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Flashcards in Exam 4 Deck (161):
1

CO=

HR x SV

2

BP=

SVR x CO

3

blood flow through the heart

RA- tricuspid valve- RV- Pulmonary Artery- lungs pulmonary vein- LA- Mitral valve- LV- Aortic valve- body

4

Preload

filling and stretch just prior to contraction

5

Afterload

resistance in the aorta, if it increases SV/CO decrease

6

Baroreceptors

Sense pressure in large vessels (aorta and internal carotid artery)
Decreased stretch because of decreased volume causes increased HR and vasoconstriction

7

ADH

potent vasoconstriction, assists kidney water conservation

8

Renin- angiotension- aldosterone system

increases CO, constricts arterioles

9

ANP or BNP

suppress ADH and aldosterone, Ventricle stretch

10

antihypertensive classifications

Adrenergic Drugs= Alpha 1 blockers (antagonist), Alpha 2 agonist, Beta Blockers
Drugs that interfere with the Renin, Angiotensin, Aldosterone System (RAAS)= Angiotensin- Converting Enzyme (ACE) Inhibitor, Angiotensin II Receptor Blockers (ARB), Direct Renin Inhibitors
Calcium Channel Blockers
Diuretics
Vasodilators

11

Adrenergic drugs categories

Centrally and peripherally acting adrenergic neuron blockers
Centrally acting alpha2 receptor agonists
Peripherally acting alpha1 receptor blockers
Peripherally acting beta receptor blockers (beta blockers)= Cardioselective (beta1 receptors), Nonselective (both beta1 and beta2 receptors)

Peripherally acting dual alpha1 and beta receptor blockers

12

Centrally acting alpha 2 receptor agonists

Stimulate alpha2-adrenergic receptors in the brain
Decrease sympathetic outflow from the CNS
Decrease norepinephrine
Stimulate alpha2-adrenergic receptors
Result in decreased bp
clonidine (Catapres) methyldopa (Aldomet)
Can be used for hypertension in pregnancy

13

Peripheral alpha 1 blocker/ agonist

Block alpha1-adrenergic receptors
doxazosin (Cardura)
terazosin (Hytrin)
prazosin (Minipress)

14

Beta blockers

Reduce BP by reducing heart rate through beta1 blockade
Cause reduced secretion of renin
Long-term use causes reduced peripheral vascular resistance
nebivolol (Bystolic), propranolol (Inderal), atenolol (Tenormin)

15

Dual-action alpha 1 and beta receptor blockers

Reduce heart rate (beta1 receptor blockade)
Cause vasodilation (alpha1 receptor blockade)
carvedilol (Coreg)
labetalol
Result in decreased blood pressure

16

Adverse effects of Adrenergic drugs

*High incidence of orthostatic hypotension

Bradycardia with reflex tachycardia, Dry mouth, Drowsiness, sedation, Constipation, Depression, Edema, Sexual dysfunction (impotence)

17

ACE inhibitors

block conversion of angiotensin I to angiotensin II, may be combined with thiazide diuretic or calcium channel blocker, vasodilation
*captopril (Capoten) benazepril (Lotensin) enalapril (Vasotec) fosinopril (Monopril) *lisinopril (Prinivil) moexipril (Univasc) quinapril (Accupril)
* can be used with liver disfunction

18

ACE inhibitors adverse effects

Fatigue Dizziness Headache Mood changes Impaired taste Possible hyperkalemia
***Dry, nonproductive cough, which reverses when therapy is stopped
Angioedema: rare but potentially fatal

19

ARBs

blocks receptors that receive angiotensin, block vasoconstriction and release of aldosterone
losartan (Cozaar) eprosartan (Teveten) valsartan (Diovan) irbesartan (Avapro) candesartan (Atacand) olmesartan (Benicar) telmisartan (Micardis) azilsartan (Edarbi)

20

ARB adverse effects

Upper respiratory infections, Headache, May cause occasional dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, fatigue
Hyperkalemia much less likely to occur

