exam 3 Flashcards
1
Q
endothelial cells
A
hyper/hypotension
2
Q
lumen
A
diameter of a blood vessel
3
Q
endothelium
A
controls vascular function, platelet function, platelet adhesion, blood clotting, modulation of flow, vascular resistance, regulation of immune and inflammatory responses
4
Q
Systole
A
-contraction
-BP rises
-left ventricle contracts
5
Q
diastole
A
-relaxation
-BP falls
-the heart relaxes
6
Q
systolic pressure
A
-less than 120 mm Hg in adults
-rapid upstroke occurs during LV contraction
7
Q
diastolic pressure
A
less than 80 mm Hg
-lowest pressure
8
Q
mean arterial pressure (MAP)
A
-average pressure in arterial system during ventricular contraction and relaxation
-indicator of tissue perfusion
-est 90-100 mm HG in adults
9
Q
vagal stimulation- neuro
A
bradycardia
10
Q
sympathetic stimulation-nuero
A
tachycardia
11
Q
baroreceptors-nuero
A
-pressure sensitive receptors located in walls of blood vessels
-carotid and aortic baroreceptors effects changes in heart rate, contraction, and vascular tone
12
Q
blood pressure regulation: Humoral
A
-RAAS
-Vasopressin (ADH)
-epinephrine-norepinephrine
13
Q
systolic and diastolic actions
A
13
Q
disorders of systemic arterial blood flow
A
disease of the arterial system affects the body function by impairing blood flow
-the effect of impaired blood flow on the body depends on the structures involved and the extent of the altered flow
13
Q
ischemia!
A
reduction in arterial flow to a level that is insufficient to meet the oxygen demands of the tissues
14
Q
infarction!
A
an area of ischemic necrosis in an organ produced by occulusion of its aterial blood supply or its venous drainage
14
Q
hyperlipidemia
A
elevated levels of lipids in the blood
-cholesterol, triglycerides, phospolipids)
14
Q
dyslipidemia
A
condition of imbalance of lipid components of the blood
15
Q
VLDL
A
very low density lipoprotein
carries large amounts of triglycerides
16
Q
low density lipoprotein (LDL)!
A
-atherogenic (forms plaques in intima layer of arteries)
-carry cholesterol to the peripheral tissues
-“bad” cholesterol
17
Q
High-density Lipoprotein (HDL)!
A
-protective
-remove cholesterol from the tissues and carry it back to the liver for disposal
-cardioprotective because it carries cholesterol away from artery walls to be excreted
-“good” cholesterol
18
Q
primary dyslipidemia
A
genetic basis
19
Q
secondary dyslipidemia
A
dietary, obesity, type II diabetes
-other factors
20
Q
metabolic syndrome
A
-elevated fasting blood glucose
-elevated BP
-elevated waist circumference
-dyslipidemia
21
atherosclerosis
formation of fibrofatty lesions in intimal lining of large and medium sized arteries
22
major risk factor of atherosclerosis
hypercholesterolemia (elevations of LDL)
-other risk factors: smoking, obesity, hypertension, diabetes
23
modifiable atherosclerosis!
hypercholesterolemia
-lifestyle changes
-diet
23
nonmodifiable atherosclerosis!
age, family history, male sex, genetics, post-menopause
24
fatty streaks: artherosclerosis
thin, flat yellow intimal discolorations that progressively enlarge
25
fibrous atheromatous plaque:artherosclerosis
the accumulation of intracellular and lipids, proliferation of vascular smooth muscle cells, and formation of scar tissue
26
complicated lesion: artherosclerosis
contains hemorrhage, ulceration, and scar tissue deposits
27
lesions with atherosclerosis
as lesion increase in size, lumen of the artery decreases (the artery constricts)
28
developmental stages of atherosclerosis
endothelial cell injury, migration of inflammatory cells,lipid accumulation and SMS proliferation, plaque structure
29
endothelial cell injury
endothelial injury occurs and then the monocytes and platelets adhere
30
migration of inflammatory cells
inflammatory cells initiate atherosclerotic lesions and then monocytes transform into macrophages which engulf lipoproteins and cause "foam cells"
31
lipid accumulation and smooth muscle cell proliferation
progressive accumulation of foam cells leads to lesion progression leading to migration of SMCs and foam cells die leading to necrotic debris in the vascular wall
32
plaque structure
aggregation of SMCs macrophages, leukocytes, collagen forms a fibrous cap (the shoulder)
33
plaque structure!
