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CPT I > CPT I - EXAM > Flashcards

CPT I - EXAM Flashcards

1
Q

What is VO2? What units is it measured in?

A

The rate of oxygen consumption in aerobic metabolism.

Absolute: L/min
Relative: ml/kg/min

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2
Q

What is the average resting VO2?

A

3.5 mL/kg/min (1 MET)

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3
Q

What is the average Max VO2?

A

30-40 mL/kg/min (10 METs)

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4
Q

When does the anaerobic metabolism come into play?

A

It works a little bit at rest but starts to work harder when the oxygen transport system can’t keep up with demand.

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5
Q

What is VO2 a function of?

A

CO x (a-vO2)

Cardiac output x how much oxygen consumed

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6
Q

What is a-vO2?

A

Oxygen in arteries - oxygen in veins

Ie, how much oxygen consumed by mitochondria in muscles

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7
Q

What are the pleural cavities composed of?

A

Visceral pleura
Pleural fluid
Parietal pleura

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8
Q

What is parenchyma?

A

Spongy structure of lung surrounding airways

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9
Q

What are the functions of the upper airways? What are the complications if they can’t do those functions?

A

Gets air from outside to lower airways

Warm, filter, humidify air

Higher risk for aspiration, pneumonia, dried out secretions, inability to talk or cough

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10
Q

What is the purpose of the epiglottis?

A

Protects the airways by preventing food from entering the trachea when swallowing

Provides an effective cough (creates pressure after deep breath in)

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11
Q

What is the glottis?

A

The opening to the trachea from the larynx. Contains the vocal cords.

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12
Q

What is the carina?

A

The bifurcation point where the trachea splits into the right/left main stem bronchus.

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13
Q

Which lung (R/L) is more likely to have pathology? Why?

A

More likely on the right because the right main stem bronchus is more straight than the left (greater chance of aspiration).

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14
Q

What happens to the diaphragm in neuro/spinal cord injuries? Clinical indication?

A

No abdominal musculature to support organs that hold the diaphragm up - sits lower.

Patients can’t breathe effectively, at risk for pneumonia.

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15
Q

What happens to the diaphragm in COPD?

A

Patients have an expanded chest that forces the diaphragm to sit lower.

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16
Q

Primary muscles of inhalation?

A

Diaphragm, external intercostals

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17
Q

Accessory muscles of inhalation?

A

SCM, scalenes, abdominals

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18
Q

Muscles of active exhalation?

A

Internal intercostals, abdominals

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19
Q

How do we work speech and cough?

A

Speech - eccentric contraction of diaphragm to control flow

Cough - isometric epiglottis and abdominals to concentric contraction

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20
Q

Lung Volume: TV

A

Tidal Volume

Volume of air inspired or expired per breath

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21
Q

Lung Volume: IRV

A

Inspiratory Reserve Volume

From end of tidal inspiration to max inspiration

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22
Q

Lung Volume: ERV

A

Expiratory Reserve Volume

From end of tidal expiration to max expiration

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23
Q

Lung Volume: RV

A

Residual Volume

Volume of air in lungs after max expiration

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24
Q

Lung Volume: TLC

A

Total Lung Capacity

Volume in lungs at end of max inspiration

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25
Q

Lung Volume: VC

A

Vital Capacity

Volume from max inspiration to max expiration

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26
Q

Lung Volume: IC

A

Inspiratory Capacity

Volume from tidal expiration to max inhalation

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27
Q

Lung Volume: FRC

A

Functional Capacity

Volume after tidal expiration

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28
Q

FEV1/FVC ratio

What is the average? What is FEV1 indicative of?

A

Forced Expiratory Volume in 1 Second
Forced Vital Capacity

Reflects pulmonary expiratory power and overall resistance to air movement upstream in lungs. Measures ability to sustain a high airflow level.

Average should be 0.75-0.8 (75-80% of air in 1 second). FEV1 is air in upper airways.

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29
Q

FEF 25-75%

A

Forced Midexpiratory Flow

Average flow rate during middle phase of max expiration. Gives better idea about small airway disease (goes from upper –> lower airway flow)

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30
Q

What is anatomical dead space?

A

Normal/fixed area where no gas exchange occurs. Includes conducting zones and upper airways.

1/3 of individual’s resting tidal volume

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31
Q

What is physiologic dead space?

A

An area that could or should be exchanging gas, but is not.

Normal - alveolar sacs not in use at rest (IRV)

Abnormal - fixed disease (cystic fibrosis)

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32
Q

What is 2/3 resting tidal volume?

A

Air movement to alveoli

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33
Q

What are the 3 forms of resistance to lung airflow?

A

Compliance - ability to expand

Elasticity - back to original shape after deformation, no energy required

Airway resistance - radius/diameter

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34
Q

Healthy Work of Breathing (WOB) is low. This is affected by? (5)

A 
Compliance
Elasticity
Resistance
Ventilatory demand
Number of intact alveoli
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35
Q

What is minute ventilation (VE)? What is maximum voluntary ventilation (MVV)?

A

VE = TV x RR
Volume of air moved in or out of lungs per minute.

MVV = TVmax x RRmax

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36
Q

What is V/Q matching? What is the average V/Q?

A

V/Q matching is attaining an adequate combination of V/Q for gas exchange.

Alveolar ventilation / cardiac output
4 L/min / 5 L/min = 0.8

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37
Q

What is Ventilatory Index?

A

VI = VE/MVV

Minute ventilation at any time divided by maximum voluntary ventilation. Should be very small at rest.

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38
Q

What is your breathing reserve?

A

MVV - VE

How much air is left at any time.

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39
Q

What is the VI during exercise? At VO2max? Dyspnea? Fatigue? Non-sustainable?

A 
60% MVV at exercise, typically
80% at VO2max
50% for dyspnea
70% for fatigue
90% for unsustainable
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40
Q

Will a patient with pulmonary pathology have a higher or lower MVV? What does this do to their VI?

A

Have a lower MVV which gives them a high VI (SOB with walking)

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41
Q

What are the 4 factors of gas exchange (passive diffusion)?

A

Partial pressures
Surface area
Diffusibility of membrane
Time (1/4s at rest)

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42
Q

What is the hypercapnic drive?

A

Primary drive in healthy ppl. Central chemoreceptors in the medulla detect CO2 levels and increase ventilation when levels are high.

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43
Q

What is the hypoxic drive?

A

Secondary drive in which peripheral chemoreceptors in carotid bifurcation and arch detect low levels of O2 to increase ventilation.

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44
Q

What is the sympathetic response to the airways?

A

Bronchodilation with decreased mucus production.

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45
Q

When HgB is fully saturated (100%), how much oxygen will it carry?

How much HgB does a person have on average?

A

HgB carries 1.34 mL O2 / g HgB

Average HgB: 15 g/dL blood

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46
Q

What is the oxygen carrying capacity of blood (CaO2)? What does this measure?

A 
CaO2 = (1.34) x (15) x (.98)
CaO2 = Amount of O2 x Amount of HgB x Saturation of HgB

Measures how well gas is exchanged.

