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NUR 942 Thurman > Exam 1 Cardiac > Flashcards

Exam 1 Cardiac Flashcards

1
Q

What is the resting coronary blood flow? Answer in ml/min, ml/gm and % of CO.

A

Approx. 250ml/min (1ml/100gm), 4-5% of CO.

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2
Q

When is angina pectoris considered “stable”?

A

Angina pectoris is considered “stable” when there has been no change in the patient’s angina symptoms for at least 60 days. Factors related to the angina that should be evaluated include the precipitating factors, frequency, and duration. (Miller, pg 416).

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3
Q

When is angina pectoris considered “unstable”?

A

When there has been a recent change in the patient’s angina symptoms. Changes that should be evaluated include the degree of activity a patient can do before the onset of angina and the duration of each anginal episode. Another Sx of angina is chest pain occurring at rest. The clinical implication of unstable angina is that the Pt. may be at risk of an impending myocardial infarction. (Miller, 416)

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4
Q

Which are exposed to higher pressures during LV contraction? Sub-endocardial or sub-epicardial vessels?

A

Sub-endocardial. Therefore, it is more susceptible to ischemia in the presence of coronary artery stenosis, pressure overload, hypertrophy, and pronounced tachycardia. (Thurman III, slide 5).

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5
Q

There is a greater amount of LV coronary flow during (systole or diastole).

A

Diastole

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6
Q

What occurs to the LV coronary artery blood flow during systole?

A

During systole, the left coronary artery blood flow to the subendocardium ceases d/t compression of the subendocardial vessels by the myocardium. Flow to the epicardial vessels are not affected to the same extent.

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7
Q

Name the factors that determine myocardial O2 SUPPLY.

A

Heart Rate, Coronary Perfusion Pressure, Arterial Oxygen Content, Diameter of Coronary Vessels

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8
Q

Name the factors that determine myocardial O2 DEMAND.

A

Basal Metabolic Requirements, Heart Rate, Wall Tension, Contractility

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9
Q

The myocardium extracts about ____% of O2 from arterial blood.

A

65-80% (she says to remember 75%)

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10
Q

What is the most important factor that negatively affects mVo2?

A

Heart Rate. Doubling the HR doubles the myocardial O2 consumption. So tachycardia is bad for Pts with coronary artery disease.

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11
Q

The difference between maximal and resting coronary blood flow is termed what?

A

Coronary Reserve

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12
Q

What is the normal heart size for males and females (in grams)

A

Females 230- 280g, Males 280-340g

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13
Q

What is the normal coronary blood flow?

A

225-250ml/min or 4-7% of CO (slightly different that previously, but this is from “a chart in naglehout”

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14
Q

Normal Myocardial 02 Consumption

A

65-70% Extraction according to NH, 75-80% according to Barash. Again…she says go with 75% (8-10ml O2/100g/min)

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15
Q

Normal Autoregulation (ie MAP of coronary arteries within the heart in mmHg)

A

60-140 mmHg (MAP)

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16
Q

Coronary Filling mostly occurs during…

A

Diastole (80-90%)

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17
Q

Determinants of Myocardial Oxygen Consumption

A

Myocardial Contractility
Myocardial Wall Tension (Preload)
Heart Rate
MAP (Afterload)

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18
Q

What is the formula for determining O2 Content in plasma (ml O2/ml plasma)???

A

O2 content (ml O2/ml plasma)=(PaO2 x 0.003) + (1.36 x Hgb)(O2 Sat/100)

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19
Q

Calculate the Plasma 02 Content using the following parameters.
Hbg 13
Sat 98%
PaO2 88

A 
17.6
(88 x 0.003) + (1.36 x 13)(98/100)
(0.264)+(17.68)(0.98)
0.264 +17.3264
17.5904
17.6
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20
Q

Coronary blood flow is autoregulated at 60-140mmHg. What occurs when the MAP falls outside of these limits?

A

It becomes PRESSURE DEPENDENT

now CBF determined by MAP - RAP

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21
Q

Coronary perfusion pressure is determined by the difference between…….

A

aortic pressure and ventricular pressure

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22
Q

Formula for calculating CPP

A

Arterial diastolic pressure - LVEDP

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23
Q

heart is bound anteriorly by

A

sternum/costal cartilages of 3rd, 4th, + 5th ribs

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24
Q

heart is bound inferiorly by

A

diaphragm

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25
Q

apex points this way

A

anteriorly/inferiorly toward left 5th intercostal space

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26
Q

S1 best heard here, or S3, S4 if present

A

PMI

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27
Q

what are the layers of pericardium

A

fibrous (tough and dense)

serous

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28
Q

2 layers of serous pericardium

A

parietal and visceral (epicardium)

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29
Q

pericardium is pierced by these vessels

A

SVC, aorta, pulm trunk

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30
Q

this layer of the heart is made of fibrocollagenous - tough, dense layer, forms outer layer of pericardial sac. continues superiorly with great vessels and adventitia & pretracheal fascia

A

fibrous pericardium

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31
Q

fibrous pericardium.. anteriorly attaches to ____ thru ____ ligaments

A

sternum

sternopericadial

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32
Q

fibrous pericardium.. posteriorly fuses with ___ ___ of the _____.

A

central tendon

diaphragm (stabilizes heart and chest)

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33
Q

Layers from Fibrous pericardium to heart chamber

A 
FP
parietal layer of pericardium
pericardial cavity
epicardium (visceral layer)
myocarium
endocardium
heart chamber
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34
Q

amount of serous fluid in pericardial cavity

A

10-35 ml

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35
Q

if CVP is 18 what is the pericardial cavity pressure

A

18 - 5 = 13 mmHg

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36
Q

Pericardial blood supply

A

branches of internal thoracic arteries, bronchial, esophageal & superior phrenic arteries

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37
Q

Pericardial venous drainage from these veins

A

azygos and pericardiophrenic veins which join internal thoracic vein

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38
Q

Has sarcomere with actin and myosin. Cardiac Muscle, Skeletal muscle, or Both.

A

Both

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39
Q

Capable of contraction

Cardiac Muscle, Skeletal muscle, or Both.

A

Both

Cardiac longer, Skeletal shorter

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40
Q

T-tubule system and SR

Cardiac Muscle, Skeletal muscle, or Both.

A

Both

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41
Q

Which has more mitochondria?

Cardiac Muscle or Skeletal muscle

A

Cardiac Muscle

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42
Q

Which has more O2 requirements?

Cardiac Muscle or Skeletal muscle.

A

Cardiac Muscle

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43
Q

Which extracts more O2 from the blood?

Cardiac Muscle or Skeletal Muscle

A

Cardiac - 75%, Skeletal only has 25% extraction of O2.

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44
Q

Has Intercalated discs?

Cardiac Muscle, Skeletal muscle, or Both.

A

Cardiac

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45
Q

Functions aerobic or anaerobic?

Cardiac Muscle, Skeletal muscle, or Both.

A

Skeletal. Cardiac is Aerobic only and requires constant supply of O2.

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46
Q

Myocardium are like smooth muscles in that they are interconnected so that action potentials can rapidly spread to adjacent cells. What is the name of this characteristic?

A

Syncytial- Thus the action potential propagation and the muscle contraction occurs as a “all or none” response.