rupture, ulceration, or erosion of an unstable of vulnerable fibrous cap leads to hemorrhage into the plaque or thrombotic occlusion
34
atherlosclerosis clinical manifestations
-narrowing of the vessel (the lumen) and production of ischemia
-sudden vessel obstruction due to plaque hemorrhage or rupture
-thrombosis andn formation of emboli resulting from damage to the vessel endothelium
-aneurysm formation due to weakening of the vessel wall
35
atherosclerosis complications
larger vessels= complications are thrombus formation and weakening of the vessel wall
-medium sized arteries (coronary and cerebral) = ischemia and infarction due to vessel occlusion is more common
-arteries supply the heart, brain, kidneys, and lower extremeties and small intestine are most frequently involved
36
aneurysm
-abnormal localized dilation of a blood vessel that occurs in arteries and veins, most commonly in the aorta
-classified according to cause, location, anatomic features
37
aneuysm etiology
congenital, trauma, infection, atherosclerosis
38
aortic aneurysm etiology
ascending, aortic arch, descending, thoracoabdominal aorta, or abominal aorta
-elevated lipids, HTN, smoking
39
aortic aneurysm clinical manifestations of a thoracic !
back, neck pain, hoarseness, brassy cough
40
aortic aneurysm clinical manifestations of a abdominal !
pulsating mass, mid abdominal or lumbar discomfort or back pain, may impinge on renal, iliac, or vertebral arteries that supply the spinal cord!
41
aortic dissection
acute, life threatening
-hemorrhage into vessel wall with longitudinal tearing of the vessel wall
42
aortic dissection etiology
hypertension, degeneration of medial layer of vessel wall leading to changes in elastic and smooth muscle layers
43
Aortic dissection clinical manifestations
excruciating pain from tearing, anterior chest, back, elevated BP (will become unatainable in one or both arms as the dissection disrupts arterial flow to arms), syncope, paralysis, heart failure
44
acute arterial occlusion etiology/patho
sudden event that interrupts arterial flow
-result of embolus or thombus
45
arterial occlusion :emboli
atrial fibrillation, ischemic heart disease
-fat, amniotic, air emboli
-emboli lodge in bifurcation of major arteries
46
acute aortic occlusion manifestations
pallor, pain, pulselessness, paresthesia, paralysis, polar
47
atherosclerotic occlusive disease (peripheral artery disease) etiology
common in lower extremity vessels (femoral, popiteal)
-advanced age
-cigarette smoking, diabetes
48
atherosclerotic occlusive disease (peripheral artery disease) manifestations
gradual s/s, intermittent claudications (pain w walking)- calf pain because highest oxygen consumption
-vague aaching/numbness
-atrophic changes
-weak pedal pulses
-ischemic pain at rest, ulceration, gangrene, necrosis
49
thromboembolism
venous thrombosis: presense of thrombus in vein and inflammation
50
thromboembolism etiology
stasis of blood- immobilization, venous pooling
-hypercoagulability, factor V leiden, BCP, smoking, cancer
-vessel wall injury- trauma, surgery, infection/inflammation
51
thromboembolism manifestations
pain, swelling (calf, posterial, tibial) deep muscle tenderness, inflammation
-asymptomatic
52
chronic venous insufficiency
persisent venous hypertension on the structure and function of the venous system of the lower extremities
53
chronic venous insuffienciey etiology
prolonged standing, incompetent valves, DVT, inflammation, endothelial dysfunction
54
chronic venous insufficiency manifestations
tissue congestion, edema, impaired tissue nutrition, skin atrophy, brown pigmentation, stasis dermatisis (thin, shiny, bluish brown, irregulary pigmented skin)
55
stages of chronic venous disease
C1- spider veins
c2- varicose
c3- swelling
c4- skin changes
c5-6- venous ulceration
56
disorders of BP regulation
-BP must be closely regualted throught the body to ensure adequate perfusion of body tissues adn to prevent damange to blood vessels
57
low BP
tissues dont receive sufficient blood flow to ensure delivery of nutrients and oxygen and removal of cellular wastes- hypoxic ischemia
58
high BP
can damage endothelial tissue, increasing likelihood of both atherosclerotic vascular disease and vascular ruptures
59
hypertension
sustained condition of elevation of the BP within arterial circuit
