the muslce contracted
this would be BAD in the heart!! this would mean the heart could stay contracted which is dangerous, the longer AP allows the heart to contract and fully relax before it can take another AP allows the heart time to fill with blood
what is the SA node depolarizing rate?
60-100 times/min
what is the AV node depolarizing rate?
40-60 times/min
what is the purkinje cell depolarizing rate?
20-40 times/min
what is the electrical conducting pathway through the heart?
where is there a delay and why is this a good thing?
- SA node (0sec)
- Far side Left atrium (.09 sec)
- AV node (.03 sec)
- bundle of HIS (.16 second)
- purkinje fibers (.19 sec)
- epicardial wall (.22 sec)
notice that there is a delay at the AV node since it takes longer to travel down the bundle of HIS, this occurs intentionallly because you want to allow enough time for the atria to contract and push the blood into the ventircles so they can fill before contracting!!
if your atrial stopped contracting would you notice it?
you wouldn’t notice it originally just at rest, but if you got up and started jogging you would notice it because the demands of the body are going up and without the atria contracting you can’t meet those demands
sympathetic stimulation on the heart…how does it effect:
- ep/NE; adrenergic receptors
- HR
- conduction velocity
- force of contraction
- increases stimulation of EP/NE receptors
2. increases HR
3. increases conduction velocity (wires to lightbulb)
4. increases force of contraction
what is the parasympathetic innervation of the heart effect:
- ACH muscarinic receptors
- HR
- conduction velocity
stimulates ACH muscarinic receptors
2. decreases HR
3. decreases conduction velocity
what receptors in the heart does sympathetic stimulation act on?
adrenergic receptors NE/EPI
what receptors in the heart does parasympathetic stimulation act on?
ACH, muscarinic receptors
explain the hormonal influence on the heart?
what is the order of organs that produce them?
what is this hormal influence on the heart important
circulating catecholamines
- epinephrine (80%)
- norepinephrine (20%)
hypothalamus->pituitary glands->adrenal glands
this is the order that is used to produce them
significance: if someone lost their sympathetic/parasympathetic control of their heart, like with a heart transplant, they are still able to control HR using circulating hormones, it might take a little time to see the response because you have to wait for them to be produced, but the can do the same time, just takes a longer work up like walking on treadmill
Case: a pt has a HR of 30 and an occlusion in the right coronary artery. ECG shows no P waves. Pt complains of being dizzy!
whats happened? what does he potentially need?
SA and AV node have been taken out and he is firing from the purkinje fibers
atria aren’t contracting anymore
likely needs a dual wire pacemaker!!
what do you need to do about the QT interval to account for HR? what is the name of this equation?
Bazetts equation
allows you to correct the QT for heart rate
divide the square root of the RR interval into the QT interval, measured in seconds
where do V1 and V2 lie?
where do V3 and V4 lie?
where do V5 and V6 lie?
v1 and v2: directly over right atrium
v3 and v4: directly over interventricular septum
v5 and v6: directly over left ventricle
the direction of the mean vector is called….
mean electrical axis
what is the leading cause of cardiovascular death?
atherosclerosis
what percent of people with PAD are asymptomatic?
50%
in a person with PAD
where are the arterial ulcers?
where are the venous ulcers?
arterial ulcers: lateral side
venous ulcers: medial side, usually painless, large and irregular
people with athlerosclerosis most likely die from….
AMI
ankle-brachial index
what is this used to diagnose? how does the test work? what value is diagnostic?
used to diagnose PAD
- BP cuff around the ankle, meausure the systolic BP using doppler (measures the PT and PD pressure)
- BP cuff around the brachial artery
ankle/brachial of .9 or less is diagnostic for PAD, since the pressure in the ankle decreases if PAD is present since the tissue isn’t being profused and there is decreased BV and pressure
if the ABI is less than .5, what is the 5 year survival rate?
63%! so hey, thats good
what does a supervised walking program do in PAD? (four things)
- improves oxygen utilization
- increases muscle anaerobic metabolism
- shifts energy of walking to muscles with higher O2 delivery
- recruits collateral blood flow
explain how the charges on the inside of the cell change through the cardiac cylcle?
Resting state: inside the cell is -negatively charged
depolarization: creates a temporary + charge inside cell
repolarization: cells go back to -negative charge
explain the properties of pacemaker cells?
(7 characteristics)
- autorythmic (can generate a AP on their own)
- coupled to myocytes via gap junctions
- no resting membrane potentional, always constantly changing with their charge in cell, constant flux
- located in SA node, AV node, purkinje cells
- under neural and hormonal imput that determines the rate of depolarization
- with each depolarization, a new AP is created that stimulates the next cell
- 5-10 ug long
explain the properties of the SA node
dominant pacemaker cells, 60-100 b
- primary pacemaker of the heart
2. slow response action potential
- no true resting membrane potential
- AV node action potential very similar
explain the properites of the electrical conducting cells
what is the electrical conducting pathway of the heart?
(7 pathways)
hard wiring of heart, long and thin, “wires to a lightbulb” they carry the messages quickly and effectively to the heart
pathway:
- interatrial pathway
- SA Node
- inter nodal pathway
- AV node
- bundle of HIS
- right and left bundle branches
- perkinje fibers
purkinje fibers are the _______ conducting system
ventricular
bachmans bundle allows for…..
activation of the left atrium from the right atria
explain the characteristics of myocardial cells
(7 things)
allow for contractility of the heart, account for 99% of the cells in the heart, THESE ARE THE WAVES YOU SEE ON THE EKG
- striated muscle with gap junctions or intercalculated disks
- fast reponse action potenitals
- NOT AUTORYTHMIC
- true resting potential unlike SA and AV
- contain actin and myosin
- depolarization causes CA TO ENTER CELL and cause it to contract
- spreads slowly across myocardial cells compared to conducting cells
explain the small and large boxes on both the X and Y axis of the EKG paper
X axis: seconds
small boxes: 1mm x 1mm, .04 seconds
larger pink boxes: 5mm X 5mm .2 seconds
Y-axis: mV
small boxes: .1 mv
large boxes: .5 mv
explain the p wave seen on the EKG
what leads do you read the p wave in?
the right atria depolarizes creating the p wave
first part of p wave is right atrial depolarization
second part of p wave is left atrial depolarization
read the p waves:
1. left lateral leads (I and aVL)
2. inferior leads (II and aVF)
explain the function of the AV node?
gate between the atria and the ventircles, slows the conduction so that the atria have time to contract and the vetnricles to fill with blood
represented by the P-R segment on the EKG
what wave represents ventricular depolarization?
where does the signal travel after AV node?
in a normal person what two leads would you expect this to be positive in?
which one would you expect this to be negative in?
