Final Flashcards
Whats the first part of the ventricular muscle mass to depolarize during contraction
Interventricular septum (left to right)
What is the first myocardial layer to receive depolarization signal in the ventricles
Subendocardial
What do we call the “flatline” when no electrical current is being detected by the ECG leads
Isoelectric line
What creates a positive deflection on the isoelectric line of an ECG
Depolarization occurring toward the lead
-OR-
Repolarizing current away from the lead
What produces a negative deflection from the ECG isoelectric line
Depolarization occurring away from the lead
-OR-
Repolarizing current toward the lead
How much electrical charge needs to be detected in the ECG leads to produce a deflection with magnitude 10 mm
1 mV
Where. Is lead 1 placed
4th intercostal space on the right (just lateral to sternum)
Where is lead 6 placed
5th intercostal space on the left midaxillary line
What happens during p wave
Atrial depolarization
When ventricular contraction begins we see positive deflection in the reading from lead __ and negative deflection from lead __
1, 6 (because its moving left to right)
Why is. Ventricular depolarization a negative deflection from the isoelectric line for lead. 1?
Because it occurs so strongly in the left ventricle, it overwhelms what happens in right ventricle (from subendocardium to epicardium occurs away from lead 1)
What type of deflection does ventricular contraction produce in v6 lead reading
Positive (subendocardium to epicardium is toward that lead)
What part of ECG measures ventricular depolarization
Qrs
In what. Direction does ventricular repolarization occur
From epicardium to subendocardium
How does ventricular repolarization appear in V1 reading? What about V6?
V1: neg
V6: pos
What is a t wave
Ventricular repolarization
Which part of the ECG is the broadest? (Aka which part of heart contraction occurs the slowest)
Ventricular repolarization (t wave)
Qrs and t waves tend to share what relationship
Concordant : they go in the same direction on ECG
Atrial repolarization occurs when
During qrs complex so we don’t see it on the ECG
Of the atria, AV node, His-Purkinje, and ventricle who has the fastest and slowest conduction velocity?
slowest- his-purkinje
ventricle and atria
fastest- AV node
Where do you find the Na (f) gates and what’s special about them?
SA and AV node where it causes SLOW depolarization during rest phase
Ventricles, atria, and purkinje system have ____ resting potentials, ____ upstroke, and ____ duration
stable
rapid
long
In APs of ventricles, atria, purkinje system What do you call the phase with resting potential and how is it sustained?
phase 4 high K (c) conductance
In APs of ventricles, atria, purkinje system What causes phase 0? What is phase 0?
rapid upstroke caused by opening of Na channels and crossing threshold
In APs of ventricles, atria, purkinje system What causes the small depolarization? What phase is that?
phase 1
Na (m) gates close
some K (a) open
In APs of ventricles, atria, purkinje system What sustains the plateau phase? What phase is that?
2
slow Ca opens and close special, voltage gated K (b) channels
In APs of ventricles, atria, purkinje system What phase is complete depolarization? What causes it?
phase 3
slow Ca channels close
special K channels open
Why is the SA node said to exhibit automaticity/
RMP gradually depolarizes until it reaches threshold and fires
Why doesn’t AV node dominate the pacemaking activity?
it gradually depolarizes too but it get stimulated by SA node’s AP before it can reach threshold on its own
What causes phase 0 in AV and SA nodes?
opening of slow Ca gates
closing of K (b) gates
What phases are you missing in SA and Av nodes? Why?
1 and 2
due to scarcity of traditional, voltage gated Na (m) channels)
What causes phase 3 in sa and AV nodes?
closing of CA gates and opening of special K (b) gates
What causes phase 4 in sa and AV nodes?
opening of special voltage na (f) gates
When do Na (f) gates open?
when membrane is repolarized
If both the SA and AV nodes fail who takes over pacemaking?
bundle of His/purkinje fibers
Why is there a pause before purkinje fibers take over?
stay polarized for a while but if not stimulated they’ll begin to spontaneously depolarize during phase 4
How can we make the conduction velocity faster?
higher inward current (Na(m)) or slow Ca
how will phase 0 look if we have a faster velocity?
steeper
What type of fiber allows for the faster transmission of ap and therefore velocity?
BIG fiber
Why is it beneficial for there to be a delay in the AV?
allows atria to empty into ventricles before ventricles contract
what is important to help prevent arrhythmias?
refractory period
What do we call effects that change rate of depolarization of SA node and therefore heart rate?
chronotropic
A positive chronoctropic makes the SA node depolarize…
faster!
