5011- Cardiac Theory 1 (overall)

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118 Terms

1
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Describe long axis imaging planes

  • POM @ 11 o’clock

  • Divides: left and right


<ul><li><p>POM @ 11 o’clock </p></li><li><p>Divides: left and right</p></li></ul><p></p>
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Describe short axis imaging planes

  • POM @ 1 o’clock

  • Divides: superior and inferior


<ul><li><p>POM @ 1 o’clock </p></li><li><p>Divides: superior and inferior </p></li></ul><p></p>
3
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Describe 4CH imaging planes

  • POM @ 3 o’clock

  • Divides: anterior and posterior


<ul><li><p>POM @ 3 o’clock </p></li><li><p>Divides: anterior and posterior</p></li></ul><p></p>
4
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Describe 2CH and 3CH imaging planes

  • 2CH: POM @ 1 o’clock

    • divides left and right

  • 3CH: POM @ 12 o’clock

    • divides anterolateral and posteriomedial


<ul><li><p>2CH: POM @ 1 o’clock </p><ul><li><p>divides left and right</p></li></ul></li><li><p>3CH: POM @ 12 o’clock</p><ul><li><p>divides anterolateral and posteriomedial </p></li></ul></li></ul><p></p>
5
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Describe subcostal imaging planes

  • POM @ 3 o’clock


<ul><li><p>POM @ 3 o’clock</p></li></ul><p></p>
6
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Describe suprasternal imaging planes

  • POM @ 1 o’clock


<ul><li><p>POM @ 1 o’clock </p></li></ul><p></p>
7
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Difference between arteries and veins?

  • veins: blood returning to the heart

  • arteries: blood moving away from the heart


8
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Which 3 structures drain into the RA?

  • SVC, IVC, and CS


9
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Describe characteristics of RA (2)

  • smooth walled except anterior surface

    • anterior surface contains pectinate muscles, prominent ridges of muscle

  • right atrial appendage (RAA) on anterior surface

    • contains pectinate muscle and increases RA volume


10
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Describe characteristics of RV (5)

  • walls lined with trabeculae carneae

  • contains moderator band

  • thick walls, but not as much as LV

  • chordae tendineae that connects TV leaflets to pap muscles

  • 3 pap muscles: anterior, posterior, and septal


11
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What are trabeculae carneaes?

  • ridges of muscle lined with endocardium

  • help push and rings out the blood


12
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What is moderator band?

  • thick band of the cardiac muscle that extends from the IVS to anterior papillary muscle

  • helps prevent over-distention of the RV, similarly to rubberband


13
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Describe characteristics of LA (3)

  • receive oxygenated blood from 4 pulmonary veins

  • smooth walled

  • left atrial appendage (LAA) contains pectinate muscles


14
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Describe characteristics of LV (4)

  • thick walls

  • contain trabeculae carneae

  • chordae tendineae connect MV to pap muscles

  • 2 pap muscles: anterolateral and posteromedial (Prime Minister At Lunch)


15
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What are the main roles of chordae tendineae and pap muscles?

prevent eversion of MV into LA and TV into RA

16
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What are the main roles of semilunar valves

the crescent shapes valves help prevent backflow

17
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Rank the valves from most superior to inferior

  1. Pulmonary

  2. Aortic

  3. Mitral

  4. Tricuspid


18
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What are the valves relation to the aortic valve?

