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N311 Cardio + Drugs + Pulmonary

Terms in this set (117)

Kidneys
renal failure, (vascular disease) // Lack of auto-regulation // HTN & atherosclerosis = end stage renal failure
Eye
blindness, (vascular disease) // Increase pressure = retinal detachment or hemorrhage → (blindness)
Hypertension
increase workload of the heart (vascular disease) = Leads to L ventricle hypertrophy
• Modifiable Risk factors
o Decrease weight, low Na diet, limit alcohol to 2/daily, aerobic exercise, stop smoking/lower cholesterol
• If ruptures = aneurysm // Progression to ischemia & HF // + atherosclerosis = problems with heart + kidneys + brain + eyes
o HTN emergency
Sudden acute elevation in BP = >180-220
evidence of end-organ damage = go to hospital [parenteral meds, rapid/controlled reduction]
o HTN urgency
Sudden acute elevation in BP = >180-220
no evidence of organ damage [assess for sources, 24-48 hour reduction, oral meds]
High BP Agents
Adrenergic antagonists
Alpha1 blockers
Alpha-2 receptor agonists
Alpha/beta blocker
ACE inhibitors
AT1 receptor blockers
Ca channel blockers
Direct-acting vasodilators
Diuretics
Adrenergic antagonists
- ßeta [reduce HR]/ alpha [reduce vascular resistance] receptor blockers → blocking SNS receptors
o Alpha 1 - arterial vasoconstriction
o Beta 1 - cardiac effects/selective, (+) chronotropic/inotropic
o Alpha 2 - (CNS) central arterial vasodilation, less epinephrine
o Beta 2 - pulmonary dilation/relaxation of bronchial smooth muscle
Alpha1 blockers
- affects baroreceptor response on periphery, "-zosins", vasodilation, for 2/3rd line agents for HTN
o ADRs - reflex tachycardia, orthostatic hypotension, sexual dysfunction,
Alpha-2 receptor agonists
blocking SNS receptors → centrally acting on NE
Alpha/beta blocker combo
combo drug (acute care), non-selective beta/alpha1 blockage
ACE inhibitors
["-prils"] & ARBs [used if unable to tolerate ACEI] - use for DM/HF
o Inhibit conversion of angiotensin I→II & decrease PVR/salt/H2O retention/preload/afterload/lowers BP/inhibit degradation of bradykinin
o ADRs - cough, rashes, angioedema, hyperkalemia, hypotension, renal failure, agranulocytosis, contraindication in pregnancy
- reduce progression/remodeling
AT1 receptor blockers (ARBs)
"-sartans", no effect on bradykinin = no cough
Ca channel blockers
vasodilating effect, vascular smooth muscle reduce vascular resistance
o Block Ca entry into smooth muscle, (-) chronotrope, inotrope, dromotrope
o Verapamil [slow down HR], diltiazemreduct workload on heart], nifedipine [vasodilators on smooth muscle]
o ADRs - hypotension, bradycardia, h/a, peripheral edema
Direct-acting vasodilators
(nitrates) [drugs do not work through SNS]- &lower BP, venodilator/reduce preload, reduce afterload // make nitric oxide = smooth muscle to relax; angina, CHF
o Nitrates→nitric oxide = increase cGMP (relaxor, decrease Ca), dilation
o ADRs - flushing, pounding h/a, postural hypotension → reflex tachycardia, drug-drug interactions, drug tolerance // Prophylaxis
o Nitroglycerine [rapid relief of angina pain] - 1 tab/decrease pain/repeat*2 q5min & if increased pain/ACS = call 911 //q8-12 chronic, lose effectiveness if leave patch on too long
Diuretics
reduce BP/Na, use for HF, affects the salt in the body
[fluid overload] -- work on kidney
• Carbonic anhydrase inhibitors- inhibit bicarbonate reab = inhibit Na reab
• Osmotic diuretics "fake sugar" - holds water = Mannitol
• Loop diuretics (Lasix) - inhibit Na/Cl transport → water stays with the ions & Mg/Ca excreted // increased dose = increase effect