21

Direct Renin inhibitor

Indication: hypertension
MOA: inhibits the release of renin and prevents the activation of the RAAS.
Example: aliskiren (Tekturna)

22

Calcium channel blockers

Cause smooth muscle relaxation
Decreased peripheral smooth muscle tone
Decreased systemic vascular resistance
Decreased blood pressure
A Very Nice Drug

23

Arteriole selective drugs (dihydropyridines)
A Nice

Relax arterial smooth muscle
Treat hypertension and angina
Nifedipine, amlodipine

24

Nonselective drugs (non-dihydropyridines)
Very Drug

Relax arterial smooth muscle
Affect myocardial contraction and heart rate
Treat hypertension and coronary artery disease
Verapamil, diltiazem

25

Diuretics

Decrease plasma and extracellular fluid volumes
Overall effect= Decreased workload of the heart and decreased blood pressure

26

Diuretic drugs

Thiazide
Potassium sparing
Loop diuretic
osmotic diuretics

27

Thiazide

Most common diuretic for hypertension
Chlorthalidone (Thalitone), Hydrochlorothiazide (Microzide) (HCTZ)
Metolazone (Zaroxolyn) is a thiazide like diuretic

28

Potassium sparing

Triamterene (Dyrenium), spironolactone (Aldactone), amiloride (Midamor), Eplerenone (Inspra)
Not as effective as others at diuresis
Risk of hyperkalemia with renal impairment, gynecomastia
Cannot use salt substitutes
Drugs like spironolactone Amiloride (Midamor) Triamterene (Dyrenium

29

Loop diuretic

Usually not used for HTN, potent diuretics
Furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex)
Cannot give IV furosemide faster the 10 mg/min

30

Osmotic diuretic

Rarely drugs of first choice
Indications= Increased intracranial pressure High intraocular pressure Renal failure
May cause fluid/electrolyte imbalance
mannitol (Osmitrol)

31

Vasodilators

diazoxide (Hyperstat) hydralazine HCl (Apresoline) minoxidil (Loniten) sodium nitroprusside (Nipride, Nitropress)

32

process of atherosclerosis

Epithelial injury- Inflammatory process- Macrophages accumulate- Action of macrophages cause more endothelial damage- Oxygen free radicals oxidize the Low Density Lipoproteins- Macrophages engulf the oxidized LDL and foam cells are formed- Foam cells form fatty streaks, Macrophages stimulate the growth of smooth muscle cells- The combination of the foam cell smooth muscle and collagen develope fibro/fatty lesion-
become fibrous plaques- fibrous plaques narrow the lumen of the arteries- Advanced fibrous lesion called atheroma are covered by a fibrous cap.

33

Plaque rupture

Occurs when strain is placed on fibrous cap, Characteristics of plaque likely to rupture: Large soft lipid core High macrophage count Relatively few smooth muscle cells A thin fibrous cap

34

stable plaque

thick fibrous caps, Partially block vessels, Do not tend to form clots or emboli

35

unstable plaque

thin fibrous caps, Plaque can rupture and cause a clot to form, May completely block the artery, The clot may break free and become an embolus

36

C-reactive protein

Nonspecific marker of inflammation
Increased in many patients with CAD
Chronic exposure to CRP triggers the rupture of plaques

37

collateral circulation CAD

Normally some arterial anastomoses (or connections) exist within the coronary circulation, When occlusion of the coronary arteries occurs slowly over a long period (chronic ischemia), there is a greater chance of adequate collateral circulation developing

38

HDL increase

decrease chance of CAD
mobilize cholesterol from the tissues

39

LDL increase

direct correlation with CAD

40

triglycerides increase

linked to CAD

41

normal serum cholesterol

less than 200

42

LDL normal

less than 100

43

HDL normal

greater than 60

44

serum triglycerides normal level

less than 149

45

drugs used to treat hyperlipidemia

Bile Acid Sequestrants, HMG-CoA Inhibitors, Fibrates, Niacin, Cholesterol Absorption Inhibitors

46

Drugs that restrict lipoprotein production:

Statins, niacin

47

Drugs that increase lipoprotein removal:

