Exam 4 Flashcards
What connects the left Atrium to the SA node & its function?
The Interatrial pathway (Bachman’s Bundle) & to facilitate coordinated electrical action potentials.
What sends the signal from the SA node to AV node?
The 3 internodal pathways (anterior, middle & posterior).
What does Isotonic contraction refer to?
Looking at contractions using the same weight but with different stimuli intensity or rate.
What is basal tension?
A muscle at rest without contraction.
What is an isometric contraction?
A contraction, in which the overall muscle length does not change.
What are iK+ ATP channels & where are they found?
Channels that open in response to low ATP or ischemia to reduce metabolic rate. They are found in nodal and ventricular tissue.
What effect do beta adrenergists have on HCN channels?
They facilitate wider opening of the channels, which results in a faster signal propagation from rest to threshold= faster HR.
How long does it take the signal to travel to the Bundle branches once the AV node receives the signal?
0.13seconds. (AV node receives the signal at 0.03 seconds and the L & R Bundle branches receive the signal at 0.16 seconds).
Through what tissue does the Bundle of His penetrate?
The Atrioventricular fibrous tissue
What is the last part to receive the action potential signal & how long does it take starting from the bundle branches?
It is the superior left lateral part of the left ventricle & it takes 0.06 seconds.
What causes the signal delay from the atria to ventricles (2 reasons)?
There are fewer gap junctions in the AV node & the penetrating part of the Bundle of His are smaller in diameter.
What is the difference of Purkinjie cells compared to Atria cells?
Purkinjie cells are wider & have lots of gap junctions
How long does the signal travel from SA to AV node?
0.03 seconds
How long does it take the for the last part of the Atria to see the electrical signal?
It takes 0.09 seconds
How long does it take the electrical signal to spread throughout the right Atrium?
0.07sec
What would cause a divided or biphasic P-wave?
Most likely a dilated left Atrium. Could be fibrosis or scar tissue of Bachman’s Bundle.
What would cause a larger P-wave?
Right Atrium hypertrophy
How long is the AV node delay?
0.09 sec
What is the combined total delay in the Bundle of His?
0.04sec
When does the conduction signal reach the Bundle branches?
0.16
What relates to the PR interval?
Signal travel from SA node to the Bundle branches
Where is the QRS initiated?
At the Bundle branches. The left bundle branch fires first, which reflects as the Q-wave.
What is indicative of a QS wave & where would one see it?
Indicative of ischemia & seen in Lead II
How long does it take for the entire depolarization to occur?
0.22sec
What prevents electrical signal travel between Atria & ventricles?
Cartilaginous rings
How does WPW present on an EKG?
Shortened PR interval or absorbed PR into QRS & widened QRS.
What are the clinical symptoms of Wolff Parkinson White?
Tachycardia, arrhythmias, EKG changes
What are accessory pathways & where are they found?
Abnormal pathways between atria and ventricles on the lateral aspects of the heart, they are called Bundle of Kent. Type-A is found between the Left atria & ventricle. Type-B is found between the Right atria & ventricle.
What is the normal Magnitude of a QRS complex?
1.5 – 2.0 mV
What would be causes of reduced voltage changes on an EKG?
Soft tissue, adipose tissue, air in lungs, COPD
When would we see the highest reading on a current meter?
When half of the tissue is depolarized & half is reset.
Where does Bachmann’s Bundle branch off?
Off the anterior intranodal pathway close to the SA node.
What are two reasons for a prolonged P wave?
Fibrosis/scar tissue of or around Bachmann’s Bundle & a dilated left atrium.
What is indicative of a peaked P wave?
Hypertrophy of the right atrium.
Which arrhythmia has circular conduction in the atria?
A-flutter
What is the difference between purkinjie cells & internodal pathways?
Purkinjie cells don’t have much actin & myosin & have lots of gap junctions & are wider to conduct very quickly.
What are the 3 LV fascicles?
Posterior (comes off early of the LBB), left lateral wall, & anterior fascicle (towards apex)
What is indicative of a QS wave is observed in Lead II?
Dead heart tissue.
How long is a perfect QT interval?
0.35sec
What is the ST segment, how long is it, & what are two other names for it?
All of the ventricle tissues are depolarized. It is 0.16sec, & it is also called the J-Point or Isoelectric point.
True or false? Infarcted tissue can reset but not depolarize.
False, it can depolarize but not reset.
On a standard 3 lead EKG which lead is least likely to have a Q wave?
