CARDIO MIDTERM EXAM Flashcards
(225 cards)
1
Q
It is characterized bv an elevation in mean pulmonary arterial pressure greater than 25 mmlic at rest or 30 mmHa during exercise. increased pulmonarv vascular resistance, and normal left heart ventricular function in the absence of other secondarv causes.
A
Pulmonary Hypertension
2
Q
Pulmonary Hypertension associated with:
A
Congenital Heart Disease, Collagen vascular disease, liver cirrhosis,
viral infection
drug effects
3
Q
more common among women than in men, with a ratio of 3 to 1.
A
Primary pulmonary hypertension
4
Q
rare and can occur at any age, although it is more common in the third and fourth decades.
A
Primary pulmonary hypertension
5
Q
Primarv pulmonarv hvpertension is characterized by:
A
Dyspnea
Angina
Syncope
Cough, hemoptysis, hoarseness and Raynaud phenomenon
6
Q
most common symptoms
A
Dyspnea (60% of patients)
7
Q
probably due to underpeftusion of the Right ventricle or stretching of the large pulmonary arteries
A
Angina (50% of patients)
8
Q
an early symptoms of PH
A
Syncope ( 8% of patients)
9
Q
Most important non-invasive test.
A
V/O scan
10
Q
Useful to determine the degree of hemodynamic impairment, the presence of vasoreactivity and the prognosis or patents win LAn.
A
Pulmonary artery catheterization
11
Q
Useful to rule out the presence of significant restrictive or obstructive airway disease
A
Pulmonary Function Test
12
Q
Rule out associated etiologies and evaluate patients with chronic interstitial disease and
normal chest radiographs.
A
High-resolution CT
13
Q
life-threatening and
has poor prognosis
A
IPAH
14
Q
improves survival. > Recommended target IN is approximately 1.5:2.5 (average 2).
A
Oral anticoagulations
15
Q
indicated for Right ventricular volume overload ( pulmonary congestion ana pedal edema)
A
Diuretics
16
Q
reserved for patients with refractory ventricular failure and for rate control in atrial fllutter or fibrillation
A
Digoxin
17
Q
Refers to a disease state characterized by the presence of incompletely reversible airflow obstruction.
A
chronic obstructive pulmonary disease
(COPD), or
18
Q
proposes a definition that focuses on the
progressive nature of airflow limitation and its association with abnormal inflammatory response of the lungs to various noxious particles or gases, primarily causes by smoking
A
Global Initiative for Chronic Obstructive Lung Disease (GOLD)
19
Q
COPD is “a disease state characterized by airflow limitation that is not fully reversible.”
A
GOLD document
20
Q
The chronic airflow limitation that is characteristic of COPD is caused by a mixture of small airways disease (e.g., obstructive bronchiolitis) and parenchymal destruction (emphysema),
A
The chronic airflow limitation that is characteristic of COPD is caused by a mixture of small airways disease (e.g., obstructive bronchiolitis) and parenchymal destruction (emphysema),
21
Q
TWO MAJOR DISEASES THAT MAKE UP COPD
A
Emphysema
Chronic Bronchitis
22
Q
defined in condition characterized by abnormal, permanent enlargement of the airspaces beyond the terminal bronchiole, accompanied by destruction of the walls of the airspaces and loss of elastance
A
Emphysema
23
Q
defined in clinical terms as a condition in which chronic productive cough is present for at least 3 months per year for at least 2 consecutive years.
A
Chronic bronchitis
24
Q
Common denominator of the 3 diseases:
A
Airflow Obstruction
25
asthma is no longer conventionally considered to be part of the spectrum of COPD, the diagram shows that there is overlap between asthma and COPD.
asthma is no longer conventionally considered to be part of the spectrum of COPD, the diagram shows that there is overlap between asthma and COPD.
26
In actual practice, it may not be possible to distinguish between individuals with a history of asthma but with incompletely reversible airflow obstruction and individuals with COPD. Recently, this overlap has been recognized with the term ________________
“asthma-COPD overlap” syndrome (ACOS)
27
Pink puffer
Cachexia
EMPHYSEMA
28
Blue bloater
Barrel chested
BRONCHITIS
29
one of the most frequent causes of morbidity and mortality worldwide.
COPD
30
will become the fifth most prevalent disease in the world and the third leading cause of worldwide mortality by 2030.
COPD
31
COPD prevalence increases with aging, with a five-fold. Increased risk for adults older than 65 years.
COPD prevalence increases with aging, with a five-fold. Increased risk for adults older than 65 years.
32
is the third leading cause of death worldwide, causing 3.23 million deaths in 2019. WHO
Chronic Bronchitis
33
Nearly 90% of COPD deaths in those under 70 years of age occur in low- and middle-income countries.