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47
Q

Name the 3 types of cardiac muscle

A
  1. Atrial muscle
  2. Ventricular muscle
  3. Excitatory and conductive muscle fibers

Atrial and ventricular muscle contract like skeletal muscle, excitatory and conductive muscle contract poorly and have fewer contractile fibrils.

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48
Q

Cell membranes separating individual cardiac muscle cells.

A

What are intercalated discs?

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49
Q

The area where intercalated discs fuse

A

Gap Junctions. (Allows for rapid diffusion of ions).

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50
Q

The heart is how many syncytiums?

A

2

  • Atrial syncytium, which constitutes the walls of the 2 atria.
  • Ventricular syncytium, which constitutes the walls of the 2 ventricles.
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51
Q

On a cellular level, name the three components of the heart.

A
  1. Cardiac muscle tissue (contracting cardio-myocytes)
  2. Conduction tissue (conducting cells)
  3. Extracellular connective tissue
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52
Q

What is a group of cardio-myocytes with its extracellular matrix (connective tissue)?

A

Myofiber

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53
Q

Myofibrils are connected to adjacent myofibrils via

A

Collagen strands

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54
Q

What 3 elements make up the structure of the myocyte?

A

Sarcolemma
Mitochondria
Sarcomere

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55
Q

What is the external membrane of the cardiac myocyte?

A

Sarcolemma

Contains ion channels, ion pumps, exchangers, G-protein coupled and other receptors, transporter enzymes and T tubules.

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56
Q

What part of the myocyte generates large amounts of high-energy phosphates?

A

Mitochondria

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57
Q

What is the fundamental contractile unit of the cardiac muscle?

A

Sarcomere

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58
Q

Cardiomyocytes are between ____um and ____um in length.

A

20um-140um. Atrial are shorter and ventricular are longer Atrial are 20 micrometers, ventricular at 140 micrometers

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59
Q

What is the rod-like bundle forming the contractile element of the cardiomyocyte?

A

Myofibril

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60
Q

The contractile proteins make up ____% of the myofibrillar protein.

A

80%

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61
Q

The ____ & _____ proteins make up the remaining 20% of the myofibrillar protein.

A

regulatory and structural

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62
Q

Separates cardiac intracellular and extracellular space

A

Sarcolemma

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63
Q

Contains ion channels, ion pumps and exchangers, G-Protein coupled and other receptors, and transporter enzymes.

A

Sarcolemma

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64
Q

The Sarcolemma is the _____ membrane of the cardiac muscle cell.

A

EXTERNAL

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65
Q

What forms specialized intracellular junctions between cells?

A

T Tubules

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66
Q

The sarcolemma surrounds the cardiomyoctes and invaginates into the myofibrils through tubular networks called…. allows for rapid, uniform impulse transmission

A

Transverse tubules (T Tubules)

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67
Q

The cardiomyocyte sarcoplasmic reticulum is subdivided into these 2 types.

A

Longitudinal and Junctional

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68
Q

Which type of SR is involved in the uptake of calcium? (helps initiate relaxation)

A

Longitudinal

think long relaxing nap

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69
Q

The junctional SR contains

A

Large calcium release channels….Ryanodine receptors (RyRs).

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70
Q

The sarcomere is the fundamental ________ unit of the myofibril.

A

contractile

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71
Q

Regarding the cardiac cycle, which of the following is FALSE.

a. LV systole has three phases
b. Isovolumic contraction occurs after mitral valve closure.
c. The decrease in ejection fraction (EF) is proportional to the decrease in LV function.
d. Isovolumic contraction occurs in both the LV and the RV.
e. Diastasis allow free blood flow through the left atrium.

A

D. True isovolumic contraction does not occur in the RV b/c of the sequential nature of inflow followed by outflow during RV contraction. See page 258, Barash for further explanation).

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72
Q

Each of the following is a characteristic of cardiac AND skeletal muscle fibers, EXCEPT?

a. both sarcolemma contain Na+ channels
b. Impulses reach the myocytes through “T transverse tubules”
c. Mitochondria are highly abundant in both types of fibers
d. Actin and myosin are the contractile proteins
e. They use transporter enzymes to regulate intracellular ion concentrations.

A

C. Unlike the skeletal muscle cell, the cardiac myocyte is densely packed with mitochondria, which are responsible for generation of large quantities of high-energy phosphates (e.g. adenosine triphosphate) that are required for the heart’s phasic cycle of contraction and relaxation.

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73
Q

Which sarcomere band contains thin filaments only, which decrease in width as the cell contracts?

A

“I” band

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74
Q

What sarcomere band is an overlap of thick and thin fibers, and lengthens as sarcomere shortens?

A

“A” band

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75
Q

What defines the border between 2 adjacent sarcomeres? (hint, each “I” band is bisected by this)

A

Z line

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76
Q

What band lies in the middle of the “A” band, and consists of thick filaments constrained by myosin-binding protein C?

A

Central “M” band

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77
Q

Found beneath the sarcolemma, wedged between the myofibrils, contain enzymes promoting ATP, and is the powerhouse of the cardiac myocyte.

A

Mitochondria

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78
Q

What part of the cardiac myocyte contains the genetic information?

A

Nucleus

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79
Q

What is the fluid-filled microenvironment of the cardiac myocyte?

A

Cytosol

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80
Q

Name the 3 different types of intercellular junctions.

A
  1. Gap junctions
  2. Spot desmosomes
  3. Sheet desmosomes
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81
Q

Which type of intercellular junction provides the mechanical linkage, has adhesion sites and anchors the filament cytoskeleton?

A

Spot desmosomes

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82
Q

Which intercellular junction anchors the contractile apparatus and is AKA fascia adherens?

A

Sheet desmosomes

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83
Q

Which type of intercellular junction is responsible for electrical coupling and transfer of small molecules between cells.

A

Gap Junctions

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84
Q

Name the 3 functional categories of the cardiomyocytes.

A
  1. Excitation system
  2. Excitation Contraction Coupling System (ECC)
  3. Contractile System
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85
Q

action potential in the muscle cell that triggers contraction, begins with depolarization and spread of the electrical excitation.

A

ECC System (excitation contraction coupling system)

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86
Q

What is the “key player” in the ECC system? Hint- electrolyte.

A

Ca++

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87
Q

Which is where cellular action potential originates in the special conduction tissue; impulses propagates to individual cells to initiate an events leading to the contraction

A

Excitation System

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88
Q

This system “basically” consists of the sarcomere

A

Contractile system

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89
Q

Which structures of the heart have “fast-response action potentials”?

A

His bundle, Purkinje system, and the Atrial and Ventricular Cardiomyocytes

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90
Q

Which structures of the heart have “slow-response action potentials”?

A

Pacemaker cells found in the SA + AV nodes

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91
Q

Which ion is responsible for establishing a resting membrane potential?

A

Potassium

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92
Q

The heart is bound anteriorly by the…

A

Sternum and costal cartilages of the third, fourth, and fifth ribs.

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93
Q

The heart is bound inferiorly by the…

A

Diaphragm.

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94
Q

Where is the “point of maximal impulse”?

A

The apex- L 5th intercostal space, midclavicular line.

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95
Q

Which heart sounds are best heard at the apex of the heart?

A

S1, S3, and S4

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96
Q

The superior aspect of the cardiac silhouette is formed by the…..