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47
Q

How much oxygen does the body extract from what is delivered to it (at rest)?

A

25%

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48
Q

What determines whether oxygen is picked up or dropped off? What affects this?

A

Affinity of HgB for O2 (high = picked up)

Affect Affinity: acidity, temp, level of O2

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49
Q

What is the main transport of metabolic CO2?

A

Bicarbonate

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50
Q

What creates non-metabolic CO2?

A

During anaerobic metabolism, the body accumulates lactic acid.

Lactic acid + bicarbonate = CO2

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51
Q

What is stroke volume? Average?

A

SV - volume of blood ejected by heart per beat

End Diastolic Vol - End Residual Vol

Avg: 70 mL

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52
Q

What is venous return?

A

Volume of blood that returns to heart per beat

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53
Q

What is cardiac output?

A

Volume of blood pumped by heart per minute

CO = HR x SV

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54
Q

What side of the heart is low/high pressure?

A

Right side: low pressure (pulmonary)

Left side: high pressure (systemic)

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55
Q

During exercise, we lose time in diastole (ventricular filling), how do we maintain stroke volume (cardiac output)?

A

Increased venous return (fill up ventricles faster)

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56
Q

What is the ejection fraction? What is the average?

A

Volume ejected from the amount available.
SV/EDV

Avg: 60-70%

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57
Q

What is the average cardiac output?

A 
CO = SV x HR
CO = 70 ml x 70 bpm = 5 L/min
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58
Q

What are the determinants of stroke volume?

A

Preload - tension before heart contraction; determined by EDV

Afterload - load against which heart contracts (right and left side); determined by vascular resistance (state of dilation/constriction)

Contracility - positive inotropic effect increases contractility

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59
Q

What happens to the 3 determinants of SV during exercise?

A

Preload - increases (venous return)
Afterload - decreases (vasodilation)
Contractility - increases (SNS)

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60
Q

What are the 3 determinants of HR?

A

Intrinsic conduction system (automaticity, rhythmicity, intercalated discs)

Autonomic NS - chronotropic effect

Chemical/hormonal response - norepi and epi from adrenal glands

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61
Q

What is the primary pace maker? How fast?

A

SA Node (60-100 bpm)

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62
Q

What is the secondary pacemaker? How fast? What else does it do?

A

AV Node (40-60 bpm). Delays impulse for fraction of a second which allows the atria to contract and complete ventricular filling.

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63
Q

What is the rest of the conduction system after the SV and AV nodes?

A

Bundle of His - left/right bundle branches through interventricular septum

Purkinje fibers - L/R ventricles; beats 20-40 bpm

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64
Q

What vessels determine vascular resistance?

A

Arterioles (resistance vessels)

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65
Q

What kind of vessels increase during aerobic training? Why?

A

Capillaries - to increase blood flow and O2 delivery and remove waste products.

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66
Q

What are the 2 main branches of the left coronary artery?

A

Circumflex

Left Anterior Descending (LAD)

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67
Q

Why does coronary perfusion decrease during exercise?

A

Heart gets its blood supply during diastole, which is shortened during exercise.

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68
Q

What is Mean Arterial Pressure (MAP)? What is the average?

A

MAP = DBP + PP/3

Pressure that maintains tissue perfusion, detected by kidneys.
PP is pulse pressure (SBP - DBP)

Avg = 93 mmHg

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69
Q

BP =?

A

BP = CO x TPR

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70
Q

If TPR decreases during exercise, why would SBP increase?

A

CO increases

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71
Q

What is the difference between the effects of the autonomic NS and hormonal response on cardiovascular function?

A

Autonomic has an immediate effect while hormonal takes time to kick in.

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72
Q

What is the parasympathetic influence on the heart? Sympathetic influence?

A

PNS: Negative chronotropic effect

SNS: Positive chronotropic and inotropic effects

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73
Q

What releases norepinephrine? Epinephrine?

A

Sympathetic NS releases NE from the adrenergic fibers.

NE stimulates adrenal release of epinephrine.

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74
Q

If the SNS causes vasoconstriction, why is their vasodilation during exercise?

A

Exercise (metabolism and PaO2) overrides the SNS response

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75
Q

What is the RPP?

A

Rate-Pressure Product
RPP = HR x SBP

Myocardial oxygen demand. This is why we measure both HR and BP to assess patient.

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76
Q

A patient has a BP of 150/84. What kind of HTN is this considered?

A

Stage I because of the SBP of 150.

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77
Q

Why is the Valsalva maneuver dangerous for cardiopulmonary patients?

A

It is an acute drop in blood pressure secondary to drop in venous return.

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78
Q

What are the 3 factors of assessing tissue perfusion?

A

Heart rate
Strength of pulse
Rhythm

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79
Q

How do you assess a patient’s reaction to exercise?

A

Before activity

During activity

After activity at 1 min intervals until back to baseline

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80
Q

What is the difference between the bell and the diaphragm on a stethoscope?

A

Diaphragm detects high frequency sounds

Bell detects low frequency sounds (better for diastolic BP)

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81
Q

How fast do you release air from the BP cuff?

A

2 mmHg per second

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82
Q

What are Korotkoff sounds?

A 
Phase 1: 1st appearance of sounds (SBP)
Phase 2: Murmur or swishing
Phase 3: Crisp and louder
Phase 4: Muffling
Phase 5: Sounds disappear (DBP)
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83
Q

What are you assessing for respiration?

A

Rate
Depth
Rhythm
Quality

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84
Q

What is the average body fat % for males/females?

A

Males: 12-15%
Females: 25-28%

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85
Q

What is body mass index?

A

BMI = body mass (kg) / Stature (m2)

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86
Q

What are the body’s goals during exercise?

A

Deliver oxygen at a rate needed to meet energy demand

Eliminate waste products at rate equal or greater than production

Dissipate heat, regulate body temp

Deliver hormones

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87
Q

What is the difference between absolute and relative intensity?

A

Absolute - actual intensity person is tested at

Relative - % of max capacity; relative to the individual

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88
Q

What is APMHR?

A

Age Predicted Max Heart Rate

APMHR = 220 - Age
only use for healthier individuals

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89
Q

What is the state of vasodilation during aerobic exercise?

A

Vasodilation throughout workout

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90
Q

What is the state of vasodilation during anaerobic exercise?

A

No vasodilation until recovery. TPR and therefore BP rises.

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91
Q

During aerobic exercise, what kind of TPR drop occurs if you are just working out arms, just legs, or both?

A

Arms: less of a drop (less area to dilate)
Legs: higher drop (more mass than arms)
Both: lowest BP response

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92
Q

What is SaO2? Does it change at max exercise?

A

Saturation of HgB molecule - ability for diffusion across alveolar membrane. Does not change at max exercise except for a couple % points. Delivery/consumption decreases, however.

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93
Q

What is typical anaerobic threshold?

A

40-60% VO2 max (4-6 METS)

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94
Q

What is ventilatory efficiency?