Nearly 90% of COPD deaths in those under 70 years of age occur in low- and middle-income countries.
34
Common Causes (COPD):
Cigarette smoking
Alpha-1 antitrypsin (AAT) deficiency
Outdoor air pollution
Long-standing asthma
Biomass and occupational exposure
35
a Genetic condition (symptoms; trouble breathing, jaundiced or yellow skin). Which can cause COPD at a young age and also damage lungs and liver.
alpha-1 antitrypsin (AAT) deficiency
36
chronic asthma
Long-standing asthma
37
Risk factors COPD
COPD is prevalent w/aging such as 65 years old, except for COPD brought by AAT because it is genetic and may occur in younger people.
38
the main component of cigarette that is mainly
causing COPD
Nicotine
39
Prevents the attack of neutrophil elastase
ALPHA 1 – ANTITRYPSIN
40
released by neutrophil, when this elastase break off from neutrophil, it destroys the bacteria and can also destroys the lungs
Neutrophil elastase
41
in the absence of a1-antitrypsin, the neutrophil elastase is increased, and the lungs is being continuously damaged and this can even invades the liver
in the absence of a1-antitrypsin, the neutrophil elastase is increased, and the lungs is being continuously damaged and this can even invades the liver
42
a condition that features a reduced amount of the protein
AAT
GENETIC EMPHYSEMA OR Α-1 ANTIPROTEASE DEFICIENCY
43
May result in the early onset of emphysema
and which is inherited
autosomal codominant condition..
44
The importance of early identification is emphasized by the need to test (by simply sending a serum level for a1- antitrypsin testing) first-degree relatives (e.g., siblings, parents, children), by the favorable effect of primary prevention of smoking among individuals identified early, and by the availability of a specific therapy
intravenous (IV) augmentation therapy
45
a major structural protein that supports the alveolar walls of the lung, is normally protected by a1-antitrypsin, a protein that opposes the degradative threat of neutrophil elastase.
lung elastin
46
a protein contained within neutrophils that is disgorged when neutrophils are attracted to the lung during inflammation or infection.
Neutrophil elastase
47
individuals with established emphysema,
consideration can be given to available specific therapy
intravenous (IV) augmentation therapy
48
COPD may also occur without active cigarette smoking or AAT deficiency. Factors such as: may contribute to airflow obstruction that is not reversible.
1.passive smoking
2.air pollution
3.occupational exposure
4.airway hyperresponsiveness
49
CLINICAL SIGNS AND SYMPTOMS (COPD)
cough
phlegm production
wheezing
shortness of breath
50
often slow "but progressive in onset and occurs later in the course of the disease, characteristically in the late sixth or seventh decade of life.
Dyspnea
51
in which dyspnea begins sooner (mean age, approximately 45).
a1-antitrypsin deficiency
52
may show wheezing or diminished breath sounds
early
COPD
53
may be evident (i.e., increased anteroposterior diameter (sometimes called barrel chest),
hyperinflation
54
diaphragm flattening, and dimpling inward of the chest wall at the level of the diaphragm on inspiration
Hoover's sign
55
is not caused by COPD alone, even if hypoxemia is present. Clubbing in a patient with COPD warrants consideration of another cause (e.g., bronchogenic cancer, bronchiectasis)
Digital clubbing
56
because of cor pulmonale
Bipedal edema
57
Other late signs of COPD include:
the use of accessory muscles of respiration,
o edema resulting from cor pulmonale,
o mental status changes caused by hypercapnia
(especially if acute, as in acute exacerbations
of chronic, severe disease),
o or asterixis (i.e., involuntary flapping of the
hands when held in an extended position, as in
"stopping traffic").
58
The goal of management is to relieve the bronchoconstriction
The goal of management is to relieve the
bronchoconstriction
59
In managing patients with chronic, stable COPD, the following goals must guide the clinician:
-Establish the diagnosis of COPD.
– Optimize lung function.
– Maximize the patient’s ability to perform daily
activities.
– Simplify the medical treatment program as
much as possible.
– Avoid exacerbations of COPD.
– Prolong survival
60
In cases of emphysema and part of the lungs is severely damaged then the patient can undergo surgical procedure, which is removal of the damaged lung portion or lobe.
In cases of emphysema and part of the lungs is severely damaged then the patient can undergo surgical procedure, which is removal of the damaged lung portion or lobe.
61
If the ordinary nasal or face mask is not effective on patient, CPAP or BIPAP is used to expel the excessive CO2 instead of intubating the patient.
If the ordinary nasal or face mask is not effective on patient, CPAP or BIPAP is used to expel the excessive CO2 instead of intubating the patient.
62
The major challenge facing the clinician who encounters a patient with airflow obstruction is to distinguish COPD (i.e., emphysema or chronic bronchitis or both) from
asthma.