60
hypertension etiology
primary (essential) HTN: clinical presence of HTN without evidence of specifc causitive condition
secondary HTN: caused by medical condition such as renal failure
61
primary HTN risk factors/etiology non modifiable
age, gender, race, fam history, genetics
62
primary HTN etiology modifiable
dietary, dyslipidemia, tobacco, alcohol consumption, fitness, obesity, Blood glucose diabetes, OSA
63
secondary HTN: risk factors
erythropoietin, renal HTN/disease, disorders of adrenal cortical hormones, oral contraceptive use, cocaine, amphetamines
64
clinical consequences of HTN
HTN increses the workload of the left ventricle, increasing the pressure against which heart must pump as it ejects blood
65
clinical consequences of HTN on organs
heart- angima, AMI, heart failure
brain- stroke
kidney- chronic disease
eye- blindness
66
normal BP
less than 120 and less than 80
67
elevated BP
120-129 and less than 80
68
stage 1 HTN
130-139 or 80-90
69
stage 2 HTN
over 140 or over 90
70
chapter 27
71
disorders of the pericardium
pericarditis
inflammation of the pericardium causes severe pain
72
pericardial sac
double layered serous membrane that isolates the heart from other thoracic structures
-barrier to infection
73
two layers of pericardium
1) visceral pericardium (thin)
2) parietal pericardium (fibrous, outer)
74
two layers separated by potential space
pericardial cavity (NML: 50 mL serous fluid)- lubricates, prevents friction
75
inflammation
viral, bacterial, rheumatic fever, uremia, AMI, cardiac surgery
76
neoplastic disease
breast cancer, lung cancer
77
congenital (from birth)
cysts
78
acute pericarditis etiology
viral most common, bacterial, uremia
79
acute pericarditisis patho
inflammation of pericardium, increased capillary permeability
80
manifestations of acute pericarditis
Triad of symptoms: sharp chest pain that radiates to shoulders, neck, back pain (gets worse with deep breathing, positional- releief when sitting up)
-pericardial friction rub
-ECG changes
81
pericardial effusion
-accumulation of fluid in pericardial cavity
-result from infection or inflammation
-small effusion: minimal symptoms
-increases intercardiac pressures
81
tamonade manifestions
-Becks triad!:
muffled heart sounds, jugular venous distention, narrowed pulse pressure (hypotension)
82
pericardial tamponade
compression of the heart due to infections, neoplasms, and bleeding into pericardial sac
83
coronary artery
supplies blood to the heart
84
coronary artery disease
heart disease caused by impaired coronary blood flow
85
CAD etiology
atherosclerosis which causes myocardial infarction, cardiac irrythmias, conduction defects, heart failure, and sudden death
86
CAD risk factors
smoking, elevated BP, elevated serum toal and LDL cholesterol, low HDL, diabetes, age, obesity, inactivity
87
assessment of coronary blood flow
12 lead ECG
excercise stress training
echocardiograph
cardiac MRI/CT
cardiac catheterization
87
determinants mv02
heart rate, left ventricular contractility, myocardial wall stress (SBP)
-as heart rate goes up, myocardial oxygen consumption and demand increases
88
pathogenesis of CAD
atherosclerosis (most common)
-chronic ischemic heart disease
-acute coronary syndrome
89
chronic ischemic heart disease
recurrent, transient, myocardial ischemia (intermittent, not permanent)
stable agina: results from narrowing of artery lumen
90
acute coronary syndrome
unstable angina, myocardial infarction
near permanent
91
atherosclerotic lesions: fixed/stable plaque
obstructs blood flow
-implicated in stable angina
92
atherosclerotic lesions: unstable plaque
-worse
-high risk plaque- abrupt changes-ruptures-causes platelt adhesion and thrombus formation
-implicated in unstable angina
-trigger event: emotion distress, physical activity
93
thrombus and vessel occlusion
thrombosis after plaque distribution: lipid core provides stimulus for platelet aggregation and thrombus formation
-thrombin and fibrin deposition
94
chronic ischemia heart disease
myocardial ischemia occurs when the ability of the coronary arteries to supply blood is inadequate to meet the metabolic demands of the heart
-atherosclerosis vs vasospasm
95
types of CIHD
chronic stable angina
variant/vasospastic angina
96
stable angina
-fixed coronary obstruction (stable!)