A

How much CO2 released (the more the better)

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95
Q

What is the difference between VO2max and VO2peak?

A

VO2max - leveling of VO2 with increasing intensity

VO2peak - exercise is stopped before seeing the O2 consumption leveling off (reach APMHR, RER > 1.15, anaerobic metab., stopped exercise)

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96
Q

What are the 4 principles of training?

A
  1. Overload
  2. Specificity
  3. Individual differences
  4. Reversibility
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97
Q

What are the 5 (or 4) exercise prescription components?

A 
Mode
Intensity
Duration
Frequency
Progression

Frequency
Intensity
Time
Type

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98
Q

Why aerobic training?

A

Enhance delivery and utilization of oxygen.

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99
Q

Physiologic effects of training

A 
Increased VO2 max
Decreased VE at submax intensity
Decreased HR/BP at submax intensity
Increased capillary density
Increased anaerobic threshold
Enhanced metabolism
Reduction of risk factors
Decrease morbidity/mortality
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100
Q

What is the respiratory quotient?

A

RQ = VCO2/VO2

CO2 production vs. O2 consumption during aerobic exercise (metabolic CO2).

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101
Q

What is respiratory exchange ratio?

A

RER = VCO2/VO2

CO2 production vs. O2 consumption during anaerobic exercise (metabolic and lactic acid buffering CO2)

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102
Q

If RER is > 1, what state is the person in?

A

Anaerobic metabolism

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103
Q

What non-exercise demands can stimulate the oxygen transport system?

A

Infection, disease, injury

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104
Q

If the quality of blood in SV is poor, what is the compensation?

A

HR increase (for CO)

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105
Q

If a patient has weakness if the cardiovascular system, what other systems should be improve to compensate and take away some physiologic stress on the body?

A

Ventilatory pump system
Neuromuscular system

(parts of the O2 transport system)

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106
Q

If there is an inability to increase CO and/or (a-vO2) is limited, what are the consequences?

A 
Decreased VO2 max
Early onset anaerobic metabolism
Inability to reach anaerobic threshold (SOB)
Increased physiologic stress
System failure
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107
Q

What increases metabolic demand?

A 
Movement
Stress, fear, yelling
Resistance/intensity
Anticipation
Anxiety
Pain
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108
Q

What limits the Oxygen Transport System response?

A 
Disease
Deconditioning
Inactivity
Bedrest
Medications
Neural control
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109
Q

Where is a voluntary ventilator tube placed? Clinical implication?

A

At the jugular notch

Affects upper airways

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110
Q

Which ribs articulate with the manubrium?

A

1 and 2

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111
Q

What does the sternal angle articulate with? What lies directly behind it?

A

Rib #2 is on either side of it

Carina and T3 vertebra are directly posterior

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112
Q

How many true ribs / false ribs / floating ribs?

A

True: 7
False: 3
Floating: 2

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113
Q

Which ribs does the body of the sternum articulate with?

A

Ribs 2-7

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114
Q

Which ribs articulate at the junction between the sternum body and xiphoid process? What structures are directly lateral to this junction?

A

Articulate with ribs 6-7

Rib 5 and the apex of the heart are lateral to this junction

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115
Q

What is the clinical implication of ribs 8-10 articulating with cartilage only?

A

Gain mobility here for rib expansion

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116
Q

What is FRC? How are the ribs angled?

A

Functional Residual Capacity - volume of air left in lungs after normal resting exhalation.

Ribs are angled downward (sagittal view) less than 90 deg. Ribs are angled downward (posterior view) about 45 deg.

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117
Q

You palpate the T4 spinous process. Which vertebral body is anterior to that?

A

T5

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118
Q

Rib 7 articulates with what structures?

A

Inferior facet of T6
Superior facet of T7
Transverse process of T7

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119
Q

Why do connective tissue disorders (RA, lupus) impact ventilation? What is a good stretch to increase ventilation?

A

Joints are made up of connective tissue. If costovertebral/costotransverse joints are limited, their ability to expand is limited.

Stretch: deep breath with lateral side bend

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120
Q

What are the 3 steps of effective breathing?

A

Belly rise
Lateral expansion
Chest rise

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121
Q

What are Type 1 and Type 2 alveoli cells?

A

Type 1: anatomical structure of alveoli (stability)

Type 2: produce surfactant

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122
Q

What is surfactant? When does this start to develop in utero?

A

Fluid that breaks up the surface tension of the alveoli and allows them to expand.

Produced at 26-28 weeks but doesn’t mature until 36.

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123
Q

What do collateral ventilatory pathways do?

A

Bypass occluded airways

Decrease resistance to airflow

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124
Q

What are the 3 types of collateral ventilation?

A

Channels of Martin - 2 bronchioles
Channels of Lambert - bronchiole to alveoli
Alveolar pores of Kohn - 2 alveoli

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125
Q

How much of VO2max goes toward the work of breathing?

A

10% (increased surface area aids in diffusion)

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126
Q

What is PO2 in venous blood, alveolus, and arterial blood?

A

Venous: 40 mmHg
Alveolus: 100 mmHg
Arterial: 100 mmHg

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127
Q

What is PCO2 in venous blood, alveolus, and arterial blood?

A

Venous: 45 mmHg
Alveolus: 40 mmHg
Arterial: 40 mmHg

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128
Q 
Arterial blood gas (at rest):
pH range?
PaCO2 range?
PaO2 range?
HCO3 range?
A

pH: 7.35-7.45
PaCO2: 35-45
PaO2: >80
HCO3: 22-26

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129
Q 
Venous blood gas (at rest):
pH range?
PaCO2 range?
PaO2 range?
HCO3 range?
A

pH: 7.31-7.41
PaCO2: 41-51
PaO2: 35-40
HCO3: 22-26

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130
Q

Why does bicarbonate levels remain unchanged between arterial blood gas and mixed venous blood gas?

A

It is affected by kidneys, not ventilation

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131
Q

Why is there residual volume when you force air out of the lungs? What is the clinical implication of pulmonary disease?

A

When air is forced out, pressure around airways increases and collapses them.

Someone with pulmonary disease starts out with narrowed airways, so they are collapsed earlier which results in less total lung capacity.

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132
Q

Which volumes are studied to determine how well a patient can get air out of their lungs?

A

Forced Vital Capacity (FVC)
Forced Expiratory Volume in 1 Sec (FEV1)
Forced Midexpiratory Flow (FEF 25-75%)
Peak Expiratory Flow (PEF)

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133
Q

What happens to PEF in those with asthmatic attack?

A

Peak Expiratory Flow is a person’s maximum speed of expiration. PEF drops in those with pulmonary issues.

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134
Q

Why is increasing volume more effective than breathing faster?

A

Increased surface area (decreased physiologic dead space). Breathing faster decreases more anatomical dead space instead of physiologic dead space.

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135
Q

What is the inhale:exhale ratio at rest? During exercise?

A

At rest: 1:2 (elastic recoil slower)

Exercise: 1:1 (active exhale)

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136
Q

What is Work of Breathing? How is efficiency determined?