The major challenge facing the clinician who encounters a patient with airflow obstruction is to distinguish COPD (i.e., emphysema or chronic bronchitis or both) from
asthma.
63
Features that tend to favor COPD include chronic daily phlegm production, which establishes the diagnosis of chronic bronchitis; diminished vascular shadows on the chest radiograph (called hyperlucency); and a decreased diffusing capacity.
Features that tend to favor COPD include chronic daily phlegm production, which establishes the diagnosis of chronic bronchitis; diminished vascular shadows on the chest radiograph (called hyperlucency); and a decreased diffusing capacity.
64
establishes the diagnosis of chronic bronchitis; diminished vascular shadows on the chest radiograph
hyperlucency
65
The diagnosis of asthma is favored if the diminished FEV obtained on spirometry returns to normal after bronchodilator treatment.
The diagnosis of asthma is favored if the diminished FEV obtained on spirometry returns to normal after bronchodilator treatment.
66
a secondary issue is for the clinician to consider whether the patient has an unusual cause for COPD, such as a1- antitrypsin deficiency or another etiology. Such underlying etiologies will be present in fewer than 5 % of patients with COPD, with a1-antitrypsin deficiency the most common.
a secondary issue is for the clinician to consider whether the patient has an unusual cause for COPD, such as a1- antitrypsin deficiency or another etiology. Such underlying etiologies will be present in fewer than 5 % of patients with COPD, with a1-antitrypsin deficiency the most common.
67
Pulmonary Disease Strategies during acute exacerbations of COPD (MEDICAL MANAGEMENT)
inhaled bronchodilators
antibiotics
corticosteroids
anti-inflammatory mediators
supplemental oxygen
68
especially beta-2 agonists
inhaled bronchodilators
69
if there’s an infection(e.g., trimethoprim-sulfamethoxazole, amoxicillin, or doxycycline)
antibiotics
70
to reduce inflammation and improve lung function (e.g., trimethoprim-sulfamethoxazole, amoxicillin, or doxycycline)
corticosteroids
71
theophylline
anti-inflammatory mediators
72
theophylline
anti-inflammatory mediators
73
to maintain arterial saturation at greater than 90%, inhaled bronchodilators, oral antibiotics, and a brief course of systemic corticosteroids
supplemental oxygen (O2)
74
recommended for px with COPD
Bronchodilator therapy
75
produce smooth muscle relaxation, resulting in improved airflow obstruction, improved
symptoms and exercise tolerance, and decrease in the frequency and severity of exacerbations, but they do not enhance survival
Bronchodilators
76
can improve airflow in patients with COPD, although many clinicians favor an inhaled
anticholinergic and sympathomimetic bronchodilators
77
first-line therapy (COPD)
anticholinergic medication (e.g., ipratropium bromide)
78
Controlled trials do show lessened dyspnea in methylxanthine recipients despite lack of measurable increases in airflow.18 Side effects of methylxanthines include anxiety, tremulousness, nausea, cardiac arrhythmias, and seizures. To minimize the chance of
toxicity, current recommendations suggest maintaining serum theophylline levels at 8 to 10 ug/mL.
Controlled trials do show lessened dyspnea in methylxanthine recipients despite lack of measurable increases in airflow.18 Side effects of methylxanthines include anxiety, tremulousness, nausea, cardiac arrhythmias, and seizures. To minimize the chance of
toxicity, current recommendations suggest maintaining serum theophylline levels at 8 to 10 ug/mL.
78
The addition of a sympathomimetic bronchodilator (e.g., a p2-agonist) may offer additive bronchodilation.
The addition of a sympathomimetic bronchodilator (e.g., a p2-agonist) may offer additive bronchodilation.
79
offers little additional bronchodilation in patients on inhaled bronchodilators and generally is reserved for patients with debilitating symptoms from stable COPD despite optimal inhaled bronchodilator therapy.
Methylxanthine therapy
80
recommend the use of short-acting β-adrenergic agents (≤6 hours) for symptomatic management of all patients with COPD.
GOLD guidelines
81
can lessen the frequency of acute exacerbations of COPD.
long-acting β agonist (e.g., salmeterol) or a long-acting anticholinergic drug (e.g., tiotropium)
82
Strategies to improve lung function in acute exacerbations of COPD generally include inhaled bronchodilators (especially (32-agonists) and systemic corticosteroids. An early randomized, controlled trial of IV methylprednisolone for patients with acute exacerbations has shown accelerated improvement in FEV1 within 72 hours.
Strategies to improve lung function in acute exacerbations of COPD generally include inhaled bronchodilators (especially (32-agonists) and systemic corticosteroids. An early randomized, controlled trial of IV methylprednisolone for patients with acute exacerbations has shown accelerated improvement in FEV1 within 72 hours.