Lead III
Which leads are used to check for ventricular hypertrophy & what is the amplitude?
Leads I, II, III & >2mV.
At what rate does EKG paper print & what does each individual horizontal box mean?
It prints at 25mm/sec. Each box is 1mm & 0.04sec.
How long is the RR interval supposed to be & what can it be used for?
0.83sec & it can be used to calculate the HR (60/RR interval= HR)
Where should leads V1 & V2 be placed?
In the 4th intercostal spaces
Where should lead V4 be placed?
In the midclavicular line/ the 5th intercostal space
Where should V6 be placed?
In line with the lateral portion of the clavicle. Also called Mid-axillary line.
Where should V5 be placed?
At the anterior axillary line
What are the reasons for left axis deviation?
Obesity, LV hypertrophy, loss of electrical activity in right side, LBBB, systemic HTN, AS, AR, age, deep exhalation, low lung volume (paralytics), lying down.
What are the causes for right axis deviation?
COPD, RV hypertrophy, RBBB, being skinny, deep inspiration, pulmonic valve stenosis, pulmonary HTN
What leads are used to evaluate axis deviation?
Lead I & III
What are the values for left axis deviation?
Anything less than +59 to -90 degrees.
What are the values for right axis deviation?
Anything greater than +59 to +180 degrees.
When is axis deviation considered extreme?
> +180 degrees.
The tallest normal T wave should be seen in what lead?
In Lead II
At what point do the contracted ventricles start to loosen?
Shortly after the end of the T-wave. (slide 12, lecture 12)
At what 3 points is no potential recorded?
When the ventricular muscle is either completely depolarized or repolarized or when current is moving perpendicular to the lead.
What is the mean electrical axis & what is it derived from?
+59 degrees & averaging out all currents.
Where does ventricular depolarization start?
At the septum & the endocardial surfaces.
What is Eindhoven’s law state?
The electrical potential of any limb equals the sum of the other two.
What are the Precordial leads?
V1 – V6
Which lead in a 12 Lead EKG will have the highest QRS complex?
V4
Where are the positive electrodes for aVR, aVL, & aVF located?
aVR= right arm, aVL= left arm, aVF= left foot
What are the axis of Lead I, II, & III?
0, 60, & 120 degrees
What gives us the S wave?
The last part to depolarize is the left lateral part of the LV, so the current flows towards the negative part of Lead III & partially towards the negative part of Lead II.
Should we see an S wave in Lead I & why?
No, current flows towards Lead I at that part of depolarization & therefore we should still see a positive deflection above baseline.
What part of the ventricles is first to repolarize?
The epicardium of the apex.
Why is the T wave positive in deflection?
Because repolarized areas have a positive charge, therefore, a (+) net vector occurs.
In a vectorcardiogram, when is the vector the largest?
When half of the ventricle is depolarized.
An axis shift will also cause what to change in an EKG?
It will slightly prolong the QRS
What EKG observations are made in V1 & V6 in a RBBB?
V1 has a positive secondary R wave & V6 has a slurred terminal S wave.
What EKG observation are made in V1 & V6 in a LBBB?
V1 has a wide negative S wave & V6 has rabbit ears
What is a high voltage EKG & what causes it?
If the sum of Leads I-III is >4mV & usually caused by increased ventricular muscle mass either due HTN or marathon runners.
What will cause decreased voltages in a standard EKG?
Cardiac muscle abnormalities, pleural effusions, emphysema, fluid in perdicardium, & anterior-posterior rotation of the apex.
What are 3 causes of current of injury?
Ischemia, mechanical trauma, & infection.
Does injured tissue emit current? If so, what kind?
Yes, it emits negative charges throughout each beat.
What type of deflection for the P wave, QRS, & T wave will we see in aVR?
Negative P, QRS, & T wave.
What degree relates to aVL?
-30 degrees.
What current of injury will be observed in Leads I, II, & III with a left lateral superior infarct on a standard EKG?
A negative deflection in Lead I, & positive deflections in Lead II & III.
If Lead I has a + current of injury & Lead III has a – current of injury, where would the infarct be & what direction is mean vector pointing at?
Infarct would be in the lower lateral area of the RV & the vector would point more towards the left shoulder.
If V2 has a prolonged depolarization & a negative deflection from the Isoelectric point, what would this be indicative of?
An anterior wall infarct.
Lead II & Lead III have negative currents of injury & V2 has a + current of injury, would be what kind of infarct?
