Med_Surge_1-1

7/21/2019 Med_Surge_1-1

http://slidepdf.com/reader/full/medsurge1-1 1/31

Congestive Heart Failure (CHF) is a state of low cardiac output – not a disease but a group ofmanifestation related to inadequate pump performance. CHF is the inability of the heart to pumpsufficient blood to meet the metabolic needs of the tissue for oxygen and nutrients.

Cardiac output is the amount of blood pumped by the ventricles in 1 minute C! " H# $ %&

For the normal adult at rest' C! is about *minute. Stroke volume is the amount of blood pumped +ith each ventricular contraction. ,he average %& is about -m*heartbeat

C! can be affected by changes in either heart rate or stro/e volume. H# regulated primarily bythe autonomic nervous system. 0arasympathetic nervous system (vagus nerve) ¯ H# %%H#. 2hen C!↓' the %% H# to maintain adequate C!.

%& is primarily determined by three factors31. Preload3 the volume of blood in the ventricles at the end of diastole' before the

next contraction. 0reload determines the amount of stretch placed on theventricles during diastole 4ust before contraction. 0reload " %tarling5s a+ of theheart the greater the amount of stretch placed on the myocardial fibers' thegreater the force of the contraction. ,hus' %& is '+hich in turn C!. 6ut thisonly +or/s up to a point. 2ith too much volume' preload' myocardial fibers

become overstretched. ,he result is a less forceful contraction. ,hus %& is ¯ '+hich in turn ¯ C! and heart failure results.7. Contractility3 the force +ith +hich the heart contracts during systole. 8ncreasing

contractility %& by ventricular emptying. 9ecreasing contractility ¯ %&.:. Afterload3 the arterial pressure against +hich the ventricles must contract to pump

blood out of the heart. 8ncreasing afterload leads to ¯ %& and ¯ C!. 9ecreasingafterload %& and C!.

8n heart failure' in +hich the primary problem is impaired contractility of the ventricular muscle'stro/e volume is impaired and normal cardiac output cannot be maintained.;ny factor that puts a continuous strain on the heart by3

a. increasing its +or/

b. decreasing its ability to contract or c. hindering or altering blood flo+ through its chambers can cause CHF.

F;C,!#% ,H;, ,H< 2!#= !F ,H< H<;#,3

a. hypertension afterload

b. demands for blood supply (high output failure >> H# to C!) r*t metabolicneed of tissues

c. fast>rate dysrhythmias +ill impair C!.

F;C,!#% ,H;, 9<C#<;%< C;#98;C C!,#;C,88,?3

a. @yocardial infarction. oss of myocardial mass ¯ contractility of involved

ventricle. 2hen cardiac muscle loses ability to maintain adequate C!' CHF

results. b. Cardiac dysrhythmias lead to ineffective mechanical pumping.

C88C; @;8F<%,;,8! !F <F,>%89<9 H<;#, F;8A#<a. 9yspnea*shortness of breath (rapid' shallo+ respirations*tachypnea)

i. 9yspnea on exertion associated +ith exertional activity such as stair climbing

ii. !rthopnea – %!6 +hile lying flat and is relieved +hen patientassumes an upright position

iii. 0aroxysmal nocturnal dyspnea occurs +hen the patient is sleeping'suddenly +a/ing up breathless at night.

7/21/2019 Med_Surge_1-1


b. Cough caused by alveolar irritation from fluid accumulation (early) dry' hac/ingcough (r*t pulmonary edema) +ith frothy' blood>tinged sputum

c. 6ilateral crac/les over lung bases basilar crac/lesd. S3 (ventricular gallop—hallmark sound of CHF) and %B (atrial gallop) diastolic

filling sound +hen blood enters a noncompliant (stiff) ventricle (8& ;morodion)e. eft ventricular hypertrophy point of maximal impulse (0@8) displaced laterally to

the left

f. pulmonary artery pressure (0;0) pulmonary capillary +edge pressure (0C20)

C88C; @;8F<%,;,8! !F #8H,>%89<9 H<;#, F;8A#<

a. 2eight gain (fluid accumulation as a result of aD

and H7! retentionE common). b. 0eripheral edema*edema of dependent body parts (ambulatory patient' feet and

an/les bed rest patient' sacrum) r*t &# due to supine position.c. ugular vein distension caused by pressure on the right side of the heart.

d. C&0 as the blood volume load in the right side of the heart increases.e. iver engorgement*enlargement – hepatomegaly and abdominal pain * tenderness

in #AG of abdomen as liver becomes congested +ith venous blood.f. ;scites – accumulation of fluid in abdominal cavity.g. 0ositive hepato4ugular reflex.h. astrointestinal complaints such as anorexia' nausea' vomiting' and bloating.

<<#; %?@0,!@ !F CHF r*t ¯ C!

a. fatigue*muscular +ea/ness b. tachycardiac. nocturia excessive urination at night*night>time diuresis r*t &# in supine positiond. behavioral changes (impaired cerebral circulation * blood flo+)e. chest pain +ith myocardial ischemia due to reduced coronary artery blood flo+f. s/in changesEpale' cool' clammy diaphoretic s/in +ith peripheral cyanosisg. delayed capillary refill time : o/ay' I: is poor.

988,;8% ursing 8mplications3

1. ,a/e apical pulse for 1 minute noting pace and rhythm7. @onitor 8J!:. 9aily +eights under standard conditions – best measure of fluid volume (before brea/fast and

defecation' after voiding on same scale' similar clothing). #eport +eight gain of 7 lbs.*day or lbs.*+ee/ or more.

B. @onitor for %J% of hypo/alemia monitor serum potassium levels.

. @onitor for %J% of digitalis toxicity monitor serum digoxin levelsK. !bserve for and report therapeutic effects of digitalis (e.g.'↑ urine output).

0atient ,eaching 0oints31. ,a/e medication at same time each day.7. Count pulse for 1 minute before ta/ing digitalis noting rate and rhythm. If rate or rhythm has

changed significantly, withhold medication and notify MD promptly.:. #eport %J% of digitalis toxicity.B. #eport %J% of hypo/alemia (e.g.' muscle +ea/ness' fatigue). 2eigh daily under standard conditions. #eport +eight gain of 7 lbs.*day or lbs.*+ee/ or more.K. @aintain daily dietary potassium inta/e as indicated.-. ;dvise patient to avoid dairy products for at least 7 hours before and after digoxin because they

reduce its absorption. (; high fiber diet may also reduce absorption).L. ,a/e digoxin at least 7 hours before or after ta/ing antacids and antidiarrheal products because they

may decrease its absorption.

98A#<,8C% ursing 8mplications3

1. @easure 8J! daily.7. 9aily +eights under standard conditions. #eport +eight gain of 7 lbs.*day or lbs.*+ee/ or more.:. @onitor 60 for hypotension*orthostatic changes. @onitor supine' sitting' and standing 60s.

Withhold medication and notify MD for BP systolic <90-00 mm !g or for a drop of "#-$0 mm !g from %aseline&

B. 8nstruct to go from a lying to sitting' or sitting to standing position slo+ly to prevent posturalhypotension.

. ,a/e diuretics early in the day to avoid nighttime diuresis' upsetting normal sleep pattern.

7/21/2019 Med_Surge_1-1


K. @onitor serum potassium levels and assess for %J% of hyper/alemia +ith potassium>sparingdiuretics.

-. !bserve for improvement of edema (pulmonary and peripheral edema).

0atient ,eaching 0oints31. @easure +eight daily under standard conditions. #eport sudden losses or gains.7. ,each symptoms of postural hypotension and advise patient to sit or lie do+n if they occur.:. #eport recurring %J% of pulmonary and peripheral edema.B. #eport recurring %J% of hypo/alemia or hyper/alemia (e.g.' muscle +ea/ness).. ,a/e potassium supplements if prescribed.K. <at a potassium>rich diet as indicated-. ,each importance of ta/ing diuretics early in day to prevent nocturia from upsetting patient5s

normal sleeping pattern.

;C< 8H868,!#% (captopril*Capoten)6y inhibiting ;C<' the drugs bloc/ conversion of angiotensin 8 to angiotensin 88' a potent vasoconstrictorand stimulant of aldosterone.0rimary <ffects3

1. &asodilation (arteriolar dilator MN afterloadO and venous dilator MN preloadO).7. #eduction of blood volume (diuretic*diuresis Mhelps reduce edemaO). 8ncreased excretion of aD and

H7! by decreasing release of aldosterone.

0rimary ;dverse <ffect of ;C< 8nhibitors3• Hypotension• Hyper/alemia secondary to decreased aldosterone release• 9ry' persistent cough

!ther ;dverse <ffects3• #enal failure in patients +ith renal artery stenosis• Hypersensitivity reaction +ith rash and angioedema• Contraindicated during the second and third trimesters of pregnancy (fetal in4ury)• 8mpaired sense of taste

7/21/2019 Med_Surge_1-1


7/21/2019 Med_Surge_1-1


• 2arm' moist compresses to relieve pain and reduce inflammation. @ild oral analgesics(acetaminophen) to relieve pain. For more severe pain' a nonsteroidal anti>inflammatoryagent (ibuprofen) to relieve pain and inflammation.