83
offer little benefit in the setting of acute exacerbations of COPD and have fallen into disfavor in this setting
IV methylxanthines
84
For patients with purulent phlegm as an underlying feature of their acute exacerbation, oral antibiotics (e.g., trimethoprim-sulfamethoxazole, amoxicillin, doxycycline) administered for 7 to 10 days have produced accelerated improvement of peak flow rates compared with the rates of placebo recipients.
For patients with purulent phlegm as an underlying feature of their acute exacerbation, oral antibiotics (e.g., trimethoprim-sulfamethoxazole, amoxicillin, doxycycline) administered for 7 to 10 days have produced accelerated improvement of peak flow rates compared with the rates of placebo recipients.
85
Criteria defining candidacy for noninvasive ventilation include:
-acute respiratory acidosis (without frank
respiratory arrest);
-hemodynamic stability;
-ability to tolerate the interface needed for
noninvasive ventilation;
-ability to protect the airway;
-and lack of craniofacial trauma or burns,
copious secretions, or massive obesity.
86
PREVENTING PROGRESSION OF COPD AND ENHANCING SURVIVAL
-Stop smoking
-Take regular exercise
-Get vaccinated
87
maximize patients ability to perform daily activities concerns COPD and other neuromuscular disease
pulmonary rehabilitation
88
IMPORTANT AREAS OF PULMONARY REHABILITATION
Exercise
Psychological counselling
Appropriate therapy/treatment
89
involving strengthening the respiratory
muscles
Exercise
90
strengthening the patients
morale
Psychological counselling
91
Asthma in childhood is reversible, but asthma in adulthood is not fully reversible and may lead to COPD
Asthma in childhood is reversible, but asthma in adulthood is not fully reversible and may lead to COPD
92
COPD AND ASTHMA SIMILARITIES
Same pathophysiology:
- Inflammation
- bronchoconstriction
93
COPD AND ASTHMA DIFFERENCES
Triggering factors and risk factors
- COPD: smoking cigarette
- Asthma: allergen
94
classification for asthma
GINA guidelines
95
classification for COPD
GOLD
96
The point of origin of pulmonary emboli is found in only one half of patients.
The point of origin of pulmonary emboli is found in only one half of patients.
97
arise from detached portions of venous thrombi that form, in most cases, in deep veins
of the lower extremities or pelvis (86%).
Pulmonary emboli
98
A small percentage of pulmonary emboli arise from the right heart chambers (3.15%) or the superior vena cava (3%).
A small percentage of pulmonary emboli arise from the right heart chambers (3.15%) or the superior vena cava (3%).
99
CAUSES OF PULMONARY EMBOLISM:
-Thrombus formation occurs by blood stasis, the presence of hypercoagulable states, or vessel wall abnormalities.
-The causes of stasis include local pressure, venous obstruction, and immobilization.
-Other causes of stasis include congestive heart failure, shock and dehydration, varicose veins, and enlargement of the right heart chambers.
99
RISK FACTORS OF THE VIRCHOWS TRIAD HYPERCOAGULABILITY
-Malignancy (cancer patient)
- Major surgery
-Infection and sepsis
-Estrogen
-dehydration
100
RISK FACTORS OF DVT FORMATION
- Dehydration – lack of water cause the blood to become thick
- Long flight (immobilization)
- Bedridden
*Stroke
*Coma
*Lower extremity disorder
- Pregnancy
- Obesity
- Blood extraction especially during searching
- Invasive catheter
101
VASCULAR DAMAGE
- thrombophlebitis
- Indwelling catheter
- actual or direct trauma
102
BLOOD STASIS
- Immobilization
- bradycardia (low heart rate)
- inadequate blood volume
103
an important factor for the formation of DVT, is rarely the only risk factor.
Stasis
104
Deposition of platelets and fibrin in the venous valve cups of the lower extremities occurs as a result of stasis
Deposition of platelets and fibrin in the venous valve cups of the lower extremities occurs as a result of stasis
105
Most PEs originate as thrombi in the deep veins (DVT) due to deposition of platelets and fibrin in the venous valve cusps of the lower extremities.
Most PEs originate as thrombi in the deep veins (DVT) due to deposition of platelets and fibrin in the venous valve cusps of the lower extremities.
106
most frequently in the calf veins, then femoropopliteal veins, and less frequently in the iliac veins.
site of thrombosis
107
Emboli detach from their point of origin and travel through the systemic venous system, through the right sided chambers of the heart, and lodge in the pulmonary arterial system.
Emboli detach from their point of origin and travel through the systemic venous system, through the right sided chambers of the heart, and lodge in the pulmonary arterial system.
