N211 -Health Differences Across the Life Span 1 Flashcards

1
Q

HTN

A

28-31% adults in US

of this , 90-95% PRIMARY HTN (unidentified cause)

remaining 5-10% SECONDARY HTN (identified cause)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Identified Causes for HTN

A

-narrowing renal arteries, renal parenchymal dis, hyperaldosteronism (mineralocorticoid HTN), Pregnancy, coarctation of aorta, certain meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ETOH and HTN linked to

A

UP triglycerides, sugars, weight gain, LDLs, cardiac function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dx someone with HTN elevation on one round. Must have average of

A

2 or more contacts w health care provider

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Normal BP

A

<120/<80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pre HTN

A

120-139/80-89

PIH (pregnancy induced HTN usually resolves after placenta expelled)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Stage 1

A

140-159 / 90-99

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Stage 2

A

160 up / 100 up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stage 1 TX

A

Medication, MD until stable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Stage 2 Tx

A

doctor and workups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

?250 - 400

A

Moderate Cardio Vas dis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

UnTx HTN

A

.UP workload to heart
.thickening of arterial wall
. etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HTN Emergency

A

BP 180/120

.pressure in head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HTN Crisis Tx.

Short lived meds (minutes - 4hrs)

A

Nitroglycerin (Nitro-Bid)
Socium Nitroprusside (nipride or nitropress)
nicardipine hydrocholoride (cardene)
enalaprilat (vasotec)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vasodilator: Fendolopam

A

Fendoldopam (Corlopam)

1.action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Alpha Adrenergic Clocker

A

WORK DIRECTLY ON BLOOD VESSELS

keeps hormone from tightening muscles and walls. counter epi and nor epi.

SE: V/N/D, urinary freq, cardio vascular collaps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Alpha Adrenergic Clocker

A

WORK DIRECTLY ON BLOOD VESSELS

keeps hormone from tightening muscles and walls. counter epi and nor epi.

SE: V/N/D, urinary freq, cardio vascular collaps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Beta Adrenergic Blocker

COREG

ALPHA and BETA

A

Dry Cough - BAD, change meds

Slow transition to get used to

SE: cardiovascular. can worsen ss. not for newly HTN patients Not first line drug.

Contracindicated in Heart failure, COPD and ?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Beta Adrenergic Blocker: Inderol

A

Propanolol

for Stage Fright, BP control,

slows HR, reduces cardiac output, fatigue, bizarre dreams

SE bradycardia, insomnia, fatigue,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Calcium Chan Blocker

A

Diltiazem

Inhibit calcium ion influx and reduce after load.

inhibit na, inhibit water.

Procardia: CHF, resistant Angina,

Some people chew to get emergency fast effects. not for normal pt as it can bottom out pressure fast.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Beta Adrenergic Blocker

A

Lopressor, Corguard, Inderol, Toprolol

slow HR. they get breathless, can’t excercise on this drug.

decrease contractions and AV signal,

SE bradycardia, insomnia, fatigue, bad dreams, sex dysf, LO HDL, GI probs, LO BP, depresson

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ACE Inhibitors

A

Angio 1 - 2.

lowers resistanece of peripheral vascular syste =less risistance

SS proteinurea, dry cough, hyperkalemia, renal damage

Catapress
Aldamet
diminish periphera outflow from brain. brain action to neurons.

dose at bedtime. monitor 30-90min for syncopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diuretics

A

Thiazides

pulling fluid from extra vascular to intra vascular spaces to rebalance lo plasma.

affect smooth muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Burn patients