- bundle of HIs
- right and left bundle branches
- purkinje fibers
positive in:
1. lateral leads (I and aVL)
2. inferior leads II, aVF
Q wave of QRS
what is this? what does it represent? what is normal mV for it? what four leads would you see it in most likely?
first downward deflection
represents septal depolarization
**not always visible** generally <.1 mV
leads:
I, aVL, V5, V6
R wave in QRS
what is it? what does it represent? what do you see it?
first deflection upwards, might be a second spike called R’
represents ventricular myocardium depolarization
leads:
left lateral (aVL, I)
inferior leads (II, aVF)
what is the S wave in QRS?
what is it?
first downard deflection AFTER UPWARD!!
what is a QS wave?
if the entire configuration is only one downward deflection
explain what these are?
wow you’re good
what part of the heart does the EKG reflect?
measures the electrical activity of the myocytes particullary the left ventricle since this is the largest, it has the most electrical activity
what does the T wave represent?
ventricular repolarization, requires energy because it uses the membrane pump
this is a active process, explaining why it takes longer with a wider wave on the EKG
typically these are positive in the same leads where the R is positive
explain what the PR interval is?
what is a normal time for this interval?
includes the p wave to the start of the QRS
atrial depolarization to just before ventricular depolarization
usually .12-.2 seconds
what does the PR segment represent?
why is this important?
from the end of atrial depolarization to the start of ventricular depolarization
represents the depolarization stimulus slowing at the AV node creating a brief pause, this allows the atrial blood to enter the ventricles before they contract, held here about .1 of a sec then travels down ventricles via bundle of his, bundle branches, terminal perkinje
what does the ST segment represent?
measures time after ventricular depolarization to the start of ventricular repolarization
what is the QT interval?
how much of the cardiac cycle should this account for? what must you control for?
begining of the QRS to the end of the T
begining of ventricular depolarization through ventricular repolarization
~40% of each cardiac cycle and varies with HR, if it repolarizes faster the QT interval becomes shorter, therefore, if the heart rate is slower the QT becomes longer, but controll for heart rate
explain how depolarization moving towards or away from a postivie electrode effects the deflection? what about perpendicular?
if moving towards: positive deflection
if away from: negative deflection
if perpendicular: get biphasic deflection
what charge is the EKG picking up?
the charge on the outisde of the cell, not the inside!!!
explain the relationship between depolarization “QRS” and repolarization T waves?
repolarization occurs in the last area of the heart to have been depolarized and travels backwards, in a direction opposit of the wave depolarization
since the same electrodes that recorded a positive depolarization, (appearing as a tall R wave), will generally record a positive deflection during repolarization
it is therefore typical to find positive T wave deflection in the same leads that have tall R waves with positive deflection!
explain how repolarization is seen when traveling toward or away from an electrode? what about perpendicular?
THIS IS OPPOSTITE OF DEPOLARIZATION!!!!
IN REPOLARIZATION:
- a wave traveling TOWARDS, is NEGATIVE
- a wave traveling AWAY is POSITIVE
- if perpendicular: biphasic, but negative inflection comes first
explain the degrees of each of the limb leads as seen on the circle?
what leads are included and called left lateral leads?
what degrees do these measure at?
what is considered a right lateral leads? what does it measure at?
what leads are considered inferior limb leads? what angle do they measure at?
lead II 60*
aVF 90*
lead III 120*
explain the placement of the 6 pericordial leads?
V1-fourth intercostal space to the right of the sternum
V2-fourth intercostal space to the left of the sternum
V3- between 2 and 4
V4-fifth intercostal space in the midclavicular line
V5- between four and 6
V6- placed in the fifth intercostal space in the midaxillary line
of the pericordial leads, which ones measure the
anterior
left lateral
right ventricular regions?
anterior: V2, V3, V4
left lateral: V5 V6
right ventricular: V1
of combined leads, which ones reads the ANTERIOR HEART?
V2, V3, V4
of the combined leads which ones read the LEFT LATERAL heart?
I, aVL, V5, V6 read left lateral
of the combined leads which ones read the INFERIOR heart?
II, III, aVF read inferior heart
of the combined leads which ones read the RIGHT VENTRICULAR of the heart?
aVR and V1
explain what a vector is that the EKG reads?
the average direction
if you have players on the a soccer field and they are running to get a goal, individually the players are running all over the place, but together they are moving down the field=average direction
explain the four rules that typically reflect R wave progression in the precordial leads?
- V1 smallest R wave
- V5 largest R wave, and builds progressively as it gets up to this
- V6 is usually a little smaller than V5
- V3/V4 R wave goes from being smaller than S wave, to larger than s wave, so S3 is usually biphasic
explain the difference between the resting state AP and the exercise state AP for pacemaker cells.
(3 things for each)
resting membrane (blue line):
- parasympathetic tone
- resting membrane potential more negative
- rate of rise to threshold, the slope becomes less steep, so it takes more time to get to threshold
exercise state (green line):
- sympathetic tone
- decreased Ca entry
- increased rate of rise to threshold, steeper slope so it takes less time to get to threshold
explain what happens at the three stages in an action potential in SA and AV pacemaker cells!
controlled by Ca and K
Phase 4: -60 mV spontaneous depolarization that triggers action potential when threshold is met at -30-40 mV
slow Na+ and Ca++ in
Phase 0: depolarization phase of AP
fast Ca++ IN
phase 3: repolarization till -60mV, cycle spontaneously repeates
Ca channels close, K+ OUT FAST (makes neg again)
what are the SA and AV node pacemaker cells depolarization depended on?