A

transverse and ascending aorta

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97
Q

The anterior surface of the cardiac silhouette is almost entirely composed of the….

A

Right Ventricle

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98
Q

The outer portion of the pericardium is called the…

A

Fibrous pericardium

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99
Q

What is the inner pericardium portions called?

A

The visceral portion, which is in intimate contact with the outer surface of the heart, and the outer parietal portions, which adheres to the fibrous pericardium.

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100
Q

The pericardial cavity is a potential space between which two layers?

A

The visceral and parietal pericardium.

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101
Q

The pericardial cavity normally contains __ - __ml (give range) of serous fluid, which provides lubrication for the free movement of the heart within the mediastinum.

A

10-25ml

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102
Q

The right coronary artery travels within this sulcus.

A

Coronary Sulcus (AV sulcus)

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103
Q

The LAD travels within this sulcus

A

Anterior interventricular sulcus.

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104
Q

What is the name of the place where the coronary and the posterior sulci meet?

A

Crux of the heart

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105
Q

What is the name of the heart’s skeleton?

A

Annulus Fibrosus

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106
Q

T/F The annulus acts as an insulator to prevent aberrant electrical conduction from the atria to the ventricles so that AV conduction moves through on pathway only: the AV node to the AV bundle (bundle of HIs)

A

TRUE

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107
Q

What is the approx. muscle thickness of the RA?

A

2mm

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108
Q

What is the name of the rudimentary valve protecting the coronary sinus?

A

Thebesian valve.

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109
Q

What is the “Gorlin” formula used to calculate?

A

Valve area (cm2)

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110
Q

Nervous innervation to heart

A

vagus
phrenic
sympathetic trunk

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111
Q

Which phase of the action potential is the “plateau phase”?

A

Phase 2- Slow Ca++ channels open and allow an influx of Ca++

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112
Q

heart receives vagal fibers via this nervous tissue

A

esophageal plexus

Left RLN

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113
Q

heart receives vagal fibers via this nervous tissue

A

esophageal plexus

Left RLN

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114
Q

these arteries provide 80% of vascular supply to pericardium from pericardial phrenic branches

A

Internal thoracic a. (left and right)

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115
Q

pericardial pain: worsens and releived by

A

worse - lies on back or left

relieved - lean forward

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116
Q

pericardial pain: worsens and releived by

A

worse - lies on back or left

relieved - lean forward

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117
Q

most lymph drainage to these ducts

A

thoracic
right lymphatic
.. also bil mediasstinal & parasternal internal thoracic lymph nodal groups

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118
Q

double layer of pericardial lymphatic vasculature surrounds the ___ pericardium and is present in ___ and loose ____ tissue

A

perietal
fat
areolar

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119
Q

this occurs when systemic and pulm pressures equalize in tamponade to prevent chamber collapse and pericardium cannot distend anymore

A 
ventricular interdependence
(also can say pulsus paradoxus)
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120
Q

define pulsus paradoxus

A

drop in SB > 10 mmHg with inspiration

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121
Q

define pulsus paradoxus

A

drop in SB > 10 mmHg with inspiration

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122
Q

becks triad

A

low bp
JVD
distand muffled heart sounds
*may not see in chronic

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123
Q

becks triad

A

low bp
JVD
distand muffled heart sounds

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124
Q

hallmark of pericardial tamponade

A

atrial & ventricular diastolic transmural pressure = 0 mmHg

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125
Q

pericardium typical max capacity

A

250 - 300 ml

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126
Q

describe filling of chambers during insp/expiration in ventricular dependence

A

inspiration: inc VR/filling to RIGHT heart bulges toward left
expiration: inc VR/filling to LEFT heart - bulges toward right

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127
Q

describe filling of chambers during insp/expiration in ventricular dependence

A

inspiration: inc VR/filling to RIGHT heart bulges toward left
expiration: inc VR/filling to LEFT heart - bulges toward right

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128
Q

how does CVP compensate for inc volume and intrapericardial pressures

A

inc CVP

maintains gradient allowing heart filling

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129
Q

What is another name for the SA node?

A

Keith-Flack Node

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130
Q

transvalvular blood flow velocities during insp and exp

A

insp: tricuspid > mitral and LV
exp: mitral and LV > tricuspid

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131
Q

What is the primary electrolyte in effect during Phase 0 of the action potential?

A

Na+ Sodium channels open and Na+ moves from the ECF to the ICF.

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132
Q

Which phase of the action potential is the “plateau phase”?

A

Phase 2- Slow Ca+ channels open and allow an influx of Ca+

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133
Q

Which phase of the action potential is the early rapid repolarization phase where the sodium gates close and the rapid influx of sodium stops and the slower influx of Ca++ begins?

A

Phase 1

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134
Q

Which phase of the action potential is the terminal repolarization phase?

A

Phase 3

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135
Q

Calcium channel blockers exert their pharmacological effects during this phase of the action potential.

A

Phase 2

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136
Q

Which phase of the action potential is the diastolic repolarization phase?

A

Phase 4

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137
Q

the flexible carilaginous (fibrous connective) structure of cardiac skeleton compose of these

A

annuli of valves
aortic & PA roots
central fibrous body
Rt & Lt trigones

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138
Q

why is left heart collapse rare

A

inc stiffness/thickness of LV

located posteriorly - not much fluid behind it

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139
Q

IF you do have LA collapse in tamponade why is this significant

A

HIGHLY SPECIFIC for tamponade

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140
Q

function of fibrous skeleton

A

valve support
prevent overstretching of valve
insertion point & anchor for muscle bundles
electrical insulation btw atria & ventricles

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141
Q

RCA in which sulcus

A

coronary sulcus

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142
Q

Circumflex in which sulcus

A

coronary sulcus

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143
Q

name location where coronary sulcus and posterior IVS meet

A

crux

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144
Q

the flexible carilaginous structure of cardiac skeleton compose of these

A

annuli of valves
aortic & PA roots
central fibrous body
Rt & Lt trigones

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145
Q

Where is the absolute refractory period lie in regards to the action potential phases?

A

Phase 0 to the middle of phase 3

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146
Q

Aortic stenosis and mitral regurgitation are (systolic/diastolic) murmurs?

A

Systolic

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147
Q

Mitral stenosis and aortic regurgitation are (systolic/diastolic) murmurs?

A

Diastolic

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148
Q

Mitral stenosis often occurs with mitral regurgitation and usually is at result what type of infection?

A

Strep

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149
Q

What murmur is a incompetent valve heard early in systole due to part of the valve prolapsing back into the atrium late in systole?

A

Mitral valve prolapse murmur

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150
Q 
in RA... valve of coronary sinus
not a true valve
semicircular fold of membrane
lies at orific of coronary sinus
varies in size or completely absent
A

Thebasian valve

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151
Q

in RA… muscular trabeculi
extend anterolaterally from Crista Terrminalis to auricle
parallel ridges in atrium walls
mainly in RA - few in LA
do not contribute much to atrial contraction
can improve ability to inc volume in RA w/o creating wall stress

A

pectinate muscles

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152
Q

function of fibrous skeleton

A

valve support
prevent overstretching of valve
insertion point for muscle bundles
electrical insulation btw atria & ventricles

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153
Q

muscle wall thickness of RA

A

2 mm

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154
Q

RA receives blood from these 4 structures

A

SVC
IVC
coronary sinus
Thebasian cardiac veins (minute valveless cardiac veins)

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155
Q

LA thickness

A

3 mm

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156
Q

only portion of LA that is trabeculated

A 
left auricle 
(longer and narrower than right auricle)
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157
Q

ventricle muscles consist of these 3 things

A

interdigitating deep sinospiral
superficial sinospiral
superficial bulbospiral

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158
Q

valve of IVC is Thebasian or Eustachain?