• <lastic compression stoc/ings after acute stage +hen patient becomes ambulatory. <lasticstoc/ings compress superficial veins' reducing pooling of venous blood and enhancingvenous return to the heart.

• ;nticoagulant therapy is usually not indicated for superficial thrombophlebitis.• ,he ris/ of superficial venous thrombi dislodging and causing emboli is very lo+ because

the ma4ority of them adhere firmly to the vein +all and undergo spontaneous lyses.

"iagnostic Studies in "eep #ein!hromophleitis oninvasive venous studies Doppler 'ltrasound – common

noninvasive test to measure blood flo+through blood vessels (arteries andveins). 8n 9&,' determines venous blood flo+ in deep veins. 8n 9opplerultrasound' a probe transmits high>frequency sound +aves through thes/in to+ard veins. ,he sound +avesstri/e the moving red blood cells andare transmitted bac/ to the probe' producing audible tone. ormal venous

blood flo+ creates a roaringsound. 8n the patient +ith 9&,' the sound of venous blood flo+ is diminished or absent.

,0; – tissue plasminogen activator – dissolves clots' bodies natural fibrinolytic

9uplex venous scanning or imaging (noninvasive) test is usually done +ith 9oppler flo+ studies.9oppler scanning produces a three>dimensional vie+ of the veins on a monitor screen' allo+ingexaminer to vie+ both vessel and any thrombus' thrombi.

"dimer test3 ; blood test to measure fibrin degradation fragments generated by fibrinolysis. <levated 9>dimer levels indicate a thrombotic process' but aren5t specific to 9&,. (9>dimer is produced by action of plasmin of fibrin clot.)

mpedance Plethysmography measures venous changes in the limbs. ,he test uses a blood pressure cuff +rapped around the patient5s thigh and inflated ( to K mm Hg) to occlude venous blood flo+ from thecalf. 8n the normal patient' venous blood volume in the calf increases mar/edly as blood becomes trapped belo+ the cuff. 8f a 9&, is present' venous volume +on5t increase as much because blood is alreadytrapped in the calf. 2hen the pressure applied by the thigh cuff is released' venous outflo+ is measured. ormally' venous volume falls dramatically as the trapped blood surges up+ard. 8n the leg +ith 9&,'venous volume remains much the same.

7/21/2019 Med_Surge_1-1


*#AS#+ P,-C+".,+ #+*-/,APH0 is the most definitive test for diagnosing 9&, but it carries several ris/s (eg' allergic reaction to dye – contrast medium>phlebitis) and so should only be doneis the patient has signs and symptoms of 9&,' but the results of noninvasive studies are ambiguous.0rocedures involves in4ecting contrast media into bloodstream' follo+ed by x>rays to identify location ofclot.

RR<dema in extremities is a vein problem' never an artery problem.

9<<0 &<8 ,H#!@6!0H<68,8% (9&,)Clinical @anifestations

!nce a thrombus becomes large enough to completely obstruct blood flo+ through a vein' signs andsymptoms develop. ,he first sign is usually edemal s+elling of affected extremity. ,he amount of s+ellingcan be determined by measuring extremity (an/le' calf' and inner thigh) circumference at various levels+ith a tape measure' compare one extremity to the other by measuring the circumference of each at thesame level for siPe differences. 8nspect legs from groin to feet' noting any unilateral or bilateral changes.Compare one leg to the other.

,he s/in over the affected area may become +armer. ,here may also be erythema (redness) in the affectedarea. ,he patient may complain of a tight or heavy sensation in the limb' heaviness in the affected limband pain or tenderness over involved vein or palpation. @alaise and fever sometimes occur. ; positiveHoman5s sign (calf pain upon dorsification of the foot) is a classic but unreliable sign for 9&, because itcan be elicited in any painful condition of the calf. 9iminished or absent 9oppler flo+ reading over veinsin affected extremity.

'anagement /oals3 Prevent e1isting thromi from ecoming emoli& 0revent ne+ thrombi from forming increase venous return to the heart decrease venous pressure. 6ed rest to prevent clotdislodgement. 6ed rest is usually required for about to - days after 9&, to give the clot time to adhereto the vein +all so it +on5t emboliPe.

<levate the affected extremity above heart level to reduce s+elling (N venous pressure) and enhancevenous return (prevents venous stasis and the formation of ne+ thrombi)

<levate the patient5s legs by elevating the foot of the bed six inches on bloc/s. ;void placing pillo+sunder patient5s /nees and use of /nee gatch to prevent compression of the popliteal vein and obstructionof venous blood flo+.

9o not elevate the head of the bed more than : degrees to prevent inguinal congestion (consult doctorregarding degree H!6 should be elevated).

;pply +arm' moist' compresses to affected extremity to relieve pain and reduce inflammation if ordered'administer mild oral analgesics (eg' acetaminophen) to relieve pain. @easure and record circumference ofextremity daily. Compare bilaterally and +ith previous measurements. ;ssess extremity color'temperature' pulses' complaint of pain.

RR9on5t give ,ylenol +ith Coumadin or 2arfarin.

"o not e1ercise affected e1tremity during acute phase of "#! to prevent clot dislodgement& 8nstruct

and assist patient to move affected extremity slo+ly and cautiously.

!he unaffected e1tremity should e e1ercised actively to promote venous blood flo+.

*ever ru or massage affected e1tremity – could dislodge clot.

,o protect affected extremity from trauma and pressure' use an air mattress' sheeps/in' heelpads' and a bed cradle or foot board.

Caution patient to avoid activities that create a #alsalva maneuver (eg' straining to have bo+el movement Mstool softenerO' holding breath +hile moving in bed Mprovide trapePeO). #alsalva maneuver 2 intraadominal pressure 4 venous return 2 venous pressure& 8nstruct patient to perform deep

breathing exercises to promote venous return.

7/21/2019 Med_Surge_1-1


'aintain ade5uate fluid intake – t+o to three liters a day unless contraindication – to prevent dehydration. <lastic compression bandages *;ce bandages are usually prescribed to promote venousreturn and decrease leg s+elling. 6andages are applied from toes up +ith uniform*even pressure. %hould be re+rapped at least once during each shift chec/ for circulatory' motor' and neurologic functions inextremity because an improperly +rapped bandage can have a tourniquet effect. !nce s+elling hassubsided' patient can be measured for an elastic support stoc/ing.

%A@@;#? on>invasive test for thrombophlebitis3

1. 9oppler ultrasound7. 9>dimer test (degraded fibrin fragments):. 0lethysmography (cuff around thigh)

8nvasive tests for thrombophlebitis3 1.&enography (ris/s " allergy to dye.

7/21/2019 Med_Surge_1-1


; dysrhythmia is defined as an abnormality in the rate or rhythm (regularity) of the heart beat or both.6ecause of their ability to lo+er cardiac output' dysrhythmias are associates +ith a high degree ofmorbidity and mortality.

!#@; C;#98;C <<C,#!0H?%8!!?@yocardial cells possess the properties of3

a. e1citaility3 ability to respond to an electrical stimulus' an electrical impulse b. automaticity3 ability to spontaneously initiate an electrical impulse (property of pace ma/er

cells in the %; node' ;& node' and 0ur/in4e fibers !?).c. conductivity3 ability to conduct or transmit an impulse from cell to cell.d. contractility3 ability to respond to an electrical impulse by contracting

,efractory period3 throughout most of repolariPation' cardiac muscle cells do not respond to any stimuli. ,he property of refractoriness of myocardium prevents uncontrolled' rapid cardiac contractions +hich+ould prove fatal +ithout immediate intervention.

Cardiac cycle consists of diastole (relaxation 7*: of heart cycle) follo+ed by systole (contraction 1*: ofheart cycle).

H<;#,5% ;C,8! 0!,<,8;;ction potential is the process of depolariPation (contraction) and repolariPation (relaxation)

+lectrical activity eforemechanical contraction

#esting polariPed cell – inside of cell is more negatively chargedthan outside.

%timulated cell depolariPed

2hen an electrical impulsestimulates a resting muscle cell'inside of cell is converted from (>)to (D)' causing depolariPation.

9epolariPed cells then contract.

,ecovered cell repolari$ed

#epolariPation " electricalrecovery returns cell5s charge tonegative.

Cell relaxes – returning to polariPed resting state untilanother impulse starts the cycle.