Bile acid sequestrants

48

Drugs that decrease cholesterol absorption:

Ezetimibe (Zetia)

49

bile acid sequestrants

increase effects of Warfarin, used for increased LDL, other meds should be taken 1 hour before or 4 hours after
cholestyramine (Questran ) colesevelam (Welchol) colestipol hydrochloride (Colestid Sequestrants)

50

HMG-CoA inhibitors

STATINS contraindicated with pregnancy and liver disease, risk for rhabdomylosis (muscle breakdown, effects kidneys) ****check creatine kinase CK
atorvastatin (Lipitor) Fluvastatin (Lescol) Lovastatin (Mevacor) Pitavastatin (Livalo)Pravastatin (Pravachol) Rosuvastatin (Crestor) Simvastatin (Zocor)

51

cholesterol absorption inhibitors

lowers serum cholesterol, ezetimibe (Zetia), Must administer concurrrently with statin

52

Niacin

B-complex vitamin, decreased production of VLDL

53

Fenofibrates

decreased LDL, Increased uric acid secretion – may stimulate triglyceride breakdown, drug interactions: with statins Increased risk of myositis and rhabdomyolysis
with anticoagulants Increased risk of bleeding
with antidiabetic agents Enhanced hypoglycemic effects

gemfibrozil (Lopid) Fenofibrate (Antara, TriCor) fenofibric acid (Trilipix)

54

Chronic stable angina

reversible myocardial ischemia= angina
O2 demand > o2 supply

55

angina Vasospastic

prinzmetal's angina, Occurs at rest usually in response to spasm of major coronary artery, Seen in patients with a history of migraine headaches and Raynaud’s phenomenon, Spasm may occur in the absence of CAD
treat with calcium channel blockers

56

silent ischemia

Ischemia that occurs in the absence of any subjective symptoms
Up to 80% of patients with myocardial ischemia are asymptomatic
Associated with diabetes mellitus and hypertension
Confirmed by ECG changes

57

drug therapy for angina

Nitrates/nitrites (acute)
Beta blockers
Calcium channel blockers

58

sublingual nitroglycerin

never chew swallow, NitroQuick Nitrostat Nitroglycerin

59

Long acting Oral agents nitorglycerin

Isosorbide dinitrate (Dilatrate, Isordil)
Isosorbide mononitrate (Imdur, Ismo, Monoket)

60

beta blockers

treats stable angina and CHF, reduces HR and contractillity, for long term treatment of angina, monitor glucose

61

Calcium channel blockers

A Very Nice Drug
amlodipine (Norvasc) nifedipine (Procardia)
verapamil (Calan, Isoptin) diltiazem (Cardizem)
used for prinzmetal angina- coronary artery spasms, Slow HR

62

ranolazine (Renexa)

used for angina, has anti-ischemic and antianginal effects that do not depend upon reductions in heart rate or blood pressure

63

enzyme PDE5

breaks down chemicals that cause the penis to relax/ erect, causes contraction and blood leaving the penis

64

Drugs used to treat ED

Sildenafil (Viagra)- used to treat hypotension in women
Tadalafil (Cialis)
Vardenafil (Levitra)
Selectively inhibits PDE5 and increases nitrous oxide levels, allowing blood flow into the corpus cavernosum

65

Ejection fraction normal range

50-70 %

66

Left-sided failure

pulmonary edema, Decreased CO, pink frothy sputum, increase BP (from fluid) or decrease BP (from pump fail)

67

Right-sided failure

dependent edema, Usually the result of left ventricular dysfunction, Isolated right sided failure can occur in patients with lung disease= cor pulmonale, increase liver size, weight gain, JVD

68

Systolic failure

Decreased contractility, Decreased ejection fraction (less than 40), symptoms of decreased CO, Volume increases because it is not moving out of the heart, Blood backs up and symptoms of pulmonary and systemic congestion develop

69

Diastolic failure

Decreased ventricular filling, Normal ejection fraction

70

tests for ejection fraction

Echocardiogram MUGA CT Scan Cardiac Catheterization Nuclear Stress Test

71

HF compensatory mechanisms

increase HR, Vasoconstriction, sodium and water retention, increase blood volume, increase BNP and ANP