A

Eustachain valve

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159
Q

valve of coronary sinus is Thebasian or Eustachain?

A

Thebasian valve

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160
Q

ridge of muscle in RA (superior portion)

divides pectinate muscles and auricle from smooth surface of RA

A

crista terminalis

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161
Q

T/F
RV is highly compliant and is able to accomadate to acute changes in intraventricular volume to a greater degree than the LV

A

true

Barash 240

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162
Q 
valve of coronary sinus
not a true valve
semicircular fold of membrane
lies at orific of coronary sinus
varies in size or completely absent
A

Thebasian valve

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163
Q

collagenous band within subendocardium of RA that is part of fibrous skeleton
originates from central fibrous body

A

Tendon of Todaro

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164
Q

osteum/skeleton of coronary sinus, antero-septum leaflet commisure & tendon of Todaro
** anatomical landmark for location of AV node for EP studies, pacing **

A

Triangle of Koch

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165
Q

orientation of LV apex

A

anterior/inferior

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166
Q

LA thickness

A

3 mm

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167
Q

LV.
upper 1/3 portion is ___ endocardium.
lower 2/3 of septum are rest of ventricular wall have ____ _____

A

upper 1/3 - smooth

lower 2/3 - trabeculae carneae

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168
Q

superior RV has a ____ appearnace as it approaches pulm orifice; called _____

A

conical

infundibulum

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169
Q

infundibulum is aka

A

conus arteriosus

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170
Q

RV thickness

A

4-5 mm

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171
Q

RV relies on this for contractility

A

interventricular septum

LV

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172
Q

T/F
RV is highly compliant and is able to accomadate to acute changes in intraventricular volume to a greater degree than the LV

A

true

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173
Q

RV outflow tract =

A

infundibulum

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174
Q

how many papillary muscles in RV and what are they

A
  1. anterior (large)
  2. posterior (large)
  3. septal (smaller)
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175
Q

chordae tendineae consist of __ % collagen and __ % elastin.

A

80% collagen

20% elastin

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176
Q

orientation of LV

A

anterior/inferior

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177
Q

LV thickness

A

8-15 mm

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178
Q

normal valve area of tricuspid

A

7 cm2

< 1.5 cm2 = symptomatic

179
Q

per Stoelting, aortic valve has these 3 semilunar cusps

A

left
right
noncoronary

180
Q

how many papillary muscles in LV

A
  1. anterior
  2. posterior
    both large
181
Q

this vessel must be carefully avoided during tricuspid valve repair or replacement surgery

A

proximal right coronary artery

located in the atrioventricular groove (coronary sulcus)

182
Q

LV contracts with this direction in shift

A

anterior and to right

183
Q

this type of activation in LV causes long axis to shorten, reduce chamber diameter, and produce rotation of apex in an anterior-right direction

A

synchronous activation of LV

184
Q

standard method to calculate valve area (cm2)

A
  • Gorlin formula (done in cath lab)

- noninvasive - echo

185
Q

one of the most accurate ways of determining the presence of valvular pathology is to

A

calculate valve area

186
Q

tricuspid valves size compared to mitral

A

thinner and more translucent

187
Q

now many tricuspid leaflets

A
  1. anterior
  2. septal
  3. posterior
    unequal sizes
188
Q

normal valve area for MV and when Sx start

A

norm 4-6 cm2

sx when decreased by 1/2

189
Q

MV - two major leaflets: anteromedial and posterolateral are connected by what
- where chordae and leaflets attached

A

commisural tissue

190
Q

this is a lateral segment of myocardium stretching btw anterior and septal papillary muscles and separates the embryonic RV inflow and outflow tracts

A

moderator band

191
Q

coronary sulcus is aka

A

atrioventricular groove

192
Q

this vessel must be carefully avoided during tricuspid valve repair or replacement surgery

A

proximal right coronary artery

located in the atrioventricular groove (coronary sulcus)

193
Q

of mitral valve leaflets and names

A
  1. anteromedial (oval)
  2. posterolateral (crescent)
    -
194
Q

above (proximal) aortic valve is a dilation know as this

A

sinus of Valsalva

195
Q

normal aortic valve area and when Sx occur

A
  • 2.5 - 3.5 cm2

- reduction by 1/3 to 1/2

196
Q

MV posterior division

A

P1, P2, P3

197
Q

MV anterior division

A

A1, A2, A3

198
Q

epicardium composed of 3 things

A

mesothelium
tissue
fat

199
Q

SNS effect inc myocardial BF due to inc in metabolic demand & predominant __ receptors activation

A

beta 2

200
Q

MV - two major leaflets: anteromedial and posterolateral are connected by what

A

commisural tissue

201
Q

LAD main branches

A

diagonals
septal perforators
RV branches

202
Q

LCX main branches

A

sinus node artery (40-50%)
obtuse marginal
posterolateral

203
Q

What is a normal LV pressure?

A

100-140/3-12 mmHg

204
Q

LCA supplies these areas

A

LA
most of IV septum
LV (septal, anterior & lat walls)

205
Q

What is a normal PCW (PAOP)?

A

6-12 mmHg

206
Q

in this artery the coronary BF is continuous throughout cardiac cycle

A

Right coronary flow - reaches peak during systole bc RV pressures remain low and cause minimal compression

207
Q

What is a normal LAP?

A

4-12 mmHg

208
Q

for MV, the primary and secondary chordae are attached to what? whereas, the teriary chordae insert into..

A

leaflet edges

distal posterior leaflet or myocardium adjacent to annulus

209
Q

each semilunar valve has __ leaflets

A
  • 3

- translucent and macroscopically avascular

210
Q

Bundle of His blood supply

A

dual BF from PDA & LAD

211
Q

which papillary muscles are vulnerable to ischemic dysfunction

A

posteromedial (PDA) because coronaries taper here in the myocardium (poorer blood supply). yet LCX will contribute some BF to posteromedial muscle regardless of dominance

212
Q

above aortic valve is a dilation know as this

A

sinus of Valsalva

213
Q

how do PM branch to chords and so on

A

1 PM = 6 heads
1 head = 12 chordae tendineae
head = “fingers”

214
Q

Sinuses of Valsalva of SL valves have ___ flow which prevents adherence of valve leaflets & aids closure (prevents occlusion of coronary ostia)

A

hydraulic

215
Q

these cardiac veins traverse the myocardium & drain into RA (40%), RV & LV (lesser extent). Also may carry 40% of blood returned to RA

A

Thebasian veins (little dudes)

216
Q

epicardium composed of 3 things

A

mesothelium
tissue
fat

217
Q

SNS effect inc myocardial BF due to inc in metabolic demand & predominant __ receptors activation

A

beta 2

218
Q

activation of SNS results in mobilization of these substances for energy use by myocardial cells.

A

fat-free acids

glycogen

219
Q

The electrical discharge during a cardioversion is timed to coincide with ________ wave
P, Q, R, S, or T?