• Thiazide diuretics - inhibit Na/Cl transport & alter Na/H2O content in arteriole walls, direct vasodilator
• Hydrochlorothiazide // high doses may have many side effects
• K+ sparing diuretics - block Na reabsorption / K excretion // COMBINED with Lasix to reduce K loss
• Spironolactone (Aldactone) used for HF
BP Targets
>60 yo = <150/9 & <60 yo = <140/90 & Diabetes = less than 140/90
• Ohm's Law
BP = CO * SVR
o
cardiac output
CO = HR * SV = how much your heart pumps out in 1 minute (4 affecting factors
• SV - (stroke volume)
amount of blood your heart pumps out in 1 beat
• (End diastolic volume - End systolic volume) / End diastolic volume = STROKE VOLUME
o Example: EDV = 160 ESV 100 SV = 60 = (160-100)/160
• Ejection Fraction (EF)
= Stroke volume / End diastolic volume = ejection fraction
• Example: SV = 60 EDV = 160 EF = 60/160=0.375 or 37.5% =
• HR [chronotropy]
primary way body changes CO via baroreceptors, intrinsic
• Contractility [inotropy]
how much squeeze pressure in ventricles [SNS/PSNS], intrinsic
• Increase Ca availability = (+)
• Decrease Ca availability = (-)
• Preload
volume work of the heart (blood left in heart after it pumps; focus on L ventricle)
• Increased by SNS [catecholamines] → fibers stretch → more CO →
• Decreased by PSNS [HF, treat with diuretics]
• Afterload
pressure work of the heart (force generated to eject blood from the heart)
• Increase with SVR→ increase work & O2 consumption & decrease SV
• Decrease → vasodilation
• Aortic stenosis
• Increase demand of these 4 factors → decrease supply [perfusion pressure/arterial oxygen]
o SVR
systemic vascular resistance
• Increase = constrict
• Decrease = dilate
hypotension /Low BP
reduce CO/HR or SVR --- Anti -hypertensive medication - affect 1+ variables
BP drops, HR increase by >10%, (vascular disease) // d/t shock, hypovolemic (blood loss), drugs, +bed rest, HF, spinal injuries
o Vasopressor
antidiuretic]- vasoconstrictor, increase HR/BP/CO && stimulate alpha/beta/DA receptor
• Dobutamine - increase HR, but less vasoconstriction
• affects Beta1 the most, then Beta2, then Alpha1 and not DA
• Dopamine - for specific DA receptors, vasoconstrictor
• affects Alpha1&Beta1 the most, then Beta2 & DA
• Epinephrine -- like our natural
• affects Alpha1&Beta1, then Beta2 and not DA
• NE - like our natural
• affects Alpha1&Beta1 but not Beta2 or DA
Poisseues Law
resistance through the vessel (radius of vessel = r4) Decrease radius of vessel=increase Resistance
• Reduce radius by 1/2 = resistance goes up 16 fold
Regulation of the heart
Intrinsic SA rate of 100bpm
• Baroreceptor reflex (mainly) — regulate the pressure
• Bainbridge (stretch) reflex - increase wall tension → increase HR = dilate vessels
SNS
• B1 receptor = increase HR (release norepinephrine)
o (+) inotropy, chronotropy, dromotropy, lusitropy ON HEART
o constrict on pulmonary/coronary vessels / most others
• Dromotropy
rate of AP conduction
PSNS
• →Acetylcholine via vagus nerve = decrease HR of 60-80bpm (conserve energy)
o (-) inotropy, chronotropy, dromotropy, lusitropy ON HEART
o dilate on pulmonary/coronary vessels
o no effect on most others
• Lusitropy
rate of relaxation
Peripheral Arterial Disease
affect the legs, (vascular disease)
DVT
• Deep Vein Thrombosis
Affect the big leg veins & obstructions to flow = clots
o 2 affected = CHF // risks - immobile // 20% (+) Homan's sign [do not check for] - push on toes = pain in calf
o Treat - elevation // Prevent - ambulation, low dose heparin, anti-platelet, Coumadin, anti-embolic devise