108
occur more frequently in the lower lobes and often found in right lung
Pulmonary emboli
109
Embolic obstruction of the pulmonary artery increases the alveolar dead space, causes bronchoconstriction, and decreases the production of alveolar surfactant
Embolic obstruction of the pulmonary artery increases the alveolar dead space, causes bronchoconstriction, and decreases the production of alveolar surfactant
110
areas occur because of the presence of ventilated but nonperfused lung parenchyma.
Wasted or dead space
111
The response is to increase total ventilation (V). The increased V contributes to the sensation of dyspnea that accompanies pulmonary embolism.
The response is to increase total ventilation (V). The increased V contributes to the sensation of dyspnea that accompanies pulmonary embolism.
112
Not all patients with pulmonary embolism have arterial hypoxemia, but the presence of a wide alveolararterial oxygen tension gradient andreduced arterial oxygen tension (Pa02) are common
Not all patients with pulmonary embolism have arterial hypoxemia, but the presence of a wide alveolararterial oxygen tension gradient and a reduced arterial oxygen tension (Pa02) are common
113
develops because of high and low V/Q mismatch, intrapulmonary shunt, or cardiogenic shock
Hypoxemia
114
caused by obstruction of the pulmonary vasculature by massive emboli or by numerous small emboli in the presence of cardiopulmonary disease
Shock
115
resulting to venous oxygen desaturation
Cardiac output decreases, and oxygen delivery falls
116
may develop because of the presence of a patent foramen ovale
intracardiac shunt
117
no specific signs or symptoms indicate the presence of venous thromboembolic disease, although most patients with DVT have pain or swelling, or both, of the extremity
no specific signs or symptoms indicate the presence of venous thromboembolic disease, although most patients with DVT have pain or swelling, or both, of the extremity
118
In patients who have swelling above and below the knee, fever, and a history of immobility and cancer, the likelihood of finding DVT on a venogram is only 42% .
In patients who have swelling above and below the knee, fever, and a history of immobility and cancer, the likelihood of finding DVT on a venogram is only 42% .
119
PHYSICAL FINDINGS OF DVT IN LOWER EXTREMITIES
* Erythema
* Warm skin
* Swelling and tenderness
120
SIGNS AND SYMPTOMS (PVD)
1) Dyspnea
2) Pleuritic chest pain
3) Cough
4) Apprehension
5) Leg swelling and Pain
6) hemoptysis
7) hypoxemia
8) tachypnea
9) tachycardia
10) wheezing
11) angina-like pain
121
The combination of dyspnea of sudden onset, fainting, and chest pain should raise suspicion of pulmonary embolism
The combination of dyspnea of sudden onset, fainting, and chest pain should raise suspicion of pulmonary embolism
122
When a pulmonary embolism is possible, the most commonly used tool to predict the clinical probability of a pulmonary embolism is the modified
Wells Scoring System
123
Chest Radiograph for PVC by itself is helpful to rule out other potentially life-threatening conditions, such as pneumothorax
Chest Radiograph for PVC by itself is helpful to rule out other potentially life-threatening conditions, such as pneumothorax
124
a normal chest radiograph may be a clue to the presence of pulmonary embolism.
Dyspneic patients
125
enlargement of the right descending pulmonary artery (66%)
Palla’s sign
126
enlargement of the heart shadow (55%)
Cardiomegaly
127
present in patients who have infarction or atelectasis
Parenchymal densities
128
Other less common findings include: PVC
Westermark sign
Hampton hump
129
helpful to rule out other diagnoses, such as acute myocardial infarction and
pericarditis
electrocardiogram
130
are the mosT common findings in PVC
tachycardia and ST-segment depression
131
Most patients with acute pulmonary embolism have _________
hypoxemia
hypocapnia
132
In an intubated patient or in patient with COPD, a decrease in PaO2 and increase in arterial carbon dioxide content should raise suspicion of pulmonary embolism
In an intubated patient or in patient with COPD, a decrease in PaO2 and increase in arterial carbon dioxide content should raise suspicion of pulmonary embolism
133
The utility of measuring ABGs is to document hypoxemia and direct oxygen supplementation. In the care of patients with limited cardiopulmonary reserve, ABG levels are used to document the level of carbon dioxide.
The utility of measuring ABGs is to document hypoxemia and direct oxygen supplementation. In the care of patients with limited cardiopulmonary reserve,
ABG levels are used to document the level of carbon dioxide.
134
Measurement of fibrin split products (D-dimers), products of cross-linked fibrin, has been found sensitive for ______________
acute venous thromboembolism
135
The most standard test is the It helps to see the segmental defect.