A

WOB: ventilatory requirement determined by VO2 demand and ventilatory efficiency.

Efficiency is how much air is moving per how much CO2 is removed (VE/VCO2)

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137
Q

What are the 3 types of V/Q mismatching?

A
  1. Ventilation in excess of perfusion (increased V without Q) - air is sent to area with no blood supply (ex: pulm embolism obstructs blood flow).
  2. Perfusion in excess of ventilation (increased Q without V) - send blood to area without ventilation (ex: secretions block airflow)
  3. Absence of perfusion and ventilation (ex: tumor obstructing V and Q).
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138
Q

Why should you assess someone’s vital signs when you reposition them?

A

Positioning can affect V/Q ratio. You need to make sure they are stable in the new position.

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139
Q

How does a patient with pulmonary disease develop secondary pulmonary hypertension?

A

If vasoconstriction does not occur in areas of dead space, they have perfusion in excess of ventilation which leads to pulmonary HTN.

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140
Q

What are the voluntary and involuntary CNS controls of ventilation?

A

Voluntary: motor cortex

Involuntary: Hypercapnic drive, hypoxic drive, peripheral mechanoreceptors (muscles)

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141
Q

Why is the yawn/sigh reflex so important?

A

It forces you to breathe into your reserve volume which prevents secretion buildup and subsequent infection.

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142
Q

What is pleural effusion?

A

Pleural fluid buildup in the potential space between visceral and parietal pleura. This can collapse the lung or prevent expansion.

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143
Q

What is the point of maximal impulse?

A

The apex of the heart

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144
Q

How does an increased afterload lead to heart failure?

A

The heart increases contractility to compensate which overloads the heart.

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145
Q

SBP reflects which determinant of SV? What else does it represent in regards to the heart?

A

Represents afterload

Also represents contractility (how hard the heart is working)

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146
Q

DBP is a good indicator of what? Why? High DBP indicates what?

A

DBP is good indicator of cardiac perfusion because it is the time that coronary arteries are supplied with blood.

High DBP can indicated trouble filling the arteries.

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147
Q

What is the normal increase in SBP during aerobic exercise? DBP?

A

SBP: 10 mmHg per MET level
DBP: rises very little

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148
Q

What is SpO2?

A

How well oxygen gets from alveolar membrane to the blood stream

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149
Q

What are the criteria for low, moderate, and high risk people for cardiopulmonary disease?

A

Low: asymptomatic, 0-1 risk factors

Moderate: asymptomatic, 2+ risk factors

High: symptomatic, known disease

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150
Q

What are symptoms of cardiovascular disease?

A 
Angina
Claudication
Orthopnea/PND
DOE/cough
Dizziness/syncope
Palpitations
Edema/skin color
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151
Q

What is angina?

A

A conglomerate of symptoms, not just chest pain.

Can be any symptom above the waist as a result of an imbalance between myocardial oxygen supply (coronary circulation) and demand (HR and SBP).

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152
Q

What is claudication?

A

Lack of blood flow to peripheral muscles which causes cramping.

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153
Q

What is orthopnea? PND?

A

SOB, trouble breathing in supine. Associated with heart failure. Supine increases venous return which increases preload.

Orthopnea - happens as soon as lay down

Paroxysmal Nocturnal Dyspnea - can handle initial rise in preload but can’t over handle it over time.

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154
Q

What is DOE?

A

Dyspnea on Exertion

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155
Q

What is syncope? Caused by?

A

Fainting, transient loss of consciousness

Result of decreased BP, CO, blood flow to brain

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156
Q

What are symptoms of pulmonary disease?

A 
SOB/DOE
Cyanosis - nails, lips, eyes
Wheezing
Cough
WOB
Sputum production
Pain
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157
Q

How does edema present when it is associated with heart failure? Which side is the heart failure?

A

Standing up - peripheral edema due to gravity

Laying down - fluid backs up the SVC and causes jugular venous distension

Right-sided heart failure

158
Q

What is digital clubbing a sign of?

A

Chronic hypoxia

159
Q

Which muscles would exhibit atrophy in cardiopulmonary disease? Hypertrophy?

A

Atrophy - peripheral muscles, pecs, abs

Hypertrophy - SCM, upper traps, scalenes

160
Q

Why is there peripheral atrophy in patients with CPD?

A

It’s hard to eat (takes too much energy just to breathe) and there is an increased metabolic demand to breath.

161
Q

How wide/deep should the chest be? What does the barrel shape indicate?

A

Chest should be 2x as wide as it is deep.

Increased AP diameter (barrel shape) indicates obstructive disease - lungs are hyperinflated because can’t get air out.

162
Q

What is a Cheyne-Stokes breathing rate?

A

Crescendo/decrescendo

Breathing with rhythmic waxing and waning of depth of breaths and regularly recurring apneic periods.

163
Q

What is Biot’s breathing rate/pattern?

A

Slow rate and depth
Irregular rhythm

Rapid, short breathing with pauses of several seconds, indicating increased intracranial pressure.

164
Q

What is paradoxical breathing?

A

That in which all or part of a lung is deflated during inhalation and inflated during exhalation, such as in flail chest or paralysis of the diaphragm.

165
Q

What is psychogenic dyspnea?

A

Dyspnea that occurs in a background of emotionally stress, characterized by irregular breathing and prominent deep sighs; severe PD may be marked by hyperventilation, light-headedness, tingling of hands and feet, tachycardia, T wave inversion, syncope.

166
Q

What are the 4 major vital signs?

A

Blood pressure
Heart rate
SpO2
Respiratory rate

167
Q

What part of the stethoscope do use to listen to S1/S2?

S3/S4/murmurs?

A

1/2: diaphragm

3/4: bell

168
Q

What is the S1 sound?

A

Closure of the AV valves (systole)

169
Q

What is the S2 sound?

A

Closure of the SV valves (diastole)

170
Q

What is the S3 sound?

A

Ventricular gallop after S2. Indicates CHF

171
Q

What is the S4 sound?

A

Atrial gallop before S1.

172
Q

What does a murmur indicate? Where is it loudest?

A

Indicates valvular dysfunction. Loudest at the valve it is affecting.

173
Q

What part of the stethoscope do you use to listen to breath sounds?

174
Q

Where is tracheal/bronchial sound normal?

175
Q

where is the bronchovesicular sound normal?

A

mainstem bronchi

176
Q

where is the vesicular breath sound normal?

A

peripheral lung areas

177
Q

What are wheeze sounds? what do they indicate?

A

high pitched sounds usually on inhalation. indicate narrowing of airways

178
Q

what are crackle lung sounds? indicate?

A

also called ronchi

bubbles/popping of air through fluid or airway opening up.

caused by fluid backup or secretions

179
Q

what is the pleural rub lung sound? indicates?

A

grating/friction that is painful. caused by inflammation that causes the visceral and parietal fluid to rub together

180
Q

what does increased voice sound mean?

A

increased lung density

181
Q

what is bronchophony?

A

increased transmission of voice sound caused by alveoli filled with fluid or replaced by solid tissue

182
Q

what is egophony?