A

hi K levels. As they stabilize, K drawn back into cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Loop Diuretics
can cause volume depletion . NOT first line. After Thiazines tried.
26
K sparing Diurents
can cause Hyper Kalemia.
27
Vasodialiators | Hydralazine
Hydralazine (Apresoline)
28
DASH Diet
reduce cholestoerol in blood
29
Chart textbook P15
MAKE CARDS
30
PTT (partial prothrombin time)
eficacy of Heparin
31
PT(C) (prothrombin time)
Efficacy of Coumadin
32
when we have a venus problem, DO NOT add heat
it will increase circulation. If arterial problem, yes warm. you want blood to go down to extremeties. in venous, the blood is pooling and we need to elevate legs to help move up blood.
33
intermitent caudicatoin
when person walks, not enough blood flow to legs. sever pain, heavy , sharp. they stand still , then it goes away, then it starts again when they walk
34
Abdominal Aortic Aneurysm
-asymptomatic Watch for clotting emboli rx for clotting SS: Abdominal pain, low back pain, feel heart beat
35
Assessing AAA
Bruit, swooshing over consicted artery. | Pain: abdominal/loabdomin
36
Calcium Channel Blockers
Tx Angina, HBP affect movement of ca in cells of heart
37
Digoxin/Linoxin
stronger heart contraction
38
Beta Blockers
Control catacholoamines
39
Beta Blockers
Control catacholoamines
40
Digoxin Antagonist
digoxinase ?
41
Hyperkalemia Antagonist
Kayexalate
42
Heparin
protamin sulfate
43
Coumadin antagonist
vit k
44
Pulse Pressure
diff between top and bottom
45
Pump Problems
cardiomyopathy
46
Cardiogenic shock
loss of hearts ability to pump enough blood to heart
47
hypovolemic shock
loss of large amount of blood or fluid
48
Distributive Shock
loss of vascular tone causing decreased peripheral resistance, larger vascular bed, result in hypovolemia
49
Class 3
9/6/18
50
Problems of intake and supply of O2
.
51
beta blockers Inderol?
non selective vs selective
52
classic angina comes from
exertion or stress
53
unstable angina pre infarction
frequent times daily with increasing severity
54
classic dysrythmias result from
hypoxia and hypercapnia
55
Digitalis preps effective in treating
CHF
56
cardiac glycoside aka
dig glycoside
57
digitalis
allows heart to work less but beat stronger
58
strted from page 24
review ABG
59
Sudden hypercapnia causes
.UP Pulse, resp, BP .Mental cloud see rest
60
Acute Respiratory Acidosis
inadequate excretion of CO2 w inadequate vent
61
Chronic Resp Acidosis
occurs w pulmonary diiseases
62
Nursing Interventions
.lo flo O2 | .monitor consiousnee, abg, ekg for dysrythmias
63
SLIDE 9
HCO3 is Bicarb not H2CO3
64
when you rae chronically aciic, hi CO2
body become used to it. It's stops becoming the hi CO2 that makes the breath, but the lo O2 levels.
65
go over respiratory vs metabolism
k
66
Respiratory Alkalosis
Carbonic Acid deficit .body loses CO2, decrease in acid, increases ph level .occurs w hyperventilation, leads to loo CO2 ......
67
Causes
.
68
SS
.
69
.
.
70
.
.
71
.
.
72
Nursing Intervention
.tx underlying cause
73
Metabolic Acidosis
.ABG .lo bicarb .lo ph
74
Metabolic Alkalosis
.hi ph > 7.45 .hi plasma bicarb (HCO3 > 26) .paCO2 INC as lungs attempt to compensate for excess bicarb by retaining CO2 compensate by blowing it off
75
Acidotic complication
.peripheral vasodilation and decrease cardiac output w Ph drops to <7.0 .chronic metabilic acidosis usually seen wtih chronic renal failure .closemonits K leves. hypokalemia
76
LOOK at old ABG slides
look at old ABG slides
77
metabolic acidosis
.see P57 in book . lo bicarb .hyperkalemia
78
SEE pg 57 in book
MAKE SLIDES
79
Adult Respiratory Failure
Slide 97
80
pg 61
beta antagonist | corticosteroids
81
Atropine
drying secretions | .......
82
PNA clsassification
``` community hospita incompromised host aspiration pna ? ? ```
83