V/Q scan
136
involves the inhalation of a radiolabeled gas (usually xenon-133, xenon-127,
krypton-181m, or technetium-99m) and the intravenous injection of macroaggregated albumin tagged with a gamma-emitting radioisotope
Ventilation/perfusion scanning
137
The distribution of lung V and lung Q is studied, and areas of mismatch where Q is less than V are sought
The distribution of lung V and lung Q is studied, and areas of mismatch where Q is less than V are sought
138
The presence of mismatches most often indicates embolic occlusion of the blood vessel
The presence of mismatches most often indicates embolic occlusion of the blood vessel
139
TREATMENT FOR PVC
Prophylactic therapy
Pharmacological choices
Mechanical measures
140
reduces the risk of venous thromboembolism in patients at risk. Preventive measures especially if there is an identified risk.
Prophylactic therapy
141
for prophylaxis include lowdose subcutaneous heparin, warfarin, low-molecularweight heparin, heparinoids, and dextran
Pharmacological choices
142
should monitor the dosage because
too much can cause massive bleeding, or GI
bleeding
Heparin
143
Simplest treatment for PVC
Aspirin
144
To reduce venous stasis include
early ambulation, wearing elastic stockings
(compressive stocking to help the muscle to contract),
pneumatic calf compression, and electrical stimulation
of calf muscles.
Mechanical measures
145
the standard therapy for
venous thromboembolic disease; it has an immediate
action and is relatively safe
Heparin (anticoagulant)
146
It potentiates the action of antithrombin and heparin
cofactor 2
It potentiates the action of antithrombin and heparin
cofactor 2
147
Clinical recurrence of DVT and PE is rare when heparin
is infused at doses of at least ___________
1250 units per hour
148
Complication of IV heparin administration includes
major bleeding
thrombocytopenia
149
Most commonly used oral anticoagulant in PVC
racemic warfarin sodium
150
MANAGEMENT OF PULMONARY EMBOLISM
Therapy with heparin followed by oral coumarin is the modality of choice
Supplemental oxygen
Analgesics
Resuscitation with fluids and vasopressor agent
151
for patients who are hypotensive and in shock
Resuscitation with fluids and vasopressor agent –
152
In the care of patients with severe hypoxemia, acute right heart failure, or shock, thrombolytic therapy may be administered for lysis of the emboli.
In the care of patients with severe hypoxemia, acute right heart failure, or shock, thrombolytic therapy may be administered for lysis of the emboli.
153
For massive pulmonary embolism:
Pulmonary Embolectomy
Catheter tip embolectomy Catheter tip fragmentation
Inferior vena caval filter
154
Surgical removal of the embolus
Pulmonary Embolectomy
155
A medical condition which causes the airway path of the lungs to swell and narrow
ASTHMA
156
hyperreactive airway disease
ASTHMA
157
a clinical syndrome characterized by airway obstruction, which is partially or completely reversible either spontaneously or with treatment; airway inflammation; and airway hyperresponsiveness (AHR) to various stimuli
Asthma
158
In the genetically susceptible host, allergens, respiratory infections, certain occupational and environmental exposures, and many unknown hosts or environmental stimuli can produce the full spectrum of asthma, with persistent airway inflammation, bronchial hyperreactivity, and consequent airflow obstruction.
In the genetically susceptible host, allergens, respiratory infections, certain occupational and environmental exposures, and many unknown hosts or environmental stimuli can produce the full spectrum of asthma, with persistent airway inflammation, bronchial hyperreactivity, and consequent airflow obstruction.
159
When inflammation and bronchial hyperreactivity are present, asthma can be triggered by additional factors, including exercise; inhalation of cold, dry air; hyperventilation; cigarette smoke; physical or emotional stress; inhalation of irritants; and pharmacologic agents, such as methacholine and histamine.
When inflammation and bronchial hyperreactivity are present, asthma can be triggered by additional factors, including exercise; inhalation of cold, dry air; hyperventilation; cigarette smoke; physical or emotional stress; inhalation of irritants; and pharmacologic agents, such as methacholine and histamine.
160
When a patient with asthma inhales an allergen to which he or she is sensitized, the antigen cross-links to specific immuno- globulin E (IgE) molecules attached to the surface of mast cells in the bronchial mucosa and submucosa.
When a patient with asthma inhales an allergen to which he or she is sensitized, the antigen cross-links to specific immuno- globulin E (IgE) molecules attached to the surface of mast cells in the bronchial mucosa and submucosa.
161
Early (acute) asthmatic response an immediate hypersensitivity reaction that usually subsides in approximately 30 to 60 minutes
Early (acute) asthmatic response an immediate hypersensitivity reaction that usually subsides in approximately 30 to 60 minutes
162
The mast cells degranulate rapidly (within 30 minutes), releasing multiple mediators including leukotrienes
slow-reacting substance of anaphylaxis [SRS-A])
163
Late asthmatic response
- usually more severe and lasts longer than the early asthmatic response
- late asthmatic response is characterized by increasing influx and activation of inflammatory cells such as mast cells, eosinophils, and lymphocytes.