CALCIUM AND K
when a ion channel is open there is increase in…
conductance
myocytes are sometimes referred to as…..
“fast reponse AP” since they have very rapid depolarization
explain the depolarization repolarization phases seen in myoctyes?
Phase 4: -90mV, with true resting potential
K conductance and currents high since K is leaving the cell, making the inside negative
Phase 0: threshold -70mV, rapid delpolarization
rapid increase in Na++ conductance, rushes in!! K conductance decreases because gates close, so the K is stuck inside of the cell, making it more positive
Phase 1: inital repolarization, plateau phase
Ca+ still moving in but K gates open, so K starts to move out, but they someone equal each other so you get a plateau
Phase 2: plateau phase prolongs the action potential since the Long type Ca gates (L-type) are still open, this distinguishes cardiac muscle from the fast muscle AP in skeletal muscle
Phase 3: repolarization
K current increases as it rushes out of the cell, Ca gates close, makes the cell negative again
what ions are the non-pacemaker heart cells (myocytes) dependent on?
depolarization-fast Na influx
plateau- slow Ca in
repolarization- Fast K out
how do you determine HR from EKG?
explain what hypertrophy of the heart is?
give two examples of conditions this is common in?
increase in muscle mass, most commonly caused by pressure overload where the heart is forced to pump blood against increase resistance in the body
Ex: hypertension or aortic stenosis
explain what englargment of the heart means?
dilation of a particular chamber, allowing it to hold more blood than a regular chamber, this usually happens because of volume overload caused by increase volume of blood
the chamber dilates in an attempt to decrease the overall pressure
what are three things on a EKG that can suggest enlargement or hypertrophy?
- chambers take longer to depolarize increase in duration
- chamber can generate more voltage higher amplitude
- change in the electrical shift
what is axis? what is normal values for this and what leads do you see it in?
axis: the average direction or mean vector of ventricular depolarization, mean electrical axis
normal 0-90*
positive in I and aVF
what two leads do you look at to determine axis deviation?
I and aVF
explain what you would see for:
left axis deviation
right axis deviation
extreme right axis devation
what specific two leads do you look at?
look at I and aVF
After finding the axis explain how you calculate the axis by degree?
- figure out which quadrant it is in
- find a biphasic wave in the limb leads
this means the axis is perpendicular to this, so add 90*
- there will be two options for this, but pick the one that is in the axis that you already defined
Ex: you know you have left axis deviation, the biphasic QRS is at aVR.
AVR is at -150, subtract 90 from it=60*
this is in the left axis deviation quadrant so you know this must be right
which is more common:
Left axis deviation or right axis deviation?
Left axis deviation is far more common than right axis
deviation, it is more likely that left ventricle has hypertrophy because of sustained hypertension than hypertrophy of the right ventricle, however, this does happen with conditions like PE, where the blood is backed up with blood
what wave do you look at to determine atrial enlargement?
what is the normal duration and ampitude for this wave?
what two leads do you look at to determine right and left atrial englargements?
Pwave for atrial englargment
normal duration: .12 seconds (3 little boxes)
normal amplitude: 2.5 mm (2.5 little boxes)
lead II=right atrial englargement
lead V1=left atrial englargement
right atrial enlargment
what lead do you look at?
what will you see?
what is the nickname for this and why?
look at lead II
greater than 2.5 in amp of pwave
commonly seen in SEVERE LUNG DISEASE so called p. pulmonade
left atrial enlargement
what lead do you look at?
what will you see? what is the nickname for this and why?
lead V1
of the biphasic p wave the second portion must:
greater that 1 mm wide**
OR
greater than 1 mm amp
Commonly seen in mitrial valve disease so nicknamed P. mitrale
right ventricular hypertrophy
what are the rules for this in the limb leads and pericordial leads?
Limb leads:
I QRS negative (since moving away from I)
Pericordial leads:
MUST HAVE RIGHT AXIS DEVIATION
THEN
A: R>S in V1
B: S>R in V6
explain how this shows right ventricular hypertrophy?
V1: R>S
V6: S>R
left ventircular hypertrophy
what are the two limb lead rules?
what are the four pericordial rules?
SPECIFIC IN LIMB, SENSITIVE IN PRECORDIAL
LIMB:
R amp in aVL exceeds 11mm
R amp in I exceeds 14 mm
pericordial:
R amp in V5 + S wave in V1= 35 mm
R amp in V5>26 mm
R amp in V6>18 mm
R amp in V6>V5
in ventricular hypertrophy
what two characteristics of the wave might you see?
what does this happen?
- downward sloping ST depression
- T wave inversion
people don’t know why it happens but it often happens with severe hypertrophy
what are the four questions you want to ask when analyzing a rythmn?
- does the rythmn appear regular/irregular? fast or slow?
- Is the QRS wide or narrow? greater than .12
- are there p waves present and what do they look like?
- what is the relationship between p waves and QRS? 1:1 etct
what are the four sinus origin rythms?
normal sinus rythmn
sinus arrythmia
sinus bradycardia
sinus tachycardia
what are the symptoms that are generally associated with the presence of arrythmia if the pt is symptomatic? 4 things
palpitations
awareness of rapid heart beat
decreased CNS profusion causing leightheadedness and syncope
sudden cardiac death
explain how enhanced automaticity leads to arythmias?
what type of depolarization do they exhibit?
what are four things that can cause this?
accounts 10% of arrythmias
property of certain cardiac cells to spontaneously initiatie an action potential
cells exhibit diastolic depolarization
cells become activated and “irritable” as a result of drug toxicity, hypoxemia, ischemia, metabolic abnormalites and more, these initiate the arrythmia
what are the three mechanisms of arrhythmias occuring outside of the sinus node?