S.''A,03 electrical activity à depolariPation à contraction*systole à repolariPation*dystole

,#<;,8 9?%#H?,H@8;%;ssess*evaluate patient for serious signs or symptoms of dysrhythmia' e.g. rapid H# I 1 bmpHemodynamically unstable patient +ith serious signs3 C;#98!&<#, F8#%,. 2hat constitutes a

hemodynamically unstable patientS Chest pain' dyspnea' ¯ level of consciousness' hypotension' shoc/'

H#' @8' acute pulmonary edema

0%&, (0;#!$?%@; %A0#;&<,#8CA;# ,;CH?C;#98;)<C3 stable narro+ G#% complex

7/21/2019 Med_Surge_1-1


&agal maneuvers I Adenosine I Cardiovert

;,#8; F86#8;,8! ormal cardiac function TBLh

1. Control rate6 beta bloc/ers calcium channel bloc/ers (&erapamil*9iltiaPem) 9igoxin7. Control rhythm6 electrical cardiovert or pharm cardiovert (;miodarone' 8lbutilide

9ofetilide):. Control clot6 anticoagulant therapy (Heparin)

ormal cardiac function IBLh1. Control rate6 beta bloc/ers calcium channel bloc/ers (verapamil*diltiaPem) digoxin7. Control clot6 anticoagulant therapy (Heparin):. Control rhythm6 delayed for fear of dislodging clot

8mpaired cardiac function TBLh1. Control rate6 ;miodarone' 9iltiaPem' 9igoxin (no beta bloc/ers)7. Control rhythm6 electrical cardiovert or pharm cardiovert (;miodarone):. Control clot6 anticoagulant therapy (Heparin)

U2hat did 8 sayS 8f someone is in HF and ;>fib' the drug of choice is (miodarone.V

8mpaired cardiac function IBLh1. Control rate6 ;miodarone' 9iltiaPem' 9igoxin (no beta bloc/ers)

7. Control clot6 anticoagulant therapy (Heparin) for B +ee/s:. Control rhythm6 delayed three +ee/s for fear of dislodging clot

0&C (0#<@;,A#< &<,#8CA;# C!,#;C,8!%);cute therapy +ith beta bloc/ers (+smolol)' ;miodarone or idocaine.

&>,;CHHemodynamically stable3 Cardiovert or Amiodarone78idocaine or Procainamide or Sotalol

Hemodynamically unstable3 Cardiovert

&>F86• ;ssess chec/ rhythm• 1 shoc/ • C0# >7 minute cycles• Chec/ rhythm• 1 shoc/ • C0# •

&asopressors3 vasopressin or epinephrine

7/21/2019 Med_Surge_1-1


• chec/ rhythm

• 1 shoc/ • C0# • ;ntiarrhythmics3 Amiodarone78idocaine• chec/ rhythm• 1 shoc/ • C0#

;%?%,!<9& Confirm asystole in more than one lead:& ,ranscutaneous pacing3& +pinephrine first' then Atropine

6#;9?C;#98;1. ;tropine7. ,ranscutaneous pacing:. 9opamine' <pinephrine

<C,A#<

2hen do you treat for dysrhythmiaS 2hen you see signs of ¯ C!.

?ou +ill be responsible ;& bloc/s' ;& +hen impulses are excessively delayed or totally bloc/ed in the;& node or 4unction (4unction involves the 6undle of His before it divides).

Sinus tachycardia ; H,<9== > %ay aove 9== > ut the rhythm %ill e regular& ?hy@ ecause itoriginates from the SA node& 0our SA node is your pacemaker so the disturance is really in rate&?hen you have automaticity of the SA node you have sinus tachycardia ut the rhythm is

regular& tBs still considered a dysrhythmia& n most cases if you have a sinus tachycardia you lookfor the underlying cause and treat it& Possile causes could e hyperthyroidism anemia hypo1ia&

Someho% there is an in sympathetic effect and a ¯ in parasympathetic effect& 'any things can

cause it including the odies o%n compensatory mechanisms to counteralance ¯ C- > rememer

that early on H, %ill C- ut overtime it %ill ¯ C-& So %hen you have SS of ¯ C- you may

need drugs that are gong to slo% the H,& What drugs can slow the SA node? Digoxin, beta blockers, and calcium channel blockers i.e. Verapamil and Diltiazem – not i!edipene. !hey %ill all slo% the SAnode and then slo% conduction through the A# node& And that %ill slo% the H,& !hose three drugsact as SA node lockade and A# node lockade& 9igoxin' 6eta bloc/ers' and Calcium channel bloc/ers.

%inus bradycardia " H# TK but the rhythm +ill be regular b*c it comes from the sinus node. 8f your rate

is so slo+ it is going to lead to ¯ C! and ¯ 60 leading to ¯ tissue perfusion. 8dentify the cause and treatthe cause. 8n some circumstances you may need a pacema/er to deliver the electrical impulse to +hich the

myocardial cells +ill react and contract. 2ith bradycardia sometimes a pacema/er +ill be used that5s one+ay to treat a bradycardia. Ho+ever' +hat drugs can +e useS

Atropine. ;tropine is a vagolytic (causing inhibition of the vagus nerve)' anti>cholinergic' anti> parasympathetic that +ill stimulate the %; node and stimulate conduction through the ;& node. 8t is ama4or drug given for bradycardia. #emember' bradycardia ends in a' a for Atropine.

Amiodarone sho+s beta bloc/er>li/e and calcium channel bloc/er>li/e actions on the %; and ;& nodes' increases the refractory' and slo+s conduction of the cardiac action potential.

• Ased for )-tach, )-fi%• %lo+s nerve impulses in the heart by acting directly on the heart tissues

7/21/2019 Med_Surge_1-1


• %ide*;dverse <ffects3 lung problems' liver problems' and ne+ or +orsening irregular heartbeats.

• 9rug of choice for life>threatening ventricular dysrhythmias.

;denosine• 9ecreased ;& nodal conduction• 8ndications3 %upraventricular tachycardias. %ince adenosine is only available as an 8&

solution' and because of its short half life (a matter of seconds) it is only used for acutetherapy.

%ometimes +hen people have 0%&, healthcare providers can do vagotonic maneuvers to slo+ the H# byvagal (vagal " parasympathetic) impulses to the heart3 carotic sinus massage' valsalva maneuver' gagging'vomiting' coughing' ice bag to face' pressure to eyeballs.

0%&,%upraventricular because the foci is above the ventricles.*reatment focus3 treat unstable patients urgently. ,here5s a rule' if the patient is hemodynamically unstable' cardiovert first to covert dysrhythmia to normal sinus rhythm. 8f H# I1bpm +ith serious

%J% such as chest pain' dyspnea' ¯ level of consciousness' hypotension' shoc/' H#' @8' acute pulmonary

edema you don5t have time for drugs. ?ou +ant to convert the rhythm as soon as possible to normal sinusrhythm. 8t5s synchronous +hen you terminate a dysrhythmia +ith a G#% complex.

2hat +e5re going to do if +e5re not hemodynamically unstable then +e5re going to use ;& nodal bloc/ingagents. ,hese ectopic foci that are firing these impulses are not in the %; node' so +e5re not tal/ing about%; nodal bloc/ing agents no+' +e5re tal/ing about these atrial impulses that are going to go do+n the ;&node to the ventricles and +e don5t +ant all those impulses to get do+n there because it5s your ventricularrate that determines C!' so +e +ant to bloc/ a lot of those impulses and prevent those impulses fromgetting out of control and sending patient into cardiac arrest. 2e5re tal/ing about foci that are no longer inthe %; node. ?our impulses from the atria +ill go do+n to your ventricles' so +e use an ;& nodal bloc/ing agent. 8n this situation +hat they do to the %; node is meaningless& !he drug of chose in PS#!is Adenosine.

2hat are other ;& nodal bloc/ing agentsS ,he calcium channel %loc+ers, %eta %loc+ers, and digoin&

,hey +or/ on both the %; and ;& node. ormal <F means you5re not in heart failure. 2hen you are in heart failure ;denosine and then

;miadoarone because +e said even in heart failure a>fib +e +ant ;miodarone. 9iltiaPem has less of aneffect on myocardium then &eramapil does' so 9iltiaPem is safer in someone +ho has HF. ;nd of courseyou see your 9igitioxin.

8f things are going to cause delay through the ;& node' in general you /no+ there is the potential adverseeffect of hypotension and bradycardia. <ven +ith a beta bloc/ers and calcium channel bloc/ers +e saidyou can have bradycardia and hypotension. #emember ;denosine is the drug of choice for 0%&,.

;,#8; F86#8;,8!,he most common dysrhythmia in ;merica.et5s loo/ at the drugs. For less than TBLh control the rate. ?our calcium channel bloc/er 9iltiaPem or &erapamil. ;gain you see your beta bloc/ers and 9igoxin. Control rhythm you can do it +ith electricalcardio vert of pharmacologic cardiovert amararodian ibutilide' dopeltilide.

2hat are +e trying to doS ,o prevent all those impulses from getting do+n there to the ventricles +here

the problem really is in terms of ma/ing them beat to fast ¯ C!' and then your going into cardiac arrest.?ou see +ith ;miodarone again the bradycardia and hypotension. 8t can also cause cardiac toxicity andvisual problems. ,he understanding +ith supraventricular tachycardias – tachycardias above the ventricles>> you don5t +ant all the impulses to get do+n to the ventricles. ,hat5s +hat all these drugs do. 6ut +ith0%&, the drug of choice is ;denosine.