-angina precipitated by situations that increase the workload of the heart
-relieved within minutes by rest or NTG
97
stable angina: angina pectoris !
-constricting/squeezing
-precordial/substernal pain
-may radiate to left shoulder, jaw, and arm
98
variant/prinzmetal angina
endothelial dysfunction, hyperactive SNS, defects in handling of calcium
-occurs during rest or with minimal exercise
-occurs nocturnally
99
acute coronary syndrome is an umbrella term for
unstable angina, non-ST segment elevation (non-Q wave), and ST-segment elevation (Q wave)
100
unstable angina (USA)
nonST segment MI (NSTEMI)
patho- 5stages
-unstable plaque ruptures/nonobstructive thrombosis
-obstruction/spasm occurs
-severe narrowing of coronary lumen
-decreased oxygen supply
101
unstable angina (USA)
nonST segment MI (NSTEMI)
patho- 5stages
subendocardial (NSTEMI) infarcts involve 1/3 to 1/2 of ventricular wall (severerly narrowed but patent arteries)
102
unstable angina (USA)
nonST segment MI (NSTEMI)
three clinical features
-occurs at rest lasting move then 20 minutes if not interrupted by NTG
-severe pain, new onset
-more severe, prolonged, or frequent then previously experienced
103
ST-segment elevation MI (STEMI)
-ischemic death of myocardial tissue
-complete coronary occlusion
-area of infarction determined by coronary artery affect and by its distribution of blood flow, duration of occlusion, metabolic needs, collateral circulation
104
STEMI patho
transmural stemi infarcts: involve full thickeness of ventricular wall (obstruction of single artery)
-aerobic- anaerobic metabolism:unable to sustain normal function
-loss of contractile function within 60 seconds
reversibile changes if blood flow restored- after 20-40 minutes of severe ischemia is irreversible the pump fails
-ventricular remodeling occurs
105
STEMI/ Acute corornary syndrome manifestations
-abrupt onset
-someones sitting on my chest
-severe crushing, constricting, suffocatnig
-radiation to left arm, neck, jaw
-STEMI progression from NSTEMI
-prolonged, no relief from resting
-GI/ N/V
-fatigue
-pale, cool, moist skin
-impending doom
-sudden death within an hour (fatal arrythmia)
106
ECG changes NSTEMI
non-stemi= no st wave
-st segment depression
-may be transient st segment elevation
107
ECG changes STEMI
-st segment elevation
-t wave inversion
-Q wave (goes down)
108
diagnosis ACS
-ECG first time sensitive
-troponin 1 (Tn1) and troponin 2 (TnT): MORE SPECIFIC (increase withing three hours)
-creatinine kinase MB (CK-MB)- less specific-found in muscle cells (4-8 hours)
-coronary angiography, stress testing
109
infection endocarditis
potentially life threatening
110
infectious endocarditis patho
colonization or invasion of the heart valves and endocardium
-formation of bulky, friable vegetations, and destruction of underlying cardiac tissues
-septic emboli: carried by the blood stream- initiate infection or ischemia in remote tissues
111
infectious endocardititis etiology
staphylococcal infections
112
portal of entries that the organism gains access to the circulatory system
valvular disease, prosthetic valves, congential heart defects provides an environment conducive to bacteria growth
-oral lesions, dental procedures
113
infectious endocarditis; manifestations
fever, chills, petechiae, splinter hemorrhages, cough
114
function of heart valves
promote directional flow of blood through the chambers of the heart
115
etiology of valvular disorders
-congenital
-trauma
-ischemic damage
-degenerative changes
-inflammation
116
mechanical disruptions: stenosis
-narrowing of the valve opening-- valves do not open properly (gets stuck)
-increasing resistance to blood flow through the valve
117
mechanical disruptions: regurgitation
-distortion of the valve-- valve does not close properly
-permits backward flow to occur when the valve should be closed
118
mitral valve
left atrium to the left ventricle
-paroxysmal nocturnal dyspnea, orthopnea, DOE, CP, fatigue
119
mitral valve stenosis
-incomplete opening of mitral valve during diastole
-left atrial distention, impaired ventricle filling
-etiology: rheumatoid heart disease
120
mitral valve regurgitation
-incomplete closure
-LF stroke volume- 1/2 goes foward 1/2 goes backward back into lungs
-etiology: rheumatoid heart disease
121
mitral valve prolapse
floppy valve which balloon back into left atrium during systole
122
aortic valve stenosis etiology
-congenital valve malformation, acquired calcification "wear and tear"
123
aortic valve stenosis patho
-increases restitance to ejection of blood from LV into aorta
-calcification develops gradually-- LV has time to adapt
-LV wall becoming thicker-- obstruction to forward flow
