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Critical Care > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

ventilatory status

A

See if they’re retaining or releasing carbon dioxide
BiPap to increase ventilation
If on ventilator, increase settings to have patient ventilate more

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2
Q

Contraindications of ABG

A

Bleeding disorder
AV fistula
Severe peripheral vascular disease, absence of an arterial pulse
Infection over site

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3
Q

Which artery to use for ABG

A

The radial artery is superficial, has collaterals, and is easily compressed. It should almost always be the first choice
Other arteries (axillary, femoral, dorsalis pedis, brachial) can be used in emergencies

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4
Q

what medicine is in ABG and what can it alter

A

heparin!
Preloaded dry heparin powder
Eliminates dilution problem
Mixing becomes more important
May alter sodium or potassium levels

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5
Q

air bubble in ABG

A

pO2 will begin to rise, pCO2 will fall
Oxygen is 21% of air
Oxygen concentration in blood is lower than air. Air goes from high concentration (bubble) to low concentration (blood), falsely elevating oxygen levels
CO2 concentration in blood is higher than air. CO2 goes from high concentration (blood) to low concentration (bubble), falsely decreasing CO2 levels
pH falsely elevated because of low CO2

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6
Q

Transporting ABG

A

After specimen is collected and air bubble is removed, gently mix and invert syringe
WBCs are active and will consume oxygen (PaO2 will decrease, PaCO2 will increase)
Get blood analyzed within 30 mins
Place ABG on ice to stop WBCs from being active

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7
Q

how to do ABG

A

Withdraw the needle and hold pressure on the site
Protect needle
Remove any air bubbles
Make sure blood is in contact with heparin
Gently mix the specimen by rolling it between your palms
Place specimen on ice and transport to the lab immediately
Pressure on the site and monitor for bleeding

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8
Q

Arterial vs venous pH

A

Arterial: 7.35-7.45
Venous: 7.32-7.42
Venous is lower because low O2 and high CO2

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9
Q

pH compatible with life

A

6.8-7.8

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10
Q

pH regulation methods

A

chemical buffer system
lungs
kidneys

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11
Q

why is bad pH harmful?

A

Bad pH denatures proteins

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12
Q

Chemical buffer system

A

Binds or releases H+
Intra and extracellular buffers

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13
Q

Three major chemical buffer systems

A

bicarb
phosphate
protein buffer systems

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14
Q

Extracellular buffer example equation

A

H2O+CO2=H2CO3=H+ +HCO3-

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15
Q

Intracellular buffers

A

Proteins, organic and inorganic phosphates, hemoglobin in RBC

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16
Q

Lungs in buffer system

A

regulates ventilation in response to CO2 in blood (CSF=central chemoreceptor)
Rise in partial pressure CO2 in arterial blood stimulates respiration, more powerful than the decrease of partial pressure of O2

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17
Q

How long do the lungs take to regulate pH

A

Takes minutes to activate, timing of peak compensation 1-24 hours

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18
Q

COPD and ventilation

A

Patients with COPD should NOT be over oxygenated because it will destimulate breathing

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19
Q

Kidneys in buffer system

A

Regulaes bicarb AND H+ by regenerating bicarb or absorbing them from renal tubular cells

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20
Q

How long do the kidneys take to regulate pH

A

hours to days (12h-5d)
Studies are done from healthy pts, no research from critically ill population

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21
Q

For which acid-base imbalance is the body’s compensatory system poorest

A

metabolic alkalosis

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22
Q

respiratory acidosis clinical manifestations

A

increased ICP (acute) due to: increased CO2 which leads to cerebrovascular dilation and increased cerebral blood flow
Papilledema and dilated conjunctival blood vessels
Hyperkalemia (H+ into cells means K+ comes out of cells and into blood)

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23
Q

Respiratory alkalosis manifestations

A

Lightheadedness from decreased cerebral blood flow
Inability to concentrate
Numbness and tingling (affect nerve function)
Dysrhythmias (hypokalemia)

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24
Q

metabolic acidosis due to loss of bicarb

A

hyperchloremic acidosis
diarrhea
lower intestinal fistula
Use of diuretics (carbonic anhydrase inhibitors such as acetazolamide, dorzolamide)
Early renal insufficiency
Excessive administration of chloride
Administration of parenteral nutrition without bicarb

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25
Q

metabolic acidosis due to excessive accumulation of acid

A

Lactic acidosis (anaerobic metabolism) (infection)
Late phase of salicylic poisoning
Kidney failure
Methanol or ethylene glycol toxicity (found in automotive antifreeze and de-icing solutions, windshield wiper fluid, solvents, cleaners, fuels, and other industrial products)
Ketoacidosis (diabetes)
Starvation

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26
Q

Clinical manifestations of metabolic acidosis

A

HA, confusion, drowsiness
Increased respiratory rate and depth
Nausea and vomiting
Peripheral vasodilation and decreased cardiac output (when pH<7)
Decreased blood pressure
Cold and clammy skin
Dysrhythmias
Shock

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27
Q

Metabolic alkalosis due to loss of H+

A

Vomiting or gastric suction most common
Hypokalemia (kidneys hold on to potassium by excreting H+, K+ moves out of cells and H+ moves in)
Too much bicarb (antacids or sodium bicarb during CPR)

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28
Q

Manifestations of metabolic alkalosis

A

Muscle twitching: affect neuromuscular function
Hypokalemia: arrhythmia

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29
Q

what kind of air do trach patients get

A

warmed and humidified
Risk for infection since nose filters the air and they can’t do that

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30
Q

What allows us to inhale

A

Pressure difference!
Chest cavity pressure has to be lower than outside air pressure
This happens when chest cavity expands