ended at laryngeal obstructino
slide 182
84
Factors Causing Hypertension
.INcreased Sympathetic stimulation .UP blood volume d.t increased renal reabsorption of Na+, CL- and H2o retention .UP activity of RAAS system, caused expansion of extracellular fluid volume. causing systemic vascular resistance .Dysfx of vascular endothelium causing decreased vasodilation of arterioles .resistance to Insulin
85
most gastric cancers are
adenocarcinomas will go through stomach and into other organs
86
most gastric cancers are
adenocarcinomas will go through stomach and into other organs
87
Ovarian Ca SS
bloating
88
to take the ovaria
.
89
Capoten
Captopril ACE inhibitor
90
Lotensin
Benazepril
91
Zestril
Lisinopril
92
Aldactone
Spironolactone ARB - Aldosterone Receptor Blocker
93
Cozaar
Losartin ARB
94
what does epinephrine do?
vasoconstrict
95
Lopressor
Metaprolol Beta Blocker
96
Tenormin
Atenolol BB
97
Norvasc
Amlodipine CCB
98
Plendil
Felodipine CCB
99
Procardia
Nifedipine
100
Catapres
Clonidine Central Alpha 2 agonist
101
Coreg
Carvedilol | alpha and BB
102
Apresoline
Hydralazine (direct vasodilator) helps body loose excess water by releasing excess salt
103
Esidrix
Hyrochlorothiazide Diuretic
104
Prinzide
Lisinopril / HCTZ (Lisinopril/HCTZ) {=Thiazide diuretic and ACE inhibitor} causes the blood vessels to loosen and dilate. This decreases the strain on the arterial walls. Therefore, the speed and pressure inside the artery walls decreases {=Vasodilators}
105
Prinzide
Lisinopril / HCTZ (Lisinopril/HCTZ) {=Thiazide diuretic and ACE inhibitor} causes the blood vessels to loosen and dilate. This decreases the strain on the arterial walls. Therefore, the speed and pressure inside the artery walls decreases {=Vasodilators}
106
Systolic heart failure
most common alteration in ventricular contractoin
107
Diastolic heart failure
stiff noncompliant heart muscle
108
Type of Heart Failure determined by EF
Ejection Fraction, vol blood ejected w each contraction of ventricular volume (normal 55-65%) determines Systolic or Diastolic heart failure HF = low EF
109
Left Sided HF
Pulmonary Edema SS: dyspnea, wet lung, cough, fatigue, tachy, anxiety, restlessness, confusion, paroxysmal nocturnal dyspnea (sudden attacks at nght), orthopnea (diff breathing lying down) Frothy pink sputum = severe Pulm Edema Dominant feature of heart failure is decreased tissue perfusion to kidney, brain, and GI system
110
Right Sided HF
Peripheral Edema SS: peripheral edema, weight gain, distended neck vain, anorexia, nausea, nocturia, weakness
111
HF
``` .decreased cardiac output .impaired urinary elim d/t decreased perfusion .activity intolerance .anxiety .ineffective tissue perfusion ``` Tx: restrict Na, to reduce salt and water retention, reducing vascular volume .assess/monitor q4hrs .assess/mon apical hr .assess for hypoxia (restlessness, tachy, chest pain) .auscultate lungs for pulmon edema (crackles/wet sounds) .admin O2
112
HF Interentions
.observe ss of edema (daily weight, monitor i&O, measure abdom girth, observe ankles/fingers for swelling. .elevate HOB to assist w breathing and limit Na intake. .check apical HR before Digitalis, HOLD if <60. .diuretics in AM .periods of rest after activity
113
Cardiomyopathy, 3 types
Disease of myocardium 1. Dilated (most common) • Causes diffuse cellular necrosis and fibrosis • Leads to decreased contractility (systolic failure) 2. Hypertrophic (rare) • A chronic disorder in which the heart muscle becomes abnormally thick. 3. Restrictive cardiomyopathies lead to decreased distensibility and ventricular filling (diastolic failure)
114
HF NURSING DX
• Altered cardiac and peripheral circulation related to decreased cardiac output • Ineffective tissue perfusion from altered circulation • Anxiety related to lack of knowledge and fear of the unknown • Activity intolerance related to decreased cardiac output