124
aortic valve stenosis manifestations
severe obstruction causes progressive pressure overload--increased heart workload--signs of heart failure
125
aortic valve regurgitation patho
result of an incompetent valve that allows blood to flow back into LV during diastole
-LV must increase its stroke volume to include blood entering from the lungs as well as that leaking back through the regurgitant valve
126
aortic valve regurgitation etiology
IE, trauma, aortic distention
127
aortic valve regurgitation manifestions
dyspnea, orthopnea, abnormal drop is diastolic pressure leads to decreased perfusion
128
heart failure
complex syndrome
-related to functional or structural disorder of the heart-- manifestations of low cardiac output and pulmonary or systemic congestion (if blood cant get back into the LA, can go back into the lungs)
129
function of the heart pertaining to heart failure
move deoxygenation blood from the venous system through the right heart into the pulmonary circulation
-move oxygenated blood from the pulmonary circulation through the left heart and into atrial circulation
130
heart failure etiology
-coronary artery disease, hypertension, dilated cardiomyopathy, valvular heart disease
131
cardiac output -- how to find
cardiac output (amount of blood ejected by ventricle per min)= HR (balance between SNS and PNS) x stroke volume (amount of blood ejected each heart beat)
132
preload
volume of blood in the ventricle at teh end of disastole
-volume of blood stretching the heart muscle at the end of diastole--determined by venous return to the heart
133
afterload
the amount of resistance that the ventricle must overcome in order to eject blood out of the heart
-peripheral vascular resitance
-ventricular wall tension
134
myocardial contractility (inotropy- heart ability to contract)
the contractile performance of the heart
-contractility increases cardiac output independent of preload and afterload
-requires ATP and calcium
135
ejection fraction (EF)
should be between 55-70%
determines systolic vs. diastolic dysfunction
136
systolic dysfunction
decrease in myocardial contractility
-decreased EF less than 40%
-ischemic heart disease
-valvular disorder
-HTN
-weak LV cannot pump blood forward
137
diastolic dysfunction
EF is preserved
-contraction is normal but ventricular relaxation is impaired
-pericardial effusion, HCM (increase wall thickness)
-aging
-less filling of blood in LV
138
right sided heart failure etiology
Left ventricle failure pulmonary hypertension, pulmonary embolus
139
right sided heart failure patho
inability to move deoxygenated blood from systemic circulation into pulmonary circulation-- then to left side--reduction of LV cardiac output
-increased ventricular end diastolic, right atrial, and systemic venous pressure
140
right sided heart failure manifestions
edema, hepatomegaly, jugular venous distention, abnominal pain, anorexia
141
left sided heart failure (ventricular dysfunction)
-hypertension, AMI
-patho: impaired movement of blood from low pressure pulmonary circulation into high pressure arterial side of system circulation
-decrease in cardaic output, blood occumulated in left ventricle, LA, and pulmonary circulation
142
left sided heart failure manifestations
-pulmonary edema (nocturnally), pulmonary symptoms
143
frank-staling mechanism
increased preload--increased stretch--increase in force of contraction
144
SNS
catecholamines elevated, stimulated HR and cardiac contractility
145
RAAS
recognizes reduced renal blood from from low CO leading to increased sodium and water retention
146
natriuretic peptides
potent diurectic hormones (anp and BNP)
147
acute heart failure syndromes
-gradual or rapid changes in heart failure signs and symptoms resulting in need for urgent therapy
-worsening dysfunction that respond to treatment
-new onset from a precipitating event (large AMI)
-worsending end stage heart failure
148
clinical manifestations AHFS
-respiratory: dyspnea, orthopnea, PND, chronic dry nonproductive cough, bronchospasm, cheney stokes
-fatigue, weakness, confusion
-fluid retention, edema, nocturia, oliguria, ascites, pleural effusion
-cachexia, malnutrition
-cyanosis,
-arrythmia, sudden cardiac death
149
clinical manifestations AHFS: pulmonary edema
-gasping for air, cyanosis, frothy/pink sputum, crackles
150
ventilation
involves the movement of atmospheric air to the alveoli for provision of oxygen and removal of carbon diox
151
adequate oxygenation adn removal of c02 depends on
-adequate circulation of blood through pulmonary blood vessels
-appropriate contact between ventilated alveoli and perfused capillaries of pulmonary circulation
-ventilation and perfusion!!