A

bleating sound often by lung consolidation and fibrosis

183
Q

what is whispered pectoriloquy?

A

increased loudness of whispering in areas of lung consolidation (pneumonia, cancer)

184
Q

what does a weak pulse mean?

A

poor perfusion

185
Q

what is tactile fremitus?

A

feeling for vibrations when patient says voice sound (assessing density)

186
Q

what would mediate percussion pick up?

A

alterations in lung density

187
Q

what is the dyspnea index? what is it used for?

A

how many breaths it takes to count to 15.

used to figure out exercise intensity during treatment

188
Q

what are the vascular tests that are used to determine perfusion (peripheral arterial disease)

A 
Ankle Brachial Index
Rubor of dependency
Venous filling time
Homan's sign
Claudication time
189
Q

What is electrocardiography? What can it diagnose?

A

12-leads (10 electrodes) that provide different views of the heart and measure electrical activity (4-beat reading).

Diagnostic for heart rate, rhythm, axis, hypertrophy, infarction, and ischemia

190
Q

What does a holter monitor do?

A

Provides 24-hour monitoring of heart rate and rhythm using 1 or 2 leads

191
Q

When is pharmacologic stress testing used? What are the typical medications?

A

If patient unable to reach at least 85% of predicted max HR on standard exercise testing

Adenosine or Persantine

192
Q

What does isotope imaging or radionuclide perfusion imaging test for? What are the typical medications?

A

Reversible vs. irreversible ischemia

Thalium or Technetium (cardiac tracers that light up on CT in coronary arteries)

If pt is ischemic during stress but perfused at rest, they have reversible ischemia

193
Q

What is echocardiography? What does it look for?

A

Ultrasound of the heart

Assesses valvular function, coordination of contraction, thickness of heart muscle, estimated ejection fraction, and estimated pulmonary artery pressure

194
Q

What does a cardiac catheterization look for?

A

Pressure in the chambers, stroke volume, ejection fraction, Pulmonary Vascular Resistance (PVR), Total Peripheral Resistance (TPR), coronary artery perfusion

195
Q

What are the precautions of a patient who just had a cardiac catheterization?

A

Patient should be on bedrest for at least 1 hour due to risk of infarction or stroke.

196
Q

What is Central Venous Pressure (CVP)?

A

Pressure in the right atrium

197
Q

Which has a higher pressure: right atrium or left atrium?

A

Left atrium

198
Q

Which has a higher pressure: right ventricle or left ventricle?

A

Left ventricle

199
Q

What is the normal measure of diffusion? What does this test?

A

25-30 mL/min/mmHg

Tests how fast Carbon Monoxide gets from alveoli to blood

200
Q

What is normal peak flow? What is it like during an asthma attack?

A

9-10 L/sec

Decreased in asthma attack

201
Q

What is the difference between reversible and irreversible ischemia?

A

Reversible: ischemia

Irreversible: necrosis due to prolonged ischemia

202
Q

What is the sign for ischemia on electrocardiogram?

A

S-T segment depressions

203
Q

What are the signs for infarction on electrocardiogram? (3)

A

Presence of pathologic Q waves

S-T segment elevations

T wave changes

204
Q

Should heart rhythm change during exercise?

205
Q

What are the tools in the metabolic cart used for?

A

Differentiating between heart issue, lung issue, vascular issue, or deconditioning

206
Q

A max VO2 of how many METs would determine disability?

207
Q

If a patient has a patent foramen ovale and had pulmonary hypertension, what direction would blood flow inside the heart? Implications?

A

Right to Left (low to high pressure)

Deoxygenated blood into left ventricle and periphery which dilutes the oxygen out of the blood. Patient will experience hypoxymia during exercise.

208
Q

What kind of study would they do with an echocardiogram to figure out if there is a R –> L shunt?

A

Bubble study (radio isotope injected on venous side)

209
Q

How would the diaphragm appear in a patient with COPD? With a flaccid diaphragm? With a spastic diaphragm?

A

COPD: flat (hyperinflation)
Flaccid: higher
Spastic: lower

210
Q

What is more accurate: echocardiogram or cardiac catheterization?

A

Cardiac catheterization

211
Q

Where does a cardiac catheterization lead travel when assessing the right side of the heart? Left side?

A

Right: subclavian vein
Left: femoral artery

212
Q

What is the normal mean PAP (Pulmonary Arterial Pressure)?

213
Q

What can a V/Q scan diagnose?

A

Pulmonary embolism

214
Q

What does a bronchoscope assess?

A

Abnormal tissue or secretions

215
Q

What is a bronchogram?

A

Glorified chest x-ray - inhale a gas that lines airways to visualize on x-ray

216
Q

What is a (+) Bronchogram Sign?

A

When you can view the airways on a regular x-ray (shouldn’t be able to). Indicates consolidation of secretions, increased density, or abnormal pathology.

217
Q

What do pulmonary function tests look for?

A

Restrictive vs. obstructive lung disease

218
Q

Why take sputum cultures?

A

Figure out what organisms are contributing to infection and select appropriate antibiotic.

219
Q

BP reading error: bladder too narrow

220
Q

BP reading error: arm below heart

221
Q

BP reading error: arm above heart

222
Q

BP reading error: back unsupported

223
Q

BP reading error: legs dangling

224
Q

BP reading error: slow inflation rate

A

DBP too high

225
Q

BP reading error: fast deflation rate

A

SBP too low, DBP too high

226
Q

BP reading error: slow deflation rate

A

DBP too high

227
Q

What is the Origin, Insertion, and Innervation of the Diaphragm?

A

Origin: xiphoid process, lower 6 costal cartilages, anterior surfaces of lumbar vertebrae

Insertion: central tendon

Innervation: phrenic nerve (C3-4-5)

228
Q

What innervates the upper trap and the SCM?

A

Spinal Accessory Nerve (CN XI)

229
Q

What nerve segments innervates the scalenes?

230
Q

What nerve segments innervate the abdominals?

231
Q

Normal Tidal Volume?

A

600 (M) 500 (F) mL

232
Q

Normal Total Lung Capacity?

A

6000 (M) 4200 (F) mL

233
Q

Normal Residual Volume?

A

1200 (M) 1000 (F) mL

234
Q

Normal Functional Residual Capacity?:

A

2400 (M) 1800 (F) mL

235
Q

Normal Forced Expiratory Volume in 1 Sec?

A

75-80% FVC (forced vital capacity)

236
Q

Normal FEV1/FVC ratio?

237
Q

Normal Peak Expiratory Flow?

A

9-10 L/sec

238
Q

Which valves are open/closed during isovolumetric relaxation?

A

AV valves open, SL valves closed

239
Q

What valves are closed during isovolumetric contraction?

A

All 4 until ventricular pressure > aortic pressure - SL valves open

240
Q

What is the “lub” sound? “Dub”?

A

Lub: AV valves close (start systole)

Dub: SL valves close (start diastole)

241
Q

What is the EF and functional capacity of a low-risk cardiac patient?

