Exam 4 Flashcards
CO=
HR x SV
BP=
SVR x CO
blood flow through the heart
RA- tricuspid valve- RV- Pulmonary Artery- lungs pulmonary vein- LA- Mitral valve- LV- Aortic valve- body
Preload
filling and stretch just prior to contraction
Afterload
resistance in the aorta, if it increases SV/CO decrease
Baroreceptors
Sense pressure in large vessels (aorta and internal carotid artery)
Decreased stretch because of decreased volume causes increased HR and vasoconstriction
ADH
potent vasoconstriction, assists kidney water conservation
Renin- angiotension- aldosterone system
increases CO, constricts arterioles
ANP or BNP
suppress ADH and aldosterone, Ventricle stretch
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
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
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
Peripheral alpha 1 blocker/ agonist
Block alpha1-adrenergic receptors
doxazosin (Cardura)
terazosin (Hytrin)
prazosin (Minipress)
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)
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
Adverse effects of Adrenergic drugs
*High incidence of orthostatic hypotension
Bradycardia with reflex tachycardia, Dry mouth, Drowsiness, sedation, Constipation, Depression, Edema, Sexual dysfunction (impotence)
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
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
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)
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
Direct Renin inhibitor
Indication: hypertension
MOA: inhibits the release of renin and prevents the activation of the RAAS.
Example: aliskiren (Tekturna)
Calcium channel blockers
Cause smooth muscle relaxation Decreased peripheral smooth muscle tone Decreased systemic vascular resistance Decreased blood pressure A Very Nice Drug
Arteriole selective drugs (dihydropyridines)
A Nice
Relax arterial smooth muscle
Treat hypertension and angina
Nifedipine, amlodipine
Nonselective drugs (non-dihydropyridines) Very Drug
Relax arterial smooth muscle
Affect myocardial contraction and heart rate
Treat hypertension and coronary artery disease
Verapamil, diltiazem
Diuretics
Decrease plasma and extracellular fluid volumes
Overall effect= Decreased workload of the heart and decreased blood pressure
Diuretic drugs
Thiazide
Potassium sparing
Loop diuretic
osmotic diuretics
Thiazide
Most common diuretic for hypertension
Chlorthalidone (Thalitone), Hydrochlorothiazide (Microzide) (HCTZ)
Metolazone (Zaroxolyn) is a thiazide like diuretic
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
Loop diuretic
Usually not used for HTN, potent diuretics
Furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex)
Cannot give IV furosemide faster the 10 mg/min
Osmotic diuretic
Rarely drugs of first choice
Indications= Increased intracranial pressure High intraocular pressure Renal failure
May cause fluid/electrolyte imbalance
mannitol (Osmitrol)
Vasodilators
diazoxide (Hyperstat) hydralazine HCl (Apresoline) minoxidil (Loniten) sodium nitroprusside (Nipride, Nitropress)
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.