- reentry (most common!)
- enhance automaticity
- afterdepolarizations
afterpolarizations
What is this caused by? what can this trigger if it is large? what about sustained? what are the two ways that this can occur by? what are 3 things that cause the first and two things that cause the second?
oscillations of membrane potential before or after completion of repolarization, if they reach threshold potential they can initiate spontaneous action potentials , can happen in any cells in the heart including nonpacemaker cells, happens in people with cardiac pathology
IF AFTERPOLARIZATION LARGE CAN TRIGGER PVC or SUSTAINED SYSTOLES WHICH MEANS SUSTAINED VTACH, this is dangerous!! THIS IS WHY IT IS DANGEROUS!
Causes:
1. prolonged APs
-long QT syndrome, genetic defects, drug induced
2. Ca overload from
-digoxin toxicity, PDE inhibitor toxicitiy
how do you preform carotid massage?
what are the 5 steps to preforming this?
- auscultate for carotid bruits, DO NOT PREFORM IF BRUITS PRESENT BECAUSE YOU DON’t want to cut off the last remain blood supply OR CAUSE STROKE
- lay patient supine, rotate head away from you
- apply gentle pressure to carotid artery at the angle of the jaw 10-15 seconds
- TRY THE RIGHT CAROTID FIRST because has higher rate of success, then move on to the left if right doesn’t work
- have rythmn strip running through the entire thing so you can see what hs happening, have defib stuff handy just in case
what rythmns can carotid massage help?
3 things
- atrial flutter
- paroxysmal supraventricular tachycardia (PVST)
- sinus tachycardia
explain how carotid massage effects narrow QRS tachycardia like:
- sinus tachycardia
- atrial flutter
- Paryoxysmal supraventricular tachycardia (PSVT)
sinus tachycardia: briefly slow rate, will return to tachycardia when carotid massage is stopped
atrial flutter with 2:1 block: increase the AV block (make there be more flutter waves make it 4:1) which in turn slows the ventricular rate because the QRS are farther apart
PSVT: may abruptly terminate the arrythmia, or not work
what are four drugs that can cause a decreased heart rate and cause bradycardia?
Beta blockers
diltiazem
verapamil
digoxin
what are the 6 drugs that can cause increased heart rate of tachycardia?
- levothroxin
- digoxin toxicitiy
- caffeine
- cocaine
- amphetamines
- sympathomimetics
what are four drugs that can cause a prolonged QT?
- antiarrythmics (class 1A, 1C, class III0
- erythromycin
- antifungals
- tricyclic antidepressants
AND MORE…naturally
what must you do if a elderly pt has sinus node dysfunction caused be medication and needs a pacemaker?
must stop the drug before getting a pacemaker
need to determine if its the persons heart or the drug….they might not need it
what are the two most common indications for a pacemaker?
- sinus node dysfunction
- AV node dysfunction
if the ventricular rate of Afib continues to exceed 200 bpm
consider…
WPW syndrome
what is the best rate control med you can give the ED for afib?
what about for acute MI or HF?
IV diltiazem for a fib
IV B-blocker for acute MI or HF
in pts with chronic/recurrent afib who can’t be cardioverted….what is their tx option?
rate control approact
leave in afib, control ventricular rate and anticoagulate with warfarin
what are the 6 risk factors for stroke that would make you want to put a patient with rate controlled afib on anticoagulation?
must put these patients on anticoagulation if at increased risk for stroke to prevent against embolism
RF for stroke:
- prior stroke/TIA
- HTN
- DM
- HF
- >75 years old
- valvular disease
what has the ability to increase contractility?
only sympathetic tone
a depolarized cell is ______ on the outside of the cell and ______ on the inside of the cell when it repolarizes?
a depolarized cell is negative on the outside of the cell and when repolarizing is negative on the inside of the cell
circulating catecholamines can cause a decrease in HR?
true or false
false, they come from the adrenal glands and they can only INCREASE the HR
if you were at the highest point of the QRS, you would be completely depolarized?
true or false?
false!!
this would mean you are only half depolarized because in order for full depolarzation you have to make it through the entire QRS, not just the top!!
what are the two parts of the cardiac cycle?
systole and diastole
refers to the ventricles
systole=when the ventricles are contracting
diastole=when the ventricles are relaxing
as you sit in a chair under parasympathetic control, what happens to the K+?
increase in K exiting the cell, makes the cell more negative which lowrs the resting membrane potential and makes the HR slower
explain the different waves of the atrial pressure curve and what is happening at each stage?
wave a: occurs in the last 1/3 of ventricular diastole, atria contract to push the remain blood that didn’t passive drain into the ventricles into the ventricles
wave C: ventricles contract, but since they do it with such force, they push the closed AV valves up into that atria increasing the pressure
wave V: occurs towards the end of ventricular systole while the AV valves are still closed and the atria steadily fill with blood, increasing their pressure, at this point atria pressure is greater than ventrcular pressure (since they have pushed everything out)
explain the ventricular pressure curve as seen in the picture?
A, B, C, D
region A: diastole, passive ventricular filling
region B: systole, isovolumic contraction meaning the ventricles are contracting, but they haven’t gained enough pressure yet to open the pulmonary or aortic valves yet!
region C: blood ejection by ventricular contraction, pressure in the ventricles is greater the in the aorta or pulmonary arteries so it pushes the semilunar valves open
region D: diastole, isovolumetric relaxtion, when ventricular blood volume stays the same (residual), muscle starts to relax decreasing the pressure in the ventricle until it becomes less than the atria causing the AV valve to open
explain the aortic pressure curve?
what does the dicrotic notch represent?
systolic peak pressure (systolic BP)
diastolic pressure
diacrotic notch: when the aortic pressure is greater than the ventricular pressure this causes the blood to come back towards the heart and the aortic valve to close
what is end diastolic volume?
what is end systolic volume?