A

R wave

220
Q

vagal innervation

sympathetic innervation

A

v - supraventricular
v - Purkinje
SNS - everywhere

221
Q

preganglionic PNS fibers originate here

A

medulla

222
Q

RCA supplies these areas (about 9)

A 
SA &amp; AV nodes
RA &amp; RV
posterior 1/3 of interventricular septum
medial portion of posterior wall
part of LV (inferior wall)
posterior fascicle of LBB
internal septum
223
Q

cell differences in conduction system

A

variable in shape
fewer myofibrils
pale staining of cytoplasm

224
Q

LCX branches

A

sinus node artery (40-50%)
obtuse marginal
posterolateral

225
Q

example of an accessory pathway that can bypass AV node, go thru skeleton, and establish conduction btw atria and ventricles

A

Bundle of Kent = supraventricular tachyarrhythmias as in WPW syndrome

226
Q

Hypokalemia _____ resting membrane potential, while Hyperkalemia ______ resting membrane potential.

A

hypokalemia decreases, hyperkalemia increases.

227
Q

SA node: 2 cell types

A

P cells = pacemaker = pale & ovoid, large round nuclei

Intermediate = transitional = elongated, conduct impulses

228
Q

obstruction in these branching arteries of LAD (go across anterior wall of LV - can be large) can produce significant damage

A

diagonals

229
Q

LCA supplies these areas

A

LA
most of IV septum
LV (septal, anterior & lat walls)

230
Q

in LCA dominant population (__ to __ %) this artery supplies the PDA

A

10-15 %

LCX

231
Q

part of conduction system with mostly transitional myocytes (on histology) and insulated with sheath of connective tissue

A

AV bundle (Budle of His)

232
Q 
The most important ion currents during the ventricular action potential phases:
Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
A 
Phase 0: Sodium In
Phase 1:  Chloride In
Phase 2: Calcium In
Phase 3: Potassium Out
Phase 4: Sodium Out
233
Q

duration of S1 and S2

A

S1 - 0.14

S2 - 0.11

234
Q

split S2 may be heard d/t

A
  • aortic valve closes sooner
  • physiologically - P2 (pulm valve closure) is later on inspiration - normal
  • best heard in young/pulmonic area
  • on inspiration inc VR to RH + dec VR to LF = Aortic v. closes earlier bc of dec blood volume in LV
235
Q

disease states with paradoxical split S2

A
  • aortic stenosis
  • hypertropic obstructive cardiomyopathy
  • LBBB
236
Q

Bundle of His blood supply

A

dual BF from PDA & LAD

237
Q

which papillary muscles are vulnerable to ischemic dysfunction

A

posteromedial (PDA) because coronaries taper here in the myocardium

238
Q

Which muscles last to be perfused

A

LV papillary

239
Q

diseases with S4 sound

A

older patient with LVH (noncompliant ventricle)
diastolic heart failure
active ischemia

240
Q

physiologically, S4 is due to this

A

during active LV filling (e.g. atrial contraction) blood is forced into a noncompliant LV - thus the sound of blood striking the noncompliant LV

241
Q

S3 + S4 =

A

summation gallop

242
Q

speed of conduction

A

dromotropic

243
Q

inc SNS causes inc in HR which is a __ effect on heart

A

chronotropic

244
Q

activation of SNS results in mobilization of these substances for energy use by myocardial cells.

A

fat-free acids

glycogen

245
Q

What is another name for the SA node?

A

Keith-Flack Node

246
Q

how does SNS stimulation effect the AV node ERP (effective refractory period) and PR interval

A
  • decreases

- vagal stimulation does the opposite (ur welcome)

247
Q

description of murmur sounds

A

harsh
blowing
musical
rumbling

248
Q

preganglionic PNS fibers originate here

A

medulla

249
Q

The SA and AV have action potentials a longer plateau than the ventricular. T/F

A

False- The SA and AV do not have plateau phases.

250
Q

diseases with holosystolic finding

A

mitral regurge

tricuspid regurge

251
Q

disease with early diastolic; blowing or swishing

A

aortic regurge

252
Q

how can you identify internodal pathways clinically

A

EP study

* not myocyte histology (rare)

253
Q

example of an accessory pathway that can bypass AV node, go thru skeleton, and establish conduction btw atria and ventricles

A

Bundle of Kent = supraventricular tachyarrhythmias

254
Q

causes of aortic regurge

A 
rheumatic
endocarditis
aortic disease (Marfan syn - connective tissue)
syphyllis
ankylosing spondylitis
aortic dissection
cardiac trauma
255
Q

SA node: 2 cell types

A

P cells = pacemaker = pale & ovoid, large round nuclei

Intermediate = transitional = elongated, conduct impulses

256
Q

The LAD provides blood supply to which structures?

A 
Anterior Interventricular septum
Apex of the Heart
L+R Bundle Branches
Anterolateral Wall
Papillary muscles of the MITRAL Valve.
257
Q

prominent artery of SA which is a branch of RCA

A

conus artery

258
Q

this part of conduction system is located in atria, is a preferential pathway btw SA and AV, composed of packed parallel myocarial fibers large pale-staining cells witih perinuclear clear zone, large nuclei, have transitional cells and spare myofibrils

A

internodal tracts

259
Q

part of conduction beneath endocardium on right side of atrial septum, multiple nerve endings including vagus, causes delay in AP transmission

A

AV

260
Q

part of conduction system with mostly transitional myocytes (on histology) and insulated with sheath of connective tissue

A

AV bundle (Budle of His)

261
Q

determinants of both supply and demand

A

HR

EDP

262
Q

duration of S1 and S2

A

S1 - 0.14

S2 - 0.11

263
Q

split S2 may be heard d/t

A

aortic valve closes sooner

264
Q

factors responsible for coronary autoregulation

A 
myocardial consumption
metabolic vasodilation (SNS, adenosine - primary vasodilator substance)
265
Q

What structures does the RCA supply?

A 
Posterior Interventricular Septum
Posterior Left Bundle Branch
Interatrial Septum
And...most of the time...
AV node in 90% of population
SA node in 60% of population
266
Q

disease states with paradoxical split S2

A
  • aortic stenosis
  • hypertropic obstructive cardiomyopathy
  • LBBB
267
Q 
Match the structures with the coronary artery that supplies it.  
Apex
AV Node
L atrial wall
(RCA, LCX, LAD)
A

Apex-LAD
AV Node- RCA
L atrial wall- LCX

268
Q

features of cardiac t-tubule that make it different from skeletal t-tubule

A

cardiac: larger, broader, fewer #

269
Q

when is S3 (sound at the beginning middle third of diastole) normal and abnormal

A

normal - children and adolescents

heart failure in older

270
Q

best patient position for S3

A

left lateral

271
Q

in ECC, transient Ca++ removed by these 3 ways

A
  1. active uptake into SR
  2. Na Ca exchanger
  3. binding of Ca to proteins
272
Q

diseases with S4 sound

A

older patient with LVH
diastolic heart failure
active ischemia

273
Q

what are the three types of ryanodine receptors

A

RyR1 - skeletal
RyR2 - heart
RyR3 - brain

274
Q

About how thick is the walls of the Right Ventricle?

A

4-5mm

275
Q

About how thick is the walls of the Left Atrium?