164
particularly involved in the pathophysiology of asthma
T lymphocytes
165
stimulated by microbes or allergens and assist B cells transform into plasma cells that produce immunoglobulin E (lgE).
Th 1 cells
166
attract mast cells, eosinophils, and basophils, which promote inflammation.
Th2 cells
167
binds to mast cells and provokes their degranulation, which releases mediators such as histamine and leukotrienes.
IgE
168
responsible for the development of bronchoconstriction, bronchial hyperreactivity, edema, and eosinophilia.
Leukotrienes
169
contributes to bronchospasm and inflammation
Histamine
170
Supposedly asthma is only common during childhood
Supposedly asthma is only common during childhood
171
CATEGORY OF ASTHMA
Intermittent (green zone)
Mild Persistent (green zone)
Moderate persistent (yellow zone)
Severe persistent (red zone)
172
The attacks are not frequent and the duration
- Not recognized early
Intermittent (green zone)
173
- 2 times a week, or symptoms at least once per week,
-Symptoms is relief after medication
Mild Persistent (green zone)
174
- Daily symptoms
- Relieve after medication
- Daily use of short-acting B2-aginist
Moderate persistent (yellow zone)
175
- Continuous symptoms
- Go to ER immediately
Severe persistent (red zone)
176
TRIGGERING FACTORS OF ASTHMA:
Allergen
Infection
Season
Exercised-induced
Stress (intrinsic)
Skin asthma
Environment (such as chemical prone places)
177
The diagnosis of asthma requires a two-pronged approach of clinical assessment supported by laboratory evaluation
The diagnosis of asthma requires a two-pronged approach of clinical assessment supported by laboratory evaluation
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physical examination can be entirely normal between episodes, the history plays a key role in suggesting
physical examination can be entirely normal between episodes, the history plays a key role in suggesting
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Laboratory Findings for ASTHMA
Spirometry
Peakflow
Methacholine challenge
Imaging tests
Allergy testing
Nitric oxide test
Provocative testing for exercise and cold- induced asthma
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The severity of the symptoms depends on the degree of bronchial hyperresponsiveness and reversibility of the bronchial obstruction
The severity of the symptoms depends on the degree of bronchial hyperresponsiveness and reversibility of the bronchial obstruction
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classic symptoms of asthma are
episodic wheezing,
shortness of breath, dyspnea
chest tightness
cough
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Patients going into respiratory failure caused by marked airway constriction have inaudible breath sounds and a repetitive, hacking cough.
Patients going into respiratory failure caused by marked airway constriction have inaudible breath sounds and a repetitive, hacking cough.
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may be present if larger bronchial airways are involved.
Rhonchi
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If the asthma is related to allergies, signs of chronic rhinitis may be present, including nasal edema, nasal polyps, rhinorrhea, and oropharyngeal erythema
If the asthma is related to allergies, signs of chronic rhinitis may be present, including nasal edema, nasal polyps, rhinorrhea, and oropharyngeal erythema
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asthma requires demonstration of a component of reversible airflow obstruction
asthma requires demonstration of a component of reversible airflow obstruction
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PFTs may be normal in asymptomatic patients with asthma, but more commonly they reveal some degree of airway obstruction manifested by a decreased FEV1 and FEV1/FVC ratio
PFTs may be normal in asymptomatic patients with asthma, but more commonly they reveal some degree of airway obstruction manifested by a decreased FEV1 and FEV1/FVC ratio
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RADIOGRAPHY (CHEST X-RAY) ASTHMA
Usually shows normal
Hyperinflation or flattening of diaphragm
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improvement in the FEV1 by at least 12% and 200 mL after administration of a short-acting bronchodilator is considered evidence of reversibility.
improvement in the FEV1 by at least 12% and 200 mL after administration of a short-acting bronchodilator is considered evidence of reversibility.
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Spontaneous variation in self-recorded PEFR by 15% or more can also provide evidence of reversibility of airway obstruction.
Spontaneous variation in self-recorded PEFR by 15% or more can also provide evidence of reversibility of airway obstruction.
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Elevated values of exhaled nitric oxide can also be used to support the diagnosis of asthma when eosinophilic inflammation is present.
Elevated values of exhaled nitric oxide can also be used to support the diagnosis of asthma when eosinophilic inflammation is present.
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a well-established method to detect and quantify AHR.
Bronchoprovocation
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Pharmacologic agents (ASTHMA):
acetylcholine, methacholine, histamine, cysteinyl leukotrienes, and prostaglandins, and physical stimuli such as exercise and isocapnic hyperventilation with cold, dry air have been used to detect, quantify, and characterize nonspecific AHR in asthma
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The goal of asthma management is to maintain a high quality of life for the patient, uninterrupted by asthma symptoms, side effects from medications, or limitations on the job or during exercise.