72

treatments for HF

Vasodilators (ACE Inhibitors, ARBs and Nitrates)
Diuretics (Loop, thiazide, potassium sparing)
Beta blockers
Cardiac glycosides
Nesiritide
Beta-Adrenergic Agonists
Non-pharmacologic - Ultrafiltration

73

acute setting HF treatments LMNOP

Lasix, Morphine (dilates), Nitroglycerin, Oxygen, Position (sit upright)

74

Morphine for HF

reduces preload HR, watch for respiratory depression

75

ACE inhibitors for HF

reduce vasoconstriction, reduce aldosterones effects (less fluid retention)

76

Diuretics for HF

reduce blood volume, lower BP, increase CO, only use for fluid overload

77

spironolactone for HF

k sparing, aldosterone antagonist

78

beta blocker for HF

Block negative effects of catecholamines- Slow heart Reduce contractility Prevent tachydysrythmias
May worsen heart failure
Initially lower CO
Must be started much lower than target dose
Cardioprotective

79

Vasodilators for HF

reduce symptoms of heart failure by reducing preload or afterload
Hydralazine with isosorbide dinitrate (BiDil)
Nesiritide (Natrecor)

80

cardiac glycosides for HF

increase contraction CO and renal perfusion, slow HR
digoxin (Lanoxin)
must be withheld HR is less than or equal to 60 apical pulse
Need lower doses with the elderly because of decreased renal clearance
*****Hypokalemia can increase Dig toxicity
Daily weights are essential (2-5 lbs in a week be reported)
do not switch brands

81

Normal blood level for cardiac glycosides

0.5 to 2 ng/ml

82

Digoxin antidote

Digoxin Immune Fab= Digibind or Digifab
Used for the treatment of life threatening digoxin intoxication (serum levels > 10 ng/mL with serum potassium > 5 mEq/L)
Patient should be on a cardiac monitor
don't check Dig levels after, will increase

83

Phosphodiesterase inhibitors

Inamrinone (Inocor): Approved only for use in patients with HF that has not responded to digoxin, diuretics, or vasodilators
Milrinone (Primacor): Short-term management of HF in patients who are receiving digoxin and diuretics
****ventricular dysrhythmias

84

Phosphodiesterase III inhibitors

Increase contractility, Cause vasodilation, CO increased, Multiple toxicities
For patients with resistant HF who have not responded to ACE inhibitors, digoxin, or other therapies

85

Heart failure cocktail

Need to be on: ACEI or ARB
-If ACEI or ARB are contraindicated then
Hydralazine with isosorbide dinitrate (BiDil)
BB (Carvedilol, Metoprolol, Bisoprolol, Atenolol)
Aldosterone Antagonist (Potassium Sparing diuretic)
Diuretic plus or minus Potassium Replacement
Possibly Digoxin (Not first line therapy)

86

Intrinsic pathway and Extrinsic pathway for coagulation

Intrinsic pathway
Takes several minutes to complete
Extrinsic pathway
Less complex, completed in seconds
The outcome of both pathways is a fibrin clot

87

clotting factor active X ----> _____ ---->_____ which turns _____ into ______

Prothrombin , thrombin, fibrinogen to fibrin

88

normal clotting takes about

6 minutes

89

clot dissolution

Tissue plasminogen activator (t-PA) released by the endothelium activates the conversion of plasminogen to plasmin (fibrinolysis)
Urokinase type plasminogen activator also activates plasminogen

90

Thromboembolic Disorder

Conditions that predispose a person to the formation of clots and emboli
CAD, STROKE, PVD, DVT

91

Hemorrhagic Disorder

Disorder in which excess bleeding occurs
Hemophilia (genetic lack of clotting factors)
Liver disease (clotting factors not produced)
Bone marrow disorders (lack of platelet formation) (thrombocytopenia)
Von Willebrand Disease

92

PT for clotting normal

Normal – 9.5-11.8
Therapeutic: 1.5 to 2 times the laboratory control value

93

INR for clotting

Normal - 1
Therapeutic: 2-3
High level therapeutic: 2.5-3.5 (4.5)

94

aPTT for clotting

Normal : 20-36 seconds
Therapeutic: 1.5-2.5 times normal

95

anti Xa for clotting

anti Xa
Therapeutic 0.3-0.7

96

Platelet counts

Normal: 150,000-400,000 cells/mm3

97

D-Dimer

measures clot formation and lysis that results from the degradation of fibrin.