2hen +e thin/ of a>fib +e thin/ of clotting and that they5re going to be on an anticoagulant. 8f they don5tconvert them into sinus rhythm and they continue +ith the a>fib because they can control it +ith the ratethey5re on Coumadin' 2arfarin or aspirin.

7/21/2019 Med_Surge_1-1


&<,#8CA;# ,;CH?C;#98;2ith ventricular dysrhythias you don5t see' Ucontrol the rate' control the rhythmV. ,hat5s because +e

have to get rid of the dysrhythmia& 6ecause ventricular rate determines C!' so no+ +e5re tal/ing realserious so +e +ant to terminate the dysrhythmia' restore normal H# and rhythm.

0&CFrequency can indicate myocardial irritability. 8n and of itself 0&C is benign' but K or more 0&C in a ro+can lead to the lethal dysrhythmias of &>tach or &>fib. ,hese predispose people to lethal dysrhythmias.;nd if you have a mild cardio infarction the last thing you +ant to see if a lot of 0&Cs in a ro+.

Ase beta bloc/ers li/e <smolol (8& version) in acute care situation. %ame drugs for ventriculardysrhythmias in general. ;mioadarone' lidocaine' procanamide' and sotalol.

8f you have stable v>tach your four ma4or drugs are ;miodarone (used for both atrial and ventriculardysrhytmias)' lidocaine' procanamide' and sotalol. Ho+ever' if they are not stable cardiovert first.

& F86#88;,8!For all of these dysrythmias the mantra is Utreat the patient' not the monitorV. Firs thing you al+ays do inthese situations is assess the patient to /no+ if they are stable or not. ,here is no contractility so there isno pulse so there is no C! so in B>K minutes pt. +ill be brain dead.

First action is defibrillation' not C0#. C0# only until defibrillator is available. %o then you give a shoc/.Ase C0# ( cycles of 1 compressions for 7 minutes)' chec/ rhythm' continue C0# +hile defib charges'give shoc/' resume cpr' +hen 8& is available give vasopressors first (vasopressin or epinephrine). ,hishappens +hile someone is giving C0#. CH<C= #H?,H@ after cycles al+ays. et5s say you maxed outthe vasopressin. ext cycle of drugs is ;miodarone (preferred to idocaine)' and then magnesium.

;%?%,!<,here is no electrical or mechanical activity. ,ranscutaneous pacing but before you do any treatment youal+ays assess the patient. Confirm asystole in more than one lead. 9rugs +ould be epinephrine andatropine. Anless someone had dro+ned or suffered an electic shoc/' you usually have died. so it5simportant to see if patient has an order for 9#. Consider +ithholding therapy if greater than 1 minutesof asystole.

C!@@! C;A%<% !F 9?%#H?,H@8;%H.ypoxia;.cid>base imbalance,.oxicity<.lectrolyte imbalances

%J% !F C;#98;C 9?%#H,@8;%

;ll relate to ¯ C!. Hypotension' ¯ urinary output' dyspneic' cool clammy s/in' capillary refill time'

diminished peripheral pulses. ;nxiety' restlessness' confusion. Chest pain.

;& 6!C=%

?eBre only doing 9st degree A# node 9st degree heart lock& Conduction time is prolonged ut allimpulses are conducted from atria to ventricles& !reatment necessary only if pt has symptomatic

radycardia %ith ¯ C-& Correct +ith ;tropine.

0;C<@;=<#%%ingle chamber pacema/er' lead is usually going to right ventricle.8nfective endocarditis. ;n invasive procedure such as dental +or/ could lead to infective endocarditis.?ou +ill be held responsible for identifying <C rhythm changes3 ;>fib' &>tach' &>fib' 0&C

%: in an early sign of HF

,he dysrhtymia commonly associated +ith HF is atrial fibrillation and the drug of choice for ;>Fib +ould

7/21/2019 Med_Surge_1-1


be 8& ;miodarone (atrial and ventricular fibrilation)

7/21/2019 Med_Surge_1-1


&asodilators' 6eta 6loc/ers' and Calcium Channel 6loc/ers'Page 9 of D

;C,8!3 nitroglycerin decreases the pain of exertion angina primarily by ¯ @?!C;#98; !7 9<@;9 via

vasodilatation. ,hese drugs ¯ !7 by ¯ preload (blood pools in veins ¯ venous return to the heart) and' to a lesserextent' afterload (dilates arterioles). *ote6 ;lthough nitroglycerin dilates coronary arteries and blood flo+ throughcollateral coronary vessels it cannot dilate atherosclerotic coronary arteries.;9&<#%< <FF<C,%3 hypotension' tachycardia' headache' flushing. #eport to doctor if blurring of vision' dry mouth'

and persistent' server headaches occur. ,hese are signs of over dosage that requires immediate attention. ;void alcoholic beveragesEbecause it is a vasodilator alcohol may exacerbate hypotension. A#%8 8@08C;,8!%3 @onitor 60 closely. 0ostural hypotension may occur caution patients to sit or lie do+n+hen ta/ing nitroglycerin.

2hen ta/ing nitroglycerin tablets % for anginal pain' instruct the patient to ta/e one % tab. 8f pain is not relieved in minutes' call W11 or report to <9. (anginal pain not relieve by nitro may indicate @8.) 2hile +aiting' ta/e one more % andthen a third tab minutes later if needed (up to : tabs min. apart)

;s a precaution' the pt. should carry % nitroglycerin at all times. ,he drug should not be carried close to the body (bodyheat) carry it in a 4ac/et poc/et or handbag. For hospitaliPed pts' physician allocates a specific number of tablets to be

placed at bedside. Count tablets.

itroglycerin is volatile and tablets are inactivated by heat' moisture' air' light' and time. 6ecause nitroglycerin tabs areaffected by cold and heat' do not store in refrigerator or bathroom medicine cabinet. %ince nitroglycerin tabs tend to lose potency' a ne+ supply should be purchased every :>K months. 8nstruct pt. to +rite date of opening on bottle and discardunused tabs after K months.

itroglycerin is unstable and is /ept in a securely capped dar/ glass bottle. itroglycerin should not be stored in metal or plastic pillboxes. ;fter the bottle is opened' remove cotton or pac/age insert these may absorb some of the drug' +hichresults 8 less potent tabs. 2hen handling the drug ma/e sure hands are dry' since moisture hastens deterioration of the drug.

#apid>acting preparations alleviate angina pain +ithin : minutes. %ublingual tabs*translingual spray has duration of :>K minutes.A%<%3 ;cute ;ntianginal ,herapy3 ,ermination or prophylaxis of an acute anginal attac/3 1) % tabs 7) ,ranslingualspray :) ,ransmucosal (6uccal) tabs (duration3 :> hrs.). ong>;cting %ustained ;ntianginal ,herapy3 %# oral tabs'

topical ointment' transdermal patches' ,ransmucosal ,abs (+hen used for prophylaxis' administer q:>Lh).

C;%%3 +!AA",+*+,/C 8-CE+,S<$;@0<3 P,-P,A*-8-8 A!+*-8-8 *onselective etalockers Cardioselective eta lockers (act more strongly on eta9 than eta: receptors)

;C,8!3 bloc/ sympathetic stimulation of beta receptors ¯ myocardial +or/load and oxygen demand by ¯ contractility' H#' and 60.

;9&<#%< <FF<C,%3 hypotension radycardia' ¯ myocardial contractility' bronchospasm' hypoglycemia

A#%8 8@08C;,8!%3 administer cautiously in clients +ith CHF and C!09 beta>bloc/ers may mas/symptoms of hypoglycemia. 9o not discontinue beta bloc/ers abruptly results in exacerbation of symptoms.

C;%%3 CA8C.' CHA**+8 8-CE+,S

<$;@0<3 "8!A+' #+,APA'8 *F+"P*+;C,8!3 these drugs inhibit calcium ion influx across cardiac and vascular smooth muscle cells. ,hey dilate coronaryarteries*arterioles and peripheral arterioles. #elief of exertion angina is produced primarily by causing dilation of

peripheral arterioles ( ¯ afterload) thereby decreasing myocardial oxygen demand.

;9&<#%< <FF<C,%3 )erapamil and Diltiaem6 hypotension radycardia& .ifedipine6 hypotension' tachycardia& A#%8 8@08C;,8!%3 monitor 60 and H#

itroglycerin itro acts directly on &%@ to promote vasodilation' acting primarily on /eins. itro ¯ the pain of exertional*acute

angina by ¯ cardiac oygen demand& !xygen demand is decrease as follo+s3

• 6y dilating veins' nitro ¯ venous return to the heart

7/21/2019 Med_Surge_1-1


• thereby ¯ ventricular filling and

• the resultant ¯ in +all tension (preload) ¯ oxygen demand. Adverse EffectsHeadache' transitory over the first fe+ +ee/s. -rthostatichypotension secondary to relaxation of &%@.

,efle1 tachycardia. itro ¯ 60 quic/ly by decreasing venous return. ,he resultant baroreceptor reflex H# and myocardial contractile force' oxygen demand and negating the benefits of therapy.Drug InteractionsHypotensive drugs such as beta bloc/ers' calcium channel bloc/ers' diuretics' and 60 lo+ering drugs are all intensified by nitro.