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31
Q

Inhalation

A

Muscles contract, diaphragm contracts (moves down), space increases
Inhalation takes effort and is shorter

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32
Q

Exhalation

A

Longer, passive movement
relaxing, everything is relaxed, space gets smaller, pressure is increased, air gets pushed out

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33
Q

anatomy of bronchi

A

Right bronchus is straight, making it more likely to choke in right lung than left
If ET tube goes too far, it can end up in the right lung and won’t help the left lung
Quick assessment, listen to lungs to make sure they’re both being ventilated

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34
Q

2 phases of respiration

A

Gas exchange between the atmosphere and the body
Gas exchange within the cells (air and blood, and blood and cells)

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35
Q

what drives respiration

A

Levels of carbon dioxide in the arteries
Very little by oxygen level: account for 10% of the total drive
COPD patient (relies on oxygen, big CO2 buildip)

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36
Q

Perfusion

A

the circulation of the blood that must be able to transport oxygen to the tissues and cells

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37
Q

Good ventilation and bad perfusion

A

heart failure, anemia, blood clots, sickle cell

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38
Q

Lung compliance

A

Lung compliance=elasticity=ability of lungs to go back to regular shape

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39
Q

Low lung compliance

A

stiff balloon, easy to get CO2 out, hard to get O2 in. Decreased ventilation. Examples are pleural effusion, obese, pulmonary fibrosis, scoliosis, etc., lung can’t expand

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40
Q

High lung compliance

A

Floppy balloon, easy to get O2 in, hard to push CO2 out. CO2 retention decreases drive to ventilate
COPD or emphysema, reduced ventilation due to decreased ventilatory drive
Alveoli inflated all the time
Can cause barotrauma

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41
Q

V/Q ratio

A

HAS TO MATCH
V=ventilation, Q=perfusion

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42
Q

Low V/Q

A

shunt perfusion–alveoli perfused but not ventilated (ET tube in mainstream bronchus (not in place, air doesn’t get to lungs), obstruction, collapsed lung

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43
Q

Normal V/Q

A

~0.8: alveoli perfused and ventilated

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44
Q

High V/Q

A

dead space ventilation–alveoli ventilated but not perfused (cardiac arrest, anemia, clots)
Poorly ventilated alveoli –> decreased ventilation –> shunt

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45
Q

Silent unit

A

In the absence of both ventilation and perfusion or with limited ventilation and perfusion
Pneumothorax (Less blood going back to the heart leading to less CO and less perfusion)
severe acute respiratory distress syndrome (Inflammation and vasoconstriction cause impaired blood distribution and less perfusion)
(Some condition that also reduce the blood flow…shocks)

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46
Q

V/Q at top/apex of lungs

A

V/Q: 3.3, PaO2: 132, PaCO2: 28

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47
Q

V/Q at middle of lungs

A

V/Q: 1.0, PaO2: 108, PaCO2: 39

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48
Q

V/Q at bottom of lungs

A

V/Q: 0.63, PaO2: 89, PaCO2: 42

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49
Q

functions of a chest tube

A

To remove air or fluid from chest
Chest tube to remove fluid is thicker than that for air
Air trapped=pneumothorax. Chest tube gets placed anterior to remove air. Posterior to remove blood (hemothorax)

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50
Q

Equation for oxygen delivery to tissues

A

Delivery=cardiac output (like perfusion) x O2 content of blood (like ventilation)

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51
Q

What 3 things determine oxygen in blood

A

O2 binding company
% saturation
Dissolved O2

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52
Q

O2 binding capacity

A

How much oxygen the blood can hold
Determined by hgb (anemics don’t have enough, although hemoglobin is well occupied by oxygen, there isn’t enough actual hemoglobin)

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53
Q

% saturation

A

% hemoglobin molecules saturated
Measured by pulse ox
Uses light and photodetector
Can’t distinguish between hgb bound to O2 and CO, so patients with CO poisoning can have an O2 sat of 100
Anmics can also have an O2 sat of 100% but have poor oxygen delivery to tissues (hypoxia without hypoxemia)

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54
Q

Dissolved O2

A

O2 directly dissolved in blood (water)-(can be used by fish, not us). Very small amount (negligible)

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55
Q

PaO2

A

partial pressure of oxygen in arteries
Higher PaO2 means more oxygen dissolved in plasma

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56
Q

SaO2

A

% oxygen saturation of blood in arteries (% of hgb carrying oxgyen

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57
Q

PO2

A

Partial pressure of oxygen in air
Air pressure at sea level: 760 mmHg
PO2 at sea level: 760x21%=160 mmHg
Air pressure at 5000 feet: 633 mmHg
PO2 at 5000 feet: 633x21%=133 mmHg

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58
Q

PO2 at sea level and 5000ft

A

PaO2 at sea level: 100 mmHg
PaO2 at an altitude of 5000 feet: 70 mmHg
Low pressure=more difficult for hemoglobin to bind (likely to have enough oxygen in blood though)
This is why it’s hard to breathe when mountain climbing

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59
Q

Low flow oxygen

A

Low CONSISTENCY
patient breathes some room air along with the oxygen
Not constant and precise concentration of inspired oxygen
Example is nasal cannula

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60
Q

High flow oxygen

A

High CONSISTENCY
Constant and precise concentration of oxygen
Example is ventura mask

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61
Q

hypoxemia

A

below normal levels of oxygen in the blood (not as important)

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62
Q

Hypoxia

A

decrease in oxygen supply to the tissues and cells (can happen even when there’s enough oxygen in the blood)