A

3mm

276
Q

contractile apparatus: 6 major componenets

A

myosin
actin
tropomyosin
3 - protein troponin complex

277
Q

How many papillary muscles in the LV?

A

Dos (anterior and posterior)

278
Q

How many papillary muscles in the RV?

A

3

279
Q

by itself, ____ is a weak inhibitor of actin-myosin interaction.. add _____, it becomes a major inhibitor

A

troponin I

tropomyosin

280
Q

What is the normal surface area of the Tricuspid Valve?

A

7 cm2

281
Q

RMP determined by these factors/forces

A
  1. chemical (ion diff btw cell membrane)
  2. electrostatic (i.e. negative pulls K+ ion into cell)
  3. Na+/K+ pump
282
Q

this equation calculates equilibrium potential if conc gradient is known and temp is 310 degrees Kelvin

A

Nernst =

Em = (-61.5/FZ) x log [K]i / [K]o

283
Q

Normal surface area of the Mitral Valve?

A

4-6 cm2

284
Q

3 factors affect the calculation due to different ions in RMP

A
  1. electric charge of each ion
  2. permeability of the membrane to each ion
  3. con gradient across membrane
285
Q

this extra heart sound is during early diastole, high pitch, sharp snap or click, not affected by respiration; early mitral stenosis

A

MV opening snap

286
Q

AP of cardiac muscle caused by opening of 2 types of channels. And.. are they fast or slow

A
  1. voltage-activated FAST Na - open/close fast
  2. L-type Ca SLOW - open slow/open longer - this prolongs depolarization = plateau phaase. Once slow Ca/Na ch closes. Rapid K out of cell = immediately restore RMP
287
Q

plateau duration of atrial and also ventricular

A

a - 0.2 sec

v - 0.3 sec

288
Q

characteristics of murmurs depend on these factors

A 
valve function
size of opening
rate of blood flow
vigor of myocardium 
thickness/consistency of tissue
289
Q

causes of murmurs

A 
high output demand
dim strength of conraction
vigorous LV ejection
persistent fetal circ - PDA 
(there are more - these stood out)
290
Q

description of murmur sounds

A

harsh
blowing
musical
rumbling

291
Q

disease with low frequency; diastolic rumble

A

mitral stenosis

292
Q

disease with midsystolic (ejection); med pitch; harsh

A

aortic stenosis

293
Q

phase 4 back to RMB at __ mV

A

-90 mV

294
Q

phase of AP that CCB work on

A

phase 2
less Ca channel influx (less contraction) and more K efflux (cell more negative - resting) to bring to relaxation sooner i suppose

295
Q

Dig effect on ion channels

A

inhibits Na/K = more Na intra cell
= more Ca intra cell
= inc contractility

296
Q

this disease with systolic ejection murmur almost always due to congenital

A

pulmonic stenosis

297
Q

cause of MR

A

rheumatic fever
MI
myxoma - tumor of connective tissue
rupture of chords

298
Q

velocity of signal conduction (atrial and ventricular)

A

a and v muscle fibers = 0.3 to 0.5 m/sec

purkinje = up to 4 m/sec

299
Q

2 determinants of coronary perfusion (things that vary)

A

CPP - LV blood supply directly depended on CPP

CVR - supply inversely related to resitance to flow - Poiseuille’s Law

300
Q

2 determinants of coronary perfusion (relatively constant)

A

vessel length

viscosity

301
Q

CPP usually determined by the diff btw ___ and ___ presssure

A

aortic

ventricular (LVEDP)

302
Q

SA node and other automatic cells have these phases of AP

A

phase 4
phase 0
phase 3
(phase 1 and 2 do not occur bc rapid depo does not occur)

303
Q

HR BMP for AV node and ventricular cells

A

AV 40-60

v 15-30

304
Q

infuencing fx of mycardial O2 demand

A

64% pressure work
20% metabolic requirements
15% volume work
1% electrical activity

305
Q

cardiac cycle lasts from

A

beginning of one beat to beginning of next

306
Q

the difference btw pulmonary arterial blood and coronary sinus

A

O2 extraction

307
Q

coronary BF determined primarily by

A

myocardial consumption

308
Q

factors responsible for coronary autoregulation

A 
myocardial consumption
metabolic vasodilation (SNS, adenosine - primary vasodilator substance)
309
Q

3 ways to optimize CPP

A
  1. low HR (avoid tachycardia)
  2. normal to high diastolic pressure (avoid hypotension)
  3. low LVEDP (avoid hypertension)
310
Q

this layer of heart is subjected to greater intramural pressures during systole and is is most vulnarable to ischemia during decreases in CPP

A

endocardium

311
Q

desmosomes are formed by ___ ___ in cell membranes linked by filaments

A

protein plaques

312
Q

features of cardiac t-tubule that make it different from skeletal t-tubule

A

cardiac: larger, broader, fewer #

313
Q

thin fibers of sarcomere contain these

A

actin
tropomycin
troponin C (complex)

314
Q

thick fibers of sarcomere contain these

A

mysoin

supporting proteins

315
Q

in ECC, transient Ca++ removed by these 3 ways

A
  1. active uptake into SR
  2. Na Ca exchanger
  3. binding of Ca to proteins
316
Q

cardiac SR compared to skeletal and implication for contraction

A

less developed than skeletal - rely on T-tubule release of Ca, otherwise contraction would be weak

317
Q

what are the three types of ryanodine receptors

A

RyR1 - skeletal
RyR2 - heart
RyR3 - brain

318
Q

2 storage proteins in SR

A

calsequestrin

calreticulin

319
Q

this important protein senses and regulates iCa++

A

calmodulin

320
Q

contractile apparatus: 6 major componenets

A

myosin
actin
tropomyosin
3 - protein troponin complex

321
Q

light chains of myosin have 2 roles

A
  1. regulatory - modulate myosin-act interaction

2. essential - undefined myosin activity

322
Q

double stranded helical chain of G-actin monomer

A

F-actin

323
Q

by itself, ____ is a weak inhibitor of actin-myosin interaction.. add _____, it becomes a major inhibitor

A

troponin I

tropomyosin

324
Q

summarize cross bridge cycling (C-BC)

A

-Ca++ released binds with Top C (C-BC starts)
-this decreases interaction btw Trop I + actin
(trop I covers up/inhibits actin so mysoin cant attach)
- once exposed mysoin binds to actin (facilitated via ATP hydrolysis + change in myosin head confirmation)
-power stroke of myosin head generated

325
Q

RMP determined by these factors/forces

A
  1. chemical (ion diff btw cell membrane)
  2. electrostatic (i.e. negative pulls K+ ion into cell)
  3. Na+/K+ pump
326
Q

this equation calculates equilibrium potential if conc gradient is known and temp is 310 degrees Kelvin

A

Nernst =

Em = (-61/FZ) x log [K]i / [K]o

327
Q

equilibrium potentials of ions Na, K, Chl, Ca…and go..