end diastolic volume: peak volume in the heart, occurs right after atrial contraction at end of diastole
end systolic volume: amount left in ventricle after contraction (residule) after systole
explain what happens to the ventricular volume during stages A, B, C, D in the picture?
what is it called when its the most? and what about when the volume is the least?
phase A: diastole peak end diastolic volume or when the ventricle has the most blood in it because the atria has just contracted and pushed all the blood in
phase B: systole, isometric contraction volume doesn’t change
phase C: stystole peak end systolic volume or the amount of blood that is left as residule or the smallest volume of blood in the ventricle
phase D: diastole isovolumetric relaxation where the volume of blood hasn’t change, because the AV valve hasn’t opened yet
what is the S1 heart sound from?
closure of the AV valves with the initiation of systole or ventricular contraction
what equation do you use to determine the stroke volume?
what does this tell you?
end diastolic volume (max volume in ventricle)-end systolic voume (minimum volume in venricle)
=stroke volume
this tells you the amount of blood that is pumped through in each stroke of the heart
what is the S2 heart sound?
closure of the semilunar valves at the end of systole and the begining of diastole
in relation to systole, where do you hear the S1 and S2 heart sounds?
s1=begining of systole when AV vavles close
S2=end of systole when semilunar valves close
when are s4 heart sounds heard?
atrial gallop, forceful contraction of atria against stiff or hypertrophic ventricle
occurs during the last 1/3 of atrial contraction in diastole
occurs just after atrial contraction and is caused by the atria contraction forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle
heard as “TEN-a-see” ten=s4 sound
explain what the S3 heart sound is?
ventricular gallop, can be associated with HF
heard immediately after the “lub dub”of a normal heart, occurs in the begining of diastole right after S2, lower in pitch and best heard with bell of stethoscope
“ken-tuck-KY” KY=s3
when is the heart tissue recieve blood during the cardiac cycle?
during diastole
the left ventricle pumps the blood up through the aorta, causing a decrease quickly in the pressure in the left ventricle and causes the blood to come back towards the heart.
simoutaneously, the aortic valve closes and stops the blood from flowing backwards. right above the valve is the enterance to the coronary arteries, so this blood flows down to feed the heart!!
how is coronary blood flow influcened in someone with aortic regurgitation?
in aortic regurgitation, the aortic vavle isn’t working right and so the blood flows back into the left ventricle, since it itsn’t being stopped by the aortic valve, the blood can’t enter the coronary arteries because the enterance to these are right about the aortic valve
they get LESS blood!!!
explain the difference between dyspnea and orthopnea?
dyspnea: shortness of breath
orthopnea: SOB while laying down
what are three ways you can increase venous return?
why is this important?
1. skeletal pump-jumping around
- respiratory and abdominal pump: breathing in and out espectially while lying down, decrease pressure in chest so blood comes back to chest rather than pooling in legs
3. venoconstriction sympathetic tone-constricts throughout the body and pushes blood back to the heart
**all of these allow you to increase your cardiac output!!**
varicose veins
what is this caused by? what does this look like? what makes this better, what makes this worse? what are 4 RF? what are the two main influencing factors for this? what is the two most common treatments for this? what about three surgical interventions?
superficial venous insufficiency and valvular incompetency
tortuous veins green blue “spider veins”, dilated in lower extermity
worsened with prolonged standing and relieved with elevation, can be related to valves or vein walls
RF: women who are pregnant, obescity, family, prolonged sitting or standing
- intrinsic weakness of vein wall and increase intraluminal pressure leads to reversal blood flow
- exposure to high pressures cause superficial veins to dilate bceause superficial veins lack support and thing walled compared to deep veins
tx: elastic stockings, leg elevation
can do laser ablation, sclerotherapy, surgical stripping
varicose veins
which vein is most common?
what are 5 things that can happen as result of having varicose veins? what test can you do?
most common is great saphenous vein
- chronic edema
- abnormal pigmentation
- fibrosis
- atrophy
- skin ulceration
brodie-tendelenburg tests: differentiates saphenofemoral valve incompetence from perforator vein incompetence (the ones that communicate between deep and superficial system)
thrombophlebitis
what is this? which vein is this most common in? what might you feel? what is the triad that puts you at higher risk for this? what is trousseaus sigh you nwa to be aware of? how do you dx? what is the TX?
partial or complete occlusion of vein and inflammatory changes“inflammatory reaction with thrombus of a being under the skin” in deep or superficial veins
most occur in saphenous vein, cord may be palpable following resolution of acute symptoms, dull pain, tenderness, asymptomatic
VIRCHOWS TRIAT (predisposes pt to this):
- stasis: >4 hrs immobolized
- vascular injury: trauma, infection, inflammation
- hypercoagubility: Factor V lieden, OCP, pregnancy
trousseau’s sign: migratory thrombophlebitis ususally associated with malignancy and vasculitis
DX: venous duplex ultrasonography (noncompressible vein with clot and vein wall thickening)
tx: supportive! elevation, rest, compression stockings, NSAIDS
where does thrombophlebitis commonly occur?
occurs frequently at the site of IV or periphreally inserted PICC lines
what is the superficial venous system?
greater/lesser saphenous veins
what is included in the deep venous system?
accompant major arteries and carry 90% of venous return, well supported
femoral, iliac, popliteal, posterior tibial, and superficial femoral
atherosclerosis
what size arteries does this involve? what forms and where? what does this make and what is it made up of? what does it lead to? what are three example conditions that are caused by atherosclerosis?
medium and large artery
gradual plaque formation on the intima of the medium/large vessels of ATERIES, material grows under the endothelia layer creating plaques: fat cholesterol and calcium
leads to:
gradual reduction in aterial lumen that prevents oxygen rish blood from geting to the tissues causing ischemia
the location of the arteries determines the name of the disease AKA
- coronary heart disease (coronary artery disease)
- cartotid artery disease
- periphreal vascular disease
periphreal vascular disease
what is this condition? what type of involvment, occuring where? what is it the leading cause of? what are the 3 MOST IMPORTANT RF? what are the four must important symptoms, which one is most important? when does this come on and when does it stop and where does it occur? in sever disease, what are four things that can happen?