o Therapeutic - high dose heparin, anti-inflammatory, rest
Anticoagulants
affect action/formation of clotting factors but not existing clots // prophylactic
Heparin
Fondaparinux
Direct thrombin inhibitors
Warfarin
Direct factor inhibitors
Heparin
SC/IV, most effective = Unfractionated heparin [higher bleeding risk]
o interact with antithrombin III & bind to natural antithombin to make it more effect to inhibit clotting factors 8+9 in intrinsic pathway, measure aPTT [1.5-prophylaxsis, 2-3 - treatment], not fibrinolytic/slows clot propagation, help treat DVT,
o ADRS - HAT [benign, transient drop in platelets d/t onset therapy] & HIT [hypersensitivity → d/c]
o Fractionated - used for DVT/Afib prevention, less effective vs. UFH, longer half life, DO NOT monitor, "-parins"
Fondaparinux
reduce risk of hypersensitivity, binds specifically/reversibly to antithrombin, no HIT risk
Direct thrombin inhibitors
bind to thrombin, used for HIT
Warfarin
(Vit K. antagonists)- oral/reduce risk of clots, monitor PT/INR, inhibit clotting factors 7, extrinsic pathway, give Vit. K to reverse, for Afib/HF/risk of DVT, interferes with Vit. K, 2-3 normal with treatment, 2.5-3.5 with heart valve, half life 20-60 hour,
Direct factor inhibitors
no monitor INR, no antidote, less bleeding risk, affect factor 10 [no conversion of prothrombin→thrombin
Antiplatelet Drugs
use for unstable angina, MI prevent, TIAs, prosthetic valves, fistulas
ASA/NSAIDs
Ticlopidine & Clopidogrel
Glycoprotein
Thrombolytic/Fibrinolytic agents
• ASA/NSAIDs
permanently inhibit thromboxane A2 synthesis
Ticlopidine & Clopidogrel
[alternate to ASA] - block ADP receptor on platelet = inhibit aggregate
Glycoprotein
blocks interaction btwn integrin receptor = abnormal platelet aggregation
Thrombolytic/Fibrinolytic agents
[Tissue plasminogen activators]/
dissolve existing clots // Higher risk of bleeding, activate plasminogen to plasmin = degraded fibrin
• For acute STEMI, pulmonary embolism, arterial occlusion, DVT
Coronary Heart disease
atherosclerotic; affect brain & heart [alter arterial body perfusion]
o Inflammatory disease of endothelial walls of big arteries →plaque for//Non/Modifiable risks // Risk >7.5% benefit to change
• Stable Angina Pectoris
• Acute Coronary Syndrome
• EKG 12 LEADS
• High lateral wall - I & aVL
• Inferior wall - II & III & aVF
• Anterior/septal wall - V1 & V2
• Anterior - V3 & V4
• Low lateral wall - V5 & V6
• Stable Angina Pectoris
Exercise = predictable pain; relived by rest
o Clot dissolves self & no necrosis - fixed stenosis, no elevated serum enzymes
o Acute - need to rest, SL Nitroglycerine = demand issue
o Chronic (prophylactic) - NTG (demand), beta blockers (reduce inotopy/chronotopy; demand), Ca channel blockers (reduce inotropy/afterload; demand), anti-platelets (no clot; supply), antilipemics/statins (lower cholesterol; supply)
o Angina Agents
decrease MVO2 demand and/or increase supply - goal: increase supply and reduce workload
• Nitrates - increase nitric oxide → vessel dilation & reduce workload, dilate coronaries
• Beta receptor blockers - reduce HR & workload
• Ca channel blockers - reduce HR→ decrease workload&afterload
• Acute Coronary Syndrome
heart attack in process [clot + plaque = thrombus] = acute ischemia
Unstable Angina
• STEMI
• NSTEMI
o MI
clot doesn't dissolve fast enough + necrosis downstream - thrombus with occlusion & BIG Q wave
• Unpredictable pain, not relieved by rest, elevated serum enzymes [cell death = big Q wave]
• CK-MB & Troponin [cardiac specific enzymes] when elevated over 48 & 96 hours