  • Most posterior: MV

    • LIMP

  • Most anterior: PV

    • PALS

  • Most inferior: TV

    • TRIP

  • Furtherest to the right: TV


19
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Difference between pericardium and heart wall

  • pericardium: sac/membrane that surrounds the heart

  • heart wall: layers of the heart


20
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What is the role of the pericardium? (4)

  • protects the heart from infection

  • protects the heart from over-distention

  • acts as lubricant to reduce friction between the heart and surrounding structures

  • made up of two layers: serious pericardium (inner) and fibrous pericardium (outer)


21
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Describe fibrous pericardium

  • outer most layer heart sac

  • tough, dense, connective tissue


22
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What are the main roles of fibrous pericardium (3)

  • protects the heart from infection

  • anchors the heart in place during beating and bouncing

  • prevents overfilling of the heart


23
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What are the 2 parts of the serous pericardium

  1. Visceral or epicardium layer - inner most layer, part of the heart wall

  2. Parietal layer - fused to fibrous pericardium

Note: pericardial fluid found between the two serous layers


24
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What are the 2 main roles of serous pericardium

  1. cushions the heart

  2. lubricates the heart


25
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What makes up the heart wall (3)

  • epicardium or visceral serous pericardium: outer most layer, but inner most layer of serous pericardium

  • myocardium: middle muscular layer

  • endocardium: inner most layer of the heart lining the chambers and valves


26
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What are the main roles of epicardium, myocardium, and endocardium?

  • Epicardium: protects heart layers, produces pericardial fluid, houses coronary blood vessels

  • myocardium: pumps blood through the heart

  • endocardium: protects the myocardium and the heart valves


27
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Why are the LV walls thicker than RV ?

  • pumps same amount of blood but LV needs to generate greater forces to overcome high resistance of the systemic circuit

  • RV needs only small amount of force to overcome the low resistance of pulmonary circuit


28
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<p>Label the correct structures of the wall </p>

Label the correct structures of the wall

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29
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Difference between coronary arteries and veins

  • coronary arteries deliver oxygen and nutrients to myocardium

  • coronary veins remove waste material


30
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What are the 3 types of sulci/grooves, and the artery and vein pairing to each?

  • anterior interventricular sulcus

    • artery: LAD

    • vein: GCV

  • posterior interventricular sulcus

    • artery: PDA

    • vein: MCV

  • coronary sulcus (left)

    • artery: CS

    • vein: GCV

  • coronary sulcus (right)

    • artery: RCA and marginal artery

    • vein: SCV


31
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<p>Label PLAX structures </p>

Label PLAX structures

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32
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<p>Label RVIT structures </p>

Label RVIT structures

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33
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<p>Label RVOT structures </p>

Label RVOT structures

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34
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<p>Label PSAX overview structures </p>

Label PSAX overview structures

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35
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<p>Label PSAX pulmonary level </p>

Label PSAX pulmonary level

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36
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<p>Label PSAX tricuspid level </p>

Label PSAX tricuspid level

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37
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<p>Label PSAX mitral level </p>

Label PSAX mitral level

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38
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How are the scallops of the mitral valves labeled

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39
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What are the two types of cardiomyocytes

  1. ventricular and atrial muscle cells

  2. pacemaker cells (SA & AV node)


40
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Describe ventricular and atrial muscle cells

  • cells shorten and lengthen to contract and relax

  • contract when they receive an electrical signal (action potential) from a neighboring cell


41
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Describe pacemaker cells (SA & AV node)

  • modified myocytes, found in specialized cells

  • autorhythmic: spontaneously generate and send out electrical signals without external stimulus

  • respond to stimulation from the brain, and continue to contract even when pulled out


42
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Describe a cardiomyocyte, what are the important structures?

  • muscle cell of the heart

  • myofibril and sarcomere structures


43
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Describe myofibril

  • contractile portion of the cell, many per cardiomyocyte

  • made of repeating contractile units called sarcomere


44
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Describe sacromere

  • contain actin/myosin myofilaments

    • thick filaments: myosin

    • thin filaments: actin


45
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How does the contraction and relaxation work in regards to cardiomyocytes

binding and unbinding of actin and myosin results in contraction and relation of muscle fibre

46
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What are intercalated discs? what are they made up of (3)?