152
gas exchange
-takes place within the lungs
-involves exchange of 02 and c02 between air in the alveoli and the blood in pulmonary capillaries
153
causes of acute respiratory failure: hypoxemic
-COPD
-severe pneumonia
-atelectasis
(retaining c02)
154
causes of acute respiratory failure: hypercapnic/hypoxic
-upper airway obstruction (laryngospasm)
-weak/paraylsis respiratory muscles
-chest wall injury
155
respiratory failure
failure in gas exchange due to heart or lung failure or both
-occurs in conditions that impair ventilation, causes a mismatches ventilation and perfusionor impaired gas diffusion
-faulure of oxygenation or failure or eliminating c02
! two types: hypoxemic
hypercapnic/hypoxic
156
hypoxemic respiratory failure
Pa02 less than 50mm Hg
hypoxia- pa02 less than 95 m Hg
157
hypoxemia results from
inadequate oxygen in air, disorder of respiratory system, dysfunction of neurological system, alterations in circulatory function
158
mechanisms by which hypoxia occurs
hypoventilation, impaired diffusion of gases, inadequate circulation of blood through the pulmonary capillaries, mismatching of ventilation and perfusion
159
hypoxemic heart failure
-tissues with the greatest need are the brain, lungs, and heart
if oxygen falls below critical level (50mm) anaerobic metabolism occurs and then releases lactic acid that causes METABOLIC ACIDOSIS
160
hypoxemic respiratory failure: mismatch of ventilation and perfusoin
lungs ventilated but not perfused and vice versa
161
hypoxemic respiratory failure: impaired diffusion
gas exchange between alveolar air and pulmonary blood impeded
162
mild hypoxemia
slight impaired mental status, vasoconstriction, tachycardia
163
chronic hypoxemia
increased RBC's, clubbing, cyanosis, pulmonary vasoconstriction
164
hypercapnia
pc02 (carbon dioxide) greater than 50mm Hg
165
hypercapnia etiology
hypoventilation in hypercapnia without hypoxemia
-mismatching of ventilation and perfusion (hypercapnia and hypoxemia)
166
hypercapnia: four factors contribute
-alterations in carbon dioxide production
-disturbance in gas excahnge function of the lungs
-abnormalities in function of teh chest wall and respiratory muscles
-changes in neural control of respiration
167
hypecapnia manifestations
decreased Ph (RESPIRATORY ACIDOSIS: pH below 7.35, pac02 above 45)
-vasodilation of blood vessels (brain)
-depression of CNS function
168
work of breathing
-shortness of breath, dyspnea, tachypnea/bradypnea, tachycardia, diaphoresis, cyanosis, use of accessory muscles, pursed lip breathing, abdominal breathing
169
disorders of lung inflation
obstruction of airway, lung compression, lung collapse
170
pleural effusion
abnormal collection of fluid within the pleural cavity that compresses lung tissue and inhibits lung inflation
171
pleural effusion patho
-rate of fluid formation exceeds rate of removal
-fluid accumulated within the pleural space (parietal/visceral pleura)
172
etiology hydrothorax
-heart failure, renal/liver failure, malignancy
173
pleural effusion: fluid
transudative: cirrhosis, CHF, nephrotic syndrome
exudative: bacterial/viral pneumonia, pulmonary infarction, malignancies
174
pleural effusion
-pleuritic chest pain, dullness/flatness to percussion, diminished breath sounds to effects area, hypoxemia
thoracentesis: releives pressure on lungs and provides for fluid analysis
175
hemothorax patho
blood in pleural cavity
176
hemothorax etiology
chest injury, complicaion of chest surgery, rupture of great vessel (aortic aneurysm)
177
hemothorax manifestations
alteration in oxygenation, venilation, respiratory effort, signs of blood loss, tachycardia
178
pneumothorax patho
presence of air in the pleural space causing partial or full collapse
179
pneumothorax etiology
primary spontaneous: bleb, smoking
secondary spontaneous: underlying patho process in the lung like TB, pneumonia, CF
traumatic: penetrating/non penetrating wound (GSW, Rib)
tension: intrapleural pressure exceeds atmospheric pressure causing buildup of air within pleural cavity that compresses lung, shifts mediastinum to opposite side of chest, compression of vena cava (life threatening)
- decreased cardiac output!