• STEMI
NSTEMI
STEMI
(ST elevation MI) - acute coronary ischemia [inverted T wave] → could result as MI, acute thrombi
NSTEMI
(no ST elevation MI) - (+) for enzymes=acute MI;
• Vulnerable plaques → MI
o Large lipid core (easily rupture), thin fibrous capsule (cause clotting), inflammation within (CRP = increase with inflammation), Ca burden, superficial platelet aggregation, fibrin deposition
• Sudden cardiac arrest
Atherosclerosis & d/t ischemia [imbalance between O2 delivery to tissue & amount needed by tissue]
o Electric abnormalities/dysrhythmias (Afib) [complicated MI] → zero CO
o Anti-arrhythmic
common cause of dysrhythmia) // last resort // need correct EKG & proarrhythmic
• Dysrhythmia associated with
• Automaticity
o Drugs = slow phase 4 depolarization, raise AP threshold
• Reentry = depolarization does not extinguish
o Drugs = alter conduction velocity & length of refractory period
• Class 1 = fast sodium channel blockers - Na channel blocked // Lidocaine
• Class 2 = Beta blockers - indirect Ca channel blocked by reducing cAMP
• Class 3 = K channel blockers // Amiodarone = inhibit P450 liver proteins [ADRs - pulmonary fibrosis, hepatitis, myopathy; need to monitor LFT, TSH, eye, PFT, chest xray, BP
• Class 4= Ca channel blockers
• Digitalis
• Chronic Ischemic heart failure
Majority of the muscle mass dies = lack of pumping
o Obstruction of blood flow through the coronary arteries d/t Atherosclerosis
o Myocardial perfusion - heart is not getting enough blood
• Arteriole insufficient
(blood obstruction away from heart to body), decrease downstream flow = ischemia, do ABI
o d/t smoking, atherosclerosis, Buergers [inflammatory], trauma, DIC, DM
o Acute = 6 Ps -- pain, pallor, pulselessness, paresis, paralysis, polar & check CSM
o Chronic = skinny hairless legs, pain with activity, decrease <1 in ABI, cramps, thick nails
o Treat - reestablish blood flow to area, thrombolytic drugs, bypass grafts, angioplasty
Heart Failure & other myocardial disease
- is a consequence d/t some other disorder (see below), increase stress = stretch = hypertrophy
• Not primary // Heart is unable to pump the blood that is coming in // Lasix // occur right after MI or later // complicated MI
• Affect baroreceptor (SNS activation), kidney (RAS activation=fluid retention) & heart wall tension (hypertrophy)
• Elevated norepinephrine [fix with beta blockers → reduce contractility], angiotensin 2 [ACEI], aldosterone [diuretics], B natriuretic peptide
• Ventricular output
maintained via preload increase sufficient to increase diastolic sarcomere length & improve force generation
o via Frank Starling law
o LV dysfx + HF = need higher preload to get the same volume
Frank Starling law
[SV increase d/t increase in blood filling heart) = The more in heart → the more it needs to pump out
• FACES for HF
[tell how bad HF is] - fatigue, activity limitation, congestion [R = body edema d/t L; L = lung fluid & JVD], edema, SOB
• Systolic dysfunction
low EF<40% d/t L ventricle has low pumping power/pressure (poor contractility/hx of MI) → shifts R
• Diastolic dysfunction
EF>50% d/t low CO& back pressure, (slow/poor relaxation/dilation&age, F, HTN) =more pressure
• L HF
d/t low CO- dyspnea, orthopnea, cough, PND, cyanosis, crackles, fatigue, increase HR, faint pulse, confusion, anxiety
• R HF
d/t lung problem- hepatomegaly, ascites, anorexia, SC edema, JVD, fatigue, increase HR, faint pulse, confusion, anxiety
• Pericarditis
inflammation pericardium → no stretch [fiction rub/squeak], occurs after MI etc.