  • found in cardiac tissues ONLY

  • communication network between cells that allows heart to work as single functioning unit

  1. gap junctions

  2. desmosomes

  3. fascia adherens


47
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Describe gap junctions

  • protein lined tunnels that directly connect the cytoplasm of the two adjoining cells

  • allow action potential to spread quickly from one cell to the next

  • lots gap junctions = faster impulse transmissions = contractions occur in unison


48
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Describe desmosomes

  • provide cell to cell adhesion

  • maintain mechanical integrity and resist shearing forces

  • bridge the space between cells


49
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Describe fascia adherens

  • anchors the actin filaments to the cell membrane


50
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Describe the conduction system in the heart

  1. SA Node (chief pacemaker, where specialized cells are located at RA)

  2. Bachmann’s Bundle

  3. AV node

  4. Bundle of His (Atrioventricular bundle)

  5. Right/Left bundle branches

  6. Purkinje Fibers

Note: higher up = faster to generate a pulse, at a higher rate and it is lower as it goes down


51
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Describe SA node, and main purpose

  • located in RA wall

  • automatically produces a consistent and constant electrical signal, 60-100 bpm

  • sends the signals to the atria, causing the atria to contract

  • natural pacemaker of the heart, it determines heart rate because reaches threshold for depolarization the fastest


52
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Describe Bachmann’s Bundle, and main purpose

  • travels from RA to LA

  • initiates contraction of the LA


53
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Describe AV node, and main purpose

  • located at the crux

  • delays electrical impulses slightly to allow atria to finish emptying before the ventricles can contract

  • sends signal down to Bundle of His


54
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Describe Bundles/Purkinje signals

  • Bundle of His: sends signal from AV to bundle branches

  • Bundle branches: signal travels down the IVS down the left and right bundle branches

  • Purkinje fibres: travel deep into the heart to supply the muscle of ventricles

    • start at apex and work their way up


55
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Briefly describe the conduction of action potential (AP) in the heart, starting with SA node

  1. SA node is primary pacemaker of the heart, fires spontaneously generating an AP that spreads thru the atria

  2. myocytes are connected via gap junctions, ions flow from one cell to another, trigger AP in neighboring cells and propagate rapidly

  3. impulse gets to AV node and slows down to allow atria to contract then goes down the conduction pathway to ventricular myocytes


56
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How do the action potential differ from pacemaker cells and cardiac myocytes?

  • pacemaker cells: creates own signal, unstable resting potential (slope on graph), autorhythmic

  • atrial and ventricular cells: needs to be stimulated to contract, stable resting potential (flat on graph), non-autorhythmic


57
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What is the unique plateau seen in atrial and ventricular cells?

  • phase that allows cells to contract and relax fully before release

  • cannot be restimulated until the end


58
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Describe action potential

  • cardiac cells are filled and surrounded by solutions that contain positive and negative ions

  • More Na+, Ca2+ outside of the cell, and more K+ inside the cell

  • electrical stimulation is created by sequence of ion fluxes through specialized channels in the membrane of cardiomyocytes that lead to contractions

  • AP: reversal of cell membrane electrical polarity due to voltage gated ion channels


59
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Describe depolarization and repolarization in relation to cell action potential

  • Depolarization: negative to positive (up the slope), cell is contracting

  • Repolarization: positive to negative (down the slope), cell is relaxing


60
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Briefly explain all 3 phases of the action potential contractile cell

  • Phase 0: AP triggered in neighboring cardiomyocyte or pacemaker cells reaches next cell via gap junction, ions leaking in raising RMP to threshold → rapid depolarization: Na and Ca in, K out

  • Phase 1: brief, early repolarization phase with some K leaving and lower transmembrane potential

  • Phase 2: plateau phase where Ca coming into cell triggers more Ca from storage → sets off muscle contractions

    • plateau caused by balance between inward movement of Ca and the outward movement of K via leaking down [gradient] and VGC

      • allows cardiac muscles cells to pump blood effectively before firing a second time

  • Phase 3: rapid repolarization phase, K leaking out and VGC slowly close, while Ca is actively leaving cell and pumps are restoring ion balance

  • Phase 4: cell goes back to rest, K leaks out following chemical gradient, Na and Ca pumps closed


61
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What is calcium doing at the muscle fiber level?