9o not ta/e nitro +ithin 7B hours of ta/ing #iagra or 8evitra' and BL hours for Cialis.eta lockers can suppress nitro>induced tachycardia by preventing %% activation of beta1 receptors of the heart.&erapamil and 9iltiaPem can suppress nitroinduced tachycardia thru direct suppression of pacemaker in SA node&

6eta bloc/ers essentially do the same thing as calcium channel bloc/ers and have identical effects and adverse effects'they 4ust do it one step earlier. 8n the heart' calcium channels are coupled to beta 1 receptors' activation of +hichenhances calcium entry.

;ngina underlying cause " C;9Anstable angina underlying cause " C;9 D vasospasm D platelet aggregation D transient coronary thrombi*emboli

%J% of unstable angina are31. %ymptoms of angina at rest7. e+>onset exertional angina or :. intensification of existing angina.

#erapamil and "iltia$emDirect Effects9ue to bloc/ade of calcium channels in the heart and blood vessels' verapamil has four direct effects3

1. ;rteriole dilation causes ¯ arterial pressure.

7. coronary perfusion (artery*arterioles bloc/ade)

:. ¯ H# (%; node bloc/ade)

B. ¯ afterload (myocardium bloc/ade' hence the bradycardia)

Indirect Effects&erapamil>induced ¯ of 60 activates the baroreceptor reflex and the %% releases norepinephrine' +hich acts to H# and force of contraction.Net Effect,he direct effects are counterbalanced by indirect effects the drug has little or no net effect on cardiac performance.

Consequently the overall C& effect of &erapmil is simply vasodialtion accompanied by ¯ arterial pressure andcoronary perfusion.

Adverse EffectsConstipation results from bloc/ade of calcium channels in smooth muscle of the intestine. ,he incidence of constipation is considerably lo+er +ith 9iltiaPem' +hich is the only significant difference bet+een the t+o drugs."i$$iness flushing' and headache occur secondary to vasodilation.radycardia (%; node bloc/ade)

¯ contractility (myocardium bloc/ade)

In patients with certain cardiac diseases, "erapamil can seriousl# exacerbate d#s!unction. 9igoxin and &erapamil both suppress ;& node conduction.

6eta bloc/ers and &erapamil both ¯ H# and contractility

ifedipine@a4or difference from &erapamil is that it does not bloc/ calcium channels in the heart – only in &%@. ,hereforenifedipine cannot be used to treat dysrhythmias' does not cause cardiac suppression' and is less li/ely to exacerate pre>existing cardiac disorders. ifedipine is more li/ely to cause reflex tachycardia.Direct Effects6loc/ade of calcium channels in the blood vessels (arteries*arterioles) causes vasodilation' resulting in3

• ¯ arterial pressure

7/21/2019 Med_Surge_1-1


• coronary perfusion

Indirect Effects

ifedipine>induced ¯ of 60 activates the baroreceptor reflex and the %% releases norepinephrine. Anli/e verapamil'nifedipine lac/s direct cardiosuppressant actions' thus cardiac stimulation is unopposed' leading to reflex tachycardia. (H# and force of contraction).Net Effect

ifedipine3

7. ¯ 60

:. H#

B. contractile force,he reflex tachycardic effects are transient and occur +ith the fast>acting formula (because the baroreceptor reflexresponds to rapid falls in 60).

Adverse Effects,efle1 tarchcardia& Combine nifedipine +ith a beta bloc/er to prevent. 6eta bloc/ers decrease the adverse cardiac effects of nifedipine.6eta bloc/ers intensify the adverse cardiac effects of verapmil and diltiaPem.

Sites of Action Hypertension Angina Dysrhythmias

ifedipine ;rterioles X G&erapamil ;rterioles*heart G G G9iltiaPem ;rterioles*heart G G G

Drug

Property Nifedipine VerapamilDiltia!em

9irect <ffects on the Heart and ;rterioles

;rteriolar dilation ?es ?es<ffects on the heart

¯ ;& conduction o ?es ¯ contractile force o ?es

@a4or 8ndicationsHypertension ?es ?es;ngina ?es ?es9ysrhythmia o ?es;dverse <ffects<xacerbation of

Heart failure o ?es<ffects secondary to vasodilation

<dema (an/les and feet) ?es ?esFlushing ?es ?esHeadaches ?es ?es9iPPiness ?es ?es#eflex tachycardia ?es o

Constipation o ?es

9rug 8nteractions8ntensifies digoxin>induced ;& bloc/ o ?es8ntensifies cardiosuppressant effects of o ?es

beat bloc/ers!ften combined +ith beta bloc/ers to ?es o

suppress reflex tachycardia

;,80;,<<, ;<,%*0;,<<, 8H868,!#%

,hese drugs suppress platelet aggregation and are used to prevent blood clot formation.

7/21/2019 Med_Surge_1-1


Aspirin L>:7mg*day0lavix/lycoprotein 7a inhiitors – bloc/ final step in platelet activation completely bloc/s fibrinogen5s ability to bind to platelets' platelets can5t clump*stic/ together. A%<9 8& for acute coronary syndrome and those undergoing 0C8.

;C< 8H868,!#% hould %e started early in post-MI sta%le, high-ris+ patients

;ngiotensin 88 is a very potent chemical that causes the muscles surrounding blood vessels to contract and therebynarro+s the blood vessels. ;C< inhibitors are medications that slo+ (inhibit) the activity of the enPyme' +hichdecreases the production of angiotensin 88. ;s a result' the blood vessels enlarge or dilate' and the blood pressure is

reduced.

B1*( B234516 %hould be started in high>ris/ post>@8 patients.,reatment of the acute @8 is geared to quic/ly dissolving the thrombus in the coronary artery and reperfusion themyocardium before cellular death occurs. ,hrombolytics must be given as soon as possible' preferably +ithin the first Khours after the onset of pain. @yocardial cells do not die instantly. 8t ta/es approximately B>K hours for the entirethic/ness of the muscle to become necrosed (transmural infarctions " G>+ave @8 " %,<@8).

,H#!@6!?,8C% (strepto/inase or ,0;s)

All thrombolytic agents work by converting plasminogen to plasmin, which dissolvesthe cross-linked fibrin mesh (the backbone of a clot). This makes the clot soluble andsubject to further proteolysis by other enymes, and restores blood flow overoccluded blood vessels. !hile other anticoagulants (such as heparin) decrease the

"growth" of a clot, thrombolytic agents actively reduce the sie of the clot. #owever,thrombolytics can only destroy existing clots$ can%t prevent new ones from forming.

,hrombolytics can3• dissolve the clot• reopen the artery

• restore blood flo+ to the heart

• limit the siPe of the infarction

• limit myocardial damage

• preserve left ventricular function

• reduce complications and

• prevent death

Criteria for thrombolytic therapy3• %,<@8

• chest pain I: minutes unrelieved by nitro' !7 supplements' or morphine sulfate.

Drug

Property Strepto"inase Alteplase #tPA$ Anistreplase

%ource %treptococcal culture #ecombinant 9; %treptococcal culture andhuman plasma

;dverse <ffects6leeding ?es ?es ?es;llegic reaction ?es o ?esHypotension ?es o ?es

8ntracranial hemorrhage ?es ?es ?es

ursing Considerations• &onitor for reperfusion (relief of chest pain is the most sensitive marker)

• Administer #eparin anticoagulation after thrombolytic therapy. Thrombolytics

can only destroy existing clots$ can%t prevent new ones from forming.• @inimiPe ris/ of bleeding complications.

%;@0< CH<%, 0;8 0#!,!C!8nitial ;ssessment&% and focused physical exam<C

7/21/2019 Med_Surge_1-1


Chest x>ray!btain 8& access!btain initial serum cardia mar/er levels

8nitial eneral ,reatment @!;@orphine!xygen' B*min' continue if %a!7 TWY itroglycerin;spirin' 1K>:7mg' che+ and s+allo+

1st

priority is chest pain assessment and then relief of chest pain' because pain leads to both ischemia and anxiety.

%pecific ,reatments#eperfusion therapy +ith thrombolytic agents door to drug T : min.Heparin 8& itro 8&6eta bloc/ers 8&' then po;C< inhibitors po (after six hours)

0C8 (6;!! ;8!0;%,?) &%. ,H#!@6!?,8C ,H<#0;?,hrombolytic therapy is preferred if3

1. 0resentation is early (: hours of less from symptom onset)7. 0C8 is not an option (e.g. due to lac/ of a 0C8 lab or vascular access is difficult:. 0C8 is an option' but cannot be done fast enough (+ithin W minutes of initial medical contact)

0C8 is preferred if31. the procedure can be started +ithin W minutes of initial medical contact7. presentation is late (I : hours but T 17 hours after symptom onset):. thrombolytic therapy is contraindicatedB. ris/ of mortality from %,<@8 is especially high. diagnosis of %,<@8 is in doubt

door>to>drug " : minutes (only for @8)door>to>0C8 " W minutes (only for @8)

8!,#!08C ;<,% to myocardial contractility and cardiac output and improve tissue perfusion."opamine +ill contractility and H#. Ase +hen 60 T1."outamine +ill only contractility. Ase +hen 60 I1.