atherosclerosis of the extremities, segmental involvement often at branching points!!!!
leading cause of occludive arterial disease in pts over 40
RF: DIABETES MELLITUS, SMOKING, >60YRS
claudication symptom most common (pain, aching, cramp, numbness or fatigue of muscle during exercise and relieved by rest!! claudication symptoms occur distal to stenosis), dimished distal pulses, hair loss with shiny skin appearance, with elevation of extremities get pallor of soles of feet and rubor (redness) in the leg, bruits in artery
in severe: pain at rest, ulceration, necrosis and gangrene from ischemia from lack of blood flow
acute aterial occlusion
what is this caused by and why is it acute? what are the 5 common causes of this? what are the four risk factors that you want to control? what are the 5 symptoms? what are the three things you use to diagnose it and which is the gold standard? what is the treatment option? and what are the 2 tx options if it is severe?
caused by embolism since happens quickly, something travels and blocks the artery , thrombus in situ
most common causes: afib, ventricular aneurysm, anterior MI, prostetic valve, thrombis at site of stenosis
RF: smoking, control of DM, HTN, hyperlipidemia so NEED TO CONTROL THESE!!!
rapid onset of pain, parenthesia, numbness, coldness in involed extremity, loss of distal pulses
DX: doppler US (DO FIRST), ABI, angiography gold standard
Tx:
1. anticoagulation with heparin to prevent propogation of the thrombus
2. if severe: reprofusion
- embolectomy
- streptokinase, urokinase, tPA
what are the symptoms that suggest an acute arterial occlusion is an emergency?
6 p’s
- pain
- pallor
- pulselessness
4. parenthesia
5. poikilothemia
6. paraylysis
these indicate tissue could die and threatens limb vitality so what to get vascular on board stat to hopefully prevent amputation
chronic venous insufficiency
what does this most commonly come from? what four other things can cause it? what are the 2 contributing factors to this? what are the 6 symptoms/exam findings you will see? when is it the worse? what can it lead to? what are the three tx options?
can result as consequence of both DVT (75% of the time) and superficial venous insufficiency
other causes: varicose veins, trauma, neoplastic venous obstruction
veins become functionally inadequate due to damage of the valves which results in bidirecitonal flow, and loss of venous wall tension that results in stasis
gradual progression of leg edema from ANKLE TO CALF!! OFTEN PAINFUL!!! NORMAL LIMB TEMP! pools at the bottom. shiny skin, skin ulcers, cyanotic aching when standing, edema worse at the end of the day, and best in the morning, secondary skin changes ulcers above the ankle on medial aspect leads to stasis dermatitis with brownish pigmentation and stippling
Tx: ruduce swelling and prevent breakdown
- intermittent leg elevation
- compression stockings
- calf exercise
explain the pathogenisis of atherosclerosis 6 steps
- endothelial dysfunction/injury that can be caused by smoking, high LDL, immune response, or mechanical stress
- macrophage infiltration to site of injury to try to clear it
- LDL oxidation (activation) by a oxidative byproduct of macrophage activation
- oxidized LDL is then aggreassively eaten by macrophages become activated to foam cells the main component of atherosclerotic lesions
- release of chemotaxins and growth factors from macrophages
- growth factors cause proliferation of smooth muscle cells and deposition of tissue, forms fibros cap, but if ruptured it can cause thrombis formation
explain the timeline of atherosclerosis in terms of a persons age?
up through most of our third decade: plaque growth mainly by lipid accumulation
end of third decade to early fourth decade: thrombosis and hematoma
mid fourth decade on: smooth muscle and collagen
explain the timeline of plaque formation from the prespective of the plaque formation.
- foam cells
- fatty streak
- intermediate lesion
- atheroma
- complicated lesion/rupture
- fibrous plaque
explain the pathway for some with a suspected MI?
frank starling mechanism
how does this work? what is it related to?
the mechanism that increases contraction when there is increased end diastolic volume, allows the heart to adjust how hard it contracts based on the amount of blood
actin and myosin filaments tension force (think of balloon blown up and wants to contract) is optimal when the distance between them is streched 2.5 times normal resting length
allows the heart to adjust pumping ability to accomodate varios levels of venous return, if not being filled enough or overstretched
as the myocardial fiber length increases in diastole, the force of contraction increases (untill stretched too far). related to preload. See pic
explain the intrinsic controls influencing stroke volume?
- increased venous return stimulates intrinsic bainbridge relex where the baroreceptors in atria sense increase pressure and increase the HR
- this increases the end diastolic volume, which stimulates the intrinsic control of frank starling mechanism and increases the strength contractility
these two together increase the stroke volume of the heart!!
explain the extrinsic controls of increase stroke volume?
the increase in venous return stimulates
sympathetic actvitiy and epinephrine, increasing the strength of the cardiac contraction
explain how the intrinsic and extrinsic factors work to increase cardiac output relative to HR and stroke volume?
how do you determine how extensive a persons MI was? what are the ranges for this?
calculate their ejection fraction, will tell you how much they are able to get out of their heart!
just a visual to think about the blood vessels
in a failing heart you get________
so the body tries to compensate by increasing ______
in a failing heart you get decreased stroke volume
so the body tries to compensate the decreased cardiac output by increasing sympathetic control to increase contractility, but the volume it is pumping out still isn’t as much as a normal heart
what drives blood towards arterioles during diastole? what is this measured by?
elastic recoil of arteries
the healthier they are the more they can push them forward
measured by the pulse pressure: Systolic BP-Diastolic BP
what is the mean arterial pressure? how do you calculate it?
diastolic pressure+ 1/3(pulse pressure=SBP-DBP)
MAP is the driving force of blood flow through the arterioles/caillaries
what is the artieral pulse pressure? what are three things it is influenced by?