Calcium influx

  • calcium binds to troponin → causes troponin to change shape, which exposes the actin-myosin binding sites in the myofibril

  • actin and myosin bind and shortens the muscle fiber → contraction!

Calcium effux

  • calcium levels drop and remainder gets used up → calcium unbinds from troponin complex → shape changes

  • shape no longer allows actin and myosin to bind together because the site is no longer exposed → cell at resting length/ relaxation


62
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What leads do sonographers use?

Lead II, strongest deflection bc it is parallel to wave of depolarization: negative to positive

63
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What does the different segments in the ECG represent?

  • P wave: atrial depolarization

  • PR segment: delay at the AV node → no electrical activity = flat line → atria contraction while ventricles filling

  • QRS complex: ventricular depolarization and atrial repolarization

    • Q: septal depolarization from left to right

    • R: ventricular depolarization (not contracting)

    • S: Purkinje fiber depolarization

  • ST segment: isoelectric period, refractory period of ventricles → contracting

  • T wave: ventricular repolarization

  • PR interval: onset of atrial depolarization to ventricular depolarization

  • QT interval: ventricular systole


64
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Based on a box grid for ECG, how to measure HR from R to R?

  • thick solid line to next until next QRS

  • 300 → 150 → 100 → 75 → 60 → 50


65
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Compare and contrast of sinus bradycardia, tachycardia and arrhythmia

  • brady: <60 bpm

  • tachy: >100 bpm

  • arrhythmia: rhythm varies with respiration


66
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What are premature atrial contractions? (PAC)

  • premature beat originates somewhere in the atria and interrupts the underlying rhythm

  • p wave may look different since its not from the SA node, but are still followed by QRS


67
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What are atrial fibrillations?

  • most common cardiac arrhythmia

  • atria receive multiple pacemaker signals, thus “quivers” instead of contracting

  • no P waves, and ventricles depolarized at irregular intervals


<ul><li><p>most common cardiac arrhythmia </p></li><li><p>atria receive multiple pacemaker signals, thus “quivers” instead of contracting </p></li><li><p>no P waves, and ventricles depolarized at irregular intervals </p></li></ul><p></p>
68
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What are atrial flutters?

  • abnormal rhythm either in RA or LA, the atria are depolarizing at an extremely rapid rate

  • “saw-like”, several P waves for each QRS, varying R-R intervals because not all electrical signals make thru the AV


<ul><li><p>abnormal rhythm either in RA or LA, the atria are depolarizing at an extremely rapid rate </p></li><li><p>“saw-like”, several P waves for each QRS, varying R-R intervals because not all electrical signals make thru the AV </p></li></ul><p></p>
69
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What are premature ventricular contractions (PVCs)

  • initiated by Purkinje Fibers in the ventricle instead of the SA node, thus ventricles contract first before the atria can fill with blood

  • “skipped beat”, usually random

  • every second beat: bigeminy

  • every third beat: trigeminy


<ul><li><p>initiated by Purkinje Fibers in the ventricle instead of the SA node, thus ventricles contract first before the atria can fill with blood </p></li><li><p>“skipped beat”, usually random</p></li><li><p>every second beat: <strong>bigeminy</strong> </p></li><li><p>every third beat: <strong>trigeminy </strong></p></li></ul><p></p>
70
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What are ventricular tachycardia (VT)

  • extremely fast heart rhythm that originates in the ventricles, either LV or RV

  • more than 3 PVCs in a row

  • since ventricles do not have enough time to fill, the blood isnt pumped to the body → can lead to emergency

  • non-sustained VT: < 30s

  • sustained VT: > 30s


71
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What are ventricular fibrillations?