A

EF > 50%

FC: > 7 METS

242
Q

What is the EF and functional capacity of a moderate risk cardiac patient? When do signs/symptoms occur?

A

EF: 40-49%
FC: < 5 METs

S/S at high levels of exertion (> 7 METs)

243
Q

What is the EF of a high risk cardiac patient? When do signs/symptoms occur?

A

EF: < 40%

S/S at low levels of exertion (< 5 METs)

244
Q

When does Phase I of cardiac rehab begin?

A

When the patient is medically stable.

245
Q

What are the goals of Phase I cardiac rehab?

A

Return to independent function
Educate on cardiac rehab & risk factors
Prevent physio/psycho effects of event
Provide home exercise program

246
Q

What kind of exercise occurs during Phase I cardiac rehab?

A

Mode: functional activities

Intensity: low level, focus is on duration not intensity

Target HR: RHR + 20 (not > 120)

Frequency: 30 min/day most days

247
Q

How long can Phase II cardiac rehab last?

A

Up to 36 weeks

248
Q

What test should be performed before beginning phase II?

A

GXT (sub-maximal)

249
Q

What are the goals of Phase II cardiac rehab?

A

Progress from low-level to moderate-level
Promote safe return to activity/exercise
Indepth education on condition management
Initiate lifestyle changes

250
Q

What kind of exercise occurs during Phase II cardiac rehab?

A

Mode: traditional aerobic/resistive

Intensity: high enough to have training effect but low enough not to evoke signs and symptoms; usually 40-50% VO2R or HRR

Frequency: 3-5 x/week

Duration 20-60 min accumlated

251
Q

What are the upper limits for exercise intensity in phase II cardiac rehab?

A

HR 10 bpm below onset of symptoms

RPP below onset of symptoms

Abnormal BP response (drop or rise > 200/100)

Certain “bad” dysrythmias

252
Q

What are some ways to prescribe exercise without a GXT?

A

Pharmacologic stress test

Duke Activity Status Index

253
Q

What are the parameters for exercising patients without a GXT?

A

Must be conservative and closely monitor pt

Start low at 2-4 METS, RHR+20

254
Q

How is activity progressed during phase II?

A

Initial phase
Improvement phase
Maintenance phase

3-6 month period of progressing from low level to moderate-vigorous level

255
Q

How long does Phase III/IV cardiac rehab last?

A

Forever, otherwise cardiac status will deteriorate again.

256
Q

What are the guidelines for progression to independent exercise?

A

Functional capacity > 8 METs
Stable VS response
No abnormal signs/symptoms

Pt demonstrates knowledge of risk factors, abnormal s/s, and disease management

257
Q

What are the guidelines for resistive training?

A

2-3 x/week

Higher reps (8-15) with lower weight

RPE: 11-14

Do not exceed RPP where s/s occur

Avoid valsalva

Use proper form with slow, controlled movements

258
Q

What is the general target of exercise in a stage III/IV cardiac patient?

A

Mode: aerobic

Intensity: 40-80% VO2R or HRR

Frequency: 3-7x/week

Duration: 30-60 min

Interval training may be effective

259
Q

A patient with CAD is at higher risk factor for MI over what MET level?

260
Q

A person who had a CABG should not perform what activities that would damage the chest wound?

A

Shoulder restrictions:

  • No push up to stand
  • No pulling on bed rails
261
Q

What should you keep in mind if exercising a patient with angina?

A 
Pt must be stable
FC must be > 3 METs
Goal is to increase anginal threshold
Prolonged warmup, cooldown
THR 10 bpm < anginal threshold
RPP below symptom level
Lower body exercises
Monitoring
Use nitroglycerin
262
Q

What should you keep in mind if exercising a patient with MI?

A

Consider size/location of MI
How is it being managed
Allow for it to heal (6-8 weeks)
Monitor for chest pain

263
Q

Can you exercise a patient with heart failure?

A

Only if they have stable/compensated heart failure.

GXT with direct gas exchange measurement is indicated. Symptoms can be used to grade intensity since they may be chronotropically incompetent.

264
Q

What is a way to differentiate between neurogenic and vascular PAD?

A

Forward flexion that relieves the pain was neurogenic (foramen opened up and relieved compression on nerve root).

265
Q

What is the main indication of peripheral artery disease?

A

Claudication, especially in the calf.

266
Q

All patients with PAD also have…?

267
Q

How should you exercise a patient with PAD?

A

Start exercise to elicit symptoms in 3-5 minutes and allow pain to reach level 3 on claudication scale followed by rest.

Promote circulation.

268
Q

What neurotransmitter stimulates cholinergic receptors?

A

Acetylcholine

269
Q

What neurotransmitter stimulates adrenergic receptors?

A

Norepinephrine

270
Q

What receptors do cholinergic drugs target?

A

Muscarinic cholinergic receptors (parasympathetic NS)

271
Q

Stimulation of Alpha-1 adrenergic receptors does…?

A

Vasoconstriction of arterioles which increases BP and workload on heart

272
Q

Stimulation of Alpha-2 adrenergic receptors does…?

A

Decreases BP by inhibiting NE

273
Q

Stimulation of the Beta-1 adrenergic receptors does…?

A

Increases HR and contracility

274
Q

Stimulation of Beta-2 adrenergic receptors does…?

A

Bronchodilation and decreased mucus production

275
Q

A cholinergic stimulant is also called what?

A

Parasympathomimetic

276
Q

An anti-cholinergic is also called?

A

Parasympatholytic

277
Q

An adrenergic stimulant is also called?

A

Sympathomimetic

278
Q

An anti-adrenergic is also called?

A

Sympatholytic

279
Q

A Beta-2 agonist would do what?

A

Bronchodilation and decreased mucus production

280
Q

What is a side effect of a beta-blocker used to decrease HR?

A

Bronchoconstriction

281
Q

What do cardiovascular medications do?

A 
Decrease MVO2
Increase myocardial oxygen supply
Control rhythm
Enhance cardiac function
Decrease clotting
Control BP
Lower cholesterol
282
Q

What kind of medication is Nitroglycerin?

A

Nitrate/Vasodilator

283
Q

What is the function of nitrates?

A 
Systemic arterial/venous vasodilation
Decreased preload
Decreased afterload
Decreased cardiac workload and MVO2
Coronary vasodilation
284
Q

Why would a nitroglycerin cause reflex tachycardia?

A

The decreased preload decreases SV and CO which is sensed by the body. This decreases BP which causes HR to increase in order to maintain CO.

285
Q

Why does nitroglycerin cause dependent edema? What can be done to counteract this?

A

Decreased venous tone - blood cannot overcome pull of gravity.

TX: lift legs, ankle pumps

286
Q

What is the procedure for sublingual nitroglycerin (NTG)?

A

Can be taken 3x total within 15 minute window (5 minute intervals) as long as BP doesn’t drop below 100 (in normotensive pt) or drop by 25% (in hypo/hypertensive pt).

If patient has cardiac event during exercise, sit them down and have them take NTG. Assess vitals and call 911 if symptoms persist.