What do we call effects that effect the speed of conduction?
dromotropic
How does the parasympathetic system slow down the heart rate? What do we call this effect
decreases opening of Na (f) gates during phase 4 in sa and av nodes
negative chronotropic
What is the neurotransmitter and receptor used by parasympathetic?
acetylcholine
muscarinic in heart
What is the receptor and neurotransmitter used by the sympathetic system to affect the heart?
norepinephrine
beta-1
How does the sympathetic system increase the heart rate? What do we call this effect?
increases opening of special Na (f)gates increases depolarization
positive chronotropy
What acts as a voltage gated Ca channel in cardiac tissue?
dihydropyridine (DHPR)
Calcium acts as a ligand for what ligand gated channel for muscle contraction?
ryanodine receptors (RyRs)
What is increased force of contraction?
positive inotropy
What is contractility of cardiac tissue proportional to?
amount of Ca available to troponin on the actin filaments
What type of an effect does sympathetic system have on heart?
positive inotropic
What does norepinephrine on beta-1 receptors cause?
more ca to enter interstitial spacedzring AP and also causes more CA to be sequestered in Sr
What does the parasympathetic innervate in the heart? What kind of an effect does it have?
atria and sparsely ventricles
negative inotropic effect
What happens with calcium when we have increased HR?
more Ca to accumulate and remain intracellularly (sequestered in SR) therefore more Ca released per AP so stronger contraction
What effect does digoxin (cardiac glycoside) have? How?
positive inotropic
blocks Na/K pump
intra Na increases decreasing gradient
Na/C exchanger less effective so intra Ca increases
What do we call the amount of wall tension in the right or left ventricle just before contraction is initiated?
preload
How does the wall tension compare between two chambers with the same chamber pressure : one is dilated and one isnt
dilated one has greater wall tension
What is the amount of chamber pressure that must be delivered to cause ejection of blood?
afterload
What is the after load a little greater than but essentially equal to?
pressure in aorta or pulmonary artery
What determines the amount of actin/myosin overlap? If this overlap is very efficient what can develop?
sarcomere length
greater tension when contraction is initiated
What is velocity of contraction inversely proportional to?
afterload
When is the velocity of contraction greatest in relation to after load?
when after load is 0
The greater the preload the more efficient the initial overlap of action and myosin causing what?
more forceful contraction
What causes greater contraction force, stroke volume, ejection fraction and cardiac output?
greater preload
Stroke volume =
EDV- ESV
Ejection fraction =
SV/EDV
Positive or negative inotropes will increase stroke volume, ejection fraction, and cardiac output?
positive
Cardiac work = work per heart beat =
stroke volume x aortic pressure
What is stroke work dependent on?
after load
diameter of chamber (greater = less efficient)
inotropic state
Minute work =
stroke work x heart rate
What are three ways to measure cardiac output? What will these show for greater cardiac output?
fick, thermodilution, dye
more diluted in blood
What do we call the technique used to measure CO by adding oxygen via lungs and measure oxygen difference before and after lungs?
fick
What do we call the way of measuring CO by adding cold fluid in pulmonary artery and measuring downstream how much it cools the blood?
dthemordilution
What do we call the way of measuring CO by adding a quantity of dye and measure how much the color change is downstream?
dye
Mean systemic is proportional to what two things?
blood volume
preload
At equilibrium cardiac output = ___?
venous return
How does increasing blood volume increase cardiac output?
increases preload increases cardiac output
Increasing total peripheral resistance does what to cardiac output
decreases
inorder for shortening to occur in muscle contraction, ca++ must bind which of the following
troponin
what attaches to the z line
actin
the A band is comprised of what
myosin
whats the major cause of phase 0 of neural action potential (depolarization)
increased Na+ conductance
what ion maintains neural resting potential
K+ conductance
whats the major cause of pass 1 (depolarization) in neural action potential
K+ gates open
4 steps of hemostasis
vascular spasm
form platelet plug
form blood clot
repair damage
what are platelets
cell fragments of megakaryocytes
we make platelets in response to what hormonal signal
thrombopoietin (TPO)
where do we make thrombopoietin?
liver
platelets, megakaryocytic, and some other hematopoietic cells contain a JAKSTAT Thrombopoeitin receptor called what
mpl (CD-110)
if thrombopoeitin binds to its receptor on a platelet what happens?
the platelet internalizes it and destroys it so it can’t tell megakaryocytes to make more platelet
mutation in TPO receptor can lead to what condition
polycythemia vera
platelets have actin and myosin which allow them to contract to perform what function
empty vesicles
what organelles remain in platelets
mitochondria, ER remnants to store Ca++
how do platelets help determine the amount of vasoconstriction/ vasodilation that occurs in vessels
COX1 (TxA2 leads to constriction and platelet aggregation), serotonin (vasoconstrictor)
what do platelets have that help them maintain stability during clot formation
fibrin stabilizing factor
how do platelets repair themselves
platelet derived growth factor
platelets have what on their membrane
glycoproteins (get sticky when activated), phospholipids, collagen receptors
what triggers EPO release? TPO release?