  • uncoordinated contraction of the cardiac muscle → ventricles quiver

  • can also quickly turn into asystole within mins

  • do not want to >5min or else brain damage


<ul><li><p>uncoordinated contraction of the cardiac muscle → ventricles quiver </p></li><li><p>can also quickly turn into asystole within mins </p></li><li><p>do not want to &gt;5min or else brain damage </p></li></ul><p></p>
72
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What are the 3 types of AV heart blocks?

  1. First degree heart blocks: AV conduction slowed

  2. Second degree heart blocks: AV conduction incompletely blocked

  3. Third degree heart blocks: AV conduction completely blocked


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Characteristic of first degree AV block

conduction at AV delayed beyond normal amount, where PR interval is longer than 0.2s followed by QRS


<p>conduction at AV delayed beyond normal amount, where PR interval is longer than 0.2s followed by QRS</p><p></p>
74
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Characteristic of second degree blocks, and what are the two types?

  • P wave is blocked from initiating a QRS complex → more p waves than QRS

  • Mobitz I/ Wenckebach and Mobitz II


75
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Explain the 2 types of second degree AV block

  • Mobitz I/ Wenckebach: PR interval gets longer with each beat until a P wave occurs, but not followed by QRS (QRS eventually dropped)

  • Mobitz II: No PR prolongation and QRS complex just fails to occur after a P wave (QRS drops occasionally)


<ul><li><p>Mobitz I/ Wenckebach: PR interval gets longer with each beat until a P wave occurs, but not followed by QRS (QRS eventually dropped) </p></li><li><p>Mobitz II: No PR prolongation and QRS complex just fails to occur after a P wave (QRS drops occasionally)</p></li></ul><p></p>
76
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Characteristic of third degree AV block

  • complete heart blocks → atria and ventricles do not communicate

  • atria controlled by one pacemaker, the ventricles by another

  • p waves occur at regular intervals with QRS, but no apparent patterns, so p waves interrupt


77
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What are bundle branch blocks

  • loss of ventricular synchrony

  • ventricular depolarization is prolonged

  • impulse has to move through muscle fibers instead of bundle

  • QRS wider than 3 squares


78
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Differentiate right vs left bundle branch blocks

  • RBBB: damage to the right:

    • RV after the LV

  • LBBB: damage to the left

    • LV contracts after the RV


<ul><li><p>RBBB: damage to the right:</p><ul><li><p>RV after the LV</p></li></ul></li><li><p>LBBB: damage to the left </p><ul><li><p>LV contracts after the RV</p></li></ul></li></ul><p></p>
79
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What is asystole

  • cardiac arrest rhythm → no electrical signal on the ECG monitor

  • flat line → code blue!


80
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What is pulseless electrical activity (PEA)

  • cardiac arrest

  • dying heart → weak electrical activity, but too dead to respond mechanically

  • no ventricular activity → no pulse


81
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Characteristic of pacemaker on ECG

  • release electrical impulses to regulate beating of the heart

  • spike on trace every time the electrode fires


<ul><li><p>release electrical impulses to regulate beating of the heart</p></li><li><p>spike on trace every time the electrode fires </p></li></ul><p></p>
82
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Compare STEMI vs NSTEMI

  • STEMI: ST segment elevation

    • coronary artery completely blocked off by clot

  • NSTEMI: depression ST segment or T wave inversion

    • partial occlusion to the coronary artery


83
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What are holter monitors

  • used to monitor ECG rhythms over 24 hrs

  • patient wear ECG leads and record activities in logbook

  • r/o structural reasons in heart causing arrhythmias and/or assess hemodynamic impacts


84
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What are stress ECH or cardiac stress tests

  • 12 lead stress test evaluates coronary circulation at rest vs maximum physical exertion

  • stress echo looks at decreased heart function during exercise


85
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What is pulse oximetry

  • measured oxygen saturation of hemoglobin relative to total hemoglobin

  • hypoxemia = insufficient oxygen in blood


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What are the 4 (7) phases of a cardiac cycle

