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CMPP > pulmonary circulation > Flashcards

pulmonary circulation Flashcards

1
Q

routine labs to diagnose Cor Pulmonale

A

CXR
EKG
Echo

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2
Q

What is the most accurate way to diagnose Cor pulmonale

A

right heart catheterization

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3
Q

how do we identify underlying lung disease of cor pulmonale?

A

spirometry
CT
V/Q scan

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4
Q

how do we treat PEs in Cor pulmonale?

A

anticoag

thrombolytics

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5
Q

How do we treat COPD in Cor Pulmonale?

A

bronchodilation and management of infxn

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6
Q

When do we give oxygen therapy to Cor Pulmonale patients?

A

<88%

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7
Q

chance of 5 year survival for COPD patients who develop cor pulmonale?

A

30%

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8
Q

how does CF cause an acid-base imbalance?

A

pooling of excessively thick mucus obstructs airways causing hypoventilation.

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9
Q

what is the single largest call of bronchiectasis

A

Cystic Fibrosis

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10
Q

why might CF cause diarrhea or weight loss?

A

thick secretions in pancreatic duct make it difficult to release digestive enzymes -> poor absorption –> diarrhea (steatorrhea)

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11
Q

VTE (venous thromboembolisms) encompass what 2 interrelated conditions?

A

DVTs and PEs

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12
Q

where do most PEs occur from?

A

DVts in deep veins of LE

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13
Q

what is the most important acute complication of DVT?

A

symptomatic PEs

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14
Q

what is the leading cause of preventable in-hospital mortality

A

PEs

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15
Q

definition of a thrombus

A

a solid mass composed of platelets and fibrin with a few trapped red and white blood cells that forms within a blood vessel

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16
Q

definition of pleural effusion

A

an abnormal colelction of fluid in the pleural space resulting from excess fluid production or decreased absorption

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17
Q

most common manifestation of pleural dz

A

pleural effusion

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18
Q

Pleural effusions are most caused by

A

CHF (most)
cancer
pneumonia

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19
Q

mechanism of pleural effusion

A 
Altered permeability of pleural membranes
     (Malignancy, PE)
Reduction in intravascular pressure
     (Cirrhosis)
Increased capillary hydrostatic pressure
     (CHF)
Reduction of pleural space pressure
     (Meosthelioma (asbestos exposure))
Decreased lymphatic drainage due to blockage
     (malignancy)
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20
Q

two types of pleural effusion

A

transudates and exudates

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21
Q

what kind of effusion does atelectasis or HF have?

A

transudates

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22
Q

extravascular fluid with low protein in Pleural effusions

A

transudates

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23
Q

what kind of effusion does Malignancy, pneumonia, PE, TB, pancreatitis have?

A

exudates

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24
Q

extravascular fluid due to vessel alteration during inflammation, high protein, in pleural effusions

A

exudates

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25
Q

sex ratio in pleural effusion

A

even

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26
Q

who gets systemic lupus more?

A

women

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27
Q

who gets mesothelioma more?

A

men

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28
Q

who gets prancreatitis more?

A

men

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29
Q

who gets malignancies more?

A

women

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30
Q

presentation of pleural effusions

A 
dyspnea
cough
chest pain
LE edema, orthopnea, PND
night sweats, fever, hemoptysis, weight loss --> TB
fever, purulent sputum --> pneumonia
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31
Q

symptoms that make you think effusion due to TB

A

night sweats
fever
hemoptysis
weight loss

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32
Q

symptoms that make you think effusion due to pneumonia

A

fever

purulent sputum

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33
Q

no physical findings of effusions below this amount

A

300mL

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34
Q

physical findings of effusions?

A 
dull to percussion
decreased tactile fremitus
diminished respiratory expansion
tracheal displacement
diminished/inaudible breath sounds
egophony
pleural friction rub
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35
Q

when does tracheal displacement occur and how?

A

when there’s >1L of liquid in effusion and displaces TOWARDS effusion

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36
Q

egophony

A

“e” to “a”

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37
Q

is thoracentesis diagnostic or therapeutic?

A

both

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38
Q

what is CXR best used for?

A

CHF

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39
Q

physical findings on CXR for effusion?

A

rarely diagnostic

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40
Q

what does the fluid look like in an effusion when there’s a malignancy?

A

redish

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41
Q

when do you do a needle biopsy with pleural effusions?

A

when you suspect TB or CA

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42
Q

normal amount to drain out of an effusion?

A

500-1000ml

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43
Q

effusion treatment

A

drainage
manage underlying etiology
pleurodesis
thoracostomy

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44
Q

installing an irritant into a space causing inflammation and fibrosis (decreases pleural space and prevents fluid buildup)

A

pleurodesis

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45
Q

what do they use to cause irritation in pleurodesis

A

talc powder

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46
Q

what meds do we use for effusions

A

antibiotics- infections
vasodilators- decrease preload
diuretics-decrease volume and edema
anticoagulants-PEs

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47
Q

most common exudative cause for effusions

A

parapneumonic

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48
Q

embolus definition

A

as a clot propagates, a piece may dislodge or fragment and embolize to pulmonary artery

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49
Q

when does a collapsed lung occur?