Posterior wall infarct
In an uninfarcted heart, what QRS currents will be seen in V1 & V2?
The QRS will be negative in nature.
What can result in recurring ischemia of a particular area recovering from a thrombus?
Exercise
RV hypertrophy would result in the QRS being ____ & the T-wave being ____?
Widened & inverted
Repolarization of the endocardium followed by the epicardium will be seen as, what?
An inverted T-wave
What are causes covered in class of tachycardia?
Increased body temp, SNS stimulation (such as reflex or blood los), toxic conditions, such as ischemia or nicotine, or caffeine (not a toxin).
How does phenylephrine affect the HR?
There is an SVR increase, the baroreceptors sense that & a reflex inhibition signal is send to nodal tissue to reduce HR.`
Bradycardia is caused by ____ K+ permeability at the _____ which _____ phase 4.
Increased, SA node, & prolongs
Inhibiting adenylate cyclase leads to reduced_____, which leads to HCN channels_____, which leads to a ______ phase 4.
cAMP, closing, & longer.
Which rhythm leads to seeing stars, decreased filling time, & a possible drop in BP?
Paroxysmal SVT
What are the treatment options for P-SVT?
Vagal maneuver, BB to shut some HCN channels –> slowing depolarization, CCB slowing action potential transmission, Digoxin, & a halter monitor.
What is the cause of P-SVT?
Abnormal atrial excitation
What will be observe in a Sinoatrial block?
Possibly no P-wave. Inverted P-wave if AP is coming from AV node, & a HR of 40-60bpm
What are the possible causes (5) of an Atrioventricular block?
Ischemia of the AV nodal tissue or fibers, compression of AV bundle from scar or calcified tissue, inflammation, excessive vagal stimulation, excess digitalis.
What do the left and right vagus nerve innervate?
Left supplies the AV node & right supplies the SA node
Why are ACE inhibitors possibly prescribed after an MI?
ACEi are growth factor inhibitors and can slow down scar tissue formation.
What is seen in an incomplete 2nd degree heart block, Mobitz Type I?
Increasing PR interval of 0.25 – 0.45sec, dropped QRS complexes.
What is seen in Mobitz type II?
Fixed & long PR interval, fixed ratio for dropped beats, which can vary.
What feedback is seen in 3rd degree HB?
An increase in SA node firing.
What happens & is observed in Atrial flutter?
Circular coordinated action potentials, which do not come from the SA node. An atrial HR of 200+ with ventricular tachycardia.
Compare how the Atria contribute to cardiac output in a healthy vs sick heart.
In a healthy heart it contributes to about 5% of CO at rest & in a sick heart it contributes to about 25% of CO.
What are some causes of A-Flutter?
Ischemia, atrial hypertrophy
How does atrial hypertrophy cause A-Flutter?
Parts of the atria may already have reset and when a close signal passes by it may depolarize.
What can cause A-Fib & how is it usually treated?
Atrial hypertrophy, stenotic valve or regurgitation. Treated with anti-coags.
What is the 5 & dime reflex?
During eye procedures if the 5th cranial nerve (Trigeminal) is pressed on it causes cranial nerve 10 (Vagus) to fire, possibly causing complete HB for a brief time.
What happens in Stokes-Adams syndrome?
An irregular AV block, the 1st beat of the ventricular escape rhythm is delayed for up to 30sec due to the purkinjie fiber’s Vrm being -90 and phase 4 slope being very gradual as there are very few Na+ leak channels. During this time it is likely to faint d/t low BP. After the first beat the rhythm is relatively regular at 15-40bpm.
What are the causes of premature atrial contractions?
Ischemia, irritation or calcified plaques.
What is a radial pulse deficit?
Early depolarization results in less filling time & lower SV, which can be felt at the left radial artery.
When would inverted P-waves be observed?
When the AP is coming from or near the AV node in PAC’s or PVC’s.
In an action potential that originates in the middle of the AV junction, what will be seen on the EKG?
A missing P-wave as it’s obscured by the QRS.
What is the source if an early & inverted P-wave are seen?
High AV junction source
What is the source if a late & inverted P-wave are seen?
Low AV junction source
Why are PVC’s wider & have a higher amplitude?
Ventricular muscle conducts slower than the purkinjie system & 1 ventricle depolarizes before the other & the currents do not cancel each other out.
What are the causes of PVC’s?
Caffeine, nicotine, stress, & lack of sleep.