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63
Q

hypoxemic hypoxia causes

A

Hypoventilation, high altitude, ventilation perfusion mismatch, shunts…

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64
Q

circulatory hypoxia

A

Decreased cardiac output, local vascular obstruction (normal PaO2, but tissue partial pressure is reduced)

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65
Q

Anemic hypoxia

A

CO poisoning (decrease in oxygen carrying capacity)

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66
Q

Histotoxic hypoxia

A

cyanide, toxic substance prevents the tissue to utilize oxygen

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67
Q

Nasal cannula FiO2

A

1 liter: 24% (21% from atmosphere)
2 liters: 28%
3 liters: 32%
4 liters: 36%
5 liters: 40%
6 liters: 44%
If patient is on ventilator, we use FiO2 instead of liters

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68
Q

Nonrebreather

A

Nonrebreathing masks have three one-way valves. Theoretically, it is possible for the patient to receive 100% oxygen. (Depends on the fit of the mask) This mask ensures the most oxygen possible (highest concentration) and is most effective besides intubation
Nonrebreather has 3 one way valves so patient can breathe out but not breathe atmosphere air back in
FiO2 82-100%

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69
Q

Partial rebreather

A

Allows a small amount of atmosphere air to be breathed

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70
Q

Oxygenation for COPD

A

Use bipap

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71
Q

thoracentesis

A

At the bedside
Sterile environment
Fluid gets sent to the lab to test
Fluid in pleural space (can’t go in each space, it’s impossible)
Air in x-ray is black, fluid is white and fluffy in the tissues as well
Crouch forward on pillow for easy access and so everything opens up
X-ray and auscultation for dull sounds to find fluid and know where to put needle

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72
Q

bronchoscopy

A

used to see what’s going on (blockage, inflammation, fluid)
X-ray to find nodules, then CT/MRI, then bronchoscopy and collecting sample
Can remove foreign objects or something blocking the airway
Gag reflex needs to be removed before bronchoscopy, need to monitor gag reflex after and keep them NPO

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73
Q

3 bottle system

A

not very advanced
Does the same stuff as drainage systems
1 bottle used when we need to get air out submerged in 2cm of water to prevent air from going back in

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74
Q

wet vs dry drainage system

A

Wet and dry do the same thing, wet one always needs fluid to maintain suction, dry doesn’t so it’s better. Dry one is also quieter
For both, check consistency and color of drainage

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75
Q

Water seal chamber

A

Has 2cm of fluid
fluctuations correspond to intrathoracic pressure during respiration
Consistent water levels mean lungs are fully expanded, tubing is blocked or disconnected, or the water seal level is incorrect
Continuous bubbling means air leak
Gentle bubbling during expiration is expected in patients with pneumothorax

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76
Q

Suction chamber

A

Slow and steady (or continuous) bubbling is expected when suction is applied
Should be 20 cm of fluid
Continuous suction: pneumothorax
Intermittent suction: fluid drainage

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77
Q

Should you clamp a chest tube?

A

ONLY UNDER CLOSE MONITORING! Very quickly to check for an air leak or change the tubing

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78
Q

Tube dislodged from patient’s side

A

Ask the patient to cough and exhale to prevent air back into the body
Cover the site with a sterile occlusive dressing to prevent air from entering the pleural space
3 sides of tape on dressing allows 1 way valve (air goes out not in)

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79
Q

Tube dislodged from drainage system side

A

Immerse the end of the tube into a bottle of sterile water (tip of the tube is about 2 cm below the water level)

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80
Q

chest tube insertion

A

slight subq emphysema might be present but should not spread. Mark it so you can monitor for spread

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81
Q

Chest tube removal

A

Ask patient to take a deep breath, hold it and bear down while the tube is removed

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82
Q

Milking the chest tube

A

NEVER

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83
Q

Chromosome

A

Microscopic structures in the cell nucleus that contain genetic information

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84
Q

Genome

A

Total genetic compliment of an individal genotype

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85
Q

Gene

A

A unit of heredity

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86
Q

Hypercholesteremia genotype

A

Mutations in low-density lipoprotein (LDL) receptors
mutations in one of the apolipoprotein genes

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87
Q

Phenotype of hypercholesteremia

A

Early onset of CVD
High level of LDL
skin xanthomas
family history of heart disease

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88
Q

Gene mutation

A

Inherited or spontaneous
Inherited: Huntington’s disease. Occurs in the DNA of all body cells
Spontaneous: achondroplasia, marfan syndrome, and neurofibromatosis type 1

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89
Q

Genetic testing vs genetic screening

A

testing: more targeted and individualized approach used to investigate known or suspected genetic disorders
Screening: a broader, systematic process applied to populations or specific groups to identify individuals at risk of genetic conditions, often in the absence of clinical systems

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90
Q

Family history consists of

A

family history 3 generations (parents, siblings, and children)
Personal and medical risk factors
Identification of associated diseases or clinical manifestations

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91
Q

Pulmonary edema

A

Abnormal accumulation of fluid in the lung tissue, the alveolar space, or both
White fluffy in x-ray
BILATERAL!!

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92
Q

Why is pulmonary edema so bad

A

Fluid in alveoli means no room for gas exchange
hypoxic, hypoxemic

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93
Q

Pneumonia vs pulmonary edema

A

PNA is one side usually
PE is both

94
Q

hydrostatic pressure

A

pushes the fluid outside the capillaries, if this was too high, fluid would go into pulmonary interstitial space

95
Q

Oncotic pressure

A

type of osmotic pressure exerted by cells and proteins that can’t cross capillary membrane, pulls fluid back
Higher in pulmonary capillaries than interstitial fluid

96
Q

Why does pulmonary edema occur in infection

A

Capillary permeability is increased in an inflammatory state, like infection, to let WBCs through–how easily fluid can get through

97
Q

If lungs are inflammatory, what side does pulmonary edema occur?