A

when air leaks in the pleural space

50
Q

causes of pneumothorax

A 
chest injury
underlying lung dz
ruptured air blebs
mechanical ventilation (PEEP)-too high
spontaneously
51
Q

who gets more pneumothoraxes?

A

men

52
Q

tall young man that comes to the ER with complaint of dyspnea

A

pneumothorax

53
Q

risk factors for pneumothorax

A 
male
smoking
20-40 yo
tall
underweight
genetics
COPD
mechanical ventilation
hx pneumo
54
Q

pneumothorax symptoms

A 
chest pain (sharp on affected side)
dyspnea (severity based on severity of pneumo)
55
Q

complications of penumos

A 
recurrence
persistent air leak
hypoxemia
cardiac arrest
respiratory failure
shock
56
Q

collapsed lung on CT or CXR

A

BLACK

57
Q

pneumothorax treatment

A

observation (most common)
needle or chest tube
surgery
**consult with surgeon

58
Q

where does a small embolism settle?

A

distal bronchioles

59
Q

where do massive emboli settle?

A

in the middle of the pulmonary trunk infarcting both lungs! AGH!

60
Q

pathophysiology of VTE

A

pulmonary artery obstruction –> platelets release serotonin –> increase in pulmonary vascular resistance

61
Q

pathophysiology of VTE

A

artery obstruction –> redistribution of blood flow –> poor gas exchange

62
Q

increased pulmonary vascular resistance leads to

A

increased RV afterload and decreased CO which leads to RV failure

63
Q

perfusion without ventilation

A

shunt

64
Q

results in blood not traveling to the lungs therefore pulmonary blood flow is abnormally reduced and blood not get oxygenated –> cyanosis and hypoxia

A

right to left shunt

65
Q

VTE risk factors (broad categories)

A

patient-related
disease states
surgical factors
hematologic d/o

66
Q

patient related VTE risk factors

A 
>40 y/o
obesity
varicose veins
OCP / HRT
immobility
long trips
pregnancy
smoking
prior DVT
antipsychotics
central venous line
admission < 6 mo
67
Q

disease states VTE risk factors

A 
malignancy
CHF
nephrotic syndrome
MI
IBD
spinal cord injury
pelvic, hip, long bone fx
COPD
paralytic stroke
chronic renal dz
68
Q

surgical factors for VTE

A 
hip surgery
pelvic surgery
CABG
urologic surgery
neurosurgery
69
Q

hematologic disorders

A 
factor 5 leiden
protein C or S deficiency
antithrombin III deficiency
antiphospholipid Ab
lupus anticoag
P-vera
70
Q

3 factors that contribute to thrombosis (virchow’s triad)

A

stasis
vessel wall injury
hypercoagulability

71
Q

venous stasis contributors in virchow’s triad

A

immobility
paralysis
a fib
LV dysfunction

72
Q

vascular injury contributors in virchow’s triad

A

indwelling
catheter
trauma
surgery

73
Q

hypercoagulability contributors in virchow’s triad

A

protein C and S
deficiency
antithrombin deficiency
malignancy

74
Q

DVT symptoms

A 
sudden swelling in affected limb
limb pain/tenderness
pain on dorsiflexion
dilated superficial collateral veins
cyanosis or pallor
warm skin over area of thrombosis
lack of distal pulses
75
Q

PE symptoms

A

dyspnea + tachypnea
syncope, hypotension, cyanosis (massive PE)
pleuritic pain, cough, hemoptysis (small peripheral PE near pleura)
leg pain/swelling
DEATH!? :(

76
Q

non thrombotic PEs

A

fat
tumor
air
catheter

77
Q

Labs to diagnose DVTs

A

D-dimer, but non-specific
ABGs not helpful
venous u/s in high probability with + d-dimer

78
Q

Labs to diagnose PEs

A

D-dimer is increased >90% in PE
not specific though, so only used to rule out PEs
ABGs not helpful
EKG nonspecific

79
Q

what do you see on a CXR for PEs

A

normal

80
Q

Venous U/S on PE diagnosis

A

loss of compressibility

81
Q

diagnostic test of choice for PE

A

CT

82
Q

most specific, gold standard for PE diagnosis

A

Pulmonary angiography

83
Q

when to do pulmonary angiography for PE diagnosis

A

if high index of suspicion and all tests are negative

84
Q

PE Diagnosis, what do we see on V/Q scan

A

if normal PE excluded

85
Q

PE outcome

A

most deaths are sudden
prognosis is good if dx made and treatmnent started
5% re-embolize