EPO- low O2 in kidney
TPO- constant release
how do we control EPO levels? TPO?
EPO- renal cells continually measure HIF accumulation
TPO- its internalized and destroyed by circulating platelets
what is the first thing that happens after a blood vessel is damaged
the smooth muscle spasms (mechanism is more effective in bigger vessels with more SM)
vascular spasm can occur by myogenic (injury to SM) or what other mechanism
platelet factor activation (serotonin and thromboxane A2)
what initiates formation of a platelet plug
break in vascular wall exposes collagen- platelets bind here
this guy is a plasma protein who binds between collagen and platelet receptor: part one of platelet plug formation
von willebrand factor
once the platelet is bound to the collagen exposed in a damaged vessel, the platelet “activates” what does this mean?
platelet swells and extends podocytes
after platelet activation, what occurs
swelling, contraction, granules leave platelet, STICKY platelets are attracted and gather at the injured area
platelets and fibrin that make up a clot interact to squeeze out plasma and then solidify the clot (thus closing wound) during what phase
clot retraction
what makes up the meshwork found in blood coagulation
fibrin and the platelets which bind it together (and RBCs)
how do the platelets go about forming a network with fibrin
they have fibrin receptors and they contract (REQUIRES CA++) to bring everything togehter
what do platelets release to being the repair of damage
platelet derived growth factor
what does platelet derived growth factor do
tells fibroblasts to differentiate into SM or whatever else is needed to close the hole
plasminogen is made in the liver, floats in plasma, is activated in the damaged tissue, and is inhibited by what?
tPA inhibitor (blood)
what does plasmin do when activated by TPA
fibrin lysis (breaks up the clot)
thrombin is floating around when we have tissue damage what is its purpose
activates protein C which activates TPA inhibitor so we can break up the clot
its important that we always try to limit clotting because the clotting factors are always present in the blood. what factors limit clotting?
- smooth endothelial vessel lining
- continuous blood flow
- glycocalyx repels platelets
- fibrin, heparin, prostacyclin, anti thrombin (anticoagulants)
- protein c (inhibits Va and VIIIa so no more fibrin is created)
whats hemostasis
maintaining intact vessel surface and blood in a fluid, clot free condition to ensure tissue perfusion
in primary hemostasis we form the platelet plug by clumping and vasoconstriction, but in secondary hemostasis what happens?
platelets are activated, undergo conformational change, expose phospholipid rich portion of membrane (phospholipid platform)
whats the purpose of the phospholipid platform
accelerate fibrin production 1000 fold
the coagulation cascade (extrinsic) can be activated by binding of factor __ to tissue factor on damaged endothelial cells
VII
what are the vitamin K dependent factors of clotting cascade
II, VII, IX, X
vitamin k dependent factors can fully function after __ binds to a glutamic acid in their active sites (this curs in liver)
ca++
vitamin k deficiency can lead to what blood condition
decreased clotting
vitamin k deficiency is common in what conditions
liver disease, malabsorption, antibiotic therapy, breast fed newborns, infants whose mother is on anticonvulsant therapy
why is thrombin (factor IIa) such a key player
activates fibrin formation,
positive feedback to upstream clotting components,
paracrine activity causes NO, tPA, ADP, vWF, and PGI2 release
which factor attaches strands of fibrin together to make a 3D mesh
XIIIa
which factor of the extrinsic pathway can be activated by intrinsic pathway components IXa and Xa
VII
what does secondary hemostasis involve
formation fo fibrin which makes the clot stick together
what are the two tests used to measure coagulation
PT (prothrombin time)
aPTT (activated partial thromboplastin time)
which coagulation test can be used to discover a problem with the intrinsic or common pathway
aPTT
which coagulation test can be used to discover a problem with the extrinsic or common pathway
PT
if a patient has a normal PT and an abnormal aPTT what does this indicate about the function of their coagulation system?