A

bilateral

98
Q

cardiogenic causes of pulmonary edema

A

coronary artery disease
cardiomyopathy
heart valve problems
HTN
Left side HF
high BNP level (brain natriuretic peptide)

99
Q

Left sided HF and pulmonary edema

A

blood volume and pressure build up in left atrium→ increase in pulmonary venous pressure→ increase in hydrostatic pressure that forces fluid out of the pulmonary capillaries

100
Q

Noncardiogenic causes of pulmonary edema

A

lung infections
exposure to certain toxins (ex. chlorine or ammonia)
kidney disease (toxin accumulation)
smoke inhalation
adverse drug reaction
Chest trauma
Sepsis
Low oncotic pressure from not making enough protein or losing too much protein
Lymphatic system problems (can’t drain fluid)

101
Q

Clinical manifestations of pulmonary edema (secretions)

A

A foam or froth is formed–foamy, frothy, blood tinged secretions
Blood and secretions mix with air

102
Q

Assessment and diagnostic findings in pulmonary edema

A

crackles in the lung bases (posterior)
rapidly progress toward the apices of the lungs
X-ray: increased interstitial markings (white fluffy)
Tachycardia from lack of gas exchange (trying to increase CO to increase gas supply)
Pulse oximetry values fall
ABG indicates worsening hypoxemia

103
Q

medical management of pulmonary edema (cardiac)

A

Improve LV function
Vasodilators: IV nitroglycerin
inotropic medications: increases pumping ability
preload reducers: (nitroglycerin and diuretics)
afterload reducers: (dilate blood vessels–nitroprusside, Vasotec, captopril
contractility medications (inotropic)

104
Q

If no response to meds for cardiogenic pulmonary edema

A

intra-aortic balloon pump (reduce afterload)
Balloon is in aorta, deflates during systole so heart can push out blood easier

105
Q

if pulmonary edema is caused by fluid overload, how do we treat it

A

diuretics
Fluid restriction

106
Q

General treatment for pulmonary edema

A

correct underlying disorder
Oxygen (relieve hypoxemia and dyspnea, go from non-rebreather to cpap to intubation)
Morphine for anxiety and to lower oxygen demand

107
Q

Acute respiratory failure (ARF)

A

sudden and life-threatening deterioration of the gas exchange function of the lung

108
Q

ARF ABGs

A

PaO2: <60 mmHg and SaO2 < 90% (Room air)
PaCO2: > 50 mmHg
pH: <7.35

109
Q

CNS ventilation patho of ARF

A

Drug overdose
Head trauma
Infection
Hemorrhage
Sleep apnea

110
Q

Neuromuscular ventilation patho of ARF

A

Myasthenia gravis
Guillain-barre syndrome
ALS (amyotrophic lateral sclerosis)
Spinal cord trauma

111
Q

musculoskeletal ventilation patho of ARF

A

Chest trauma (chest can’t expand)
Kyphoscoliosis
Malnutrition–weak muscles, can’t contract well

112
Q

impaired oxygenation patho of ARF (perfusion)

A

pneumonia
acute respiratory distress syndrome
heart failure
COPD
pulmonary embolism
restrictive lung diseases (restricted lung expansion)

113
Q

postop patho of ARF

A

anesthetic, analgesic, and sedative agents–depress respiration or enhance the effects of opioids and lead to hypoventilation
pain: interfere with deep breathing and coughing
ventilation-perfusion mismatch

114
Q

early clinical manifestations of ARF

A

restlessness
fatigue
HA
dyspnea
air hunger
tachycardia
increased blood pressure

115
Q

late clinical manifestations of ARF

A

confusion
lethargy
tachypnea
central cyanosis
diaphoresis
resp arrest
use of accessory muscles, decreased breath sounds

116
Q

medical management of ARF

A

Correct underlying cause (identify what it is!)
Intubation (non rebreather, then this, gives us time to figure out what’s wrong) and mechanical ventilation
Oxygenation

117
Q

monitoring of ARF

A

ICU
Level of responsiveness (sedated if they’re on vent)
ABG
Pulse oximetry
Vital signs

118
Q

preventing complications of ARF

A

Turning schedule
Mouth care (prevent ventilator associated pneumonia)
Skin care
Range of motion exercises

119
Q

Acute respiratory distress syndrome (ARDS)

A

a severe inflammatory process causing diffuse alveolar damage that results in sudden and progressive pulmonary edema

120
Q

diagnostic criteria of ARDS

A

refractory hypoxemia
chest x-ray with bilateral infiltrates
exclusion of cardiogenic pulmonary edema (no cardiac history and testing looks fine)

121
Q

patho of ARDS

A

damaged capillary membrane greatly increase capillary membrane permeability, causing fluid to get into alveoli
fluids, proteins, and blood cells leak from the capillary bed into the pulmonary interstitium and alveoli
reduced lung compliance: “stiff lungs”
impaired alveolar ventilation

122
Q

acute phase of ARDS

A

rapid onset of severe dyspnea 12-48 hours after the initiating event
aspiration
drug ingestion and overdose
hematologic disorders
prolonged inhalation of high concentration of O2 (oxygen is a drug, too much for too long can lead to ARDS)
shock
trauma or major surgery
fat or air embolism
systemic sepsis