9#A ,H<#;0? F!# @8

• Aspirin to ¯ ris/ of thrombosis and reinfarction

• etalockers to ¯ pain' infarction siPe' mortality.

• *itrates to ¯ chest pain from post>@8 ischemia.

• AC+ inhiitors to ¯ 60

%<#A@ @;#=<#% (see Cardiac mar/ers at a glance handout from class -' W*7*K)C=>@6 (d/antages3 it appears soon after an @8' pea/s quic/ly' and returns to baseline in 7>: days useful in ruling out an acute

@8. 2or/s +ell in con4unction +ith ,roponin 8 to document consecutive @8s that ,roponin is incapable of catching dueto its extended length of elevation in the blood (- days).

Disad/antages3 not 1Y cardio>specific also occurs in s/eletal muscle

,roponin 8 (d/antages3 most cardiac>specific enPyme can help 9x an @8 K>- days after the event. Disad/antage3 because reading remains for so many days' it is difficult to 9x a consecutive @8 +ithin seven days.

@yoglobin

7/21/2019 Med_Surge_1-1


(d/antages3 serum levels rapidly normal reading at :>K hours can reliably rule out @8.

Disad/antages3 not cardio>specific' produces false>positive results tests diagnostic value ends 7Bh after @8.

C;%% !,<% itro primarily acts to dilate veins.

B 9eterminants of myocardial !7 demand can be influenced +ith drugs to relieve*prevent anginal pain31. H# 7. Force of myocardial contraction:. 0reload (venous return to heart)

B. ;fterload (force against +hich heart must pump)

↓ myocardial +or/load à N myocardial !7 demand à relieve*prevent anginal pain.

,ransmucosal (buccal) tablets are the exception to the rule – they are fast>acting and long>lasting.

=no+ side*adverse effects bac/+ard and for+ard of itro.

@a4ority are secondary to vasodilatation' e.g.• Hypotension• #eflex tachycardia

• ,ransient headache due to cerebral vasodilatation• Flushing to due to cutaneous vasodilatation

itro ointment and patch are long>lasting med for long>term prophylaxis – 17 hours on' 17 hours off.

6eta1 receptors in heart are Q by %%' Q force of myocardial contraction' H#' and %; node conduction speed.

,his Q myocardial !7 demand.

%o' beta bloc/ers do the opposite of all that.

6eta1 bloc/ade N C! by N H# and contractility. N C! à N 60

;ll these drugs reduce3

%60 T W>1 mmHg or 7>: mmHg T patient5s baseline

9espite baseline' a H# T 8% never acceptable but for test purposes the limit is K.

#ebound excitation. 9o not abruptly stop ta/ing beta bloc/ers. 0atient +ill most li/ely suffer an @8.

Calcium causes contraction in a myocardial cell. %o a CC6loc/er decreases myocardial contractility.

itros 6eta 6loc/ers CaD channel bloc/ers ifedipeneH# QR N N QR

60 N N N N

)erapamil and Diltiaem cause bradycardia by bloc/ade of %; node through the bloc/ade of calcium channels. ,hey

also cause constipation.

<very drug causes hypotension (N60). ,hey all cause gingival hyperplasia and peripheral edema.

Rthrough reflex tachycardia

7/21/2019 Med_Surge_1-1


9ysrhythmias are the most common cause of death after an @8.

%trepto/inase can cause an allergic reaction. ursing Consideration3 Has pt had a streptococcal infection or receivedstrepto/inase in past K monthsS

;ll thrombolytics cause bleeding

A; %,<@8;nti>ischemic3 nitro' beta bloc/ers;nti>platelet3 aspirin' 0lavix;nti>coagulants3 2arfarin' Heparin' Coumadin

%J% of reperfusion3 relief of %, +ave elevation' relief of chest pain.

: parameters to 9x @83%ub4ective data3 have patient describe chest pain to differentiate pain of angina vs. pain of @8.

1. ,;=< H<;,H H8%,!#?7. <C:. Cardiac mar/ers

schemia causes inversion of ,>+ave'uscle inury causes %,>elevation' causes G>+aves

Fever as high as 17Z is normal 7B>BL hours after @8

7/21/2019 Med_Surge_1-1


hyperglycemia.doc' 0age 1 of :

,he pancreas lies retroperitoneal behind the stomach' +ith its head and nec/ in the curveof the duodenum' its body extending horiPontally across the posterior abdominal +all' andits tail touching the spleen. ,he pancreas performs both endocrine and exocrine functions.,he islets of angerhans are the cells involved in the endocrine function of the pancreas.8nsulin' a protein' is an anabolic (synthesis and storage of nutrients) hormone synthesiPedand secreted by the beta cells of the islets of angerhans. lucagon' a protein' is acatabolic (brea/do+n of nutrients) hormone synthesiPed and secreted by the alpha cells ofthe islets of angerhans.

8nsulin and glucagons have a significant effect on carbohydrate' protein' and fatmetabolism. ;lthough they can affect every cell in the body' their ma4or effects are seenon the liver' muscle' and adipose tissue.

;;6!8C ;C,8! !F 8%A8Carbohydrate8nsulin – a hypoglycemic agent – lo+ers blood glucose levels by3

a. promoting transport of glucose into the cells b. Q glycogenesis – the conversion of glucose to glycogen' the storage form of

glucose' for storage in the liver and musclesc.N glycogenolysis – the conversion of glycogen to glucose andd. N gluconeogenesis – the synthesis of glucose from non>carbohydrate

sources' such as protein (amino acids) and fat (fatty acids) in the liver.

0rotein8nsulin amino acid upta/e and protein synthesis it inhi%its the brea/do+n of protein

into amino acids.

Fat8nsulin lipogenesis – the formation of fat – and promotes storage of fat in adipose

tissue. 8t ¯ lipolysis – the brea/do+n of fat.

%o insulin ¯ blood glucose by facilitating glucose transport into cells and promoting the

storage of glucose (glycogenesis)' protein' and fat.

C;,;6!8C ;C,8! !F AC;!lucagon is a hyperglycemic agent that +or/s to counter the effects of insulinCarbohydratelucagon blood glucose levels by3

a. glycogenolysis and

b. gluconeogenesis

0roteinlucagon protein brea/do+n and amino acid transport from the muscles to provide

the substance necessary for gluconeogenesis.

Fatlucagaon lipolysis and /etogenesis (increased brea/do+n of fats to /etone bodies in

liver to provide an alternative energy sources +hen glucose is unavailable. RR8mportantas it relates to diabetic /etoacidosis)

%o glucagons blood glucose by facilitating the release of stored glucose from the liver'

protein from muscle' and fat from adipose tissue.

7/21/2019 Med_Surge_1-1


8nsulin and glucagon secretion depend on blood glucose levels.

8nsulin secretion rises in response to an in blood glucose.

lucagon is stimulated by a ¯ in blood glucose.

ac/ of insulin ¯

lucose is prevented from entering the cells

¯ 9ecreased glycogenesis

formation of glycogen from glucose ¯

8ncreased glycogenolysis biochemical brea/do+n of Hepatic production of glucose

glycogen to glucose ¯

8ncreased gluconeogenesisglucose formation from noncarbohydrate source'

i.e. proteins or fats ¯

Hyperglycemia 6ecause glucose still can5t getinto the cells +ithout insulin

¯

,he cells are in a state of starvation +hile anexcess of glucose is present in the body

¯

,he body uses fat as an alternative fuel source ¯

8ncreased lipolysis and /etogenesis (liver brea/sdo+n fatty acids into /etone bodies)

¯

@etabolic /etoacidosis Coma and death could result

,?0<% !F 8%A8

%H!#, 9A#;,8!eneric 0ea/ ;dministration

,rade name

,apid Acting (all three are clear)8nsulin lispro 1>:h subG3 1 min before meals !umalog

Insulin aspart 1>:h subG3 1 min before meals ovolog

Insulin glulisine 1>:h subG3 1 min before meals;pidra

%lo+er ;cting

6eg& insulin 1>: h subG3 : min before mealsHumulin # 8&3 the only insulin given 8&

8,<#@<98;,< 9A#;,8! .P! insulin7 K>1Bh subG3 bid' same times each day

Humulin

7/21/2019 Med_Surge_1-1


! 9A#;,8! Insulin glargine one subG3 once daily at same time

antus

0H insulin is con4ugated regular insulin +ith protamine' a large protein. ,he protein ¯

solubility of 0H thereby slo+ing its absorption. 8t is supplied as a cloudy suspensionand must be gently agitated before use & .P! is the only insulin suita%le for miing with

short-acting insulins 8ie& regular, lispro, aspart, and glulisine& Al%ays dra+ the short>acting insulin into the syringe first to avoid contaminating it +ith 0H.

