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1230 Testing (Semester 2) > Cardiac Test > Flashcards

Cardiac Test Flashcards

1
Q

Cardiac Ischemia ASA Conditions

A

Age: > or equal to 18
LOA: Unaltered
Other: Able to chew and swallow
Everything else is N/A

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2
Q

Cardiac Ischemia ASA Contraindications

A

Allergy or sensitivity to NSAIDs
If asthmatic, no prior use of ASA
Current active bleeding
CVA (stroke) or TBI (traumatic brain injury) in the previous 24 hours

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3
Q

Cardiac Ischemia ASA Dosing

A

Route: PO (by mouth)
Dose: 160-162 mg
Max. Single Dose: 162 mg
Dosing Interval: N/A
Max. # of Doses: 1

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4
Q

Cardiac Ischemia Nitroglycerin Conditions

A

Age: > or equal to 18
LOA: Unaltered
HR: 60-159 bpm
SBP: Normotension
Other: Prior history of nitroglycerin use OR IV access obtained

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5
Q

Cardiac Ischemia Nitroglycerin Contraindications

A

Allergy or sensitivity to nitrates
Phosphodiesterase inhibitor use within the previous 48 hours
SBP drops by one-third or more of its initial value after nitroglycerin is administered
12-lead ECG compatible with Right Ventricular MI

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6
Q

Cardiac Ischemia Nitroglycerin Dosing - No STEMI

A

SBP: > or equal to 100 mmHg
Route: SL (sublingual, beneath the tongue)
Dose: 0.3 mg or 0.4 mg
Max. Single Dose: 0.4 mg
Dosing Interval: 5 min
Max. # of Doses: 6

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7
Q

Cardiac Ischemia Nitroglycerin Dosing - STEMI

A

Do NOT administer nitroglycerin if patient has RVI
SBP: > or equal to 100 mmHg
Route: SL (sublingual, beneath the tongue)
Dose: 0.3 mg or 0.4 mg
Max. Single Dose: 0.4 mg
Dosing Interval: 5 min
Max. # of Doses: 3

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8
Q

Systemic Circulation

A

To the body
Left side of heart

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9
Q

Pulmonary Circulation

A

To the lungs
Right side of heart

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10
Q

Pericardial Cavity

A

Space filled with fluid (approx.10-15 mls)

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11
Q

Pericardial Sac

A

Double layered closed sac that surrounds and anchors the heart

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12
Q

Pericardium

A

Loose fitting, inextensible
Fibrous pericardium outside
Serous pericardium inside 2 layers

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13
Q

Outer Layer of Pericardium

A

Tough fibrous layer attached to the diaphragm, inner surfaces of the sternum and vertebral column

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14
Q

Inner Layer of Pericardium

A

Thin outer layer of heart wall

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15
Q

Serous Membranes (Part of Pericardium)

A

Secrete fluid to lubricate the membranes to reduce friction during contraction

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16
Q

3 Layers of the Heart Wall

A

Endocardium (inner)
Myocardium (middle)
Epicardium (outer)
Pericardium surrounds all layers and encloses the coronary vessels

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17
Q

Epicardium

A

Outer layer of the heart
Thin membrane attached to the outer surface of the myocardium.
Blood vessels that nourish the heart are inside the pericardium.

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18
Q

Myocardium

A

Sandwiched between the 2 layers of membranes (middle layer)
Thickest wall of the heart
Contraction of the myocardium provides the force that pumps the blood through the blood vessels

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19
Q

Endocardium

A

Single layer of the squamous epithelium on the internal surface of the myocardium.
Lines the chambers of the heart
Continuous with the internal lining of the blood vessels attached to the heart.

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20
Q

Heart Valves

A

Pulmonary, aortic, bicuspid, tricuspid

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21
Q

Heart Vessels

A

Aorta, pulmonary arteries and veins, superior and inferior vena cava

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22
Q

Pulmonary Arteries

A

Carry deoxygenated blood away from the heart, to the lungs.

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23
Q

Aorta

A

Carries oxygenated blood away from the heart, to the rest of the body.

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24
Q

Atria

A

Only job is to pump blood to the ventricles
2 superior chambers, right and left
Receive blood from the veins
Walls are relatively thin - they don’t need to generate much impulse as they are only moving blood a small distance to the ventricles.