• Pericardial effusion
non-inflammatory fluid collection [space occulting problem] →cannot contract properly → increase HR, JVD
o Cardiac tamponade (fluid prevent heart from filling) & pulsus paradoxus (extreme change BP when breathing)
Venous insufficiency
(blood obstruction from body to heart), increase in hydrostatic pressure
o d/t immobility, R HF, standing, obesity, pregnancy, trauma, hyper-coaguable (clot in brain)
o Pain, swelling/edema in legs, risk of DVT/pulmonary embolus, stasis ulcers/skin changes [brown blotchy]
o Thrombophlebitis - clot/inflammation in a vein [DVT or superficial] // Treat - the risk factors, immobilize if have DVT, anti-coagulate (heparins), RICE if superficial
• HF Agents
Diuretics
ACEI/ARBs
Beta blockers
Spironolactone antagonists
Direct vasodilators
Digitalis
Digoxin
• Goal - improve activity tolerance, SOB, reduce edema, weight reduction, BNP normalizing, Chest x-ray clear
beta blockers
reduce progression/remodeling, (-) inotropic, "-olols", selective for Beta1, non-selective → effect Beta1&2 / blockade of beta receptor = decrease HR, SV, kidney renin release, SVR // for HF, angina, acute MI, HTN
• ADRs - bradycardia, decreased AV node conduction, reduced contractility, bronchoconstriction, mask s/s hypoglycemia, depression, sexual dysfunction, fatigue
o Spironolactone antagonists
d/t high potassium (K sparing diuretics)
digitalis
anti-rhythmic, for Afib/HF, reduce arterial beats/HR/conduction rate, block AV node, (+) inotropic effect [inhibit Ca] // pro-arrhythmic effects
• Digoxin - inhibit Na/K pump // cardiac glycosides
• low K = more digitalis effect @ same dose
• high K = less digitalis effect @ same dose
• need to check apical pulse
Valve disorders
Congenital — R/Lside)
Rheumatic — (type 2 hypersensitivity, if not treated strep)
Infective carditits — (congenital abnormal valve structure, collect infection on it)
Degenerative calcification
focus on L [d/t wear & tear]/murmurs → HF // Stenosis (failure to open) & Regurgitation (failure to close)
o Mitral stenosis
LA/RV, diastolic murmur, "SNAP", increase L atrial pressure, Afib
o Mitral regurgitation
systolic murmur, radiate to L axilla, pansystolic(blowing), S3, L ventricle back flowing into L atrium
o Aortic stenosis
LA [high pressure]/aorta, systolic murmur, crescendo-decrescendo, radiate to neck, S4, angina/syncope [dangerous]
o Aortic regurgitation
diastolic murmur, bounding pulse, SBP/high&DBP/low, big SV, → HF
• Cardiomyopathy
stiffening/hypertrophy of ventricles → murmurs/HF
o Restrictive - impaired diastolic filling (affect Vs), stiffness/scar tissue/unable to contract
o Dilated - enlarged heart chambers (all), poor contractility, low EF
o Hypertrophic - outflow obstruction, ischemia, thick LV/septum, problems getting blood out
Congenital Anomalies/heart defects
Cyanotic-venous blood getting into the periphery
• Acyanotic defects
o Atrial Septal defect - hole between As, blood LA → RA = XS volume in RA & RV → HF
o Ventricular septal defect - hole btwn Vs, blood goes L→R via ventricles, loud murmur, increase pressure in LV
o Patent ductus arteriosus - open btwn aorta/pulmonary artery, O2 blood from L to flow back to lungs via aorta to pulmonary artery
• Cyanotic defects
doesn't go through lungs // R→Lshunt=cyanosis//R deO2 blood to L side → deO2 deliver to body // SERIOUS
o Transposition - aorta off of RV vs. LV & pulmonary artery off of LV vs. RV = 2 separate circulations
o Tetrology of Fallot - 4 different defects, aorta takes from R&LV, pulmonary stenosis [hard to get blood into lungs]
Circulatory shock
d/t neurogenic, hypotension // Factors - BP & fluid management
• O2 delivery is below basal requirement → hypoxic & immunologic injury // assess for lactic acid [marker] - contributor to the problem // baroreceptor as CO falls (bleed internal) & BP does not fall until 20% of blood volume is gone