8& infusion of insulin is used to treat dia%etic +etoacidosis and hyper+alemia' the lattero+ing to insulin5s ability to promote cellular upta/e of potassium.

8t used to be that short>acting insulins +ere clear and all others +ere cloudy. ,hat is nolonger the case only 0H is cloudy. Patient teaching may %e necessary for longtime insulin users who still associate clear with rapid acting and cloudy with long duration&

7/21/2019 Med_Surge_1-1


-ral hypoglycemic agents enhance the release of insulin from the eta cells in the pancreas inhiithepatic release of glucose (glycogenolyis and gluconeogenesis) and increase the sensitivity to insulinin ody tissues& ,herefore' they reduce blood glucose in persons +ith a functioning pancreas' and they C;!, be used in the treatment of patients +ho have type 1 diabetes.

;,8H?0<#?C<@8C ;<,%

Anli/e sulfonylureas these drugs don:t stimulate the secretion of insulin. ,hey reduce blood glucoselevels by reducing glucose production and increasing glucose upta/e by the cells. ,he follo+ing drugscan be used alone or in combination +ith sulfonylureas' secretagogues' or insulin.

9#A @<,H!9 !C;,8! @<; ;9&<#%<iguanide ¯ hepatic glucose production and iver

metformin HCl ,a/en +ith meals ,hrombocytopenia(/lucophage) upta/e by cells diarrhea

alpha glucosidase inhiotrs (A/) /ut reaction

Acarose (Precose)I ,hey interfere +ith the brea/do+n 8ntestine ,a/en +ith the first Hepatotoxicitymiglitol (/lyset) of complex carbohydrates to simple bite of a meal flatulence abdominal

sugars' resulting in a smaller rise in pain diarrhea

blood glucose follo+ing mealsthia$olidinediones ,hey insulin sensitivity at insulin

pioglitaPone (;ctos) iver ;dminister daily +ith Headache edemarosiglitaPone (;vandia) receptor sites depends on presence or +ithout food nausea' hepatotoxicity –

of insulin but does not stimulate nausea' vomiting'insulin production. abdominal pain' and

dar/ urine.

8%A8 %<C#<,;!A<%

9#A @<,H!9 !C;,8! @<; ;9&<#%<

insulin secretagogues6 li/e sulfonylureas these drugs do stimulate insulin release from pancreas. Anli/e sulfonylureas theyare rapid>acting and short>lasting.#epaglinide (0randin) 9esigned to treat postprandial 0ancreas :x day +ithin : Hypoglycemia +eight

nateglinide (%tarlix) hperglycemia and indicated to t1 minutes of each meal gaintype : only' because actiondepends on functioning beta cellsin pancreas.

;CA,< C!@08C;,8!% !F 98;6<,<% @<8,A%1. Hypoglycemia – abnormally lo+ blood glucose levels less than >K mg*1m. ;lso

/no+n as hypoglycemic reaction' insulin reaction' insulin shoc/.7. Hyperglycemia – high blood glucose ≥ 7>: mg*1m. @ay lead to diabetic

/etoacidiosis in type 1 9@' hyperglycemic hyperosmolality non>/etotic coma (HH=) in

type 7 9@.

C;A%<% !F H?0!?C<@8;• ,oo little food – delayed' omitted' inadequate inta/e.• ,oo much insulin or oral hypoglycemic agents.• ,oo much exercise +ithout additional carbohydrate compensation.

98;6<,8 =<,!;C898!% (9=;)9=; is a severe metabolic disorder characteriPed by hyperglycemia and metabolic acidosis (from production of /etoacids*/etone bodies) as a result of severe insulin deficiency.

C;A%<% !F 9=;

7/21/2019 Med_Surge_1-1


• 8nfection – a ma4or cause• <motional or physical stress – anxiety' illness' surgery' trauma' etc. trigger the stress

response' greatly increasing the patient5s insulin needs.• Precipitating factors3

o too little insulin

o too much food

o too little exercise

,herapy is directed to+ard correction of hyperglycemia' dehydration' electrolyte imbalance' acidosis' and precipitating factors.

8,<#&<,8!• #eplace fluids and electrolytes +ith 8& .WY % (isotonic) or 8& .BY % (hypotonic).• 8& regular insulin (fast>acting)

• = D +hen urine output is adequate• %odium bicarbonate if pH is T -.

7/21/2019 Med_Surge_1-1


hyperthyroidism.doc' 0age 1 of 1

,6 " thyroxine binding (binds to) globulin

Ho+ do +e ma/e thyroid hormone (,H)S 8odine is a /ey component. @a4or sourcesinclude seafood' +ater' green leafy vegetables' and iodiPed salt.

¯ iodine à enlarged thyroid " goiter

2hat does ,H doS 8t regulates basal metabolic rate (6@#)' +hich tissue !7 demand

and heat production.

<xcess 0roduction and %ecretion of ,H (+hich includes ,: and ,B)0rimary problem – +ithin gland itself %econdary problem – problem +ith anterior pituitary,ertiary problem – hypothalamus

%J% of hyperthyroidism – thyrotoxicosis (toxic thyroid gland) the most common form ofthyrotoxicosis " raves5 disease.

raves disease is an autoimmune disorder. ,%8 antibodies attac/ ,%H receptor sites onthyroid (/noc/ing ,%H off). ,his stimulates thyroid cells to increase in siPe and activityresulting in increased ,H.

%tatistically +omen age 7>B are more afflicted than men.

%J% of hyperthyroidism r*t accelerated body processes. !ypothyroidism is the opposite.

raves5 disease is a form of hyperthyroidism +ith three characteristic signs.& *oic goiter

7. 1ophthalmos (protruding eyes) +ith periorbital edema' +hich could

damage optic nerve and cause blindness. ,reating raves5 disease does

not necessarily reverse exophthalmos it is an associated autoimmune process.:. ocaliPed myxedema – U2e +on5t focus on thisV

!ther %J% of raves5 disease include3

• 8id lag " lid lags behind eyeball +hen patient loo/s do+n because it can5t go over the eyeball a*/*a Ueyelid retractionV.

• /loe lag is +hen the patient loo/s up.• / system3 appetite due to 6@#' but no matter ho+ much you eat you

can5t meet the needs of the tissue' so +eight loss despite appetite

diarrhea.

7/21/2019 Med_Surge_1-1


7/21/2019 Med_Surge_1-1


adrenalectomy.doc' 0age 1 of 1

;9#<;<C,!@?3 P,+-P+,A!#+ CA,+0reoperative care focuses on the physical and emotional stabiliPation of the patient. 6efore surgery the patient should be brought to optimal physical condition to +ithstand the stress of surgery and improve+ound healing postoperatively.

1. Fluid and electrolyte imbalances are corrected before surgery 8J!' daily +eights' assess60 for H,' edema' monitor = D and aD values' administer antihypertensive agents'diuretics +ith = D replacement aD and fluid restrictions.

7. !ptimal nutritional status3 high protein for protein depletion +ith adequate mineral and

vitamins Q = D for hypo/alemia' N aD for H, and fluid retention prescribed calorie diet+ith reduced CH!s for hyperglycemia.

:. Control hyperglycemia3 insulin dietary modifications monitor blood glucose.B. @easure to N ris/ of infection hand+ashing' aseptic techniques. @onitor for %J% of

infection report to @9.. @easure to N ris/ of falls*fractures. 0rovide safe environment guard individuals from falls

and accidents3 side rails up' /eep bed in lo+est position' assist +ith ambulation as needed –cane' +al/er' etc.

K. Asual pre>op teaching3 deep breathing and coughing exercises to prevent thrombosisdiscuss +hat to expect and expected post>op activities.

-. 8&*8@ glucocorticoid preparation administered preoperatively and during surgery to preventadrenal insufficiency during adrenalectomy and post>op period.

L. 0rovide emotional rest for patient. 0rovide support' reassurance' explanations.

P-S!-P+,A!#+ CA,+,he greatest postoperative concern after adrenalectomy is adrenal insufficiency with reduction;loss of circulating adrenocortical hormones& %ymptoms may begin to appear 17>BL hours after surgery. ;ssess for and report3 hypotension fever rapid' +ea/ pulse nausea vomiting unusual +ea/ness. First 7Bh postsurgery is a critical period for circulatory instability*circulatory collapse*shoc/' so 60 is very important.

#eplacement glucocorticoids are given 8& until oral doses are tolerated. 9extrose*saline 8& solution areadministered until oral inta/e is possible. Hemodynamic monitoring3 C&0' 60' pulse' respirations' andtemperature. ;lso 8J!' daily +eights' monitor serum electrolyte and glucose levels' monitor and recordurine output. 6ed rest until 60 stabiliPes. ;s the patient begins ambulation' provide measures to minimiPeeffects of postural hypotension.

;ssess for %J% of shoc/ due to hemorrhage. #ecord &%' report hypotension' +ea/' rapid pulse.@easure*record urine output report oliguria. 0rovide measure to reduce ris/ of infection3 turn' cough'deep breathing exercises to prevent respiratory tract infection. %trict aseptic technique is used +ith+ound care to prevent +ound infection. Control pain*abdominal discomfort at incision site. ;dminister prescribed analgesics splint incision' avoid stressful situation for patient and provide sufficient rest periods. <xplain treatments.