180
atelectasis
incomplete expansion of a lung or portion of lung
180
acelectasis etiology
airway obstruction, lung compression, loss of pulmonary surfactant
-narcotics, anestesia, post-surgical pateint, malignancy
181
atelectasis manifestations
retractions, decreased breath sounds
182
obstructive airway disorders
-caused by disorders that limit expiratory airflow
-asthma, obstructive airway disorders, emphysema, chronic bronchitis
183
obstructive airway disorders
-acute and chronic
-contraction of smooth muscle layer controls diameter of airways
-PNS stimulation=bronchial constriction
-SNS stimulation= bronchial dilation
184
asthma
-chronic disorder of airways that causes episodic:
- airway obstruction, bronchial hyperresponsiveness, airway inflammation, reversible, symptom free between attacks, airway remodelings
185
asthma patho
-exaggerated hyperresponsiveness to a variety of stimuli
-IgE mediated (eosinophils, mast cells)
-TNF-a and IL 4 and IL5-- amplification of airway inflammation
-eosinophils generate inflammatory enzymes and release leukotrienes causing incresed mucous secretion-- obstruction and further release of histamine from mast cells
-chronic inflammation: leads to airway remodelling
-short acting B2 adrenergic agonist relaxes bronchial smooth muscle
186
asthma genetic and environmental
allergens, exercise, aspirin, emotional, hormones (premenstrual), weather
187
manifestatiton of asthma
-wheezing
-prolonged expiration
-use of accessory muscles
-chest tightness
-distant or absent breath sounds
-able to speak only one to two words
188
refractory asthma
-persistant bronchoconstriction despite attempts to treat the attack with varous medication
-high medications requirements
-increased risk for fatal or near fatal asthma
189
COPD
chronic and recurrent obstruction of airflow in pulmonary airways
-accompanied by inflammatory responses
-leading cause of M and M
-is a combo of chronic bronchitis and emphysema
190
copd risk factors
tobacco, genetics (alpha 1 deficiency), hyperresponsive airway
191
COPD patho
obstruction of airflow- ventilation/perfusion mismatch
-inflammation and fibrosis of bronchial wall
-hypersecretion of mucous
-loss of elastic lung fibers and alveolar tissue
-loss of elastic fibers impairs expiratory flow rate increasing air trapping and airway collapse
(think decrease expiration = higher c02)
192
emphysema patho
loss of elasticity, abnormal enlargement of airspace distal to terminal bronchioles, destruction of alveolar walls
-over-distention of alveoli with air trapping--hyperinflation of lungs
-hyperreactive airways- leads to broncho constriction
193
chronic bronchitis patho
airway obstruction of the major and small airways
-increse in goblet cells-- hypersecretion of mucus in large airways-results in mucous plugging
-Diagnosis: cough for 3 months out of the year for 2 consecutive years
194
COPD manifestations
fatigue, exercise intolerance, cough w sputum, shortness of breath, frequent infection, respiratory failire, air hunger, tripod, hypoxemia/hypercapnia
195
emphysema
-no cyanosis
-pursed lip puffer breathing
-prolonged exhaling
-barrel shaped chest
-diaphragm pushed downward
-PINK PUFFER
196
chronic bronchitis manifestations
cyanosis
-fluid retention from right sided heart failure
BLUE BLOATER
197
disorders of pulmonary circulation
blood moves through the pulmonary capillaries-- oxygen content increases and c02 decreases
-dependent on ventilation (gas exchange) and perfussion (blood flow)
198
pulmonary embolism
develops when blood borne substance lodges in a branch of the pulmonary artery and obstructs blood flow
-thrombus, air, fat, amniotic fluid
-thromboemboli occur from deep vein thrombosis which lodge in pulmonary blood vessel as they move from right heart to pulmonary circulation
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pulmonary embolism patho
-obstruction of pulmonary blood flow--bronchoconstriction, impaired gas exchange, wasted ventilation, loss of alveolar surfactant
200
pulmonary embolism complication
pulmonary hypertension, right heart failure
201
pulmonary embolism etiology
VIRchows triad: venous stasis (immobility, chf), venous endothelial injury (trauma, surgery), and hypercoagulability states (protein C deficiency, cancer, BCP, pregnancy)
202
pulmonary embolism manifestations
-depends on size and location
-dyspnea, chest pain, tachypnea