• Hypovolemic - blood loss (reversible), treat: replace loss fluid, vasopressors (constrict)
• Cardiogenic - heart pump failure (chronic HF), try to keep CO=hurt heart/body unable; treat- (+) inotropic drugs, support device
• Distributive - abnormal vasodilation = big vascular system & need more O2 & CO to the tissues
o Anaphylactic - immune mediated/inflammation, treat-remove antigen, maintain airway, epinephrine
o Septic - overwhelming infection, treat: give fluids to increase CO, antibiotics
o Neurogenic - d/t spinal injury, vasodilate d/t loss of SNS arterial tone, treat: lie down/elevate feet/compression stockings
Lipids
LDL - (bad) go to periphery to deliver cholesterol = 130 (normal)
HDL - (good) returned cholesterol to the liver
Antilipemics
used for levels of lipidemias
HMG-CoA reductase inhibitors
Bile acid sequesterants
Fibrates
Niacin
HMG-CoA reductase inhibitors
("-statins") - increased LDL catabolism & decreased LDL synthesis = decreased total & LDL cholesterol
o Inhibits the enzyme that makes cholesterol
o ADRs - Rhabdomyolysis (elevated CK, skeletal muscle pain = muscle degradation), elevated LFTs, muscle achs
Bile acid sequesterants
inhibit intestinal absorption & accelerates LDL catabolism = decrease total & LDL
o Trap fat in gut = liver pull lipoproteins from blood = clear blood of cholesterol
o Decrease in bile acid = remove LDL from plasma d/t more cholesterol = more LDL receptors
• Fibrates
(Fibric Acid Derivatives) - increased VLDL clearance & decrease VLDL synthesis = decreased TG, VLDL,, LDL, increased HDL
o Activate lipoprotein lipase promoting the delivery of TGs to adipose tissue & interfere with the VLDL formation
o ADRs - Rhabdomyolysis, elevated LFTs
• Niacin
(nicotinic acid) - decrease LDL & VLDL synthesis = decrease VLDL, TG, increase HDL
o Specifically on TGs
o ADRs - vasodilate, elevate LFT, raise glucose, uric acid
• Pulmonary edema
L HF when fluid builds up in independent places
o Hear crackles (interfere with gas exchange) in dependent fields [bases]
o Cardiogenic (High LA pressure / mitral stenosis) - increase capillary pressure = fluid into alveoli, transudative fluid; HF
o Non-cardiogenic (inflammation) - exudative fluid [not dependent], leaky capillaries; ARDS d/t lack of surfactant
• Pulmonary embolus
embolus originates in the lungs and travels to the lung
o Material in blood occlude pulmonary vessels
o d/t DVT, fractures, childbirth, venous air, endocarditis; SOB, sudden severe dyspnea, hemoptysis, chest pain
o determine with xray, angiogram, perfusion scan, CT/MRI
• Pulmonary HTN
sustained elevation of pulmonary arterial pressure
o Primary (idiopathic/uncommon) Cor-pulmonary = long term high BP of lungs & RVentricle
• Drugs - Ca channel blockers, alpha blockers
o Secondary - to another condition causing
• Increase flow viscosity/ LA pressure = increase workload // increased resistance= hypoxia
Dynamic Compression
pressure gradient in lungs // equal pressure point [when you cannot breathe out any more d/t pressure in lungs = pressure outside the body]
Ventilation [mix gases] distribution
to dependent lung fields & affects CO2
• Apex - distended, less compliant alveoli
• Base - small, highly compliant alveoli
• Top lung = more negative pressure
• Bottom lung = less negative pressure
Perfusion distribution
dependent on the lung you breathe on // position diff to help gas exchange = lie on opposite non-fluid lung
• Zone 1 - top of the lung, DEAD SPACE, no flow/low blood flow
o Capillaries collapsed, no fresh air in alveoli, respiratory reserve
• Zone 2 - intermittent flow// diastole won't flow, systole will flow
• Zone 3 - continuous flow, at the bottom of the lung
o Pressure higher, dependent blood flow
Pulmonary Function Test
• Tidal volume - normal inhalation & exhalation
• IRV [inhalatory reserve volume] - difference between normal inhalation & max. inhale