98

signs and symptoms of coagulation disorders

Elevated PT/INR, aPTT
Bleeding, Easy bruising, Petechiae, Fecal occult blood
Bleeding from surgical wounds and IV sites

99

drugs the prevent clot formation

anticoagulants antiplatelet agents

100

drugs for removal of existing clot

thrombolytics

101

drugs that promote clot formation

hemostatics and clotting factor concertrates

102

Anticoagulant meds

Parenteral
Heparin
Low-molecular-weight heparins (No PTT monitoring)
Fondaparinux
Direct thrombin inhibitors
Oral
Warfarin

103

Antidote for heparin

protamine sulfate

104

antidote for Warfarin

vitamin K

105

Low-Molecular-Weight Heparins

prevent clots, NO PTT monitoring
enoxaparin(Lovenox) tinzaparin (Innohep) dalteparin (Fragmin)

106

warfarin (Coumadin)

Oral, Decreases the production of Vitamin K dependent clotting factors in the liver, not used in acute situation

107

Rivaroxaban (Xarelto)

Similar to warfarin, inhibits factor Xa, No INR or aPT monitoring, Bleeding most common side effect, No specific antidote

108

Direct thrombin inhibitors

Dabigatran (Pradaxa-U.S.)
oral
Indicated for reducing the risk of stoke and systemic embolism in patient s with non-valvular atrial fibrillation
Adverse reactions- bleeding, dyspepsia
No INR monitoring
No antidote
others: apixaban (Eliquis) lepirudin (Refludan)

109

Antiplatelet drugs

Interfere with platelet aggregation, Prevent clot formation
Agents include: Aspirin, ADP receptor blockers:
Ticlipidine (Ticlid)
Clopidogrel (Plavix)
Prasugrel (Effient)
Glycoprotein IIb/IIIa receptor blockers:
Abciximab (ReoPro)
Eptifibitide (Integrelin)
Trifiban (Aggrastat)

110

oral antiplatelet drugs

anagrelide (Agrylin)
Aspirin
cilostazol (Pletal)
clopidogrel (Plavix)
prasugrel (Effient)
Ticagrelor (Brilinta)
ticlopidine (Ticlid)
dipyridamole (Persantine) (can also be given IV)

111

GP IIB/ IIIA Inhibitors

All given IV
Usually in combination with ASA and heparin
Indicated for Acute coronary syndrome
Unstable angina and non-Q wave MI
Percutaneous coronary interventions
Adverse events: Bleeding
Especially from PCI or IV site

112

drugs for intermittent claudication

is pain or cramping in the lower legs that worsens with walking or exercise
Primary symptoms of (PVD)
Pentoxifylline (Trental) cilostazol (Pletal)
Aspirin and clopidogrel are also used to manage IC

113

thrombolytic agents

alteplase (Activase) reteplase (Retavase) Tissue plasminogen activator (t-PA) streptokinase (Streptase) urokinase (Abbokinase) Anistreplase (Eminase) Tenecteplase (TNKase)

114

bleeding disorders treated with clotting factors

Hemophilia, Liver Disease, Bone Marrow Disorders, von Willebrand’s Disease

115

von Willebrand’s Disease

Hereditary bleeding disorder
characterized by a deficiency of or a defect in a protein termed vonWillebrand factor
Characterized by bleeding, Epistaxis, Bleeding gums, Easy bruising, Excessive menstual bleeding