issue is with intrinsic pathway
what do we use in the lab to anti coagulate a blood sample so that we can loo at plasma only
agent that chelates Ca++ (such as sodium citrate)
which factors need to be individually analyzed for an abnormal aPTT test
(intrinsic&common) 8, 9, 11, 12, 10, 5, 2, 1
what is an anticoagulant therapy that inhibits factors IIa, IX, and Xa
heparin
what condition has been discovered to include a deficiency of factor VIII
hemophilia A
what condition has been discovered to include a deficiency of factor IX
hemophilia B
what lab test would we use to test coagulation in heparin therapy patients
aPTT
which factors need to be individually analyzed for an abnormal PT test (abnormal if clot time >13 seconds)
VII, X, V, II, I
what type of anticoagulant therapy inhibits vitamin k thus inhibiting II, VII, IX, and X
coumadin (warfarin)
what can cause coagulation factor deficiency
liver disease, wash out (after hemorrhage), disseminated intravascular coagulation, inherited deficiency
What is the first to depolarize and thus considered the pacemaker of the heart
SA node
depolarization of the SA node causes what two results to simultaneously happen
atrial depolarization, AP travels in intermodal pathway to AV node
What ECG wave occurs when Na+ influx occurs in atrial myocytes
P
AV conduction is slow causing a pause between atria and ventricle depolarization: how do we measure this on ECG
PR interval
Describe. The path of depolarization in the ventricles
Septum first then free walls of ventricles from apex up
Contraction of heart
Systole
Relaxation of heart
Diastole
Why does atrial pressure increase during ventricular systole
Blood continues to flow into atria via veins even though AV valves are closed
What is. Occurring anatomically when the pressure curves of atrium and ventricle cross
AV valve opens or closes
The first heart sound (luv) is. Associated with what anatomic change in heart
AV valve closure (when Ventricle pressure Exceeds atrial)
What is occurring during the QRS. Wave of an ECG
Isovolumetric contraction of ventricle
What pressure does L ventricle need to reach before valves open? R ventricle?
Diastolic pressure must be reached
L- 70
R- 15
What do we call the point on the aortic pressure wave (mirrored also in atrial pressure curve) when the aortic valve closes
Dicrotic notch
What creates the second heart sound (dub)
Closing aortic and pulmonary valves
After closure of aortic and pulmonary valves, we see a major decrease in ventricular pressure that is associated with what action
Isovolumetric relaxation of ventricle
What creates the third heart. Sound (normal in children, may be heard in adults)
Blood rushing into ventricle after opening of AV valve
Why does aortic pressure slowly drop after ventricular contraction?
Blood flows into small peripheral vessels (rate is determined by resistance)
In congenital heart failure patients, it is important to check for what peripheral blood vessel abnormality
Jugular venous distension
When/ why does jugular pressure increase during atrial contraction (called the “a wave” on jugular pressure curve)
No valve between atria and superior vena cava means pressure is reflected into jugular during atrial contraction
What is the “c wave” of jugular pressure (occurring after the “a wave” indicating?
Isovolumetric contraction of ventricles (increases pressure in atria and thus jugular vein as well)
The final notable feature of jugular pressure graph is a slow increase in pressure called the “v wave” what is happening in the heart at this time?
Blood returns to atrium at this time but cannot yet enter ventricle (AV valve still closed)
What is the fourth heart sound (normal in children but not adults)
Atrial contraction (last bit of blood is being squeezed into ventricle)
If blood is moving in a direction where it shouldn’t or having a hard time moving in the correct direction: what do we hear
Murmur
A murmur heard after S2 indicates backflow of blood in what area
Aortic or pulmonary valve backflow
A murmur heard after S1 (diastole murmur) indicates backflow of blood in what area
AV valve (likely mitral valve stenosis)
term: formation of new vascular channels by assembly of individual cell precursors called angioblasts which are derived from mesoderm (week 3)
vasculogenesis
term: development of blood vessels from pre-existing vessels
angiogenesis
which vessels in our body are created by vasculogenesis
dorsal aorta, cardinal veins
what happens to the paired dorsal aortae in week 4
fuse to become abdominal aorta
these primitive arteries are derived from splanchnic layer of lateral plate mesoderm and endoderm and eventually become celiac a, superior mesenteric a, and inferior mesenteric a
ventral segmental aa
these primitive arteries are derived from intermediate mesoderm and eventually become renal and gonadal arteries
lateral segmental aa
these primitive arteries supply derivatives of the somites and eventually become posterior intercostal, lumbar, and vertebral arteries
dorsal segmental arteries
when do we complete the aortic arches to give off branches that enter developing head
end of wk 5 into 6 (day 32-37)
artery derivatives of 1st aortic arch
external carotid and maxillary a
artery derivatives of 2nd aortic arch
stapedial artery
artery derivatives of 3rd aortic arch
common carotid and internal carotid aa
artery derivatives of 4th aortic arch
left: medial aortic arch
right: proximal R subclavian a
artery derivatives of aortic sac
brachiocephalic a, base of arch of aorta
artery derivatives of 6th aortic arch
pulmonary arteries (Left: ductus arteriosus)
what eventually becomes the distal part of R subclavian a and the entire L subclavian a
7th intersegmental a
the ductus arterioles in a developing fetus allows baby’s circulation to skip over what part of adult circulation
bypass R atrium (and thus lungs)
aeration of the lungs at birth decreases pulmonary vascular resistance and encourages blood flow to lungs and thinning of walls of pulmonary arteries. at this time what happens in the heart?