Describe the EKG of a PVC?
Normal P wave, QRS widened & higher amplitude, & T wave inverted.
When do the coronary arteries perfuse?
Diastole= End of the T wave to the start of QRS
What is a regular QT interval & when is it considered long?
Regular is <40% of RR interval & >50% is considered long QT.
An EKG says long QT interval, in basic terms what is happening?
Early afterdepolarization
Relate Fast Na+ & L-type Ca2+ channels to EAD’s?
Dysfunctional Na+ & Ca2+ channels have not reset properly & open on their own causing an EAD.
Relate beta agonists to EAD’s?
A beta agonist causes phosphorylation of Ca2+ channels, which increase sensitivity, which can cause EAD’s.
How can antihistamines cause EAD’s?
1st Gen block muscarinic receptors –> decrease K+ permeability of nodal tissue –> longer time in phase 3.
Relate hyperkalemia to DAD’s?
The Vrm shifts up closer to threshold & leads to increased K+ permeability thru simple Ion channels, delayed K+ & K+ir channels.
How does low ECF K+ relate to EAD’s?
Closure of K+ir & delayed rectifier K+ channels lead to longer time in phase 3.
What kind of current and voltage is used in defibrillation?
DC current & high voltage (increase voltage with successive shocks).
Delineate the pathway of extreme hyperkalemia & what it leads to in relation to cardiac action potentials?
The Vrm shifts up & V-G K+ Ion channels do not reset. Eventually lose the ability of fast Na+ channels causing a gradual phase 0 slope. If the Vrm shifts higher, then the Ca2+ channels cannot reset either, that will lead to loss of action potential generation.
Describe Type 1 antiarrhythmic drugs?
They are fast Na+ channel blockers. Manipulate speed of conduction but not the HR. – Caine drugs
Describe type 2 antiarrhythmic drugs?
Beta blockers. Slow down nodal tissue via reducing HCN mediated Na+ influx during phase 4. Also, reduce the SERCA pump longer AP, & limit phosphorylation of Ca2+.
Describe type 3 antiarrhythmic drugs?
K+ channel blockers. TEA, 4,5 diamino pyridine, Amiodarone
Describe type 4 antiarrhythmic drugs?
CCB’s reduce force & slow down nodal action potential.
What does adenosine do?
Bind to A1 receptors & slows down HR or reset thru greatly increasing K+ conductance.
What is inotropy & chronotropy?
Inotropy= increase contractile force or Ca2+ sensitivity. Chronotropy= mediates HR
What is Dromotropy?
Conductance speed. Beta agonsits increase conductance speed.
What is Lusitropy?
Resetting of the heart. Beta agonists speed up SERCA pumps= faster reset.
How does general anesthesia affect arrhythmias?
Causes an increased sensitivity to catecholamines & a reduction of NE reuptake.
How do CVL’s or contact with the heart affect the EKG?
There may be a missed beat or two.
How does the ventilator rate relate to arrhythmias?
An increase in ventilator rate will cause breathing off CO2, which causes the plasma proteins to lose attached protons causing Ca2+ attraction & binding to the protein. This bond causes a decreased ionized(free) Ca2+ level. Hypoventilation may increase plasma Ca2+ but will lead to acidosis.
How does insulin relate to arrhythmias?
Insulin receptors are tethered to the Na+/K+ ATPase. An increase in insulin will increase Na+/K+ ATPase cycling.
What are the two atrial stretch reflexes called?
Direct atrial stretch & Bainbridge reflex
Differentiate between Bainbridge & Direct atrial reflex?
Direct stretch does not rely on outside signals & can increase the HR by 15%. Bainbridge reflex is mediated via the CNS sensors that feedback via the vagus nerve to slow firing. It can increase the HR by 50%.
What energy products are carried to the tissues by the CV system?
Glucose, fatty acids, cholesterol, O2
What waste products are carried away from the tissues via the CV system?
CO2, urates, nitrates, acids, lactate, lactic acid.
How is velocity measured?
In distance/time
What would cardiac output be during a workout?
20 – 25L/min (CO increases 4-5 times during workouts)
How is blood flow measured?
In volume/time
Which system is the least linked to metabolism?
The renal system
What are the #1 & #2 vascular tone regulators?
1 arterioles & #2 is the nervous system
The nervous system is in contact with everything except?
Brain vessels & capillaries
The arterioles determine ____ within a given _____?
Blood flow & system/organ
The highest blood velocity is in the _____ & the lowest velocity is in the ______?