115
PAC
Preatrial Contraction normal electrophysiological phenomenon frequent PACs may cause palpitations, or sense of "skipping a beat" can trigger afib, aflutter etc.
116
Atrial Fibrillation (Afib)
Electrocardiogram – Chaotic activity from the AV node – No true P wave visible – Irregular ventricular rhythm TX: – Anticoagulant therapy due to risk of stroke – Antidysrhythmic drugs – Cardioversion to treat atrial dysrhythmia – Ablation of atria
117
Preventricular Contraction
Ectopic firing
118
Ventricular Tachycardia
Electrocardiogram – Wide bizarre QRS – Pulse erratic and with impaired cardiac output Treatment: – Synchronized cardioversion if pulse present – If no pulse, treat as ventricular fibrillation – Antidysrhythmics
119
Ventricular Fibrillation
``` Cardiac Emergency Electrocardiogram – Irregular undulations of varyious amplitudes from coarse to fine – No cardiac output Treatment: – CPR – Defibrillation as quickly as possible – Antidysrhythmic drugs ```
120
Myocardial Infaction
Part of myocardium permanently destroyed ``` • Caused by reduced blood flow in coronary artery • Due to rupture of atherosclerotic plaque • Subsequent occlusion of artery by thrombus ```
121
ACS, Acute Coronary Symdrome
Unstable Angina: plaque rupture, but artery not completely occluded or also ``` • Vasospasm (sudden narrowing) • Decreased oxygen supply (from acute blood loss, anemia, or low BP) • Increased demand for 02 (rapid heart rate, thyrotoxicosis, or ingestion of cocaine) ```
122
Cardiac Markers for Dx and MI
1. Troponin (cTc1 and cTnT) – will be evident 3-4 hours after a heart attack, peak in 12-16 hrs and stay elevated for 2 – 3 weeks 2. Myoglobin (Mb) can elevate in other conditions; troponin level is taken to confirm MI (1-3 hrs and peaks in 12 hrs) 3. Creatine kinase (CK), an enzyme found in heart muscle cells and other cells of the body, so a more specific level of elevation in cardiac cell must be obtained (peaks in 24 hrs)
123
3 Cardiac Markers for MI
1. Troponin, 3-4 hrs after attack 2. Myoglobin 3. Creatine Kinase
124
Electrocardiogram
note dysrhythmias, changes in T wave and SG segment and presence of Q wave
125
Echocardiogram
to assess cardiac muscular function and valves
126
Types of Schock
Cardiogenic: loss of heart ability to pump Hypovolemic: loss of blood Distributive: loss of vascular tone
127
Cardiogenic Shock SS
.sinus tachycardia, weak, thready pulse, tachypnea .S3 and S4 heart sound .hypotension .Oliguria (<30ml/hr) ``` NI: NPO, reduce risk of aspiration .admin/monitor fluids to avoid fluid overload .admin 02 to maximize cardiac .mon pulmonary and renal fx .monitor intra-aortic balloon pump (IABP) .Digitalis .Vasoconstriction agents .dopamine ```
128
Iron Deficiency Anemia
MEN: Normal 13-31 Umole/L WOMEN: 11-29 umole/L
129
Megaloblastic Anemia
.caused by deficiencies of Vit B12 or Folic Acid .changes in bone marrow, peripheral blood .abnormally large Erythrocytes called Megaloblastic red cells SS: weakness, listlessness, fatigue NI: DO NOT admin RBC transfusion because body w compensate and go into fluid overload.
130
Low Hemoglobin
heart compensates by pumping faster/harder to deliver more blood to hypoxic tissue SS: tachy, palpitation, dyspnea, dizzy, orthopnea, exertional dyspnea
131
Sickle Cell Disease
.inherited Autosomal Recessive disorder of HgB .African/eastern mediterranean descent .after 6 mos age .hemoglobin S replace all or part of normal HgB, causes RBCs to sickle w O2 is released into tissue
132
Sickle Cell Anemia
if both parents have sickle cell train, children may inheri 2 abnormal HbS genes and w have sickle cell anemia, most severe form of disease
133
Sickle Cell Anemia SS