closure of foramen oval
aeration of the lungs at birth decreases pulmonary vascular resistance and encourages blood flow to lungs and thinning of walls of pulmonary arteries. at this time what happens in the liver?
sphincter of ductus venous constricts until occluding it (this used to bring in mom’s blood from umbilicus)
when and why does ductus arteriosus close ? (to become ligamentum arteriosum)
after the first breath, O2 levels increase and cause bradykinin release in lungs. smooth muscle in ductus arterioles constricts until it closes.
a persistent ductus arteriosus causes what in newborn babies
left to right shunt (acyanotic)
abnormal narrowing of the aorta is called ___ and can happen in what two places?
coarctation
can be pre ductal or post ductal
what is the clinical presentation of coarctation of the aorta
hypertension in upper extremities, hypotension in lower extremities
why can it be problematic to have a persistent right dorsal aorta
forms ring around trachea and esophagus
what symptoms present for someone with a double aortic arch
stridor, respiratory infections or distress, wheezing, cough, dysphagia, vomitting
sometimes the right subclavian artery arises from distal part of 7th intersegmental artery and this is a problem because
it passes behind esophagus and trachea (could be occluded)
if you develop a right aortic arch, your trachea and esophagus may be occluded in a small space between aortic arch, pulmonary trunk, and what other structure
ligamentum arteriosum
when does remodeling of inflow to the heart occur
wk 4-8
whats the name of the vein that carries blood from yolk sac to the liver of the developing fetus
vitelline duct
how does a developing fetus get oxygenated blood
from mom via umbilical vein
what are the 3 most primitive veins in the developing fetus
cardinal veins (anterior, posterior, common)
what do vitelline veins become
right hepatic vein, portal vein (gut to liver)
what do umbilical veins become
right- degenerates
left- ductus venous within liver
what do cardinal veins become
anterior- internal jugular, SVC, L brachiocephalic
posterior- root of azygos and common iliac
common- coronary sinus, contributes to SVC
persistence of left anterior cardinal vein and failure of left brachiocephalic vein to form results in what venous system defect
double superior vena cava
what embryonic vein contributes to the hepatic segment of the IVC
R vitelline and hepatic veins
what embryonic vein contributes to the prerenal segment of the IVC
R subcardinal
what embryonic vein contributes to the renal segment of the IVC
subcardinal - supracardinal anastemosis
what embryonic vein contributes to the postrenal segment of the IVC
R supracardinal v
Sinus bradycardia corresponds to. What HR
Less than 60 beats/// minute
Sinus bradycardia most often results from excess ___ stimulation
Parasympathetic
Who often has sinus bradycardia
Conditioned athletes at rest
Extreme bradycardia may reduce blood flow to the brain causing loss of consciousness. What s the term for this
Syncope
Excersize produces sympathetic stimulation to the SA node which commonly causes
Sinus tachycardia (greater than 100 beats/ min)
What do you call areas in the heart that are capable of pacing in emergent situations
Automaticity foci
What are the automaticity foci in the heart (they function if the SA node gives up)
Atrial conduction system, distal portion of AV node, purkinje fibers, bundle of his, bundle branches
Automaticity centers express. This characteristic. Which. Means that the rapid activity suppresses slower activity
Overdrive suppression
What do we call it when sympathetics slightly increase HR based on phases of respiration
Sinus arrhythmia (not a true arrhythmia)
Whats the name of the part of the atrial conduction system that supplies the left atrium
Bachmann’s bundle
normal pace of the ventricular automaticity foci
20-40 beats per minute
when would a ventricular automaticity foci control heart rate
only if all pacemaking centers above failed OR complete conduction block below AV node (prevents pacing stimulus from reaching ventricles)
if the SA node fails to pace the heart rate, what is the order in which automaticity centers take over pacemaking and what are their inherent rates
atrial 60-80
AV junctional 40-60
ventricular 20-40
the P wave is upright in the readings from which ECG leads
1, 2, V4-V6, AVF
the P wave is inverted in the readings from which ECG leads
AVR