• ERV [exhalatory reserve volume] -- difference between normal exhalation & max. exhale
• RV [residual volume] - forced // volume left in lungs after take a breathe & exhale as much as you can
• FCV [force vital capacity] - IRV+ERV // force inhalation & exhalation
• FRC [functional residual capacity] - amount of volume left after normal exhale
Ventilation-perfusion imbalances
[V/Q matching] - wrong amount of blood going to the wrong ventilation area
Low V/Q
High V/Q
No ventilation with continued perfusion
Low V/Q
- normal alveolar perfusion, INADEQUATE alveolar VENTILATION = hypoxemia
o Asthma, lung disorders // Low air/ventilation = Give OXYGEN to improve levels
High V/Q
adequate alveolar ventilation, DECREASED alveolar PERFUSION [dead space]; over distended alveoli & ventilators // no blood/ getting to area = no O2
No ventilation with continued perfusion
no air movement/O2 to alveoli [inter-pulmonary shunt] = severe hypoxia
o Atelectasis, consolidation with exudate, if position on the side with consolidation
Pressure gradient
diffusion between alveoli and capillary blood [artery to vein]
• Hyperventilation → reduce alveolar PCO2 = result in alkalosis [passout]
• O2 mask → increase PO2 and improve gradient for O2 exchange
• Law of 5s - [tells how bad lung fx is] estimates how much of an increase in PaO2 is expected = 5 * % inspired O2 = PaO2 [goal >65]
o If not as expected - A-aDO2 = calculated PAO2 - measured PaO2
Central Chemoreceptors
(CNS)—response to increase PaCO2 & H+ // tell us to breathe
• → Hypercarbic drive [Co2 = acid] = d/t hypoventilate= increases in PaCO2 → feel urge to breath when CO2 is too high
• Hypercarbia = elevated PaCO2, higher than 45, CO2 will raise faster = NEED A VENITILATOR
Peripheral Chemoreceptors
(mechanical) - response to decreased PaO2, pH, increase PaCO2 // tell us to breathe
• → Hypoxic drive = feel urge to breathe when O2 is low
• Hypoxemia - low PaO2, 80-100, varies per altitude
o Dyspnea, SOB, restlessness, impaired judgement, tachycardia, acidosis, accessory muscle, cyanosis, clubbing
Obstructive Disorders
problem with exhalation / AIR TRAPPING [cannot get air out]
• High airway resistance work d/t airway radius // Mechanical problems = increase the work of breathing
• → Flow volume loop = normal inspiration/ low & abnormal expiration = baby buggy pattern
• PFTs for mild = normal FVC, FRC, RV, TLC & low FEV1, FEV1/FVC
• PFTs for severe = low FVC, extremely low FEV1, FEV1/FVC & increase FRC, RV, TLC
• Asthma
intermittent acute airway obstruction [mucus plugs]/inflammation, type 1 hypersensitivity, broncho-spastic problem // reversible
o Types: Allergic - where there are exposures & Non-allergic - exercise induced, after viral infections
o FOCUS on inflammation/airway remodeling
o Chronic cough, wheeze on beginning/throughout expiration, check PEFR often
• Bronchodilators
• Bronchodilators
• Acute management - inhaled short acting Beta 2 agonist [albuterol]
• Status management - nebulized beta 2 agonist [albuterol], O2, Epinephrine [Beta 2 Agonist]
asthma Chronic management - avoid trigger
• Inhaled corticosteroid - anti-inflammatory drug, localized effects; need to rinse mouth out to avoid systemic effects // prevent airway remodeling
• Mast cell stabilizers - anti-inflammatory drug
• Inhaled anticholinergic (ipratropium) - Bronchodilators, relaxes bronchial smooth muscle via block PSNS
• Leukotriene inhibitors [antagonists]- anti-inflammatory drug; inhibit leukotriene binding at target cells/block synthesis // bronchoconstriction, decrease edema, mucus formation
• Immunomodulators (Xolair) - anti-inflammatory drug; monoclonal Ab binds to circulating IgE = no binding to mast cell; less IgE = mast cells desensitized
• Combo agents = bronchodilator + anti-inflammatory
o Glucocorticoid + Beta 2 agonist