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25
Q

Ventricles

A

2 lower chambers of the heart
Considered to be the primary “pumping chambers” as they are responsible to pump the blood out of the heart
Walls are thicker as a result of this
Myocardium of the left ventricle is thicker than the right as it is responsible to push blood to the entire body.

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26
Q

Atrioventricular (AV) Valves

A

Formed of fibrous connective tissue
2 AV Valves - mitral (bicuspid) and tricuspid
Allows blood from the atrium to the ventricles but not back

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27
Q

Tricuspid Valve (AV Valve)

A

Right side, 3 cusps of tissue from the fibrous tissues that separate the atria and ventricles

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28
Q

Bicuspid Valve (AV Valve)

A

A.K.A Mitral valve
Left side, between the left atria and left ventricle; 2 cusps
Strands of tissue - called the chordae tendineae - extend from the cusps to the papillary muscles (located in the walls of the ventricles).
Prevent the valves from being forced into the atria during ventricular contraction.
They are just the right length to allow the cusps to close and seal tightly.

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29
Q

Semilunar Valves

A

In the bases of the large arteries that carry blood from the ventricles.
2 in the arteries leaving the heart:
1) Pulmonary: at the opening between the right ventricle and the pulmonary trunk.
2) Aortic Semilunar Valves: at the opening between the left ventricle and the aorta
3 pocket like cusps (half moon shaped) allow blood to exit the ventricles and prevent blood flow back into the ventricles.

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30
Q

Left Coronary Artery

A

Originates at the left cusp of the aortic valve.
Divides into the left anterior descending artery (anterior interventricular)
Supplies 65-75% of the blood supply to the left ventricle and septum
Oxygenation and nourishment to the myocardial cells

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31
Q

Right Coronary Artery

A

Originates at the right cusp of the aortic valve
Divides into the right marginal artery and posterior interventricular artery
Supplies 25-35% of the blood supply to the left ventricle and all of the right ventricle

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32
Q

Contraction and Relaxation

A

Contraction - systole
Relaxation - diastole
Atria and ventricles contract alternately. Both relax between beats (left and right atria pump at the same time and left and right ventricle pump at the same time; ventricles pump while atria contract)

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33
Q

Cardiac Cycle Steps

A
  1. Blood enters the heart via the vena cava, enters the right atrium
  2. Goes through the tricuspid valve into the right ventricle
  3. The deoxygenated blood then leaves the heart through the pulmonary artery.
  4. The blood then goes to the lungs to get oxygenated.
  5. Back into the pulmonary veins - towards the heart
  6. Into the left atrium (oxygenated now).
  7. Through the mitral valve
  8. Into the left ventricle
  9. Out the aorta and to the body/organs.
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34
Q

Regulation of the Heart

A

The heart is regulated by your autonomic nervous system (involuntary). This is controlled in the medulla of the brain.

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35
Q

Baroreceptors

A

Senses pressure changes and tells the body what to do because of them (higher or lower the blood pressure)

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36
Q

SNS and Heart Rate

A

SNS innervation causes an increase in heart rate (tachycardia) and contractility.
Sympathetic = not calm (release of epinephrine and norepinephrine).
Epi/norepi is secreted at the synapses in the heart -> increases heart rate and strength of contraction.

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37
Q

PNS and Heart Rate

A

Parasympathetic = calm (release of acetylcholine (blocks the release of epi and norepi)).
PNS innervation causes a decrease in heart rate (bradycardia) and contractility (vagus nerve stimulation).
Acetylcholine is secreted at the synapses -> slows the rate (acts on muscarinic and nicotinic cholinergic receptors)
Leaning forward stimulates the vagus nerve which can cause someone to pass out.
Instead of speeding everything up (sympathetic) it slows everything down (eg. heart rate).

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37
Q

Acute Cardiogenic Pulmonary Edema Indications

A

Moderate to severe respiratory distress
AND
Suspected acute cardiogenic pulmonary edema

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37
Q

Acute Cardiogenic Pulmonary Edema Conditions (Nitro)

A

Age: > or equal to 18
LOA: N/A
HR: 60-159 bpm
RR: N/A
SBP: Normotension
Other: N/A

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38
Q

Acute Cardiogenic Pulmonary Edema Contraindications (Nitro)

A

Allergy or sensitivity to nitrates.
Phosphodiesterase inhibitor use within the previous 48 hours.
SBP drops by one-third or more of its initial value after nitroglycerin is administered.