A 
intra cell // extra cell // equilib pot
Na -- 10  145  60
K    -- 135  4  -94
Cl   -- 4   114   -97
Ca  -- 0.0010  2   132
328
Q

3 factors affect the calculation due to different ions in RMP

A
  1. electric activity of each ion
  2. permeability of the membrane to each ion
  3. con gradient across membrane
329
Q

membrane potential equilibrium of K+ =

A

-90 mV

slide on K+ equilibrium potential

330
Q

AP of cardiac muscle caused by opening of 2 types of channels. And.. are they fast or slow

A
  1. voltage-activated FAST Na - open/close fast
  2. L-type Ca SLOW - open slow/open longer - this prolongs depolarization = plateau phaase. Once slow Ca/Na ch closes. Rapid K out of cell = immediately restore RMP
331
Q

plateau duration of atrial and also ventricular

A

a - 0.2 sec

v - 0.3 sec

332
Q

anti-arrhythmic that has inhibitory effect on phase 0 of cardiac muscle AP

A

lidocaine

decreases Na influx

333
Q

phase 0 Na channels open btw __- __ mV threshold potential

A

-70 & -65 mV

334
Q

phase 0 __ mV is the membrane potential that is reached

A

+20 mV

335
Q

phase 1 fast Na channels close at __ mV

A

+2 to +3 mV

336
Q

phase 2 slow Ca open at __ to __ mV

A

-30 to -40 mV

337
Q

phase 4 back to RMB at __ mV

A

-90 mV

338
Q

phase of AP that CCB work on

A

phase 2
less Ca channel influx (less contraction) and more K efflux (cell more negative - resting) to bring to relaxation sooner i suppose

339
Q

Dig effect on ion channels

A

inhibits Na/K = more Na intra cell
= more Ca intra cell
= inc contractility

340
Q

absolute refractory period (time) in ventricles

A

0.25 to 0.3 sec

this is close to duration of plateau time of AP

341
Q
  • time of relative refractory period (i suppose the total)

- time of atrial and also ventricle RR

A 
RR = 0.5 sec
atrial = 0.15 sec
ventr = 0.25 - 0.30 sec
342
Q

velocity of signal conduction (atrial and ventricular)

A

a and v muscle fibers = 0.3 to 0.5 m/sec

purkinje = up to 4 m/sec

343
Q

SA node AP characteristics of myocardium

A

contractility
automaticity
conductivity

344
Q

SA node has lower/higher RMP

A

higher

345
Q

SA node more permeable to which ion = more than other atrial myocardial cells which is capable of raising MP close to threshhold pot (-55 to -60) that CAN INITIATE AP.

A

sodium

346
Q

SA node adn other automatic cells have these phases of AP

A

phase 4
phase 0
phase 3
(phase 1 and 2 do not occur bc rapid depo does not occur)

347
Q

HR BMP for AV node and ventricular cells

A

AV 40-60

v 15-30

348
Q

time of delay of impulse from atria to ventricles

A

> 0.1 sec

349
Q

cardiac cycle lasts from

A

beginning of one beat to beginning of next

350
Q

duration of sys or diastole with HR = 72

answer in min/beat and sec/beat

A

reciprocal of HR
1/72 = 0.0139 min/beat
0.0139 x 60 sec = 0.833 sec/beat

351
Q

during tachycardia compare dec in duration of systole to diastole

A

dec in diastole > dec in systole time

352
Q

phases of diastole

A

prodiastole - SL valves close
isovolumetric relaxation
rapid v-filling

353
Q

during isovolumetric relaxation of diastole this relaxation occurs during phases 2 - 4 of AP. give duration as well.

A

auxotonic relaxation

0.03 - 0.06 second

354
Q

early filling of ventricles accounts for how much % of final SV

A

70-75%

355
Q

period of diasole. aka time of “slow fillling”

… and how much % of total SV

A

diastasis

<5%

356
Q

aka for atrial kick, what wave on ECG, how much of final SV

A

final filling
P-wave (that was a hard one)
15-25% (20-30% per NH)

357
Q

6 factors influencing diastolic function

A
  1. magnitude of systolic volume
  2. passive LV chamber stiffness
  3. elastic recoil of ventricles
  4. diastolic interaction btw RV and LV
  5. atrial properties
  6. prescense of CATs
358
Q

** primary cause of heart failure w/ normal EF **

A

LV diastolic dysfunction

aka diastolic HF

359
Q

common causes of lV diastolic dysfunction (bunch of em)

A

> 60 yo
acute MI
stunning, hibernation
remodeling
pressure-overlaod hypertrophy (aortic stenosis, HTN)
volume-overload hypertophy (regurge)
hypertrophic obstructive cardiomyopathy
dilated cardiomyopathy
restrictive cardiomyopathy (amyloidosis, hemochromatosis)
pericardial disease (tamponade, constrictive pericarditis)

360
Q

determinants of ventricular diastolic fx (bunch)

A 
rate and rhythm
LV sys fx
wall thickness
chamber geometry
myocyte relaxation factors
LV untwisting/recoil
diastolic suction magnitude
LA-LV pressure gradient
passive elastic properties of LV myocardium
viscoelastic effects (rapid LV fill, atrial systole)
LA &amp; MV structure and fx
pulm venous blood flow
pericardial restraint
RV loading conditions and fx
ventricular interdependence
CBF and vascular engorgement
compression by mediastinal masses
361
Q

ventricular ejection phases

A
  1. rapid - first 1/3

2. reduced - last 2/3

362
Q

(systolic fx slide) 3 factors combine with HR and rhythm to determine CO

A
  1. preload
  2. afterload
  3. contractility
363
Q

normal LV pressure during filling

A

10 mm Hg

364
Q

normal volumes: give em to me (EDV, SV, ESV, EF)

A

EDV 110 - 120 ml
SV 70 ml
ESV 40-50 ml
EF 60%

365
Q

all the waves of atrial pressures

A

a - atrial
c - TV closure (begin of v-contraction) - main cause of bulging of AV into atria.
v - passive a - filling (ending of v-contraction)
x - atrial diastole (trough of pressure)
y - atrial emptying (opening of TV)

366
Q

RAP and LAP pressures inc during atrial contraction (a wave)

A

RAP inc 4-6 mmHg

LAP inc 7-8 mmHg

367
Q

pressure norms: RV, LV, PAP, PCW (PAOP), CVP, RAP, LAP

A 
RV 15-30/2-8
LV 100-140/3-12
PAP 15-25/8-15
PCW (PAOP) 6-12
CVP 3-8
RAP 2-6
LAP 4-12
368
Q

describes ventricular ejection

A

systolic upstroke

369
Q

describes max pressure during systolic ejection

A

peak systolic press

370
Q

describes rapid decline in atrial press as ventricular contraction ends

A

systolic decline

371
Q

describes roughly the area under the arterial curve

A

MAP

372
Q

describes closing of aortic valve

A

dicrotic notch

373
Q

aka dicrotic notch

A

incisora

374
Q

preload formula using PCW + PAD & based on what law

A

(LVEDP x LVEDR) / 2h
h= thickness of ventricle
Laplace (pressure x radius)/2x wall thickness

375
Q

noninvasive ways to measure LVEDV

A

radionuclide angiography

dynamic MRI

376
Q

4 components determine LV afterload

A
  1. aortic compliance
  2. total arterial resistance
  3. LVES wall stress
  4. SV
377
Q

formula to estimate LV afterload

A

SVR = [80(MAP - RAP)]/CO

clinically can use SBP if aortic stenosis not present

378
Q

RV afterload (RVA) compared to LV afterload

A

pulm-arterial circ more compliant (RVA)

RV more sensitive to changes in afterload (maybe bc not as strong as LV)