systolic BP-diastolic BP
influenced by elasticity, regidity, and resistance
IF YOUR INCREASE RESISTANCE YOU DECREASE PULSE PRESSURE, or the pressure pushing the blood through the arteries to arterioles
pulse pressures also decrease as you move farther away from the heart
describe the difference between lamenallar and turbulent flow?
lamellar flow:
Laminar flow is parabolic, highest velocity in center (least resistance), lowest adjacent to vessel walls, most efficient
turbulent flow:
Turbulent flow is disoriented, no longer parabolic, energy wasted, thus more pressure required to drive blood flow. DETECHED WITH STETHOSCOPE, like bruits or valve dysfunction
explain how arterioles help to control BP? what are the 5 factors that contibute to arterial constriction and dilation?
this is where the majority of the smooth muscle is, so the dilation/contriction of these and letting blood into the capillaries help to determine the overal BP
vasoconstriction: lets less blood into the capillaries, increasing BP
caused by increase O2
increase myogenic activity
decreased CO2
sympathetic stimulation vasopressin and angtiotensin II
cold
angiotensin II
vasodilation: lets more blood into the capilarries decreasing bp
decrease myogenic activity
decreased O2
increase CO2
sympathetic release histamine
heat
explain what korotkoff sounds are and what the sounds are you hear when taking the BP
korotkoff sounds are the turbulent flow you hear through the stethoscope with each ventricular contraction, when it goes silent that is when the flow has become lamellar
the first sound: systolic BP, the amount of pressure needed to push the blood out of the ventricles
the last sound: diastolic BP, point at whic disastole occurs and the ventricles relax as blood is continuring through aorta and into periphrealy circulation
why is local control of the arterioles important to bp?
because if there is more resitance (vasconstriction) it increases BP so you get moderate flow into the capillaries
if there is less resistance (vasodilation) it decreases BP and you get large flow into the capillaries
what is a major venodilator naturally occurin in the body that is released by endothelia cells? what three things stimulate it? if you dont have this what do you have?
nitric oxide, potent smooth muscle vasodilator produced by endothelia cells and stimulated to relase by autonomic neurons, viagra, nitro
if this doesn’t work, then you get endothelia dysfunction
sympathetic stimulation causes the _____ of veins to increase so more blood can get back to the heart
sympathetic stimulation causes the decrease capitance of LARGE veins (volume of blood it contains) to increase venous return to heart
explain blood flow velocity across a capillary? explain how cross section influences velocity? what does this look like from flow of blood through vascular system?
velocity across capillary is slow to allow exchange…lake like cross section
TOTAL FLOW IS CONSTANT!!
velocity is dependent on cross sectional area if this is smaller it is like moving quickly down a river, if this is wide it is slower like moving down a lake
velocity decreases from aorta to capillaries and then increase from cappilaries back to heart!
what can increase the capillary blood flow? (3)
increase tissue metabolic activity
- decrease O2
- increase CO2
- other metabolites
these all cause increase capillary blood flow
oncotic or colloid osmotic pressure at capillaries
what does this favor? what is the most influential protein in the blood that causes this? what are the 2 mechniasm is this caused by?
“forces favoring reabsorption”…pulling fluid back into circulation
Most influential protein: ALBUMIN IN THE BLOOD
1. plasma oncotic pressure (water pulling)
2. interstital/tissue hydrostatic pressure (stagnant)
interstitial colloid osmotic pressure at capillaries
what is this? what are the two mechanisms by which this occurs?
forces favoring filtration, or fluid moving out of the capillary
- capillary hydrostatic pressure, pushing out or stagnant
- intersitial/tissue oncotic pressure (water pulling)
sinus rythmn
rate?
rythmn?
p waves?
QRS?
rate 60-100
rythmn regular
p waves yes and upright
QRS narrow
sinus tachycardia
rate?
rythmn?
p waves?
QRS?
causes?
rate >100 bpm
rythmn regular
p waves yes
QRS narrow
causes:
1. normal, seen with exercise
2. changes in SA node firing seen with CHF, lung disease, hyperthyroidism in eldery
sinus bradycardia
rate?
rythmn?
p waves?
QRS?
causes?
rate? <60
rythmn? regular
p waves? yes
QRS? narrow
causes? common rythmn seen in early stage of acute MI
sinus arrythmia
rate?
rythmn?
p waves?
QRS?
causes?
rate? slight irregularity of sinus rythmn
rythmn? slightly irregular
p waves? yes
QRS? narrow
1. phasic speeding up with inspiration and slowing down with expiration
2. variation in vagal tone as result of herring breuer reflex
what is this
junctional escape rythmn, no p waves
explain how reentry works works?
- impulse formation other than SA node, creating a new focus
- two adjacent pathways that are connected proximally and distally
- first step: get unilateral block from premature AP that causes prolonged refractory or prolonged repolarization, basically it can’t accept new stimuli
- if path B becomes slowed, currrent A can travel up it and make a reentry loop, can hapen at specific site like AV node or entire chamber
what are the three requirements for reentry loop? this accounts for what percent of arrythmias? where can this occur and what can this cause for arythmias?
requirements:
1. loop circuit
2. unidirectional block
3. zone of slowed conduction
accounts for 90% of arrythmias!!!
in atria causes: afib, aflutter, PACs
in AV nodal reentry causes: supraventricular tachycardia (polarizes from below) and vtach
explain what happens in AV nodal reentry and what can this cause for arrythmia?
- an atrial extrasytole blocks conduction in one limb of the AV node, blocking conduction in that pathway
- normal impulses travels retrograde up the blocked limb, if recoverd allows for transmision, purpetuating the arrythmia
- atria are polarized from below
ex arrythmias: supraventricular tachycardia, ventricular tachycardia
premature atrial contractions
rate?
rythmn?
p waves?
QRS?
other? 3
ATRIAL RE-ENTRY or increase AUTOMATICITY, premature atrial depolarization
rate? single beat
rythmn? premature complex
p waves? yes, but looks different than a regular p wave
QRS? narrow
other?