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38
Q

Acute Cardiogenic Pulmonary Edema Treatment if SBP ≥ 100 mmHg to <140 mm Hg

A

IV or Hx: Yes
Route: SL
Dose: 0.3 mg or 0.4 mg
Max. Single Dose: 0.4 mg
Dosing Interval: 5 min
Max. # of Doses: 6

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39
Q

Acute Cardiogenic Pulmonary Edema Treatment if SBP ≥ 140 mm Hg

A

IV or Hx: No
Route: SL
Dose: 0.3 mg or 0.4 mg
Max. Single Dose: 0.4 mg
Dosing Interval: 5 min
Max. # of Doses: 6
IV or Hx: Yes
Route: SL
Dose: 0.6 mg or 0.8 mg
Max. Single Dose: 0.8 mg
Dosing Interval: 5 min
Max. # of Doses: 6

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40
Q

Continuous Positive Airway Pressure (CPAP) Indications

A

Severe respiratory distress
AND
Signs and/or symptoms of acute pulmonary edema or COPD

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41
Q

Continuous Positive Airway Pressure (CPAP) Conditions

A

Age: ≥ 18
LOA: N/A
HR: N/A
RR: Tachypnea ( ≥ 28 breaths/min)
SBP: Normotension
Other: SpO2 <90% or accessory muscle use

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42
Q

Continuous Positive Airway Pressure (CPAP) Contraindications

A

Asthma exacerbation
Suspected pneumothorax
Unprotected or unstable airway
Major trauma or burns to the head or torso
Tracheostomy
Inability to sit upright
Unable to cooperate

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43
Q

Continuous Positive Airway Pressure (CPAP) Treatment

A

Initial Setting: 5 cm H2O OR equivalent flow rate of device as per RBHP direction
Titration Increment: 2.5 cm H2O OR equivalent flow rate of device as per RBHP direction
Titration Interval: 5 min
Max. Setting: 15 cm H2O OR equivalent flow rate of device as per RBHP direction

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44
Q

Continuous Positive Airway Pressure (CPAP) Treatment FiO2

A

Consider increasing FiO2 (if available):
Initial FiO2: 50-100%
FiO2 Increment (if available on device): SpO3 <92% despite treatment and/or 10 cm H2O pressure or equivalent flow rate of device as per RBHP direction
Max. FiO2: 100%

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45
Q

What Beta Blockers Do

A

Beta blockers block the effects of epi and norepi (the body still sends them out but they block the effects of it). Someone on beta blockers may get dizzy when exercising because they aren’t getting enough blood/oxygen when they exercise/move because the beta blockers stop the heart from being able to pump fast which normally happens from epi and norepi.

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46
Q

Factors that Increase Heart Rate

A

Elevated body temp (fever)
Increased environmental temp (humidity)
Exercise
Smoking
Stress

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47
Q

Factors Affecting Heart Rate

A

Age (HR declines) (as you get older everything slows down)
Sex (faster in females)
Physical conditioning (slower with good conditioning)
Temperature (increases with temperature)
Blood levels of K+ (excessive decreases HR and contraction, low levels can lead to lethal rhythms)
Blood levels of CA++ ions (increased CA++ increases the HR and prolongs contraction)
Potassium is the most dangerous hormone that can affect your heart.

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48
Q

Properties of Cardiac Cells

A
  1. Contractility - ability to respond to an impulse by contracting
  2. Automaticity - ability to generate their own impulses
  3. Rhythmicity - regular impulse generation
  4. Conductivity - ability to transmit impulses to adjacent cells
  5. Refractory period - relaxation without response to another stimulation
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49
Q

Cardiac Output

A

The volume of blood ejected by a ventricle in one minute. Depends on the heart rate and stroke volume.
CO = HR * SV
SV is the volume pumped from one ventricle in one contraction.

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50
Q

Starlings Law

A

The more the muscle fibers are stretched, the greater their force of contraction - this is based on an increase in blood volume (like stretching and releasing an elastic).