123
Q

24-48 hours after acute phase of ARDS

A

hyaline membranes form

124
Q

7 days after acute phase of ARDS

A

Fibrosis develops

125
Q

assessment and diagnostic findings of ARDS

A

Intercostal retractions
Crackles
Tests
BNP levels (rule out hemodynamic pulmonary edema–heart failure)
If it’s high, it indicates cardiac involvement. Increases when heart gets stretched out. If bnp normal, it’s pulmonary
echocardiography
pulmonary artery catheterization–definitive method to distinguish between hemodynamic (heart failure) and permeability pulmonary edema (ARDS), very risky, check risk vs benefit

126
Q

medical management of ARDS

A

Intubation IMMEDIATELY and increase PEEP so pressure of air can remove fluid
Can’t use diuretics or chest tube
Circulatory support and adequate fluid volume
Nutritional support
Supplemental oxygen

127
Q

PEEP goals and warning

A

PaO2 >60 mmHg or an oxygen saturation level of greater than 90% at the lowest possible FiO2
Reduced CO can happen due to heart damage from pressure (WATCH HR AND URINE OUTPUT)

128
Q

systemic hypotension and ARDS

A

Hypovolemia from increased capillary permeability, less fluid in vessels and more in alveoli
Pushing fluid out of alveoli can put it back into circulation

129
Q

pulmonary embolism

A

obstruction of the pulmonary artery
Air, fat, amniotic fluid, and septic (bacteria invasion of the thrombus)
Alveolar dead space (because no perfusion)
Substances released from the clot and surrounding area→ regional vasoconstriction
Decreased PERFUSION not ventilation since clot is blocking pulmonary artery

130
Q

pain and d dimer in PE

A

SEVERE STABBING CHEST PAIN just there, not inspiration
Normal D-dimer results can rule out a PE

131
Q

What is seen in a PE

A

Tachypnea, decreased PCO2
Hypoxia, decreased PO2
Alkalosis
Dyspnea
Tachycardia
Hemoptysis
Decreased cardiac output

132
Q

Heparin for PE

A

IV HEPARIN AND NORMAL SALINE ARE SEPARATE LINES!! DON’T MIX

133
Q

Risk factors for PE

A

Immobility, obesity, DVT, postop/partum, oral contraceptives, venous pooling with emboli formation

134
Q

Pulmonary HTN

A

mean pulmonary artery pressure exceeds 25 mmHg
normal pressure 15-18 mmHg

135
Q

How to confirm pulmonary HTN diagnosis

A

Right heart catheterization to confirm the diagnosis (deflate immediately after testing pressure)

136
Q

primary and secondary pulmonary HTN

A

primary: women 20-40y fatal in 5 years (rare)
secondary: existing cardiac or pulmonary disease (COPD)
increases the volume or pressure of blood entering the pulmonary arteries
narrows or obstructs the pulmonary arteries

137
Q

Patho of pulmonary HTN

A

progressive remodeling of pulmonary vasculature→ increase resistance of pulmonary vasculature → won’t make it better, just slows progression
collagen vascular disease
congenital heart disease
anorexigens
chronic use of stimulants
portal hypertension
HIV
vascular injury

138
Q

clinical manifestations of pulmonary HTN

A

Dyspnea!! NUMBER ONE
substernal chest pain
weakness
fatigue
syncope
occasional hemoptysis
signs of right-sided heart failure
anorexia
abdominal pain in RUQ

139
Q

assessment and diagnostic findings of pulmonary HTN

A

chest x-ray
Pulmonary function studies
ECG
Echo
Ventilation-perfusion scan
sleep studies
autoantibody tests (women 20-40 w lupus)
HIV tests
LFT
cardiac cath

140
Q

what does pulmonary function study show in pulmonary HTN

A

may be normal or have slight decrease in lung compliance and vital capacity, with mild decrease in diffusing capacity

141
Q

what does ECG show in portal HTN

A

right ventricular hypertrophy (blood coming back from)
right axis deviation (increase the chance of MI)
tall peaked P waves in inferior leads
tall anterior R waves
ST-segment depression
T-wave inversion

142
Q

what does echo show in pHTN

A

assess the progression of the disease and rule out other conditions with similar signs and symptoms

143
Q

what does ventilation-perfusion scan show in pHTN

A

detects defects in pulmonary vasculature, such as pulmonary emboli

144
Q

what do sleep studies show in pHTN

A

Want to rule out other factors such as apnea, something obstructive or central

145
Q

why LFTs for pHTN

A

Cirrhosis leads to engorgement of the liver. Used to r/o portal HTN

146
Q

cardiac cath for pHTN

A

right side of the heart: elevated pulmonary arterial pressure-determine whether there is a vasoactive component to the pulmonary hypertension by using vasodilating medications such as nitric oxide
Indirectly tests pressure in lungs

147
Q

medical management of pHTN

A

vasodilation of pulmonary arteries
anticoags
oxygen and exercise
diuretics
ca+ channel blockers

148
Q

vasodilator for pHTN

A

phosphodiesterase-5 inhibitors
sildenafil

149
Q

epoprostenol (Flolan)

A

For pHTN
flow to blood vessels
Continuously injected through an IV***
Potential side effects of epoprostenol include jaw pain, nausea, diarrhea, leg cramps

150
Q

Iloprost (Ventavis)

A

For pHTN
inhaled every three hours through a nebulizer
Side effects associated with iloprost include chest pain — often accompanied by headache and nausea — and breathlessness.
Expensive
avoid it when you are pregnant or breastfeeding

151
Q

Mucolytics

A

For resp tract
Hypertonic saline (3%) inhalation
Acetylcysteine (Mucomyst) inhalation (sulfur content, smelling like rotten eggs)
Both of the above can trigger bronchospasm.
Brings out sputum

152
Q

Ipratropium (Atrovent)

A

anticholinergic
for resp tract
Adverse effect: dry mouth and irritation of pharynx
Too much can raise intraocular pressure in patients with glaucoma