the P wave is variable (sometimes absent) in the readings from which ECG leads
3, AVL
PR interval is time between SA node to ventricular muscle fiber firing : normal PR interval time
0.12 to 0.2 seconds (3-5 tiny boxes)
short PR interval indicates what kind of arrhythmia
pre-excitation syndrome or nodal rhythms
prolonged PR interval indicates what kind of arrhythmia
AV conduction disease
a prolonged QRS complex indicates what kind of abnormality
bundle branch block, hypertrophy
if there are no Q waves in leads V5 or V6 then we have what abnormality
left bundle branch block
whats normal duration for QRS complex
0.05 to 0.1 seconds (1-3 tiny boxes)
the ST segment should be found where in relation to baseline of ECG
isoelectric or a little elevated is normal
it should NEVER normally be depressed
if the patients ST segment is elevated above baseline and/ or they are experiencing chest pain what do we call it
subepicardial injury / ischemia / infarction until proven otherwise (can be normal)
if the patients ST segment is depressed below baseline what do we call it
subendocardial injury
the T wave (ventricular repolarization) is upright in the readings from which leads
1, 2, V3-V6
the T wave (ventricular repolarization) is inverted in the readings from which leads
AVR
what is a normal amplitude for the T wave on an ECG reading
5 mm maximum- standard leads
10 mm max- precordial leads
QT duration is the length of what action of the heart
ventricular systole
the T wave is not normally depressed or inverted but if it is what should we expect
ischemic injury
we can expect tall pointy T waves in what patients
athletes, hyperkalemia
whats the ECG indicator for necrosis or infarction
Q wave or QS complex elongation
normally the QT interval is how long?
less than 50% R-R segment
how does hypokalemia show up on ECG
low T wave and U wave is present
how do we know patient has left atrial enlargement? (in the condition p mitrale)
notched p wave (looks like an m) - leads 1-2
how do we know a patient has p pulmonale? (right atrial enlargement)
tall pointy p waves in leads 2, 3, and AVF
how can we identify AV junctional rhythm aside from counting the rate of ECG
inverted P waves in leads 2 and 3 (and short PR interval)
prolonged PR interval means what
AV block
shortened PR interval means what
AV junctional rhythm, wolff-Parkinson-White syndrome, Lown-ganong-levine syndrome
whats treatment for sinus tachycardia (HR >100)
TREAT THE CAUSE- labor, anxiety, pneumonia, whatever
if we see rhythms in addition to waves PQRST then what should be included in the differential
ectopic atrial rhythm, multifocal atrial tachycardia, wandering atrial pacemaker
if we see no P waves then what should be included in the differential
A fib, A flutter, junctional or ventricular escape rhythms, junctional tachycardia, VT
if we see inverted P waves after the QRS complex then what should be included in the differential
SVT (AV nodal re-entry tachycardia)
junctional rhythm
How easy it is to cause a vessel to expand in response to change in lumen hydrostatic pressure
Compliance
Equation for compliance
Change in vol/ change in pressure
What type of vessel has the most compliance
Veins
Smooth muscle contraction in veins decreases compliance making it harder to expand. Where does the blood go in this case?
To arteries (increasing pressure)
The largest pressure drop in the circulatory system occurs where?
Arterioles
Largest pressure reached in a large artery is reported as
Systolic pressure (120)
Lowest pressure reached in large arteries is reported as
Diastolic pressure (80)
How do you calculate pulse pressure
Systolic - diastolic pressure (120-80=40)
How do you calculate mean pressure
Diastolic + 1/3 pulse pressure = 80 + (40/3) = 93.3
What. Happens to pulse pressure when compliance decreases
Increase in pulse pressure
What would increase in stroke volume do to pulse pressure
Increase
What would increase in resistance do to pulse pressure
No change (compliance stays the same with increased resistance)
What exactly is an ECG measuring?
extracellular potential
when is the only time an ECG will cause a deflection?
there is a different membrane potential at part of the heart compared to the rest
current is flowing
The ECG will not cause a deflection if there is a difference in potentials where? Why?
just between atria and ventricles
no current flowing between them
At rest the extracellular potential in the heart is?