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51
Q

Pacemaker Settings

A

SA Node: 60-100 bpm
Atrial Cells: 55-60 bpm
AV Node: 40-60 bpm
Bundle of His: 40-45 bpm
Bundle Branch: 40-45 bpm
Purkinje Fibers: 20-40 bpm
As you move down the pacemaker, the beat gets slower and slower.

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52
Q

Sinoatrial (SA) Node

A

Hearts natural pacemaker
Found in the upper part of the wall of the right atrium at its junction with the superior vena cava.
The further away the impulse is generated from the SA node the slower it becomes.
If the SA nodes fail to generate an impulse, the atrial cells will take over; pulse should always be started in the SA node.

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53
Q

Internodal Pathways

A

There are three main ones, then a bunch of other ones.
Main purpose: to transmit the pacing impulse from the SA node to the AV node.
Found in the walls of the right atrium and inter-atrial septum.
Three main pathways:
Anterior
Middle
Posterior

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54
Q

Bachmann Bundle

A

Small tract of specialized cells that transmits impulses through the inter-atrial septum, preferred path for electrical activity for left atrium. (Bundle branches and bachmann bundle are different; bachmann bundle goes off the SA node).

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55
Q

Atrioventricular (AV) Node

A

The AV node stops the pulse for a millisecond to make sure the pulse is good and what’s supposed to happen and the sends it down to the ventricle.
Controls heartrate (electrical relay station)
Slows down conduction from atria to ventricles long enough for atrial contraction - then allows the signal to pass into the ventricles.
Always supplied by right coronary artery.

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56
Q

The Bundle of His

A

Starts at the AV node.
Collection of heart muscle cells specialized for electrical conduction.
Found partially in right atrium, and interventricular septum.
Transmits impulses from the AV node to purkinje fibres, then to the ventricles.
The only route of communication between the atria and ventricles.

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57
Q

Left Bundle Branch (LBB)

A

Begins at the end of bundle of HIS.
Travels through interventricular septum.
First area to depolarize.

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58
Q

Right Bundle Branch (RBB)

A

Also starts at the bundle of HIS
Gives rise to fibers that innervate RV and right face of interventricular septum.
Terminates in the purkinje fibers.

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59
Q

Purkinje System

A

Made up of individual cells just beneath endocardium.
Carry contraction impulses from the left and right bundle branches to the ventricles.
Directly innervates myocardial cells.
Initiates ventricular depolarization cycle (ventricular depolarization is the contraction of the ventricles).

60
Q

Phases of Normal Electrical Activity of the Heart

A

Cardiac conduction is split into 2 phases: systole (contraction) and diastole (relaxation).

61
Q

Phases of Normal Electrical Activity of the Heart: Polarization

A

State of readiness
Muscle is relaxed and ready to receive electrical impulses
Potassium inside
Sodium outside
Calcium outside
Ready to respond to an electrical charge based on sodium and potassium.
Resting stage of the heart

62
Q

Phases of Normal Electrical Activity of the Heart: Depolarization

A

Contraction portion
Electrical impulse transmitted
1 - opening of sodium channels to allow sodium to move inside the cell.
2 - Potassium moves to the outside
Ca++ moves inside and stays longer
Refractory period
Sodium channels open, they are positively charged and this starts the electrical generation. Sodium starts on the inside then potassium moves out.

63
Q

Phases of Normal Electrical Activity of the Heart: Repolarization

A

Recovery phase, trying to get back to polarization
Cells returning to a ready state
After a delay (absolute refractory) termination of action potential occurs as potassium channels open allowing K+ to leave the cell.
Potassium out, sodium in

64
Q

Action Potential - Electrical Activity of a Single Cell

A

Phase 4 - Polarized; resting membrane potential
Phase 0 - Depolarization (Na inside)
Phase 1 - Early repolarization (K out)
Phase 2 - Plateau phase (Ca moves in)
Phase 3 - Rapid repolarization

65
Q

Refractory Period

A

Brief period during which the cells will resist re-stimulation.
Lasts approx. 0.5 ms after the membrane reaches the threshold potential.

66
Q

Absolute Refractory

A

Will not respond to any stimulus, no matter how strong.

67
Q

Relative Refractory

A

Few ms after the absolute - the membrane is repolarizing and restoring the membrane potential.
During this time, the membrane will only respond to very strong stimuli.