.bone marrow expand in childhood, compensate to offset anemia .anemia (7-10 g/dL) .jaundice .enlarged facial bones and skull .tachy, enlarged heart, murmurs
134
Hand-Foot Syndrome
swollen hands
135
Sickle Cell Crisis
1. Sickle cell crisis: tissue hypoxia and necrosis in tissue or organ 2. Aplastic crisis: infec w human parvovirus 3. Sequestration crisis: other organs pool sickled cells Most kids with SC will have a Splenic Infarction by age 10 and it becomes non functional (liver and lungs in adults)
136
Splenic infaction
a condition in which oxygen supply to the spleen is interrupted, leading to partial or complete infarction (tissue death due to oxygen shortage) in the organ. Splenic infarction occurs when the splenic artery or one of its branches are occluded, for example by a blood clot.
137
Acute Chest Syndrome
Rapid decrease in hemoglobin, fever, tachi, bilateral inflitrates .mimics infection but are infarctions withing pulmonary Image result for acute chest syndromethorax.bmj.com
138
Pulmonary HTN
sequel to sickle cell disease
139
4 Sickle Cell Txs
``` .Bone Marrow Trans .Hydroxyurea: (Hydrea): chemotherapy agent – increases hemoglobin F levels and decreased formation of sickled cells .Arginine: antisickling properties; used in combination with Hydrea to manage pulmonary hypertension .Long-term RBC transfusions ```
140
Sickle Cell NI's
manage pain, swollen joints, elevate extremities .relaxation .manage infection .promote coping skills
141
Chronic myeloproliferative disorder
``` • Increased RBCs • .Leukocytosis • Thrombocytosis • Increased hemoglobin concentration • Occurs between ages 40-60 in males of Jewish ancestry (mortality high if not treated) ```
142
Polycythemia SS & TX
``` SS: • Clubbing of digits • Dizziness • Headache • Hypertension • Ruddy cyanosis of nose • Thrombosis of smaller vessels • Visual disturbances ``` ``` Tx: • Phlebotomy • Chemotherapy • Myelosuppressive drugs • Anti-gout agents (Allopurinol) • Replace fluid volume lost during procedure ```
143
Polycythemia SS & TX
``` SS: • Clubbing of digits • Dizziness • Headache • Hypertension • Ruddy cyanosis of nose • Thrombosis of smaller vessels • Visual disturbances ``` ``` Tx: • Phlebotomy • Chemotherapy • Myelosuppressive drugs • Anti-gout agents (Allopurinol) • Replace fluid volume lost during procedure ```
144
Idiopathic Thrombocytopenic Purpura (ITP)
Auto Immune .Idiopathic SS: – Too few platelets – Bruising, petechiae, and internal bleeding TX: – Steroids – Immune globulins – Splenectomy
145
Thrombocytopenio: Low Platelet Count
.lo platelet production in marrow .up destruction of platelets .up consumption of platelets SS: .<20K/mm3 petechiae .nasal/gum bleeding .hi menstrual bleed .monitor dental and Sx. Tx: .teach avoid substance that lo platelet fx. (i.e. otc meds, herbs, supplements etoh) .inform med providors
146
Disseminated Intravascular Coagulation (DIV)
massive amt of tiny clots form in microcirculatotion triggered by: trauma, sepsis, shock, ca, abruptio placentae, toxins, allerg reactions Initially normal clotting time, then as the many clots forming use u the plateletes and clotting factors, coag time starts to fail. PARADOXICAL result of up clotting is bleeding
147
DIC more
pt bleed from mucous membranes, venipuncture site, gi, urinary tract
148
Hemophelia
bleeding disorder, males contracted by x-linked recessive chromosome (mother carrier) normla factor activity 50-200%, Hemophelia 0-25% Dx: PTT prolonged, factor VIII assays <25% of normal factor
149
class 2, pg 80
.
150
AICD:Automatic Implanted Cardioverter Defibrillator:
A device that detects and terminates life-threatening episodes of ventricular tachycardia (VT) or fibrillation (VF)
151
Pacemaker
an electronic instrument that supplies electrical stimuli to the heart muscle
152