1. if early coduction can be blocked at AV node
2. if there is no preceeding p wave then it is called junctional premature beat (only difference)
3. can appear as bigeminy, trigeminy
atrial fib
rate?
rythmn?
p waves?
QRS?
other? 3
MULTIPLE REENTRANT CIRCUITS IN THE ATRIA
rate? 400-600 atrial contractions (blocked at AV by refractory period)
rythmn? irregullarly iregular supraventricular
p waves? NO!!! undulating baseline
QRS? narrow QRS
other:
- in new onset without med control: ventricular rate is very fast 120-180 bpm
- goal in ED: slow rate with meds
- Risk: BLOOD CLOT and stroke if they break off
atrial flutter
rate?
rythmn?
p waves?
QRS?
other? 4 things!
RENTRY CIRCUIT around annulus of tricuspid valve
250-350 flutter waves
regular
no p waves, flutter waves
QRS narrow
- most common presentation is 2:1 AV block with QRS ~150 bpm
- SAW TOOTH APPEARANCE in II, III, aVF
- after meds given to slow AV conduction given, most common form of block is 4:1 with ventricular rate ~75
- carotid masage can help slow VR down, allowing flutter waves to be seen
paroxysmal supraventricular tachycardia (PSVT)
rate?
rythmn?
p waves?
QRS?
who is it in? tx? 3 causes?
AV NODAL REENTRY!
abrupt onset and termination
carotid massage may help terminate
150-220
regular
not usually present
narrow QRS
- most in young healthy people without cardiac disease, can tell you the second it started and stopped. cardiovert with adenosine 90-95% of the time if carotid massage doesn’t work
- can be caused by coffee, alcohol, and excitement
just some svt for you
multifocal atrial tachycardia
what must be present?
rate?
rythmn?
cause?
what is it connected to?
enhanced automaticity
3 or more p wave morphologies present, irregullarly irregular, >100 bpm
usually underlying pulmonary pathology present
junctional escape rythmn
what is this caused by?
when can it happen?
rate?
QRS?
p waves?
what can happen if sinus rate and AV rate are similar?
caused by the sinus slowing or sinus arrest so that the AV node takes over
**can occur during sleep due to increased vagal tone, if sinus rate slows during sleep, this takes over**
40-60 bpm
narrow QRS
no p waves usually seen
ususally well tolerated
may compete with sinus rythmn if rates similar
premature ventricular contractions (PVCs)
what is this the most common of?
reentry or automaticity?
QRS? p waves? rythmn? after? shape? what type of hearts? pattern?
most common ventricular rythmn
reentry more than automaticity
premature QRS complex that is wide and biazarre
no p waves
WIDE QRS >.12
irregularlly iregular, or regularly irregular (trigeminiy)
often followed by a pause
uniform or multiform
healthy and diseased hearts
bigeminy and trigeminy
ventricular tachycardia
what is this defined as?
what is sustained mean?
is the heart diseased?
hemodynamicaly stable?
what does it deteriorate into?
3 or more consective PVCs at rate >100
sustained: >30 seconds
more often uniform and regular, but can be irregular like torsades
seen in presence of structual cardiac pathology
rarely hemodynamically stable
deteriorates into vfib
torsades de points
what type of vtach is this?
what is it associated with?
what does it turn into?
“twisting of the fingers”
polymorphic vtach, very fast, very dangerous, 200-300, pt unconcious
associated with prolonged QT interval
difficult to treat and turns into vfib
ventricular fibrillation
what is this? does it contain any waves?
terminal arrhythmia associated with death
DEFIB ASAP (if you are outside the hospital pt will likely die but if happens at the hospital, the pt will likely live depending on how long it takes you to defib them)
UNDILATIONS ONLY, choatic oftren preceeded with vtach
rarely seen in pts with structually normal hearts
SICK SINUS SYNDROME
WHat does it encompass?
who do we see it in? why?
what can cause it or it be a result from?
is it reversible?
what is it characterized by and what are the three types?
CLinical presentaiton?
DX
TX
- encompasses physiologically inappropriate sinus bradycardia, sinus pause, sinus, arrest, or episodes of alternating sinus tachy and brady.
most often in elderly: caused by scaring of the hearts conduction system
could occur in an infant who had heart surgery
- may be causes of exacerbated by digitalis, calcium channel blockers, beta blockers… so on and so on.
- also could result from underlying collagen vascular or metatastic disease or surgical injury
REVERSIBLE if caused by digitlalis, quinidine, beat blockers , or aerosol propellants
- AV block is characterized by refractory conduction of impulses from the atria to the ventricles through the AV node or bundle of HIS and divided into 1st degree, 2nd degree (Mobitz 1 or mobitz II) and complete 3rd block
- FIRST degree heart block: all atrial beats conducted to the ventricles, PR interval is greater than 0.21 seconds
- SECOND degree heart block: not all atrial beats are conducted to the ventricles
- Mobitz type 1 (wenckebach) is has lengthening of PR interval with shortening of RR interval. All atrial impulses will not be conducted to the ventricles. Typical pattern is repeated cycle of: normal PR interval, long PR, longer PR, even longer PR, and dropped beat. This is due to abnormal conduction in AV node
- Mobitz type II: non conducted atrial beats. block within HIS bundle system. secondary to organic disease involving infra nodal system. can progress to complete heart block
- THIRD degree heart block: (complete) complete dislocation between atria and ventricles. due to lesion distal to the HIS bundle
Clinical Prenenstation:
most asymptomatic, but may have syncope, dizziness, confusion, HF, palpitations, or decreased exercise tolerance
- 1st degree AV conduction block usually asymptomatic.
- higher grade blocks may have weakness, fatigue, light headedness, syncope
DX: ECG changes (SEE PICTURE)
TX:
permiinnant pacing
1st degree AV conduction block require no tx
- only effective long term tx for other AV conduction disorders is permanent cardiac pacing
- temporary transthoracic or transvenous pacing should be followed by permanent pacing when Mobitz type II or complete heart block dx.