68
Q

What does the P Wave Represent on an ECG

A

Atrial depolarization (atrial contraction)

69
Q

What does the QRS Complex Represent on an ECG

A

Ventricular depolarization (ventricular contraction)
QRS complexes in ECG’s are really important: if the QRS complex is super wide it would tell you that your heart (specifically your ventricles) is taking longer to contract.

70
Q

What does the T Wave on an ECG Represent

A

Ventricular repolarization
Ventricles relax during this phase.

71
Q

What does the U Wave on an ECG Represent

A

Repolarization of purkinje fibers (not always visible on ECG and if visible, very small).

72
Q

Three Layers of Blood Vessel Walls

A
  1. Tunica Adventia (outside)
  2. Tunica Media (middle)
  3. Tunica Intima (interior)
73
Q

Which Artery goes from the Heart to the Lungs

A

Pulmonary Artery

74
Q

Lining Endothelial Cells

A

Lines the entire vessel. Provides a smooth luminal surface by inhibiting intravascular coagulation. It’s smooth so blood can go through it nicely, if it was rough you’d get clots.

75
Q

Collagen Fibers

A

Allows the vessels to keep their shape.
Minimally stretch - approx. 2-3%
Function to keep the lumen of the vessel open and strengthen the walls.

76
Q

Elastic Fibers

A

Made of elastin
Allow the vessels to expand and ‘contract’ back to normal size. Highly elastic and capable of stretching more than 100%.
Maintains passive tension - maintains normal blood pressure.

77
Q

Smooth Muscle Fibers

A

Found in the wall of all segments of the vascular system except capillaries.
Exert active tension when vessels contracted.

78
Q

Outer Layer of Vessel Walls

A

Tunica Adventitia (Externa)
Made of strong, flexible connective tissue
Helps hold the vessel open and prevents tearing during body movements
In veins - thickest of all 3 layers
In arteries - 2nd thickest, next to middle layer

79
Q

Middle Layer of Vessel Walls

A

Tunica Media (muscular portion)
Made of smooth muscle tissue sandwiched together with layers of elastic connective tissue.
The muscle allows for changes in blood vessel diameter.
Arteries have a thicker tunica media than veins because they need an ability to take on higher pressures.

80
Q

Inner Layer of Vessel Walls

A

Tunica Intima
Made up of endothelial cells (extremely thin)
In capillaries, this is the only layer.

81
Q

Arteries

A

Thick walled, muscular vessels.
All carry Oxygenated blood away from the heart except the pulmonary artery which carries deoxygenated blood from the heart to the lungs.
Arterial walls are extremely sensitive to stimulation from the ANS. Causes change in diameter as they expand and contract.
Regulate blood pressure.

82
Q

Elastic Arteries

A

Takes on the most pressure, is able to stretch the most and contract back down as the heart beats.
Largest in the body, includes the aorta and some of its major branches.

83
Q

Muscular Arteries (A.K.A. Distributing Arteries)

A

Have less stretch so they can have thicker walls.
Carry blood further away from the heart to specific organs.
Ex: brachial artery, gastric artery, mesenteric artery

84
Q

Arterioles

A

Also called resistance vessels.
Smallest arteries
Basically a pathway from artery to venule which goes to the vein
Main function is to regulate blood flow through the body.

85
Q

Veins

A

Main purpose is to carry deoxygenated blood back to the heart to get reoxygenated.
Operate on the low pressure side of the system (thinner walls since they don’t have to take on as much pressure)
The size changes to be larger closer to the heart but hey don’t get any more muscular/elastic throughout the body.

86
Q

Venules

A

First venous structure to receive blood after it leaves the capillaries.

87
Q

Capillaries

A

Microscopic blood vessels.
Carry blood from the arteries to the venules.
Walls extremely thin (1 cell thick)
Transfer of nutrients and other vital substances between blood and tissue cells.
Over 1 billion in the body - not evenly distributed because the more capillaries there are the more Oxygen in and Carbon Dioxide out which is why there’s so many at the lungs.

88
Q

Peripheral Resistance

A

Resistance to blood flow imposed by the force of friction between the blood and vessel walls.

88
Q

Vasomotor Mechanism

A

Tells the blood vessels to constrict or dilate based on the bodies needs

88
Q

Vasoconstriction

A

Reduction in blood vessel diameter caused by an increased contraction of the muscular wall.
Increases resistance to blood flow thereby decreasing blood flow to the tissues.