116

systemic hemostatic agents

Aminocaporic Acid
Actions: Stop the natural plasminogen clot-dissolving mechanism by blocking its activation or by directly inhibiting plasmin.
Indications: Prevent or treat excess bleeding
Adverse effects: Excessive clotting
similar drugs: Desmopressin (DDAVP, Stimate) Thrombin, topical (Evithrom, Recothrom, Thrombinar) Tranexamic acid (Cyklokapron, Lysteda)

117

Erythocytes

Made of Hemoglobin molecules
Made of two pairs of polypeptide chains ( the globins)
Four complexes of iron plus protoporphyrin (the heme)

118

Each erythrocyte has as may as

300 hemoglobin molecules that carry oxygen

119

Total Iron-binding capacity (TIBC)

TIBC provides a measurement of all proteins that act to bind or transport iron between the tissues and bone marrow

120

Serum Ferritin

Correlates with body iron stores

121

Transferrin saturation

Measurement of iron available for erythropoiesis (ready for use to make RBC)

122

RBC count

men 4.2-5.4 x 10^6/uL
women 3.6-5.0 x 10^6/uL

123

Hemoglobin levels

Men 14-16.5g/dL
Women 12-15 g/dL
O2 capacity

124

Hematocrit levels

Men 40%-50%
Women 37%-47%
RBC mass

125

most RBC break down in the

spleen and is processed into bilirubin

126

what is needed to have RBC

iron, B12 and folic acid, essential amino acids and carbs

127

anemia

Deficiency in: the number of erythrocytes (Red Blood Cells) The quantitiy of hemoglobinThe volume of the Packed RBC’s (hematocrit)
Leads to:
Tissue Hypoxia – resulting in signs and symptoms of anemia

128

types of anemia

Macrocytic – large size of RBC
Normochormic – normal color (Hemoglobin content is normal)
Microcytic – small size of RBC
Hypochromic – reduced Hemoglobin cause a light color of the cells pale

129

iron deficiency anemia

Hypochromic and microcytic erythrocytes

130

b12 deficiency anemia

Megaloblastic anemia
Erythrocytes are large, often with oval shape
Poikilocytosis and teardrop shapes
Neutrophils are hypersegmented
Manifestations: smooth beefy tongue, paresthesia of hands and feet

131

Erythopoietin Drugs

Epoetin Alfa (Epogen) (Procrit)
Treats anemia associated with renal failure, AIDS, chemotherapy, and decreases need for blood transfusions in patients undergoing surgery
Darbopoetin Alfa (Aranesp)
Treats anemia associated with chronic renal failure, including patients on dialysis
** can cause hypertension HF and thrombotic events

132

normal serum iron

60-170 mcg/dL

133

drugs for iron deficiency anemia

Oral Iron Preparations include:
Ferrous Fumarate (Feostat)
Ferrous Gluconate (Fergon)
Ferrous Sulfate (Feosol)
Ferrous Sulfate Exsiccated (Feratab, Slow FE)
Parenteral Iron Preparation Include:
Iron Dextran (InFed) given IM using z-track method
Used in clients with severe GI malabsoption problems

134

treat vitamin B12 deficiency

hydroxycobalamin, cyanocobalamin (Nascobal)

135

polycythemia

a blood disorder characterized by high red blood cell count
Primary Polycythemia Vera-neoplastic disease resulting in an increase of all blood components
Secondary Polycythemia Vera-results from a physiologic increase in the level of erythropoietin usually secondary to hypoxia

136

allergic rhinitis

Inflammation of mucous membranes in nose, throat, and airways by allergens

137

allergic rhinitis drugs

Drugs fall into two categories:
Preventors, used for prophylaxis
-Antihistamines, Intranasal corticosteroids, Mast cell stabilizers
Relievers, used for acute symptom relief
-Oral and nasal decongestants, usually drugs from sympathomimetic class

138

antihistamines

Examples: chlorpheniramine, fexofenadine (Allegra), loratadine (Claritin), cetirizine (Zyrtec),diphenhydramine (Benadryl)
compete with histamine to bind to receptors

139

types of decongestants

Three main types are used
Adrenergics- Largest group, Sympathomimetics
Anticholinergics- Less commonly used, Parasympatholytics
Corticosteroids- Topical, intranasal steroids