  1. isovolumetric relaxation phase (part of diastole)

  2. ventricular filling:

    1. rapid filling

    2. diastasis

    3. atrial systole

  3. isovolumetric contraction phase (part of systole)

  4. ventricular ejection


87
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Elaborate the 4 stages of diastole briefly

  1. IVRT: all valves closed as ventricles just finished contracting, dicrotic notch

  2. Rapid filling stage: MV opens, blood leaves LA and pressure drops rapidly

  3. diastasis: mid diastole, pressure in LA and LV almost equal, MV leaflets start to close

  4. atrial kick: end of diastole, second push of blood, a wave= atrial contraction


88
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What are the 2 phases in systole?

  1. IVCT: all valves closed, ventricles preparing to contract, c wave is the MV buldging back

  2. Ventricular ejection: blood is being ejected, eventually v wave to signify LA pressure slowly rising as blood enters LA


89
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Whats the lub and dub sounds

  • Lub: 1st heart sound for closure of AV valves

  • Dub: 2nd heart sound for closure of semilunar valves


90
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<p>What does the DEFAC signify in m-mode of mitral leaflets? </p>

What does the DEFAC signify in m-mode of mitral leaflets?

  • D:valve opens, onset of diastole

  • E: rapid filling, maximal opening

  • F: end rapid filling, diastasis

  • A: atrial kick/atrial systole, MV reopens after atrial contraction to eject more blood into LV

  • B: seldom seen, elevated LV end diastole pressure shown as 3rd bump, usually absent

  • C: valve closes, final leaflet position before LV systole


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<p>What does the ABCDEF signify in m-mode of pulmonary level? </p>

What does the ABCDEF signify in m-mode of pulmonary level?

  • a: follows atrial contraction, increasing RV pressure with extra blood

  • b: denotes small anterior deflection occurring at onset of ventricular systole

  • c: large posterior deflection immediately following ventricular ejection, abrupt opening

  • d: gradual anterior motion of leaflets during ejection period as the RV pressure decreases, valve moves to center of the root

  • e: denotes closed position of leaflet upon completion of ventricular ejection

  • f: slight posterior movement of leaflet during diastole immediately prior to atrial contraction


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Why do we wanna assess pulmonary valve with m-mode?

  • pulmonary hypertension: early systolic closure and absent A wave

    • severe PHT, PA diastolic pressure is higher than RV, so RA contraction will have no effect on PV → no A

    • Flying “W” = mid systolic closure and late systolic opening

      • can help confirm PHT in absence of TR

  • pulmonary stenosis:

    • increased A wave

    • look for valve thickening, doming, veg


<ul><li><p><strong>pulmonary hypertension:</strong> early systolic closure and absent A wave </p><ul><li><p>severe PHT, PA diastolic pressure is higher than RV, so RA contraction will have no effect on PV → no A </p></li><li><p>Flying “W” = mid systolic closure and late systolic opening </p><ul><li><p>can help confirm PHT in absence of TR</p></li></ul></li></ul></li><li><p><strong>pulmonary stenosis: </strong></p><ul><li><p>increased A wave</p></li><li><p>look for valve thickening, doming, veg</p></li></ul></li></ul><p></p>
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<p>Label Apical 4CH structures </p>

Label Apical 4CH structures

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<p>Label Apical 2CH </p>

Label Apical 2CH

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<p>Label Apical 3CH</p>

Label Apical 3CH

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<p>Label Apical 5Ch</p>

Label Apical 5Ch

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<p>Label subcostal 4CH</p>

Label subcostal 4CH

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<p>Label suprasternal notch </p>

Label suprasternal notch

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What are the 3 types of effusions

  1. pericardial effusion: fluid in the pericardial sac above normal levels

  2. pleural effusion: fluid around lungs

  3. ascites: fluid in abdominal cavity


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<p>Name all 17 wall segments </p>

Name all 17 wall segments

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