89
Q

Vasodilation

A

Increases vessel diameter by relaxation of the muscular wall. Causes an increase in blood flow to the tissues.

89
Q

Vasomotor Pressor flexes

A

Changes in arterial blood oxygen or carbon dioxide content sets a chemical vasomotor control mechanism into operation.
Basically if there’s too much CO2 in the blood, HR will increase to try and get rid of it causing an increase in BP. If BP is too low, HR will also increase.

90
Q

Vasomotor Chemoreflexes

A

Changes within seconds, will increase or decrease rate according to bodies needs.
Sensitive to excess blood CO2 levels (hypercapnia), less sensitive to low levels of O2 (hypoxia).

91
Q

Gravity

A

Naturally, when a person stands - blood wants to pool in the lower extremities as a result of gravity.
This is controlled by venous pumps - 2 types; respiratory and skeletal.

92
Q

Respiratory Venous Pump

A

Caused by increasing the pressure gradient between the peripheral veins and the vena cava.
Inspiration - diaphragm contracts and the thoracis cavity becomes larger and abdominal smaller. Pressure in the thoracic cavity decreases and pressure in the abdominal cavity increases.
Expiration - opposite

93
Q

Skeletal Muscles

A

Serve as “booster pumps”
As each skeletal muscle contracts, it squeezes the veins inside, thereby “milking” the blood upward/towards the heart.
The semilunar valves in veins then close and prevent blood from flowing back as the muscle relaxes.

94
Q

Diffusion

A

Oxygen and carbon dioxide pass through capillary walls from higher to lower concentration.

95
Q

Osmotic Pressure

A

Movement of water into and out of the cell from high concentration to low.

96
Q

Filtration

A

Is forcing of some water and dissolved substances through capillary walls by blood pressure.

97
Q

Pulse Pressure

A

Difference between systolic and diastolic pressure (systolic - diastolic)

98
Q

What are the Two Most Important Factors Affecting BP?

A

Cardiac output and peripheral resistance.

99
Q

What are the Four Factors Affecting BP?

A

Cardiac output, blood volume, peripheral resistance and blood viscosity.

100
Q

Antidiuretic Hormone (ADH)

A

Increases water reabsorption in the kidneys, thus increasing blood volume.
Response to decrease in blood volume and BP.
Works to vasoconstrict blood vessels as well to raise BP (known as vasopressor)

101
Q

Aldosterone

A

If a decrease in BP is detected, works to increase blood volume by increasing reabsorption of sodium ions and water (from sweat, urine and the GI system).

102
Q

What does Blood Transport

A

Oxygen is the biggest thing it’s transporting but it also transports glucose and other nutrients, hormones and electrolytes.

103
Q

Hemocrit

A

Proportion of RBC (erythrocytes).
Elevated hemocrit can indicate dehydration or excess RBC.
Low hemocrit can result from blood loss or anemia.

104
Q

Plasma

A

Makes up part of the 55% of non blood cells in the blood proportion.
Includes proteins, water and other electrolytes.
Albumin - maintains osmotic pressure in the blood.
Antibodies (Globulins) - fight off infection
Fibrinogen - blood clotting

105
Q

How much Oxygen can Hemoglobin Carry?

A

4

106
Q

Anemia

A

Lack of Oxygen carrying capacity due to a lack of red blood cells.
Causes a reduction in Oxygen transport in the blood caused by a decrease in hemoglobin content.

107
Q

Signs and Symptoms of Anemia

A

Body compensates to improve the oxygen supply by increasing HR and peripheral vasoconstriction.
These changes lead to symptoms such as fatigue, pallor, dyspnea and tachycardia.
Epithelial cells in the GI system cause inflammation and ulcers on the skin, dry lips, and hair and skin may begin to show degeneration.
In cases of severe anemia, chest pain during exercise.

108
Q

Iron Deficient Anemia

A

Insufficient iron impedes the creation of hemoglobin in the blood. This then reduces the amount of oxygen carried in the blood.

109
Q

Causes of Iron Deficient Anemia

A

Diets low in iron, chronic blood loss from things such as ulcers, hemorrhoids, cancers and excessive menstrual flow.