153
Q

adverse effects of albuterol (proventil)

A

tachycardia, angina, tremor

154
Q

Penetrating trauma management

A

restore and maintain cardiopulmonary function.
Chest tube: re-expansion of lungs

155
Q

Simple pneumothorax

A

More likely in tall young male caucasian smokers
air enters the pleural space through a breach of either the parietal or visceral pleura
through the rupture of bleb (blister) or bronchopleural fistula
healthy person in the absence of trauma due to rupture of an air-filled bleb, or blister, on the surface of the lung
may associated with diffuse interstitial lung disease and severe emphysema (lung structure is full of blisters)

156
Q

Procedure for simple pneumothorax

A

2nd intercostal space is where needle goes bc thinner skin
Device used to get rid of air
Stable: hemodynamically stable (pressure, sats, HR, conscious)
Vasovagal response can happen when putting in and taking out chest tube
May wear nonrebreather during procedure

157
Q

Tension pneumothorax

A

The air that enters the chest cavity with each inspiration is trapped
Usually due to trauma
LIFE-THREATENING

158
Q

Initial assessment of tension pneumo

A

Inspection of the airway, thorax, neck veins, and breathing difficulty
Asymmetrical movement of the chest, breath sounds, tracheal shift
No breath sounds on the affected side
Nasotracheal and mediastinal deviation EMERGENCY!! Tracheostomy necessary, intubation wouldn’t work
Black lung on x-ray

159
Q

Treatment of tension pneumo

A

immediately relieve pressure!

160
Q

Clinical manifestations of tension pneumothorax

A

depends on the size and cause
the clinical picture is: air hunger, agitation, increasing hypoxemia, central cyanosis, hypotension, tachycardia, and profuse diaphoresis
With trauma, there’s blood in the pleural space

161
Q

Medical management of tension pneumothorax

A

Small chest tube: 2nd intercostal space anterior to get rid of air
inserting a large-bore needle (14-gauge)
large chest tube: if hemothorax also
fourth or fifth intercostal space at the midaxillary line
O2

162
Q

When is chest wall opened up for tension pneumo

A

If more than 1500 mL of blood is aspirated initially by thoracentesis or if chest tube output continues at greater than 200mL/h

163
Q

Open pneumo

A

Pneumothorax associated with a chest wall defect, such that the pneumothorax communicates with the exterior
a kind of traumatic pneumothorax: the wound is large enough to allow air to pass freely in and out of the thoracic cavity with each attempted respiration.

164
Q

treatment of open pneumo

A

Seal the wound immediately with vented chest seal (or tape 3 sides of a large occlusive dressing and create a one way valve to allow air to get out and not in
Asherman Chest Seal

165
Q

sternal and rib fractures

A

most common in motor vehicle crashes with a direct blow to the sternum via the steering wheel
rib fractures are the most common type of chest trauma
5th-9th ribs are the most common sites of fractures
fractures of the lower ribs are associated with injury to the spleen and liver (dangerous!)

166
Q

Clinical manifestations of sternal fractures

A

anterior chest pain
overlying tenderness
ecchymosis
crepitus
swelling
possible chest wall deformity

167
Q

clinical manifestations of rib fractures

A

similar to sternal fractures
severe pain
point tenderness
muscle spasm over the area of the fracture that are aggravated by coughing, deep breathing, and movement
the area around the fracture may be bruised
Possible atelectasis from lung not expanding (they don’t want to take deep breaths because it hurts)

168
Q

medical management of rib/sternal fractures

A

relieving pain is #1
sedation
intercostal nerve block
ice over the fracture site
chest binder to stabilize chest
pain abate 5-7 days
Avoiding excessive activity
Treating any associated injuries
Surgical fixation is rarely necessary unless fragments are grossly displaced and pose a potential for further injury
Healed in 3-6 weeks (very vascular area)
Bump may be left on affected side after healing

169
Q

flail chest

A

free-floating segment of rib cage resulting from multiple rib fractures
may result as a combination fracture of ribs and costal cartilages or sternum

170
Q

chest wall in flail chest

A

chest wall loses stability (opposite movement, peridiscal movements, chest wall moves out during inspiration EXCEPT that part where the rib is. This is bc pressure is lower so the higher atmosphere pressure pushes the piece IN. Opposite on exhalation), causing respiratory impairment and usually severe respiratory distress

171
Q

supportive care for flail chest

A

Ventilatory support, clearing secretions, controlling pain (nerve blocking, high thoracic epidural blocks, PCA)

172
Q

care for severe flail chest

A

endotracheal intubation and mechanical ventilation, chest binder
surgery is rare

173
Q

pulmonary contusion

A

Blunt trauma to the chest, resulting in hemorrhage and localized edema–leakage of serum protein
most common potentially life-threatening chest injury
may not be evident initially
may involve a small portion of one lung, a massive section of a lung, one entire lung or both lungs
Common in athletes
motor vehicle accident: most common cause
damage to the capillaries
no cut or tear, just a bruise

174
Q

clinical manifestations of pulmonary contusion

A

Decreased breath sounds, tachypnea, tachycardia, chest pain, hypoxemia, and blood-tinged secretions to more severe tachypnea, tachycardia, crackles, frank bleeding, severe hypoxemia, and respiratory acidosis
Signs of hypoxemia: agitation or combative irrational behavior
Productive cough with frothy, bloody secretions (Severe)

175
Q

medical management of pulmonary contusion

A

maintaining the airway
providing adequate oxygenation
controlling pain
antimicrobial therapy

176
Q

cardiac tamponade

A

compression of the heart resulting from fluid or blood within the pericardial sac
caused by blunt, penetrating trauma, diagnostic cardiac catheterization, angiographic procedures, and pacemaker insertion