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
stable plaque
thick fibrous caps, Partially block vessels, Do not tend to form clots or emboli
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
C-reactive protein
Nonspecific marker of inflammation
Increased in many patients with CAD
Chronic exposure to CRP triggers the rupture of plaques
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
HDL increase
decrease chance of CAD
mobilize cholesterol from the tissues
LDL increase
direct correlation with CAD
triglycerides increase
linked to CAD
normal serum cholesterol
less than 200
LDL normal
less than 100
HDL normal
greater than 60
serum triglycerides normal level
less than 149
drugs used to treat hyperlipidemia
Bile Acid Sequestrants, HMG-CoA Inhibitors, Fibrates, Niacin, Cholesterol Absorption Inhibitors
Drugs that restrict lipoprotein production:
Statins, niacin
Drugs that increase lipoprotein removal:
Bile acid sequestrants
Drugs that decrease cholesterol absorption:
Ezetimibe (Zetia)
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)
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)
cholesterol absorption inhibitors
lowers serum cholesterol, ezetimibe (Zetia), Must administer concurrrently with statin
Niacin
B-complex vitamin, decreased production of VLDL
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)
Chronic stable angina
reversible myocardial ischemia= angina
O2 demand > o2 supply
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
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
drug therapy for angina
Nitrates/nitrites (acute)
Beta blockers
Calcium channel blockers
sublingual nitroglycerin
never chew swallow, NitroQuick Nitrostat Nitroglycerin
Long acting Oral agents nitorglycerin
Isosorbide dinitrate (Dilatrate, Isordil) Isosorbide mononitrate (Imdur, Ismo, Monoket)
beta blockers
treats stable angina and CHF, reduces HR and contractillity, for long term treatment of angina, monitor glucose
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
ranolazine (Renexa)
used for angina, has anti-ischemic and antianginal effects that do not depend upon reductions in heart rate or blood pressure
enzyme PDE5
breaks down chemicals that cause the penis to relax/ erect, causes contraction and blood leaving the penis
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
Ejection fraction normal range
50-70 %
Left-sided failure
pulmonary edema, Decreased CO, pink frothy sputum, increase BP (from fluid) or decrease BP (from pump fail)
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
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
Diastolic failure
Decreased ventricular filling, Normal ejection fraction
tests for ejection fraction
Echocardiogram MUGA CT Scan Cardiac Catheterization Nuclear Stress Test
HF compensatory mechanisms
increase HR, Vasoconstriction, sodium and water retention, increase blood volume, increase BNP and ANP
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
acute setting HF treatments LMNOP
Lasix, Morphine (dilates), Nitroglycerin, Oxygen, Position (sit upright)
Morphine for HF
reduces preload HR, watch for respiratory depression
ACE inhibitors for HF
reduce vasoconstriction, reduce aldosterones effects (less fluid retention)
Diuretics for HF
reduce blood volume, lower BP, increase CO, only use for fluid overload
spironolactone for HF
k sparing, aldosterone antagonist
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
Vasodilators for HF
reduce symptoms of heart failure by reducing preload or afterload
Hydralazine with isosorbide dinitrate (BiDil)
Nesiritide (Natrecor)
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
Normal blood level for cardiac glycosides
0.5 to 2 ng/ml
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
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
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
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)
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
clotting factor active X —-> _____ —->_____ which turns _____ into ______
Prothrombin , thrombin, fibrinogen to fibrin
normal clotting takes about
6 minutes
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
Thromboembolic Disorder
Conditions that predispose a person to the formation of clots and emboli
CAD, STROKE, PVD, DVT
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
PT for clotting normal
Normal – 9.5-11.8
Therapeutic: 1.5 to 2 times the laboratory control value
INR for clotting
Normal - 1
Therapeutic: 2-3
High level therapeutic: 2.5-3.5 (4.5)
aPTT for clotting
Normal : 20-36 seconds
Therapeutic: 1.5-2.5 times normal
anti Xa for clotting
anti Xa
Therapeutic 0.3-0.7
Platelet counts
Normal: 150,000-400,000 cells/mm3
D-Dimer
measures clot formation and lysis that results from the degradation of fibrin.