Aorta & capillaries
Arterioles have _____ inside diameters & ____ walls?
Small & thick
Larger arteries have _____ walls?
Thick
Capillaries have ____ walls with ____ inside diameters?
Thin & large
Veins have ____walls with a small layer of _____?
Thin & smooth muscle
How long does it take blood to flow thru a capillary?
2-3 seconds
Where is the highest pressure fluctuation & what is the range?
In the LV. 120mmHg at systole & 2mmHg @ diastole.
When does the aortic valve close?
@ 100mmHg
What is the best MAP & how is it calculated?
93.3mmHg. MAP= diastolic + 1/3(systolic – diastolic)
Where is pulse pressure the second highest?
In the large arteries
What is the most important reason that BP drops?
Blood encounters more resistance & energy is reduced.
How is pressure lost through the pulmonary system?
Equal pressure is lost throughout the system.
Why is pulmonary pressure so low?
There are many parallel pathways for blood to flow through. Also there is minimal resistance.
How is resistance calculated?
Delta P divided by Blood Flow
What are these two items called?
Left= Ultrasonic Doppler flowmeter & Right= Electromagnetic flowmeter probe
What is the LV diastolic pressure?
2mmHg
What is the normal range for SVR in CGS units?
800 – 1600 dynes x sec/cm-5
How is SVR calculated in PRU?
(Beginning pressure – end pressure) divided by 5L/min x (80)
What is normal wedge pressure?
8mmHg
What is a normal PVRI range in CGS units?
40 – 180 dynes x sec/cm-5
How are PRU converted to CGS units?
Take PRU units and multiple by 1333
What is the formula for Poiseulle’s law?
n= viscosity, l= length of vessel
What is a normal Hct & how do changes affect blood flow?
Normal is 0.4L/L & a lower Hct will decrease viscosity
What is the formula blood flow?
v= velocity, d= diameter, p= density, n= viscosity
Where is turbulent flow most likely & what decreases the chance of turbulent flow?
In the aorta & higher viscosity= less turbulence
Spell the law that relates to blood flow?
Poiseulle
How many capillaries do we have & what does relate to in surface area?
10 billion & 500 – 700 square meters of surface area
What 2 things does vascular smooth muscle rely on?
ECF calcium & tone from SNS
Which part of the CV system lacks the endothelial layer?
None, it is a continuous layer
What determines constriction of upstream arterioles?
Tissue factors
What all is part of the interstitial fluid?
Collagen, proteoglycan filaments, hyaluronic acid, & free fluid rivulets
What is the purpose of ECF proteoglycan filaments?
Provide hydration & swelling pressure to tissue enabling it wo withstand compression forces.
Arrange the following substances from lowest to highest molecular weight, Myoglobin, Albumin, Hemoglobin, Inulin, Sucrose?
Sucrose < Inulin < Myoglobin < Hemoglobin < Albumin
Which is the least permeable substance, Glucose, urea, NaCl, inulin, sucrose?
Inulin is the least permeable substance
What is the Delta P in capillaries?
20mmHg
What is hydrostatic pressure (Pcap) & what value goes with it?
Physical fluid pressure inside the capillaries generated by the heart & after SVR is applied. The value is 30mmHg
What pressure relates to interstitial fluid pressure & what are the abbreviations for it?
-3mmHg & Pif or Pisf
What is the value for oncotic pressure & the abbreviations?
28mmHg, & πp or πcap
What value does the interstitial fluid colloid osmotic pressure have & what are the abbreviations?
8mmHg & πif or πisf
What is the average pressure along an entire capillary?
17.3mmHg
What compounds constitute the oncotic pressure?
Albumin, globulins, & fibrinogen
What is the Donnan effect & its contribution?
Charged plasma proteins that have electrolytes bind to them & keep them from crossing into the interstitial space. It contributes 9mmHg of the total 28mmHg.
A healthy lymphatic system has an average flow rate of ____ mL/hr & can increase up to ___ times?
120mL/hr & 20 fold
What is the purpose of the lymphatic system & where does it empty into?
Collect excessive filtration (incl. proteins, colloids, etc) & empties into the subclavian veins.
What two conditions adversely affect Pcap?
HTN= increased extremity fluid &
CHF= volume expanded & getting blood out of venous system.
What 2 conditions affect πcap?
Liver failure= reduced oncotic pressure &
Burns= colloids spilling into interstitial space.