177
Q

symptoms of cardiac tamponade

A

Sudden hypotension, distended neck veins, muffled heart sound

178
Q

treatment of cardiac tamponade

A

pericardiocentesis

179
Q

subq emphysema

A

with chest trauma, air may enter the tissue planes and pass for some distance under the skin (e.g, neck, chest)
Skin under eyes and scrotum are thin so air will likely go under there
the tissues give a crackling sensation when palpated
the subcutaneous air produces an alarming appearance as the face, neck, body, and scrotum become misshapen by subcutaneous air
not a serious complication
spontaneously absorbed, no treatment needed

180
Q

when is treatment needed for subq emphysema

A

a trach is indicated if airway patency is threatened by pressure of the trapped air on the trachea (tracheal deviation, tracheostomy)

181
Q

Positive pressure MV

A

Pushes air into lungs

182
Q

Negative pressure MV how it works

A

Works like a vacuum to suck air out and pull chest open (makes chest more negative)
Likely for patients with thoracic deformities (kyphosis or distortion of spine)

183
Q

Negative pressure MV used for who

A

Used for chronic respiratory failure associated with neuromuscular conditions
Not for unstable conditions

184
Q

Important things about negative MV

A

Made of fiberglass
Has to fit the patient’s chest cavity perfectly to create a good seal. If a patient grows, they need to readjust the cuirass
For patients with a deformity of chest wall
Wearing this at home when they are stable
More likely to have PNA or another disease, they come to hospital for acute situations
Goes over clothes, doesn’t have to be on skin

185
Q

noninvasive positive pressure MV (NPPV)

A

Delivers positive pressure via masks
Eliminates the need for ET intubation or trach
Decreases the risk of nosocomial infections such as PNA since it’s noninvasive

186
Q

Contraindications of NPPV

A

Respiratory arrest
Serious dysrhythmias
Cognitive impairment
Head or facial trauma
Aspiration pneumonia if they are nauseous and throw up

187
Q

CPAP

A

NPPV
Oxygenation
Obstructive sleep apnea (obese patients)
Same pressure

188
Q

BiPAP

A

NPPV
Ventilation
Central sleep apnea
Makes alveoli big and small (makes alveoli TWO sizes)
TWO different pressures (inhalation and exhalation)
COPD

189
Q

when to intubate pt

A

Worsening ABGs
Worsening encephalopathy or agitation
Inability to tolerate the mask
Hemodynamically unstable

190
Q

meds for intubation

A

Sedative induction agent: propofol: onset 15-45 seconds, duration 5-10 minutes, adverse effect: hypotension
Paralytic induction agent: succinylcholine: onset 45 seconds, duration 6-10 minutes, adverse effect: hyperkalemia

191
Q

how to assess for placement of intubation

A

Check symmetry of chest expansion, auscultate breath sounds or anterior and lateral chest bilaterally
Obtain order for chest x-ray to verify proper tube placement

192
Q

Documentation of intubation

A

Depth of tube (markings)
Size of tube (nursing note)
Chest x-ray taken

193
Q

Normal cuff pressure for intubation

A

20-25 mmHg

194
Q

high cuff pressure

A

Tracheal bleeding
Ischemia
Pressure necrosis (pressure ulcer)

195
Q

low cuff pressure leads to

A

Air leak
Aspiration pneumonia

196
Q

When does a patient get a trach

A

After 2 weeks of intubation
Happens in the OR

197
Q

Life threatening complications of ET intubation

A

Unintentional removal of tube (Patient not being sedated long enough so they try to remove the tube before deflating)
Laryngeal swelling
Hypoxemia
Most likely during 8-10AM during change of shift, have someone watch patient

198
Q

extubation process

A

Give heated humidified oxygen and maintain the patient in a sitting or high fowler’s position
Monitor VS
Keep NPO for the next few hours
Teach pt to perform coughing and deep breathing exercises

199
Q

ET vs trach

A

ET tube can only be left in place for up to 2 weeks

Tracheostomy:
Increase patient comfort and oral hygiene
Lower hospital mortality
Higher successful weaning rates in ICU patients receiving prolonged MV

200
Q

Indications for trach

A

Bypass an upper airway obstruction
Removal of secretions
Long term use of mechanical ventilation
Neuromuscular disease can cause paralysis of muscles responsible for breathing
Monitor q6-8h!!

201
Q

Early complications of trach

A

Bleeding
Pneumothorax
Air embolism
Aspiration
Subq or mediastinal emphysema (only serious when it leads to tracheal deviation, you would have a trach but we’re already trach’ed, make sure tube is working)
Recurrent laryngeal nerve damage
Posterior tracheal wall penetration

202
Q

long term complications of trach tube

A

Airway obstruction from accumulation of secretions of protrusion of the cuff over the opening of the tube
Infection
Rupture of the innominate artery
Dysphagia
Tracheoesophageal fistula
Tracheal dilation
Tracheal ischemia
Necrosis

203
Q

Complication prevention of trach

A

Administer adequate warmed humidity
Maintain cuff pressure at appropriate level
Suctions as needed per assessment findings
Maintain skin integrity. Change tape and dressing as needed or per protocol
Auscultate lung sounds
Monitor for s/s of infection, including temperature and WBC count
Administer prescribed oxygen and monitor oxygen saturation
Monitor for cyanosis
Maintain adequate hydration of the patient (helps loosen secretions)
Use sterile technique when suctioning and performing trach care

204
Q

Closed suctioning of trach

A

Allow rapid suction when needed and to minimize cross-contamination by airborne pathogens
Decreases hypoxemia, sustain PEEP, decrease patient anxiety
Protects staff from patient secretions