Intra-Aortic Balloon Pump (IABP)
.facilitate UP myocardial O2 supply | .LO myocardial O2 demand
153
IABP Compmlications
``` Transient loss of peripheral pulse Limb ischemia; compartment syndrome Thromboembolism; cardiac tamponade Compartment syndrome Aortic dissection Local vascular injury— false aneurysm, hematoma, bleeding from the wound Infection Balloon rupture (can cause gas embolus) or balloon entrapment Hematological changes, i.e., thrombocytopenia Malpositioning causing cerebral or renal compromise ```
154
IABP NI
.monitor pulmonary pressure .treat arrhythmias. >106 .monitor HgB and Hct for anemia .monitor complication of cardiogenic shock .monitor for impending renal compromise <30cc/hr
155
Intracoronary Stent
stent placed in artery to maintain patency.
156
Stent complication
``` .bleeding/hematoma .weak pulse distal to insertion site .pseudoaneurysm and arteriovenous fistula .retroperitoneal bleeding .acute renal failure ```
157
Normal ABGs
pH 7.35 – 7.45 Kids 7.36 – 7.44 PCO2 34 – 45 mmHg (ACID) PO2 80 – 100 mmHg HCO3 21 – 28 mEq/L (BASE)
158
Respiratory Acidosis
response to HYPOventilation 1. pH < 7.53 2. PaCO2 > 45mmHg 3. UP CO2, UP Carbonic Acid 4. Hyperkalemia COMPENSATION: .UP respirations to blow off CO2 .Bicarb UP to compensate Med Tx: Calcium, Insulin, glucose, NaO2, Dialysis
159
Acidosis SS
h/a, sleepiness, confusion, loc, coma, sob, cough, seizure, weakness, diarrhea, arrhythmia, up hr, N/V
160
Causes of Resp Acidosis
Hypoventilation .severe pna, ards, impairment of resp muscles, pulmonary edema, aspiration of foreign object, atelectasis, pneumothorax, od sedatives, sleep apnea, non therapeutic O2, COPD pts
161
COPD and Chronic Hypercapnia
COPD pts gradually accumulate CO2 over time, may not develop hypercapnia d/t compensatory renal changes.
162
Respiratory Alkalosis
Carbon Acid deficit lo CO2, decrease in acid, UP pH >7.45, PaCO2 < 38mmhg .HYPERventilation, LO CO2 .Lo Carbonic Acid
163
Causes of Respiratory Alkalosis
``` .extreme anxiety . blow off excess CO2 .Hypoxemia .Gram Neg bacteremia .salicylate intox, ventilator settings ```
164
SS of Respiratory Alkalosis
ha, sleepy, confusion, loc, coma, sob, cough, arrhythmia, up hr, seizures, weakness, n/v/d, light headed, stupor, coma, hand tremor, parestesia, twitching, spasms,
165
Respiratory Alkalosos
Dx: .UP Ph >7.45 .
166
continue on Pg 25
pg 25
167
Adult Respiratory Failure (ARF)
sudden, life threat deterioration of gas exchange of O2 for CO2 in lungs can not keep up w rate of O2 consumption and CO2 production CONDITION not a disease. any disease w disorder of nerves, spinal cord, muscles or neuromuscular junction involved in respiration Muscular dystrophy, myasthenia gravis, poliomyelitis, ALS (amyotrophic lateral sclerosis, Guillain-Barre syndrome, and cervical spinal cord injuries
168
Chronic Respiratory Failure (CRF)
CRF is a deterioration in the gas exchange function of the lung, which develops insidiously, OR has persisted for a long period after an episode of ARF
169
Acute Respiratory Distress Syndrome
severe form of acute lung injury Major cause of death: non pulmonary multiple system organ failure
170
Suctioning
.apply suction ONLY when REMOVING catheter, gently rotating while withdraw .NO more than 10-15sec, 3-4 times .O2 1-2 min before and after suction
171
O2 Administration
Nasal Cannula, Simple face mask, non rebreather mask, partial rebreather mask, , venturi mask
172
PNA risks
pt w .alteration in LOC .LO/NO gag reflex .immobile Raise head of bed when feeding.
173
PNA
Inflammation of lower resp track. Bacterial, Viral, Fungal (rare), Chemical
174
Types of PNA
.community acquired . hospital acquired .PNA in immunocompromised host .aspiration pna
175
CAP
Community Aquired PNA .reside naturally in upper resp tract, then colonizes. .causes lobar or bronchopneumonia . after recent resp illness