+90mv
During phase 2 the extracellular potential is?
-15mv
The delay in signal due to the AV node is what on the ECG?
PR interval
Phase 2 causes a delay in the action potential on the ECG which we call?
ST segment
The right ventricle depolarizes before the left ventricle. Which repolarizes first and why?
left ventricle
shorter AP
Which phase of the action potential in the atrial muscle is represented by the P wave?
phase 0
Which phase of the AP in the ventricular muscle is represented by QRS complex?
phase 0
What phase of the AP in the ventricular muscle is represented by the T wave?
phase 3
repolarization
Where are the K+ goes closed in the atria on the ECG?
p wave
When is the Na+ most permeable in atrium on the ECG?
initial depolarization so p wave
When is Na+ most permeable in the ventricles on the ECG?
QRS
Segments represent what? Intervals represent what?
segment- single event
interval- several events
What is the end of atrial depolarization until beginning of ventricular depolarization on ECG?
PR segment
What is the end of the ventricular depolarization until beginning for ventricular repolarization on the ECG?
ST segment
What is the beginning of the atrial depolarization until the beginning of the ventricular depolarization?
PR interval
What is the beginning of the ventricular depolarization until the end of ventricular repolarization?
QT interval
Time between dark lines on ECG is? Light lines?
.2 sec
.04 sec
What is the grounding electrode? it is NOT recording!
RL
What are the three standard limb leads used?
1: RA to LA
2: RA to LL
3: LA to LL
What are the three augmented limb leads?
aVF: RA+LA to LL
aVR: LL+LA to RA
aVL: LL+RA to LA
What leads do we look at to evaluate the inferior region of the heart?
II, III, aVF
What leads do we look at to evaluate the septal region of the heart?
V1, V2
What leads do we look at to evaluate the anterior region of the heart?
V2, V3, V4
What leads do we look at to evaluate the lateral region of the heart?
I, aVL, V4-6
What does the mean electrical axis represent? What leads do we look at to evaluate it?
mean electrical axis
I and aVF
If both I and aVF are positive what do we say about the mean electrical axis?
normal
If I is negative what do we say about mean electrical axis? What causes this?
right axis deviation
right ventricular hypertrophy
If I is positive and aVF is negative what do we say about the mean electrical axis? What causes this?
left axis deviation
left ventricular hypertrophy
What is the relationship of electrical event to mechanical event?
electrical event before mechanical
so ECG is ahead of mechanical events
If the AP is extra slow getting through the AV node what will the ECG show?
prolonged PR interval
If there is an ectopic pacemaker in the atrium what will the QRS and QT interval look like?
NORMAL
What gates are open for the QRS segment?
sodium gates
What gates are open for the ST segment?
calcium
Sympathetic nervous system innervates what part of the heart?
BOTH atrium and ventricles
which vessels contain the highest volume
veins (lowest pressure)
which vessels contain the most area
capillaries
how can we calculate velocity of blood flow
V=Q/A
perfusion/area
at rest, which body systems receive the largest percentage of blood flow? (25% each)
renal
GI
skeletal muscle
how do we calculate flow through a vessel
Q= change in pressure / resistance
how do we calculate cardiac output
CO = BP / TPR(total peripheral resistance)
how do we calculate resistance
R= (8viscositylength of vessel) / (pi*radius^4)
whats the easiest way to change vascular resistance
change radius of the vessel
how does resistance change if we add vasculature in series
add resistances for a total (increases total R when you add in series)
how does resistance change if we add vasculature in parallel
decreases total resistance (like with pregnancy)
flow becomes ___ with high velocity, large area, low viscosity
turbulent
whats the equation used to predict when turbulence will occur (reynolds number)
[density * diameter * velocity / viscosity] = turbulent if over 2000
what do we hear upon auscultation when turbulent flow is present
bruits
what occurs in the vasculature when turbulent flow is present
arteriosclerosis
what angle is lead II at?
60
what angle is lead III at?
120
what angle is lead I at?
0
what angle is lead avF at?
90
What are two ways that an antagonist works?
- binds receptor but doesn’t activate it so agonist can’t
- suppress basal signaling of receptors that are constitutively active
What do we call drugs that mimic ACh? What affect do they have on AChR?
cholinomimemtic agents
agonists
What do affect do cholinoceptor-blocking drugs have on AChR?
antagonists
What do we call drugs that mimic or enhance a and B receptor stimulation? Are they antagonists or agonists?
sympathomimetic agents
agonists
What effects does the sympathetic system have on the SA node and atria? on what receptors does it act?