• Long acting beta agonists (LABA) = fluticasone + salmuterol = Advair
• Long acting antimuscarinic agents (LAMA) = fluticasone + vilanterol
o Anticholinergic + Beta 2 Agonost = blocking PSNS & activating SNS
o LAMA + LABA = Anoro Ellipta
• Xanethine (theophylline) - Bronchodilators, increase cAMP via inhibit phosphodiesterase = relax smooth muscle & inhibit release of inflammatory cytokines
• COPD
remodeling of the lung structure, O2 sats = 88-92% (normal) d/t inhalation of irritants
Chronic bronchitis
Emphysema
o Chronic bronchitis
airway remodeled, stiffer alveoli & bronchus, chronic airway inflammation, loss of surface area for gas exchange (Co2 retainers) // productive cough for 3 months*2years
• Low V/Q (decreased ventilation [low O2] = chronic hypoxemia/hypercarbia//unable to do mechanics), SOB on exertion, increased sputum, excess body fluids
• Seconday - polycythemia (kidneys do not think you have enough RBC = thick blood)
• Prolonged hypoxic pulmonary vasoconstriction → pulmonary HTN → R HF
o Emphysema
progressively lose of lung tissue, irreversible destruction of alveoli walls = stiff [easy to rupture = pneumothorax] // air trapping, decreased gas exchange surface area, decreased alveolar perfusion // clubbing, DOE, pursed breathing, accessory muscle
o Drugs - bronchodilators (ß2 agonists, anticholinergis, theophylline), Glucocorticoids, O2, Pulmonary rehab
Restrictive Disorders
problem with inhalation // trouble getting air in // tidal volume
High elastic forces d/t addition of non-stretchy collagen/fibrin // Mechanical problems = increase the work of breathing
• → Flow volume loop = low inhale & exhale [but can blow out fast]
• PFTs = normal FEV1/FVC & low FVC, FEV1 & low FRC, RV, TLC
• Pleural
o Effusions
- fluid in the pleural area = increase pressure on the lungs
• Transudate -- edema in the pleural space [low in protein], HF
• Exudate - inflammation, high in protein → hear friction rub (painful to breathe)
• Hemothorax - blood
• Empyema - infected material [pus/abscess], [stick, protein, WBC, bacteria] cannot drain out; absent breathing sounds, decreased tactile fremitus, asymmetric chest expansion
o Pneumothorax
• Simple open - air at top without pressure
• Tension - develop positive pressure = more air build up, collapse lung, push heart/trachea
• Spontaneous --
• Parenchymal
o Restrictive -- pneumoconioses
• Occupational/dust diseases - inhalation of particles
• Fibrosis - inert particles are walled off by immune cells that lay down fibrin
o ARDS/IRDS [adult/infant respiratory distress syndrome] - immune trigger → leaky capillary [non-cardiogenic, pulmonary, edema], lack of surfactant to reduce surface tension = Surface forces are high [atelectasis], injury repair [fibrosis] = high work of breathing, shut, hypoxemia
o Atelectasis - partial / complete collapse of alveoli; V/Q shunt imbalance; WILL NOT RESPOND TO O2, d/t pneumothorax, fluid; retained secretions, CNS depression, airway obstruction, decreased surfactants, more rest; decreased excursion, diminished breath sounds in affected area, hypoxemia; turn, cough, and deep breathing
Infectious
• Pneumonia
• TB
• Pneumonia
[problem in lung fields- lung inflammation; cough, viral, bacterial, dullness, egophony, increase tactile fremitus
o Bacterial - productive cough, elevated WBC, consolidation (dull, e →a) xray infiltrates, Antibiotics are helpful
• TB
lung destruction leads to cavitation and white calcificed lesions → "Ghon tubercule" [doesn't mean active]
o Low grade fever, night sweats, weight loss; positive ppd test; reportable disease, multidrug therapy
o Isoniazid (INH) - interferes with cell wall synthesis, narrow spectrum, +ppd, primary TB to prevent activation
o Rifampin - bacteriocidal by inhibition RNA synthesis, broader spectrum, combination therapy with INH
THIS SET IS OFTEN IN FOLDERS WITH...