signs and symptoms of coagulation disorders
Elevated PT/INR, aPTT
Bleeding, Easy bruising, Petechiae, Fecal occult blood
Bleeding from surgical wounds and IV sites
drugs the prevent clot formation
anticoagulants antiplatelet agents
drugs for removal of existing clot
thrombolytics
drugs that promote clot formation
hemostatics and clotting factor concertrates
Anticoagulant meds
Parenteral Heparin Low-molecular-weight heparins (No PTT monitoring) Fondaparinux Direct thrombin inhibitors Oral Warfarin
Antidote for heparin
protamine sulfate
antidote for Warfarin
vitamin K
Low-Molecular-Weight Heparins
prevent clots, NO PTT monitoring
enoxaparin(Lovenox) tinzaparin (Innohep) dalteparin (Fragmin)
warfarin (Coumadin)
Oral, Decreases the production of Vitamin K dependent clotting factors in the liver, not used in acute situation
Rivaroxaban (Xarelto)
Similar to warfarin, inhibits factor Xa, No INR or aPT monitoring, Bleeding most common side effect, No specific antidote
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)
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)
oral antiplatelet drugs
anagrelide (Agrylin) Aspirin cilostazol (Pletal) clopidogrel (Plavix) prasugrel (Effient) Ticagrelor (Brilinta) ticlopidine (Ticlid) dipyridamole (Persantine) (can also be given IV)
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
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
thrombolytic agents
alteplase (Activase) reteplase (Retavase) Tissue plasminogen activator (t-PA) streptokinase (Streptase) urokinase (Abbokinase) Anistreplase (Eminase) Tenecteplase (TNKase)
bleeding disorders treated with clotting factors
Hemophilia, Liver Disease, Bone Marrow Disorders, von Willebrand’s Disease
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
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)
Erythocytes
Made of Hemoglobin molecules
Made of two pairs of polypeptide chains ( the globins)
Four complexes of iron plus protoporphyrin (the heme)
Each erythrocyte has as may as
300 hemoglobin molecules that carry oxygen
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
Serum Ferritin
Correlates with body iron stores
Transferrin saturation
Measurement of iron available for erythropoiesis (ready for use to make RBC)
RBC count
men 4.2-5.4 x 10^6/uL
women 3.6-5.0 x 10^6/uL
Hemoglobin levels
Men 14-16.5g/dL
Women 12-15 g/dL
O2 capacity
Hematocrit levels
Men 40%-50%
Women 37%-47%
RBC mass
most RBC break down in the
spleen and is processed into bilirubin
what is needed to have RBC
iron, B12 and folic acid, essential amino acids and carbs
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
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
iron deficiency anemia
Hypochromic and microcytic erythrocytes
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
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
normal serum iron
60-170 mcg/dL
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
treat vitamin B12 deficiency
hydroxycobalamin, cyanocobalamin (Nascobal)
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
allergic rhinitis
Inflammation of mucous membranes in nose, throat, and airways by allergens
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
antihistamines
Examples: chlorpheniramine, fexofenadine (Allegra), loratadine (Claritin), cetirizine (Zyrtec),diphenhydramine (Benadryl)
compete with histamine to bind to receptors
types of decongestants
Three main types are used
Adrenergics- Largest group, Sympathomimetics
Anticholinergics- Less commonly used, Parasympatholytics
Corticosteroids- Topical, intranasal steroids
oral decongestants
Prolonged decongestant effects, but delayed onset Effect less potent than topical No rebound congestion Exclusively adrenergics Example: pseudoephedrine (Sudafed)
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)
antitussives
used only for non productive cough
opioid antitussive
Suppress the cough reflex by direct action on the cough center in the medulla
Examples:
codeine (Robitussin A-C, Dimetane-DC), hydrocodone
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)
expectorants
Drugs that aid in the expectoration (removal) of mucus
Reduce the viscosity of secretions
Disintegrate and thin secretions
Example: guaifenesin (Mucinex)
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
Tidal volume
the volume or amount of air per breath, normal breath
Minute volume
the respiratory rate X tidal volume, efficiency of breathing
PFT (pulmonary function tests)
measure lung volumes and flow rates and can be used to diagnose lung disease.
Compliance
Compliance is the measure of lung and chest wall dispensability
FEV1
forced expiratory volume in 1 second. push out of air quickly
FIO2
fraction of inspired oxygen (.21 is room air)
right side aspiration
more common than left, shorter and more straight
Cheyne-Stokes ventilations
alternating periods of deep and shallow breathing with apnea lasting from 15-60 seconds. impending death
Alveolar dead space
area where alveoli are ventilated but not perfused.
Classic example is pulmonary embolus
Can diagnose with VQ scan (high V/Q)
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
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
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
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
Emphysema
Enlargement of air spaces and destruction of lung tissue
Decreased surface area of alveoli decrease area for gas exchange
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