287
Q

What medications end in “-olol”?

A

Beta-blockers

288
Q

What are the functions of beta-blockers?

A 
Decrease HR
Decrease contractility
Decrease lipid metabolism
Decrease insulin sensitivity
Bronchoconstriction if non-selective
Decrease myocardial oxygen consumption
289
Q

What are the rehab concerns of beta-blockers?

A

Blunted HR response
Improved tolerance but still less than normal
Watch for s/s of CHF/CMD and dysrhythmias

290
Q

What are the functions of Calcium channel blockers?

A

Block entrance of calcium to vascular smooth ms (increase vasodilation)
Improve coronary blood flow
Decrease preload/afterload
Prolong AV node refractory period (decreases HR)

291
Q

What are the rehab concerns of Ca channel blockers?

A

Some HR blunting, but not signif
Normal BP/HR response
Use HR to monitor exercise

292
Q

Where are drugs metabolized?

A

Liver and kidneys

293
Q

What are Digoxin and Digitalis?

A

Cardiac Glycosides

294
Q

What are the functions of cardiac glycosides?

A

Increase contractility in impaired heart (CHF)
Inhibit Na/K pump
Intracellular Ca results
Slowing of AV node conduction (increased ventricular filling time)

295
Q

Cardiac glycosides have a low therapeutic index, what does this mean?

A

The therapeutic dose is close to the toxic dose.

296
Q

What are the rehab concerns of cardiac glycosides?

A

Improved ejection fraction
Improved exercise tolerance
Can use HR/BP for monitoring
Watch for digitoxiicity

297
Q

What are the symptoms of Digtoxicity?

A 
Nausea
Vomiting
Diarrhea
CNS changes
Syncope
Dysrhythmias
298
Q

What medications end in “-pril”?

A

ACE inhibitors

299
Q

What is ACE?

A

Angiotensin Converting Enzyme

300
Q

What is the function of an ACE inhibitor?

A

Prevents conversion of angio I –> II

Vasodilation decreases preload and afterload

301
Q

What are the rehab concerns of ACE inhibitors?

A

Minimal side effects (ACE cough)
Takes longer to affect exercise tolerance
Decreased MAP and PAP
Increased CO

302
Q

What are sodium channel blockers?

A

Anti-arrythmics

303
Q

What are the classifications of sodium channel blockers?

A

Ia - slow phase 0, slow conduction, prolongs refractory period (increased ventricular filling)

Ib - minimal slowing of phase 0, minimal slowing of conduction, shortened refractory period

Ic - significant slowing of phase 0, moderate effect on conduction, no effect on refractory period

304
Q

What ions regulate action potentials?

A

Ca2+, Na+, K+, Cl-

305
Q

Why would you use beta-blockers as anti-arrhythmics?

A

Decrease automaticity
Prolong refractory period
Slow HR and conduction
Used in atrial dysrhythmias

306
Q

What does Amiodarone do?

A

Prolongs repolarization. Commonly used for A-fib.

307
Q

What is the problem with using Amiodarone as an anti-arrhythmic?

A

May induce dysrhythmias before reaching therapeutic effect. May also cause liver damage

308
Q

What kind of drugs are Dopamine and Dobutamine?

A

Sympathomimetics

309
Q

What are the functions of sympathomimetics?

A

Stimulate B1 - increase Ca influx, SA node activity, conduction, and contractility

Stimulate B2 - dilation of smooth muscle in bronchioles

Stimulate alpha receptors - increase peripheral vasoconstriction to increase BP

310
Q

What are Alpha-1 blockers usually used for?

A

Hypertension

311
Q

What are the functions of alpha adrenergic blockers?

A

Decrease TPR (vasodilation)
Cause arteriole relaxation
Decrease afterload

312
Q

What are the rehab concerns of alpha blockers?

A

Hypotension
BP may be lower
BP should have normal rise with activity

313
Q

What kind of drug is Atropine?

A

Anti-cholinergic

314
Q

What does an anti-cholinergic do?

A

Increase HR, block parasympathetic outflow (vagal stimulation).

Used in bradycardias and other dysrhythmias.

315
Q

What kind of drug is lasix?

316
Q

What does a diuretic do?

A

Decreases BP

Fluid released from kidney which decreases blood volume and therefore preload.

317
Q

What are the 3 types of diuretics?

A

Loop-Diuretic - acts on ascending loop of Henle (Lasix)

Thiazides - inhibit Na+ resorption

K sparing - weaker, excretes fluid but spares K+

318
Q

Why is important that diuretics are taken on schedule?

A

Orthostatic hypotension
Electrolyte imbalance
Weakness, fatigue, irritability
Lower BP but should respond appropriately to exercise

319
Q

Patients with artificial valves are at risk for what complication?

320
Q

What are anticoagulants?

A

Blood thinners - prevent clots

321
Q

How does Heparin work?

A

Inactivates thrombin

322
Q

What are the 2 types of Heparin? Which one is better?

A

Unfractionated Heparin - IV, more unpredictable

Low molecular weight Heparin - preferred; subcutaneous injection; immediate effect and easier to reach therapeutic level; can mobilize pt with DVT earlier

323
Q

How does Coumadin work?

A

Oral anti-coagulant. Inhibits K+ function.

324
Q

What are you at risk for when you are on anti-coagulants?

325
Q

What are anti-thrombotics? Name 2.

A

Blood thinners

Aspirin and Plavix

326
Q

What are thrombolytics? Name 2.

A

Clot busters

Streptokinase
Tissue Plasminogen Activator (tPA)

327
Q

What are “-statins”?

A

Lipid lowering medications. Lower LDLs

328
Q

What are fibric acids?

A

Lower triglycerides

329
Q

What are the rehab concerns with statins?

A

Neuromuscular problems (myopathy, pain, weakness, paresthesais) or GI upset

330
Q

Beta blockers
Ca channel blockers
Nitrates

A

Decrease O2 demand

331
Q 
Thrombolytics
Antithrombotics
Anticoagulants
Ca channel blockers
Nitrates
A

Increase O2 supply

332
Q

Diuretics
ACE inhibitors
Cardiac glycosides
Beta-blockers

A

Treat heart failure

333
Q 
Diuretics
ACE inhibitors
Sympatholytics
Vasodilators
Ca channel blockers
Alpha-2 adrenergic
A

Anti-hypertensives

334
Q

Class I: Na channel blockers
Class II: beta-blockers
Class III: drugs prolong repolarization
Class IV: Ca channel blockers

A

Anti-arrythmics

335
Q

If a patient is gaining 2 lbs per day… what could this indicate?

A

Fluid retention –> heart failure

336
Q

What are the 4 types of organ transplant medications?

A

Corticosteroids
Cyclosporine
Tacrolimus
Azathioprine

337
Q

What are the side effects of corticosteroids?

A

Osteoporosis, muscle wasting, mood changes, glucose control more difficult

338
Q

What is the #1 cause of death?

A

Heart disease

339
Q

What is Class I heart disease?