-pleuritic pain change changes w respiration
-moderate hypoxemia wo c02 retention
-apprehension
-blood streaks sputum
203
massive emboli
-sudden collapse, hypotension, JVD
-often fatal
-D-dimer, helical chest CT, lower limb ultrasound, ventilation-perfusion scans, pulmonary angioangraphy
204
Acute respiratory distress syndrome
-most severe form of acute lung injury
-severity is measured by pa02/fi02 (how much oxygen on) = P/F ratio
205
ARDS etiology
A: aspiration(drowning, gastric)
I:infection (sepsis)
D: drugs (coke, smoke, raditation)
S: shock/trauma (burns, embolism)
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adult respiratory distress syndrome
-rapid onset of respiratory distress (12-18 hours)
-increase in RR
signs of respiratory failure
-Marked hypoxemia- refractory to treatment decreaed PF ratio
-bilateral infiltrated in tje absence of cardiac failure
-noncompliant lung (stiff lungs) difficult to ventilate
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respiratory defense mechanisms
-glottic and cough reflexes
-mucociliary blanket
-phagocytic and bacterialcidial action of alveolar macrophages
-immune defenses
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pneumonia
inflammation of the parenchymal structures of the lung in the lower respiratory trac (alveoli, bronchioles)
209
pneumonia etiologic agents
infections: psuedomonas, candida, other fungi
non infectious: inhalation of fumes, aspiration of gastric contents
-consider immune status of pt
210
pneumonia setting classification
-community acquired
-hospital acquired
211
pneumonia agent class
-typical
-atypical
212
pneumonia distribution class
-lobar: consolidation of a part of all of a lung lobe
-bronchopneumonia: patchy consolidation involving more than one lobe
213
typical pneumonia agent
-bacteria cause inflammation and exudates of fluid into air filled alveoli
214
atypical pnuemonia agent
-viral/mycoplasma that involves intersititum of the lung
-less striking symptoms
-lac of purulent sputum
-NO alveolar inflitration
215
community acquired pneumonia
-infections from organisms found in the community rather than in hospital/nursing home
-infection that begins outside of the hospital or is diagnosed within 48 hours of admission
-no residence in LTC facility for 14 days or more
-s.pneumoniae, H.infleunza, mycoplasma, legonella, RSV
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hospital acquired
lower respiratory tract infection that was not present or incubating on admission
-infections occuring after 48 hours of admission
-2nd most common hospital acquired infection
-most are bacterial: P. aeruginosa, S.aureus, Klebsiella
217
acute bacterial/typical pneumonia
-lung below main bronchi normally sterile
-microorganism enter air passages during ventilation/aspiration
-loss of cough reflex, damage to ciliated endothelium, impaired immune defenses predispose to colonization and infection-diabetes, smoking, antibiotics that alter normal flora
-pneumococcal pneumonia- gram positive- spleen plays a major role in elimination of the organism
-legionnaire disease (gram negative)-infection occurs when water that contains pathogen is aerosolized into droplets and is inhaled
218
primary atypical pneumonia
etiologic agents: M. pneumoniae( mycoplasma infections), influenza, RSV
-patchy involvement of the lung
-moderate sputum
-moderate leukocytosis
-no alveolar infiltrates
-cough?dry and hacking
219
tuberculosis
worlds foremost cause of death from a single infectious agent
-M.tuberculosis (rod shaped, aerobic bacteria)
-outer waxy capsure that makes them resistant to destruction
-can persis in old necrotic and calcified lesions adn remain capable of reinitiating growth
-referred to as acid fast bacilli
-strict aerobes that thrive in oxygen rich environment
-airborne, droplet nuclei
220
TB
caseating necrosis and cavitation resulting from hypersensitivity immune response
-macrophages are the primary cell infected- they cannot kill the organism but they initiate a cell-mediated immune response that eventually contains the infection
-in patients with intact cell-mediated immunity a granulomatous lesion (Ghon focus) develops caseous cheese like
221
TB manifestations
inhaled droplet nuclei with contain tubercle bacillus
-latet TB -cannot transmit no symtoms
-fever, weight loss, fatigue, night sweats, blond-tinged sputum (rusty)