176
PNA SS
``` Streptoccal (pneumococcal) PNA: .sudden onset of chills .rapid fever (101-105) .patient severely ill .tachypnea (25-45bmp) .UP plulse ```
177
VAP
Ventilator Assisted PNA
178
VAP SS
``` .bradycardia (viral) .mycoplasma infection .legionella organim .may URI, Mucopurulent sputum .h/a, lo fever, pleuritic pain, myalgia, rash, pharyngitis ``` .SEVERE: flushed cheeks, OLDER adults: .lethargy, confusion, anorexia, rapid hr .pain/dullness during percussion over affected lung area .bronchial breath sounds, crackles Xray: infiltrates w consolidation or pleural effusion
179
PNA NIs
``` .monitor abx .deep breathing q 2hrs .humidity to loosen secretions .suction airway PRN .up to 3L/day fluid .encourage flu shot ```
180
Chronic Bronchitis
``` .chronic sputum w cough production on daily basis for min of 3 mos - 1yr .chronic hypoxemia . UP mucous .UP bronchial wall thickness . ```
181
Blue bloater
``` chronic bronchitis .excessive mucous .airway obstruction .hypoxia .residual lung volume UP ```
182
Pink Puffer
``` emphysema .hyperventilation .muscle wasting .weight loss .less hypoxia, work neck and chest muscles ```
183
Tripod Position
sitting in chair, hands on knees (tripod)
184
TB
infection w Mycobacterium Tuberculosis bacteria .AIRBORNE .after initial exposure, bacteria encapsulates (form GHON lesion) .bac dormant until later when ss appear.
185
TB SS
``` .asymptomatic .fever, night sweats .anorexia .malaise .cough, sputum .dyspnea, pleuritic chest pain .cavitation or calcification per Xray .positive sputum culture ```
186
TB Skin Test
Bacillus Calmette Guerin (BCG) vaccine test w be positive positive = induratio 10mm or greater in 48-72hrs
187
TB NIs
``` • Risk for infection • Ineffective Airway Clearance • Activity Intolerance • Anxiety • Imbalanced nutrition: less than body requirements • Impaired Gas Exchange • Knowledge deficit ```
188
TB Interventions
``` .H, isolation .cough into tissue and dispose immediately in to special basket .meds for 9-12mos .hand washing .report ss of deteriorating/hemorrhage .collect sputum culture .return to work after 3 neg cultures ```
189
Cystic Fibrosis
.Autosomal recessive disease, cause dysfx of exocrine gland .tenacious mucus production, obstructs vital structures .lung insufficiency .pancreatic insuff .UP los of Na+ and Cl- in sweat
190
Cystic Fibrosis SS
usually dx in white infant or child ``` .meconium ileus at birth (10-20%) .chronic resp infection .pulmonary congestion .steatorrhea (fatty stool) .foul smelling stool .LO growth and weight .skin salty when kissed ```
191
Cystic Fibrosis NIs
.monitor respiration .IV abx .pancreatic enzymes .fat soluble vits A, D, E, K in water soluble form .nebulizer and O2 tx .percussion and postural drainage .DIET: HI cal, HI protein, MOD/HI fat, MOD/LO carbs child needs 150% of usual calorie intake for normal growth and dev.
192
Sleep Apnea
sleeping, loud snoring, breathing cessation for 10sec or longer .awaken abruptly w loud snort as O2 level drops .5-several hundred events per night. .HI risk for CAD, cerebrovascular disease, premature death .repeated apneic events cause hypoxia and hypercapnia .daytime sleepiness and fatigue
193
Types of Sleep Apnea
Central and Obstructive
194
Obstructive Sleep Apnea
most common .reduced diameter of upper airway or reduced upper airway muscle tone TX: nasal CPAP or BiPAP w supplemental O2 for severe hypoxia and hypercapnia .weight loss recommended for obese .no ETOH and sedatives
195
Central Sleep Apnea
simultaneous suspension of both airflow and respiratory mvmt Sx: – Uvulopalatopharyngoplasty to correct obstruction – Tracheostomy to bypass obstruction for respiratory failure or life-threatening dysrhythmias; unplugged during sleep NI: .avoid ETOH and respiratory suppressive drugs .weight loss .notify re potential daytime sleepiness