86
Q

PE treatment

A

anti-coags
thrombolytics
thrombectomy/embolectomy
inpatient vs outpatient

87
Q

anti-coagulants for PE

A

heparin or LMWH x5d

overlap with coumadin for 1st 4-5 days, continue for atleast 3 months (INR 2-3)

88
Q

thrombolytics for PE

A

dissolves clots by activating plasminogen to plasmin, plasmin degrades fibrin

administer for hemodynamically unstable patients

89
Q

ABSOLUTE contraindications for thrombolytics

A 
GI bleed within 6 months
Active or recent internal bleeding
Hx of hemorrhagic stroke
Intracranial or intraspinal dz
Recent cranial surgery or head trauma
Pregnancy
90
Q

thombectomy/embolectomy

A

Used less frequently due to incidence of rethrombosis

Reserved for massive PE when absolute contraindication for thrombolysis is present

91
Q

IVC filter as a treatment for PE treatment

A

Used for unstable PE
When there is a contraindication to anticoagulation
Or treatment failure to anticoagulation

92
Q

when do we admit patients for PE?

A

when they need anticoagulants
massive PEs
hemodynamically instable

93
Q

when do we send PE patients home?

A

hemodynamically stable

94
Q

help of thromboprophylaxis for PE

A

reduces DVT

reduces PE

95
Q

Medical prophylaxis for PE

A

12 hours before surgery

immediately after 7-10 days

96
Q

mechanical prevention for PE

A

pneumatic compression
early ambulation
TED stockings
Exercise while sedentary

97
Q

definition of pulmonary HTN

A

characterized by elevated pulmonary arterial pressure and secondary right ventricular failure

98
Q

what’s the outcome of pulmonary HTN when untreated?

A

progressively fatal if untreated

99
Q

what is primary pulmonary HTN

A

idiopathic pulmonary arterial HTN

100
Q

causes of secondary pulmonary hypertention (PH)

A 
PE
COPD
connective tissue disorder
sleep apea
congenital heart defects
sickle cell anemia
cirrhosis
AIDS
living at high altitudes
cocaine
pulmonary fibrosis
left-sided heart failure
101
Q

what is PH pathophysiology

A

endothelial insult (hormonal or mechanical) causing vascular scarring, endothelial dysfunction, and intimal and smooth muscle proliferation

102
Q

does IPAH have a cure?

A

no

103
Q

what does untreated IPAH lead to

A

right sided heart failure and death

104
Q

average time from symptom onset to disease is?

A

approximately 2 years

105
Q

what are early symptoms like?

A

non-specific
dyspnea
weakness
recurrent syncope

106
Q

is a CXR helpful for PH workup?

A

maybe

107
Q

what imaging is extremely helpful if underlying problem of PH is right and left ventricular dysfunction?

A

echo

108
Q

what imaging is helpful if the underlying problem for PH is interstitial or thromboembolic disease?

A

high resolution CT and VQ scan

109
Q

what imaging is helpful if underlying problem in PH is thromboembolic disease

A

pulmonary angiography

110
Q

what should we do to treat PH?

A

refer to a specialist!

111
Q

what medications treat PH?

A 
CCB
vasodilators
PDE-5 inhibitors
endothelial receptor agonists
diuretics
anticoagulants
soluble guanylate cyclase (sGC)
112
Q

definition of Cor pulmonale

A

an alteration in the structure and function of the right ventricle secondary to disease of the lung, thorax, or pulmonary circulation

113
Q

what does chronic cor pulmonale result in?

A

right ventricular hypertrophy

114
Q

pathophysiology behind right ventricular hypertrophy in cor pulmonale

A

adaptive response to long-term increase in pressure
individual muscle cells grow thicker and change to drive the increased contractile force required to move blood against greater resistance

115
Q

what does acute core pulmonale result in

A

dilation in response to acute increased pressure (PE or acute respiratory distress syndrome) (ARDS)

116
Q

is pulmonary vascular resistance increased or decreased in cor pulmonale?

A

increased

117
Q 
relative levels of..
RV afterload
CO
RV failure..
in Cor pulmonale
A

increased RV afterload
decreased CO
decreased RV failure

118
Q

two major causes of cor pulmonale

A

pulmonary vascular changes

chronic hypoxic pulmonary vasoconstriction

119
Q

what vascular changes cause cor pulmonale?

A

PE
chemical agents
disease

120
Q

what is the most common cause of cor pulmonale?

A

COPD

121
Q

nonspecific symptoms of cor pulmonale

A 
fatigue
tachypnea
exertional dyspnea
cough
anginal chest pain
hemoptysis
hoarseness
122
Q

nonspecific signs of cor pulmonale

A 
increased chest diameter
labored respiratory efforts with chest wall retractions
distended neck veins
cyanosis
wheezes or crackles
split S2
systolic ejection murmur with click
S3/4 with systolic tricuspid regurg
pitting edema

CMPP (17 decks)

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