SA node: increase heart rate, B1>B2
atria: increase contractility and conduction velocity, B1>B2
What effects does the parasympathetic system have on the SA node and atria? What receptors does it work on?
atria: decrease in contractility, M2»M3
SA node: decrease in heart rate M2»M3
What nervous system uses dopamine?
sympathetic
What nervous system controls sweat glands with what neurotransmitter and receptors?
sympathetic
ach
muscarinic
What is the MAJOR neurotransmitter of the sympathetic nervous system?
norepinephrine
Where does synthesis of epinephrine occur?
adrenal medulla
few neuronal pathways in brainstem
What is dopamine the precursor of? Where does it act?
NE and epic
acts on CNS and renal vascular smooth muscle
What are the functions of the nAChR and mAChR?
n- excitatory, release of catecholamines (in adrenal medulla)
m- excitatory and inhibitory
The cholinergic receptors M1, M3, M5 are associated with what G protein? What do they result in?
Gq-> activation of PLC: IP3 and DAG cascade
smooth muscle contraction
Cholinergic receptors M2 and M4 are associated with what G protein? What do they result in?
Gi/o inhibition of AC: decreased cAMP production so decrease in contractility
Where do we find M2?
heart, nerves, smooth muscle
Where does the synthesis of dopamine from tyrosine occur?
nerve cytoplasm
Where does the conversion of dopamine to nor then epic occur?
vesicle
Where does the conversion of norepi to epic mainly occur?
in vesicles in adrenal medulla
The tyrosine transporter transports tyrosine into the cell. What ion is it dependent on?
Na
What is the function of the vesicular monoamine transporter (VMAT-2)?
transports NE, epic, DA, and serotonin into vesicles
What is the function of NE transporter (NET)?
imports NE into nerve terminal
What is the effect of cocaine one neurons?
increases concentration of catecholamines in the synapse by blocking NET
What is the major way of termination of catecholamine signaling?
reuptake via NET or DAT
then storage in VMAT-2
What are the two main enzymes that metabolize catecholamines?
monoamine oxidase (MAO) catechol-O-methyltransferase (COMT)
Where doe we find a1 receptors? what does activation of them cause?
smooth muscle (around vasculature) constriction
Where do we find B2 receptors? What do they cause?
smooth muscle
relaxation
Where do we find B1 receptors? What do they cause?
heart
increase HR and contractility
What effect do muscarinic receptors have when activated on smooth muscle?
contract
don’t always cause vasoconstriction like a1
Ach and muscarinic agonists given IV will cause vasodilation. Why?
release of NO
What nervous systems does not innervate smooth muscles on blood vessels? What receptors will you not find there?
parasympathetic
mAChRs nor nAChRs
Blood vessels relax in response to parasympathetic releasing ACh as long as the endothelium is intact. Why?
mAChRs on endothelial cells cause production and release of NO
The release of what NT causes adrenal medulla to release epi and norepi?
ACh from preganglionic fibers
What kind of receptor is found on adrenal medulla?
nAChR
how do we know when we have a left axis deviation (0 to -90)
+ read in lead I
- read in lead AVF
how do we know when we have right axis deviation (90 to 180)
- read in lead I
+ read in lead AVF
how do we treat sinus tachycardia
treat the CAUSE
which automaticity foci in the heart serves as an O2 sensor: meaning it will fire spontaneously under hypoxic conditions
ventricular foci
consuming what can lead to premature atrial contraction
alcohol, tobacco, COPD, and CAD in people without heart disease
what stimulus can lead to premature ventricular contraction
hypoxia, nicotine, thyroid, aminophylline, digitalis, intoxication, electrolyte disorder
at what point do premature ventricular contractions become ventricular tachycardia
lasts more than 30 seconds
jugular vein distension indicates problems with which side of the heart
right side
if there is an absence of p waves, we assume what condition unless proven otherwise
atrial fibrillation (can appear as undulating baseline up to 600 per minute)
why do we have to worry about embolism in patients with atrial fibrillation
blood remains in atrium and can clot: pieces break off and emboli occur
what causes ventricular tachycardia
irritable ventricular foci that decides to pace quickly
what condition is occurring in the heart when both PAT (premature atrial tachycardia) and PJT (premature junctional tachycardia) are taking place
paroxysmal supraventricular tachycardia