196
Sleep Apnea MEDS
• Modafinil (Provigil) to reduce daytime sleepiness • Protriptyline (Triptil) HS to increase respiratory drive; improve upper airway muscle tone • Patient may require nasal continuous positive airway pressure (CPAP)
197
Childhood Upper Airway Disorders
``` .Croup .Epiglottis tis .Laryngotracheobronchitis .Spasmodic Laryngitis .Tracheitis ```
198
Epiglottitis
infection of epiglottis. caused by H. Influenzae type B ``` SS: .sudden onset .restlessness .hi fever .dysphagia .drooling .muffled voice .child assumes upright position w chin out and tongue protruding ```
199
Epiglottitis
• Epiglottis cherry red, swollen and edematous and can obstruct airway • Secretions pool in pharynx and larynx above epiglottis • Child has sore throat and unable to swallow • Can have airway obstruction within 2-6 hours • Hib vaccine has reduced incidence
200
Bronchiolitis
RSV, Respiratory Syncytial Virus .young infants . HIGHLY contagious .thick secretions .paroxysmal coughing, nasal flaring, prolonged expiratory phase, wheezing, rales .deteriorates to rapid, shallow respiration
201
Bronchitis NIs
``` .upright position .intubation/Trach .IV abx .NPR, I7o .antipyretics, cotiscosteroids to decrease edema .manage sore throat pain ```
202
Croup in kids
Laryngotracehobronchitis
203
Laryngotracheobrochitis
viral infection inflammation, edema and narrowing of larynx, trachea and bronchi .3mos - 8yrs .most common croup syndrome .inspiratory stridor and suprasternal retractions upon inhalation (barking cough)
204
Tonsilitis ss
``` sore throat fever snoring diff swallow enlarged adenoids cause mouth breathing, head colds, earaches ```
205
SARS
Severe Acute Respiratory Syndrome
206
SARS
.discovered asia, 2/2003 .RESPIRATORY, droplet .spread by contaminated surfaces then touching mucous membranes
207
SARS SS
``` .HI fever .H/a body aches .mild respiratory ss . 10-20% have diarrhea .after 2-7 days, dry cough ```
208
SARS Contaigion
``` • More contagious when symptoms present • Most contagious during second week of illness • Limit contact until ten days after fever no longer present and respiratory symptoms improved • Treatment same as CAP ```
209
Nursing Process
ADPIE ``` Assess Dx Planning Implementation Evaluation ```
210
Leading Cause death for MEN
Lung, Prostrate, Colorectal
211
Leading Cause death for WOMEN
Lung, Breast, Colorectal
212
Cell membrane of malignant cells contain
proteins tha develop over tikme called "tumor-specific antigens" i.e. prostate-specific antigen (psa)
213
Malignant Cells
.grow and divind w glucose, O2 | .mali`gnant cells us ANEROBIC metabolism
214
Malignant cells attatch to endothelium and
attract fibrin, platelets and clotting factors to seal off from immune system. Endothelium retracts, mal cells secret LYSOSOMAL ENZYME tha destroys body sys and allow implantation
215
Angiogenesis
development of new capillaries from host tissue by release of growth factors and enzymes such as vascular endothelial growth factor (VEGF) .These proteins rapidly stimulate formation of new blood vessels that help malignant cells obtain nutrients and oxygen • Through vascular network, the tumor emboli enter systemic circulation and travel to distant sites. Therapies target VEGF or its receptors.
216
Carcinogenesis
malignant transformation .Imitation: chemicals, physical factors, biologic agents, escape normal enzymatic mechanisms and alter genetic structure of cellular DNA .Promotion: repeated exposure to promoting agents (co-carcinogens) causes expression of abnormal or mutant genetics information (different latency periods) .Progression: • cells that changed during imitation and promotion invade adjacent tissues and metastasize