140

oral decongestants

Prolonged decongestant effects, but delayed onset
Effect less potent than topical
No rebound congestion
Exclusively adrenergics
Example: pseudoephedrine (Sudafed)

141

topical nasal decongestants

Adrenergics- phenylephrine (Neo-Synephrine)

Intranasal steroids- beclomethasone dipropionate (Beconase), budesonide (Rhinocort), flunisolide (Nasalide), fluticasone (Flonase), triamcinolone (Nasacort), ciclesonide (Omnaris)

Intranasal anticholinergic- ipratropium (Atrovent)

142

antitussives

used only for non productive cough

143

opioid antitussive

Suppress the cough reflex by direct action on the cough center in the medulla
Examples:
codeine (Robitussin A-C, Dimetane-DC), hydrocodone

144

nonopioid antitussive

Suppress the cough reflex by numbing the stretch receptors in the respiratory tract and preventing the cough reflex from being stimulated
Examples:
benzonatate (Tessalon Perles), dextromethorphan (Vicks Formula 44, Robitussin-DM)

145

expectorants

Drugs that aid in the expectoration (removal) of mucus
Reduce the viscosity of secretions
Disintegrate and thin secretions
Example: guaifenesin (Mucinex)

146

mucolytics

Loosen thick, viscous bronchial secretions
Two versions:
Acetylcysteine (Mucomyst)
Administered PO, inhalation, or IV
Not available OTC
Used in patients with cystic fibrosis, chronic bronchitis, and other diseases with large amounts of bronchial secretions

Dornase alfa (Pulmozyme)
Oral inhalation
Approved for management of cystic fibrosis

147

Tidal volume

the volume or amount of air per breath, normal breath

148

Minute volume

the respiratory rate X tidal volume, efficiency of breathing

149

PFT (pulmonary function tests)

measure lung volumes and flow rates and can be used to diagnose lung disease.

150

Compliance

Compliance is the measure of lung and chest wall dispensability

151

FEV1

forced expiratory volume in 1 second. push out of air quickly

152

FIO2

fraction of inspired oxygen (.21 is room air)

153

right side aspiration

more common than left, shorter and more straight

154

Cheyne-Stokes ventilations

alternating periods of deep and shallow breathing with apnea lasting from 15-60 seconds. impending death

155

Alveolar dead space

area where alveoli are ventilated but not perfused.
Classic example is pulmonary embolus
Can diagnose with VQ scan (high V/Q)

156

Pulmonary Embolism

blockage of the pulmonary artery by a thrombus, fat, air embolus, bacterial vegetation, or tumor tissue
most arise from deep vein thrombosis (DVT)
Venous thromboembolism (VTE)

Virchow triad- increased risk of PE
-Venous stasis, Hypercoagulability, Injury to the endothelial cells that line the vessels

157

COPD

Three mechanisms of chronic obstructive pulmonary disease (chronic airflow limitation)
*Bronchospasm -Sudden contraction of smooth muscle that causes acute dyspnea, Drugs targeted at relaxing the smooth muscle
*Thick, viscous secretions- Block the airway, Treatment may involve antibiotics or mucolytics
*Edema- Caused by engorgement of pulmonary blood vessels, Treatment may include diuretics and corticosteroids
includes emphysema and chronic obstructive bronchitis

158

Bronchial asthma

inflammation of the airways, characterized by airflow obstruction, increased bronchial responsiveness, increased mucous production, and edema of the airway

expiratory wheezing, dyspnea, tachypnea, tachycardia

159

extrinsic (atopic) asthma

Type I hypersensitivity, Mast cells’ inflammatory mediators cause acute response within 10–20 minutes, Airway inflammation causes late phase response in 4–8 hours

160

Emphysema

Enlargement of air spaces and destruction of lung tissue
Decreased surface area of alveoli decrease area for gas exchange

161

Chronic obstructive bronchitis

Obstruction of small airways, the presence of excessive mucous and chronic productive cough for 3 months in each of two consecutive years in a patient for whom other causes of cough have been excluded