The goal of asthma management is to maintain a high quality of life for the patient, uninterrupted by asthma symptoms, side effects from medications, or limitations on the job or during exercise.
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Asthma management relies on the following four important components recommended by the National Asthma Education Program (NAEP) expert panel:
1) Objective measurements and monitoring of lung function
2) Pharmacologic therapy
3) Environmental control
4) Patient education
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LONG-TERM ASTHMA CONTROL MEDICATIONS: keep asthma under control on a day-to-day basis and make it less likely you'll have an asthma attack
Inhaled corticosteroids Leukotriene modifiers Combination inhalers Theophylline
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recommended as part of the initial assessment of all patients being evaluated for asthma and peri- odically thereafter as needed.
Spirometry
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recommend that home PEFR measurement be used for patients with moderate to severe asthma
NAEP guidelines
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the baseline diagnosis for ASTHMA
PFT
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Simple device used in emergency setting
peak
flow meter (portable spirometer) or asthma meter
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the best personal blow
Personal best
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used for promoting deep breathing exercise especially for patient who undergone surgical procedure in thorax or abdomen
Incentive spirometry
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Get the baseline pre and post the medication using the peak flow meter. After medications there should be an improvement.
Get the baseline pre and post the medication using the peak flow meter. After medications there should be an improvement.
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-to monitor if the O2 saturation is good
* to see if there is an evident increase of CO2
o revealing hypoxia or hypercapnia
ABG ANALYSIS
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PHARMACOTHERAPY (ASTHMA)
anti-inflammatory agents
Bronchodilators
inhalation therapy
Inhaled therapy
Spacer devices
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corticosteroids that suppress the primary disease process and its resultant airway hyperreactivity
anti-inflammatory agents
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β-2–adrenergic agonists and anticholinergics relieve asthma symptoms
Bronchodilators
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preferred to oral or other systemic therapy
inhalation therapy
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using metered dose inhalers or dry powder inhalers allows high concentration of the medication to be delivered directly to the airways, resulting in fewer systemic side effects
Inhaled therapy
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used to improve delivery of inhaled medication, but training and coordination are still required for patients using metered dose inhalers
Spacer devices
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Step-by-step treatment: ASTHMA
1) If the medication did not work combine with other medication
2) If still not responding to any medication then the patient may be status asthmaticus
* This is the time you intubate the patient
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plays a key role in the pathogenesis of asthma, and many asthmatic patients have elevated levels of IgE.
IgE
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Studies have shown that treatment with omalizumab allows reduction of the dose of inhaled glucocorticoids required to control symptoms and also a decrease in the number of asthma exacerbation episodes
Studies have shown that treatment with omalizumab allows reduction of the dose of inhaled glucocorticoids required to control symptoms and also a decrease in the number of asthma exacerbation episodes
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recommend that omalizumab should be considered as adjunctive therapy for patients with severe persistent asthma
NAEP asthma guidelines
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a cytokine that promotes eosinophilic inflammation of the airway
IL-5
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Shown to decrease oral corticosteroid use and reduce exacerbations in patients with severe persistent asthma and an eosinophilic phenotype
Mepolizumab
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Works in a slightly different way than the other two drugs, in that it blocks the IL-5 receptor on immune cells and is considered to be more effective in lowering the number of eosinophils.
Benralizumab
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Emergency management of acute asthma should include early and frequent administration of aerosolized β-2 agonists and therapy with systemic corticosteroids.
Emergency management of acute asthma should include early and frequent administration of aerosolized β-2 agonists and therapy with systemic corticosteroids.
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an approved addition to treatment options for adults whose asthma remains uncontrolled despite use of inhaled steroids and long- acting β agonists.
Bronchial thermoplasty
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procedure in which a probe is introduced into the central airways through a bronchoscope and heat is applied (through radiofrequency waves) to airways of 3 to 10 mm diameter with the goal to reduce the airway smooth muscle mass, reducing the ability of the airways to constrict.
Bronchial thermoplasty
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based on the theoretical rationale that part of the immunologic response to an administered allergen is the production of an IgG-specific antibody to the allergen injected
Immunotherapy (called “allergy shots” by patients)
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environmental control measures to reduce exposure to indoor and outdoor allergens and irritants are essential
environmental control measures to reduce exposure to indoor and outdoor allergens and irritants are essential
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Patients should be advised to avoid outdoor antigens, primarily ragweed, grass, pollens, and molds.
Patients should be advised to avoid outdoor antigens, primarily ragweed, grass, pollens, and molds.
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Exposure to outdoor allergens is best reduced by staying indoors with the windows closed, in an air- conditioned environment, particularly during the midday and afternoon, when pollen and some mold counts are highest
Exposure to outdoor allergens is best reduced by staying indoors with the windows closed, in an air- conditioned environment, particularly during the midday and afternoon, when pollen and some mold counts are highest