205
Q

lab values indications for MV

A

PaO2: <55 mmHg
PaCO2: >50 mmHg and pH <7.32
Vital capacity (the total amount of air exhaled after maximal inhalation): <10 mL/kg
Negative inspiratory force: <25 cm H2O
FEV1 (forced expiratory volume of the 1st second): <10 mL/kg

206
Q

Ventilator modes

A

Most to least support:
Assist control (AC)
Synchronized intermittent mandatory ventilation (SIMV)
Pressure support ventilation (for when they’re ready to be weaned)

207
Q

Volume cycled MV

A

delivers a preset volume of air with each inspiration

208
Q

Pressure cycled MV

A

delivers a flow of air (inspiration) until it reaches a preset pressure

209
Q

A/C ventilation

A

Assumes patient isn’t breathing on their own, does all breathing for them
Patients may try to take a breath on their own. Machine senses a dip in pressure and delivers the breath for patient (not recommended for patients who try to breathe on their own)

210
Q

SIMV MV

A

Between ventilator delivered breaths, the patient can breathe spontaneously with NO assistance from the ventilator on those extra breaths
Bucking (patient-ventilator dyssynchrony) is reduced
Preset number of ventilator breaths is decreased
patient does more of the work of breathing

211
Q

PSV MV

A

Applies a pressure plateau to the airway to decrease resistance within the tracheal tube and ventilator tubing (this is similar to CPAP!)
No mandatory breaths
Pressure support is reduced gradually as the patient’s strength increases
A SIMV backup rate may be added for extra support

212
Q

If patient becomes confused or starts bucking what do we do

A

assess for hypoxia and manually ventilate on 100% oxygen with a resuscitation bag***

213
Q

Monitoring patient on a ventilator

A

Ventilator settings
Water in the tubing, disconnection, or kinking of the tubing
Humidification and temperature
Alarms (turned on and functioning properly)
Pulmonary auscultation
Interpretation of ABGs

214
Q

complications of MV

A

alterations in cardiac function (hypotension)
barotrauma and pneumothorax (open pressure relief valves to allow air to escape)
Pulmonary infection
Abdominal distension

215
Q

minute volume

A

Volume of air moved out of the lungs per unit of time
Tidal volume * frequency
Tidal volume is determined by weight of the patient

216
Q

High pressure alarm in ventilator

A

Increase in peak airway pressure (high pressure alarms) (machine says woah something is preventing me from getting air in, I need to pump harder)
Causes:
Coughing
Pneumothorax
Kinking of tubing

217
Q

Low pressure alarm in ventilator

A

tubing disconnected

218
Q

How do you know when to wean patient from ventilator

A

VS and spontaneous breathing trial

219
Q

weaning criteria for ventilator

A

Emphasize the importance of checking ABGs
Improvement of respiratory failure
Absence of major organ failure
Intact ventilatory drive: ability to control their own level of ventilation
Functional respiratory muscles
Appropriate LOC
Cooperation
Intact cough and gag reflex
Ale to expectorate secretions
Functional respiratory muscles with ability to support a strong and effective cough

220
Q

Weaning criteria for ventilator (numbers)

A

Vital capacity 10-15 ml/kg
Maximum inspiratory pressure at least -20 cm H2O
Tidal volume: 7-9 ml/kg
Minute ventilation: 6L/min
Rapid/shallow breathing index: below 100 breaths/min/L; PaO2 >60 mmHg with FiO2 <50%

221
Q

weaning to exhaustion

A

RR> 35/min
SpO2 <90%
HR >140/min
Sustained 20% increase in HR
SBP >180 mmHg, DBP>90 mmHg
Anxiety
Diaphoresis

222
Q

how to wean for A/C and SIMV

A

A/C: control rate decreased
SIMV: decrease until pt breaths spontaneously

223
Q

Weaning trials for ventilation

A

Using a T-piece of trach mask disconnected from the ventilator, receiving humidified oxygen only and performing all work of breathing
ABG after 20 mins
Watch for distress
If clinically stable, the patient can be extubated within 2-3 hours after weaning and allowed spontaneous ventilation by means of a mask with humidified oxygen
Closely monitor their VS and ABGs

224
Q

weaning from tube

A

If frequent suctioning is needed to clear secretions, tube weaning may be unsuccessful
Secretion clearance and aspiration risks are assessed to determine whether active pharyngeal and laryngeal reflexes are intact
Once the patient can clear secretions adequately, a trial period of mouth breathing or nose breathing is conducted
Downsize the tubing
Replaced by a cuffless trach tube
Change to a fenestrated tube

225
Q

passy muir valve

A

Helps them speak by covering hole
Improved senses, oxygenation, PEEP, aspiration, etc. Patients like this more in terms of quality of life

226
Q

contraindications of passy-muir

A

inflated cuff
excessive secretions
Severely ill pts

227
Q

Sedatives for MV

A

Decreases anxiety
Lorazepam
Midazolam (versed)
Dexmedetomidine (precedex)
Propofol (diprivan)
short acting barbiturates

228
Q

short acting barbiturates

A

Pentobarbital
Methohexital
Thiopental

229
Q

Neuromuscular blocking agents

A

Paralyzes patients if they’re fighting ventilator
Pancuronium (pavulon)
Vecuronium (norcuron)
Atracurium (tracrium)
recoronium (zemuron)

230
Q

Unwanted side effects of neuromuscular blocking agents

A

Make sure always connect to the vent
More chance for skin breakdown
Eye care (corneal abrasions)
Venous thromboembolism (turn the patient)

Critical Care (5 decks)

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