110
Q

Signs and Symptoms of Iron Deficient Anemia

A

Mild - typically asymptomatic
Pallor of the skin and mucous membranes
Fatigue, lethargy and cold intolerance
Irritability (CNS response to hypoxia)
Brittle hair, rigid nails, dry skin
Inflammation of the oral mucosa and tongue
Menstrual irregularities
Delayed healing
Tachycardia, syncope and dyspnea

111
Q

Pernicious Anemia B12 Deficiency

A

Caused by large, immature RBC’s.
Typically results from a deficiency of folic acid (B9) or B12.
Body has enough RBC’s but they’re too big and not developed properly.

112
Q

Signs and Symptoms of Pernicious Anemia B12 Deficiency

A

Same as anemia.
Additionally:
Enlarged tongue; red, sore and shiny
Decrease in gastric acid leads to digestive discomfort often with nausea and diarrhea.
Tingling and burning sensations to the extremities or loss of coordination.

113
Q

Aplastic Anemia

A

Impairment or failure of bone marrow function. This leads to a loss of stem cells and decreased numbers of RBC’s, leukocytes and platelets.

114
Q

Signs and Symptoms of Aplastic Anemia

A

Because the entire bone marrow is affected:
Pallor, weakness and dyspnea
Multiple and recurrent infections (don’t have enough white blood cells to fight infection so they can be sick for weeks).
Tendency to bleed excessively (bruising from something like bumping their arm).
As white blood cells diminish, uncontrolled hemorrhage and infection are likely

115
Q

Sickle Cell Anemia

A

Inherited characteristic (genetic) leads to abnormal hemoglobin; instead of being round they are crescent shaped.
Shape of them often causes clots since they’re not round, they can easily get caught in vasculature.
When it’s deoxygenated it changes its chape from a disc to a crescent.
RBC can only live for 20 days opposed to the normal 120 day lifespan.

116
Q

Signs and Symptoms of Sickle Cell Anemia

A

Usually evident at approx. 12 months old
Severe anemia symptoms such as pallor, weakness and dyspnea.
High bilirubin - evidenced by yellowing of skin and whites of the eyes.
Vasculature occlusions and infarcts can often lead to periodic, painful crises and permanent damage to organs and tissues.
Chest - SOB, pain, fever
Vessels of hands and feet - pain and swelling, ulcers.
Growth and development are late

117
Q

Hemolytic Anemia

A

RBC’s are normal but only living for 20 days instead of 120 so the body may or may not be able to keep up with the loss.

118
Q

Polycythemia

A

Blood flow is sluggish because it’s thicker/more viscous because of an increased production of RBC’s.
Primary: Increased production of RBC’s in the bone marrow.
Secondary: Increase in RBC secondary to hypoxia.

119
Q

Signs and Symptoms of Polycythemia

A

Cyanotic - bluish/red tone to the skin
High BP
HR - full and bounding
Dyspnea
Headaches and visual disturbances
Clots
Infarctions

120
Q

Hemophilia

A

Deficiency of clotting factor
Most common inherited clotting disorder
In mild forms, excessive bleeding occurs only after trauma
In severe forms - frequent, spontaneous bleeding is common

121
Q

Signs and Symptoms of Hemophilia

A

Prolonged or severe hemorrhage after minor tissue trauma
Persistent oozing of blood after minor injuries
Spontaneous bleeding may occur - in urine, feces; sometimes in joints causing chronic pain and crippling deformities from the recurrent inflammation

122
Q

Disseminated Intravascular Coagulation

A

Body unnecessarily clots so when it actually needs to form a clot it loses its factors and isn’t able to clot.
Involves both excessive clotting and excessive bleeding.

123
Q

Signs and Symptoms of Disseminated Intravascular Coagulation

A

Presentation depends on underlying cause
Obstetrical patients often manifest increased bleeding
Cancer patients often manifest more thromboses
Hemorrhage is usually the critical issue
Low clotting factor levels and prolonged bleeding
Creates low BP
Multiple bleeding sites are common

124
Q

Multiple Myeloma

A

Too many white blood cells and they’re too big.
These cells are taking place of red blood cells.
More antibodies (WBC’s), in the blood the more good cells will get attacked

125
Q

Leukemia

A

Disorder involving the white blood cells
Immature, non function and multiply uncontrollably in the marrow and are released into circulation.
This leads to anemia because they suppress the production of other normal cells.