;ssist patient*family*%! in learning about required hormonal replacement.68;,<#; ;9#<;<C,!@?3 patient requires lifelong hormone replacement therapy +ith both aglucocorticoid and mineralocorticoid.A8;,<#; ;9#<;<C,!@?3 patient requires temporary glucocorticoid replacement therapyuntil normal function of the other adrenal gland returns. (,hey don5t require mineralocorticoids becauseglucocorticoids have some mineralocorticoid properties – enough for the short>term).

7/21/2019 Med_Surge_1-1


cushings.doc' 0age 1 of 1

,he secretion of ;C,H is regulated by31. ,he circadian diurnal pattern*sleep>+a/e cycle. 9iurnal secretion is a pattern that rises and falls +ithin a

7Bh period. ;C,H and cortisol levels rise in the early morning and fall in the evening.7. %erum concentration of cortisolEthe negative feedbac/ system3 high serum levels of cortisol inhibit the

secretion of ;C,H (and thus its o+n secretion) lo+ serum levels of cortisol stimulate the secretion of;C,H (and then' as a result' its o+n secretion).

:. %tress3 physiologic*environmental*emotional stressors' e.g. infection' temperature extremes' anxiety' Q;C,H secretion. ,he stress response overrides the usual negative feedbac/ system.

lucocorticoid replacement therapy is based on the normal natural diurnal secretion of cortisol. #eplacement therapymimics the normal diurnal adrenal rhythm to prevent insomnia and suppression of adrenal cortex activity. ,he diurnalrhythm is abolished by Cushing5s syndrome and unconsciousness.

;C,H regulates the gro+th' development' and functioning of the adrenal cortex. 0resence of large amounts ofexogenously administered cortisol inhibits the release of ;C,H and thus endogenous cortisol release. ;s a result' theadrenal cortex atrophies. %o' if exogenous cortisol is abruptly discontinued' adrenal insufficiently results due to theinability of the atrophied adrenal cortex to respond adequately. ,o prevent this' cortisol must be +ithdra+n gradually

before stopping its administration altogether to allo+ normal adrenal function to return.

;drenocortical excess or Cushing5s syndrome is a functional disorder characteriPed by over secretion of adrenal cortexhormones' primarily glucocorticoids (cortisol) and to some degree adrenal androgens. Cushing5s syndrome is a relativelyrare condition. 8t occurs mainly in +omen' and the average age of onset is 7>B years ho+ever' it can be seen up to ageK years. !,<3 @ost adrenal disorders have a gradual onset and slo+*insidious progression.

<,8!!?,he causes of Cushing5s syndrome may be divided into three ma4or groups3

1. Primary CushingBs syndrome3 +ithin the gland itself' excessive cortisol production from adrenaltumors (benign or malignant' unilateral or bilateral)

7. Secondary CushingBs syndrome3 excessive cortisol production resulting from3a. <xcessive pituitary secretion of ;C,H because pituitary or hypothalamic problems'

e.g. pituitary tumor or b. <xcessive secretion of ;C,H from non>pituitary sites' e.g. bronchogenic carcinoma

(ectopic secretion of ;C,H by a tumor in the lung).:. atrogenic CushingBs syndrome3 excessive cortisol levels from prolonged administration of glucocorticoids.

8atrogenic Cushing5s syndrome is the most frequently seen syndrome in clinical practice.

@;;<@<, !F CA%H85% %?9#!@<@easures may include one or more of the follo+ing3

1. Anilateral or bilateral adrenalectomy (adrenal tumors) RR@ust /no+ procedure' pre> J post>op care7. 0ituitary surgery or radiation:. %urgery to remove ectopic source of ;C,H (ectopic ;C,H>producing tumors)B. 9rug therapy to suppress or bloc/ synthesis of cortisol (inoperable adrenal tumor or ;C,H>producing tumors

5. 8atrogenic Cushing5s syndrome3 reduce or terminate chronic therapy. 2hen corrective treatment is notfeasibly' measures include those that control the side effects of glucocorticoid therapy.

7/21/2019 Med_Surge_1-1


addisons.doc' 0age 1 of 7

0H;#@;C!!8C; @;;<@<, !F ;998%!5% 98%<;%<0rimary adrenal insufficiency. ;ddison5s disease requires lifelong replacement therapy +ith a glucocorticoid Ehydrocortisone' prednisone' cortisone' and a mineralocorticoid' i.e. Florinef.

lucocorticoid dosage schedules are designed to mimic the normal diurnal pattern of cortisol productionEhigher levels in the early morning and lo+er in the afternoon. %o 7*: of the glucocorticoid dose should be ta/enin the morning upon rising (L a.m.)' and 1*: in the afternoon (B>K p.m.). ,his N side effects associated +ithsteroid replacement therapy and prevents insomnia (because glucocorticoids stimulate the C%).

When any illness or stress occurs, e&g& flu infection, eertion, surgery, etc& glucocorticoid dosage must %e

increased to pre/ent adrenal (ddisonian crisis& ;t times of stress' patients +ill need to Q their glucocorticoid

dosage failure to do so can be fatal.

Healthy adrenals Q secretion of glucocorticoids in response to stress. For patients +ith adrenal insufficiency'glucocorticoids must be provided through supplemental dosing. 0atients should have an emergency /it +iththem at all times to ensure availability of glucocorticoids in emergencies.

=its should consist of in4ectable 8@ preparation (1mg) of hydrocortisone plus an oral agent. 0atients' family'%!s should be instructed on proper technique of administering in4ectable hormones. ,he patient should +earsome form of identification' e.g. @edic ;lert bracelet.

8nform emergency health care personnel of patient5s glucocorticoids requirements. %upplementalmineralocorticoid – hydrocortisone' Florinef – to maintain electrolyte balance is given one daily or :x +ee/.

;d4ustments in mineralocorticoid dosage may be necessary in extra +arm +eather +hen loss of sodiumincreases because of excessive perspiration. Q salt and fluid inta/e during hot*humid +eather' and if fever'vomiting' or diarrhea occur. !vertreatment can result in edema' +eight gain' and H, due to excessive sodiumand +ater retention and muscle +ea/ness and dysrhythmias due to excessive potassium excretion(hypo/alemia). @onitor aD and = D closely.

;998%!8; C#8%8% !# ;CA,< ;9#<; C#8%8%0atients +ith adrenocortical insufficiency are at ris/ for ;ddisonian crisis' +hich is a life>threatening

emergency caused by insufficient adrenocortical hormones or a sudden' mar/ed decrease in these hormones. 8tmay occur due to3

1. %tress' e.g. from infection' surgery' trauma' psychological distress – remem%er glucocorticoid

dosage must %e increased at times of stress.7. %udden +ithdra+al of adrenocortical hormone replacement therapy – steroid therapy must %e

withdrawn gradually.:. ;drenal surgery.

@anifestation of cortisol and aldosterone deficiencies include3 hypotensionI confusion (maor sign) pro!ound %eakness nausea vomiting fever hyponatremia hypoglycemia hyperkalemia shock&

8eft untreated hypotension %ill progress to circulatory7vascular collapse hypovolemic shock and death&Classic signs and symptoms of shock6 rapid' +ea/ pulse tachycardia rapid respirations lo+ 60 pallor*cyanosis N urine output restlessness' apprehension' confusion.

@;;<@<, !F ;998%!8; C#8%8%0atients experiencing acute adrenal insufficiency require rapid replacement of glucocorticoids' fluids' sodium'and glucose. ,hese goals are accomplished by administering hydrocortisone' 1>:mg as an 8& bolus' andthen 1mg 8& qLh' and 8& infusion of % +ith Y dextrose (to restore sodium and glucose and return 60 tonormal). 8f 60 does not return to normal' then vasopressors.

,reatment is also directed to+ard combating shoc/3• @aintain patent air+ay• ;dminister !7 as ordered• #estore circulation +ith 8& fluids

7/21/2019 Med_Surge_1-1


• 0lace patient in shoc/ positionEsupine +ith legs elevated' trun/ horiPontal' head slightly elevated.• @onitor &%' urinary output' etc.• &asopressors if hypotension persists.

@anagement priorities in ;drenal Crisis31. #eplacement of glucocorticoids7. #estoration of fluid volume and electrolyte balance:. administration of glucoseB. administration of vasopressors. ,reatment of cause andK. ;voiding additional stressors +ith support to patient and family.

0atients usually respond by second day and can start oral corticosteroid replacement (dosage N over several daysas maintenance levels are reached). !ral inta/e' e.g. salted broth' ta/en as soon as tolerated by patient. 8& fluidsN gradually as oral fluids are accepted.

9uring the acute crisis' a quiet' non>stressful environment maintained. ;ll ;9s for the patient are carried out by others. ;ttempts are made to detect presence of stressors' e.g. infection that may have triggered crisis in thefirst place.

Documents

Med_Surge_1-1