379
Q

LV diastolic pressure immediately before contraction (LV pressure loop)

A

diastolic pressure curve

380
Q

systolic pressure achieved during contraction

A

systolic pressure curve

381
Q

EF value assoc with significant LV impairment

A

EF < 40%

norm (60-70%)

382
Q

percentage of EDV ejected durign systole

A

EF

383
Q

CI and CO formula

A 
CI = CO/BSA
CO = HR x SV
384
Q

CO determined by 4 factors:

A

intrinsic: HR & contractility
extrinsic: preload & afterload

385
Q

norm CO and CI

A

Co ~ 5 L/min

CI ~ 2.5 L/min/sqm surface

386
Q

what does ol Frank Starlin say about CO

A
  • change in intrinsic contractile performance is based on changes in preload.
  • inc preload = greater contractility force
387
Q

preload can exist in these two ways

A

passive (flow from atria)

active (atrial contraction)

388
Q

CO formula accoring to Fick principle (which assumes normal resp fx)

A 
CO = VO2/(Ca - Cv)
VO2 = O2 consumption in ml/min
Ca = arterial O2 content
Cv = venous O2 content
389
Q

oculocardiac reflex via what efferent and afferent nerves

A

5 and dime
tri - afferent
vagus - efferent

390
Q

traction on mesentery or gall bladder, or stimulation of vagus in other areas of body such as thorax/abdoment = bradycardia hypotension apnea

A

celiac reflex

391
Q

“atrial stretch reflex” - increased volume of blood in heart.. SNS stimulation causes inc HR

A

Bainbridge reflex

392
Q

(reflex) inc ICP -> SNS stimulation cause vasoconstriction in attempt to decrease ICP

A

Cushing reflex

393
Q

chemoreceptors located in these two sites - response to hypoxia, hypercarbia and acidosis

A

central - medulla

peripheral - carotid /aortic bodies

394
Q

does wave of atrial recovery exist?

A

“too small”

395
Q

duration of QRS

A

0.7 - 0.11 sec

396
Q

characteristics of pathological q wave

A

> 1mm wide
2 mm deep
25 % of QRS size
present in V1-3

397
Q

QT normal if

A

when 1/2 of R to R interval at normal rates

398
Q

describe PR interval

A

p wave to QRS

399
Q

describe RP segment

A

end of P to QRS

400
Q

describe QRS interval

A

time from beginning to end of ventricular contraction

401
Q

describe ST segment

A

end of ventricular activation (end of S) & begin of recovery (beg of T)

402
Q

describe J point

A

junction of QRS & ST segment

403
Q

describe QT interval

A

activation to recovery (beg of Q to end of T)

404
Q

reasons for ST segment elevation

A

ischemia
pericarditis
aneurysma cordis
normal variant

405
Q

reasons for ST depression

A 
ischemia
LVH
digitalis
low K+/low Mg+
neurologic
406
Q

causes of T-wave changes

A 
ischemia
pericarditis
myocarditis
LVH/RVH
electrolyte changes (esp K+)
407
Q

significant ST depression

A

> 0.5mm

408
Q

significant ST elevation in standard vs precordial leads

A

standard > 1mm

precordial > 2mm (healthy young black american > 4mm)

409
Q

cause of … depressed upsloping ST, low T wave , prominent U wave

A

low K+

410
Q

cause of … depressed , upsloping ST, “tent-like” symmetric wide T wave, apparent long QT

A

low K+ with T-U fusion, the most common pattern,

411
Q

cause of … wide QRS, horizontally depressed ST, low T wave amp, prominent U, long QT

A

class Ia drug: quin, proc, diso

412
Q

cause of … bowl-shape ST seg, low amp T wave, prominent U wave, short QT int

A

Digitalis

413
Q

cause of … “checkmark” shaped ST seg, T low to absent, 1 degree A-V bloc, QT int short

A

Digitalis (possible toxicity)

414
Q

cause of … long, straight ST seg, normal T, long QT int

A

low Ca+

415
Q

cause of … abbreviated ST segment, short or normal QT

A

high Ca+

416
Q

ECG: arrow pointing direction of electrical potential

A

vector

417
Q

mean QRS vector in degrees

A

+59

418
Q

ECG (axis): length of arrow =

A

voltage of electrical potential

419
Q

sum of vectors generating potential at one particular instant is called

A

instantateous mean vector

420
Q

3 standard limb leads + 3 augmented leads is referred to as this system

A

Hexaxial reference system

421
Q

3 things that cause LAD (left axis dev) in 90% of folks

A

normal varient
mechanical shift of heart
LVH

422
Q

other causes of LAD (left axis dev)

A 
LBBB
LAFB (left ant fascicular block)
congenital HD (eg ASD)
high K+
inferior MI
preexisting syndromes (eg WPW)
ventricular rhythm
pacemaker rhythm
423
Q

causes of RAD (right axis)

A 
normal
mechanical shifts
RVH
RBBB
LPFB (Left post fascicular block)
dextrocardia (heart apex points to right)
ventricular rhythm
lateral wall MI
preexcitation syndrome (WPW)  
right heart strain (Cor Pulmonale, PE)
424
Q

indeterminate axis causes (no mans land - “northwest axis”)

A

ventriular rhythms
paced rhythms
lead misplacement
some congenital

425
Q

2 most important risk factors for atherosclerosis

A

male

inc age

426
Q

often 1st sx of HD

A

angina pectoris
acute MI
sudden death (dysrhythmia)

427
Q

“other causes of CAD”

A

CVA
PVD (undocumented CAD)
menopause
estrogen contraception (esp. smoking)

428
Q

most common cause of stable MI (angina pectoris)

A

atherosclerosis

429
Q

max compensatory dilation how much occusion % reached

A

70%

BF only adequate at rest

430
Q

ischemia releases these substances

A

adenosine
bradykinin
“other substances”

431
Q

cardiac causes of acute CP

A

angina
rest or unstable angina
actute mi
pericarditis

432
Q

vascular causes of acute CP

A

aortic dissection
PE
pulm HTN

433
Q

pulmonary causes of acute CP

A

pleuritis/pneumonia
tracheobronchitis
spontaneous pneumo

434
Q

GI causes of acute CP

A 
reflux
esophageal spasm - severe substernal pressure
peptic ulcer
chole
pancreatitis
435
Q

Musculoskeletal causes of acute CP

A

costochondritis
cervical disk disease
trauma or strain

436
Q

infection causes of acute CP

A

herpes zoster

437
Q

phych causes of acute CP

A

panic

438
Q

characteristics that rarely cause myocardial ischemia

A

sharp pain x few seconds

dull ache x hours

439
Q

causes of angina / ischemic HD not related to lesion

A

spasm
vasculitis
trauma
ventricular hypertrophy

440
Q

ace-inhibitors assist in what after MI

prescribed to what comorbidity patients

A

ventricular remodeling

DM, HF

441
Q

coronary spasm w/ w/o plaque

A

printzmetal

occurs usually at night, 5-15 min, ST elev during attack

442
Q

cause of printzmetal

tx

A

cold weather, stress, smoking!!!! (major), cocaine and vasoconstrictors. TREATMENT - Ca+ antagonist & nitrates

443
Q

onset, frequency and duration of unstable angina

A

sudden inc severity
> 3x/day
> 30 min

NUR 942 Thurman (6 decks)

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