126
Q

Signs and Symptoms of Leukemia

A

Typically marked initially by an infection that is unresponsive to treatment of by excess bleeding.
Multiple infections (non-function WBC’s)
Hemorrhage
Signs of anemia
Bone pain - even during rest
Weight loss and fatigue
Fever
Enlarged lymph nodes
If the cells infiltrate the nervous system - headaches, drowsiness, vomiting, visual disturbances

127
Q

Hodgkin’s Lymphoma

A

Initially involves a single lymph node.
Spreads systemically to multiple and then to organs via the lymphatics.

128
Q

Stages of Hodgkin’s Lymphoma

A

Stage 1: Single lymph node or area
Stage 2: 2 or more regions on the same side of the diaphragm
Stage 3: Affects lymph nodes on both sides of the diaphragm
Stage 4: Involvement of bone, liver or lungs

129
Q

Signs and Symptoms of Hodgkin’s Lymphoma

A

Initially - usually a lymph node that is large, painless and non tender.
Later, enlarged lymph nodes at other locations may cause pressure effects.
General signs of cancer such as weight loss, fever, fatigue and night sweats.
Recurrent infection - abnormal lymphocytes interfere with the immune response.
Pruritus (itching)

130
Q

Non Hodgkin’s Lymphoma

A

Multiple node involvement scattered throughout the body.
Non organized pattern of widespread metastases.
Often involves intestinal nodes and organs.
More difficult to treat due to its nature.

131
Q

HIV

A

Human Immune Deficiency from a virus that affects the lymphocytes and suppresses the immune system.
Attacks the T-cells, leading to low numbers of increased risk of infections and cancers.

132
Q

AIDS

A

Acquired Immune Deficiency Syndrome
Usually acquired in 10 years after HIV

133
Q

Any Patient Presenting with any Problems Related to Blood Disorders Should be Treated with:

A
  1. Oxygen - amount needed based on condition
  2. Fluids - IV
  3. ECG - monitor and treat rhythms
  4. Transport - closest most appropriate facility
  5. Pharmacology - pain management - NO advil
  6. Psychological support - be supportive and communicative with the patient.
134
Q

P Wave Length

A

Less than 0.11 seconds
Height is less than 2.5 mm (1 small box = 1 mm)

135
Q

PR Interval Length

A

Normally between 0.12 and 0.2 seconds
If the length of the PR interval exceeds 0.2 seconds, you have a first-degree AV block.

136
Q

QRS Complex Length

A

Duration of less than 0.12 seconds

137
Q

QT Interval Length

A

Usually lasts 0.36 - 0.44 seconds

138
Q

Sequence Numbers for Determining HR on an ECG

A

300, 150, 100, 75, 60, 50, 43, 38, 33

139
Q

Sinus Bradycardia

A

Complexes and morphology the same as NSR
Rate less than 60 beats/minute

140
Q

Sinus Tachycardia

A

Rate over 100 beats/minute

141
Q

Sinus Arrest

A

SA node fails to initiate an impulse
Length can vary depending on number of missed beats (a rhythm, long pause in it then back to another rhythm)

142
Q

Sinoatrial Block

A

Dropped beat, then back to normal rhythm (missing P wave)
Rate: Varies
Irregular
P waves: Present, except when dropped
P:QRS - 1:1
QRS width is normal

143
Q

Wandering Atrial Pacemaker

A

Pacemaker moves from the SA node to various areas within the atria.
P waves are all different

144
Q

Premature Atrial Complex (PAC’s)

A

Existence of a particular complex within another rhythm.
Also known as ectopic complexes.

145
Q

Supraventricular Tachycardia (SVT)

A

Heart rate must exceed 150 beats/minute
P waves are hidden because it happens so fast
P waves are hidden on paper because it happens so fast
Rate typically 140-280 bpm

146
Q

Atrial Flutter

A

Known as flutter or F waves
Degenerates into atrial fibrillation
Atrial commonly 250-350 bpm
Usually regular but may be variable
P waves - “saw tooth” appearance
QRS width is normal
P:QRS ratio - variable, most commonly 2:1 but can go higher

147
Q

Atrial Fibrillation

A

No discernable P waves
QRS complexes are innervated haphazardly in an irregularly irregular pattern.

1230 Testing (Semester 2) (1 decks)

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