A

No limitation in physical activity

340
Q

What is a Class II heart disease?

A

Slight limitation in activity, no problem at rest

341
Q

Class III heart disease?

A

Marked limitation, symptoms with minimal activity, no problem at rest

342
Q

Class IV heart disease?

A

Symptoms at rest with ANY activity

343
Q

How prevalent is primary hypertension? What is it?

A

95% of all cases

Systemic HTN with no known cause

344
Q

What is secondary HTN?

A

HTN with known underlying disease

345
Q

What are the lifestyle modifications for HTN?

A 
DASH eating plan
Weight reduction
Physical activity
Sodium reduction
Limit alcohol consumption
346
Q

What is a relative contraindication for exercise (resting BP)

A

Resting BP 165-180/89-100

347
Q

What is an absolute contraindication for exercise (resting BP)

A

Resting BP > 180/100

Stop exercise if 200/100

348
Q

What is idiopathic pulmonary arterial hypertension (IAPH)?

A

Primary pulmonary HTN - no known cause

349
Q

What is secondary PHTN

A

Secondary pulmonary HTN with known cause, commonly pulmonary disease (excessive vasoconstriction due to decreased O2 levels)

350
Q

What happens to the aorta from atherosclerosis?

A

Thinning of the media, weakening of the wall, aneurysm, rupture

351
Q

What is the atherosclerotic process?

A

Increased permeability to lipoproteins at intima layer of vessel (lesion of intima)

“Response to injury” cycle (platelet aggregation, increased permeability, thrombus formation)

352
Q

What are risk factors for cardiovascular disease?

A 
Cholesterol
Smoking
HTN
Inactivity
Diabetes
Obesity
Family history
Age
Gender
Stress
353
Q

What do HDLs do?

A

Remove cholesterol, block LDLs from smooth muscle wall

354
Q

What are the target numbers for total cholesterol, triglycerides, LDL, HDL?

A

Total cholesterol: < 200 mg/dL
Triglycerides: < 150
LDL: < 100
HDL: > 60

355
Q

How does smoking lead to CVD?

A

Chemicals in tobacco + alterations in blood gases damage vessels and increase permeability to LDLs (lowers HDLs)

356
Q

How does stress lead to cardiovascular disease?

A

Increased circulating catecholamines

357
Q

What is stable angina?

A

Symptoms are reproducible at certain workloads (easier to predict what intensity to avoid)

358
Q

What is unstable angina?

A

Symptoms are unpredictable, occur at random

359
Q

What is Prinzmetal’s angina?

A

Occur due to coronary vasospasm

360
Q

What is silent angina?

A

Coronary insufficiency without pain

361
Q

What is the anginal scale?

A
  1. Light, barely noticeable
  2. Moderate, bothersome
  3. Severe, very uncomfortable
  4. Most severe pain ever
362
Q

How is myocardial infarction diagnosed?

A

EKG and cardiac enzymes

363
Q

What is subendocardial MI?

A

Non-Q Wave MI - involves small area of inner layer of heart; particularly susceptible to ischemia

ST depression

364
Q

What is trans-mural MI?

A

Q-Wave MI - associated with atherosclerosis involving major coronary artery. Extends through whole thickness of heart muscle and usually results in complete occlusion

ST elevation and Q waves

365
Q

How do echocardiogram and cardiac cath look at MI?

A

Echo - ejection fraction, contraction quality

Cath - extent of damage

366
Q

What is medical management for CAD/MI?

A

Acute - supportive measures, restore blood flow and prevent damage

Meds to increase myocardial oxygen supply

Meds to decrease/limit oxygen demand

367
Q

What are the surgical procedures that treat MI?

A

Percutaneous transluminal coronary angioplasty (PTCA)

Coronary artery bypass graft (CABG)

368
Q

What are the PT considerations of CABG?

A 
No lifting more than 5-10 lbs
Limited shoulder ROM
No driving
Hug me pillow
Pain/bronchial hygiene (get pt to cough)
369
Q

Where are pacemakers placed?

A

Infraclavicular fossa into the SVC

370
Q

What are the types of placing of pacemakers?

A

Atrial
Ventricular
Atrial and ventricular
Biventricular

371
Q

What are the 5 pacemaker codes?

A 
Pacing location
Sensing location
Response to pacing
Programmability
Anti-tachyarrythmic function
372
Q

What are acute pacer precautions?

A

Arm sling 24-48 hours
No shoulder elevation above 90 deg for 2 wks
No lifting 5-10 lbs for 2 weeks

373
Q

What are internal defibrillators (AICD)?

A

Similar to pacemaker

Detect lethal arrhythmias and defibrillate to correct

374
Q

An ejection fraction of what percent has an increased risk for lethal arrhythmias or sudden death?

375
Q

What are AICD precautions?

A

Same as pacemaker but longer

Know settings and avoid rate that causes it to fire

376
Q

If the ICD fires, what do you do?

A 
Stop and assess
Provide reassurance
Note what pt was doing
Single shock - consult with doc
Multiple or s/s - ER
377
Q

What are the 3 types of valvular dysfunction?

A

Prolapse (balloons backwards but still closed)

Regurgitation (inadequate seal or closes too slowly)

Stenosis (abnormal narrowing or stiffening)

378
Q

What is Cardiac Muscle Dysfunction?

A

Impaired ability of the heart to EJECT and/or ACCEPT blood

379
Q

What is Congestive Heart Failure?

A

Decreased ability to maintain cardiac output secondary to CMD

380
Q

What is normal cardiac index?

A

2.7-4.0 L/min/m2

< 2.2 = cardiogenic shock

381
Q

What is systolic dysfunction?

A

Inefficient expulsion of blood

382
Q

What is diastolic dysfunction?

A

Decreased ventricular filling

383
Q

CMD is caused by?

A

HTN and CAD

384
Q

HTN leads to…?

A

Excessive workload and over time leads to heart failure

385
Q

CAD leads to…

A

Ischemia and/or MI

386
Q

What is treatment for cardiomyopathy?

A

Heart transplant

387
Q

What is cardiomyopathy?

A

Contraction/relaxation is impaired

Dilaterd (ventricle becomes floppy)
Hypertrophic (dysfunctional ms)
Restrictive

388
Q

What are the PT considerations of heart transplant patient?

A

It is a denervated heart

Sternal precautions

Elevated resting HR from lack of parasympathetic input (100-120 bpm)

Use RPE scale for monitoring

SBP same, DBP elevated

Needs longer warmup/cooldown

389
Q

What is PAD?

A

Peripheral Arterial Disease

Obstruction of the large or medium sized arteries

S/S: intermittent claudication, skin changes, necrosis/amputation

390
Q

Venous insufficiency leads to…?

A

Incompetent veins
LE edema (dependent)
Stasis ulcers
Poor healing

391
Q

DVT is a risk for…?

A

Pulmonary embolism

392
Q

S/S of metabolic syndrome?

A 
Elevated waist circumference
Elevated triglycerides
Decreased HDLs
Elevated BP
Elevated fasting blood glucose

CPT I (4 decks)

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