cardiac combined powerpoint

7/25/2019 Cardiac Combined Powerpoint

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HCA Critical Care College

Disorders of the Cardiovascular System Fall 14


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Assessment

Current or chief complaint Past medical history

Diagnostic Studies

Vital signs

Cardiovascular inspection/auscultation

Murmurs, Extra heart sounds

Palpation of extremities Skin turgor, edema, pulses


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Chest Pain Assessment

P!S" Pneumonic#P$ Precipitators %hat &ere you doing &hen it started Does it go any&here

$ uality %hat does it feel like' !ate on scale of ()*(

!$ !egion/!adiation Point to &here else it hurts'


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Chest Pain Assessment

S$ Signs/Symptoms +ave you had any other signs or symptoms'

"$ "ime/"reatment %hen did it start' Does it come and go'

s it &orse &hen you take a deep -reath'

+o& long does it last'

%hat makes it &orse or -etter'


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CP Assessment

Chief complaints

f patient has prior history of chest

pain or cardiac disease, assume it iscardiac pain until proven other&ise

.ssess for shortness of -reath S012,

dyspnea on exertion, and dyspnea&hen lying or sitting.ssess for history of C+3


7/162HCA Critical Care College

Assessment

Syncope Period of unconsciousnessDue to decreased perfusion to head

Determine Cardiac vs4 5eurologic

Palpitations

.&areness of 67uttering or racing8 heartDetermine if precipitated -y

stress/anxiety



Assessment

Edema

Determine degree and ho&

long present Cardiac related ascends from

feet and ankles up&ard to&ardheart

May -e dependent edema

seen in sacrum, posterior legs,a-domen &hen lying in -ed

9VD

!ecent &eight gain



Assessment

+eart SoundsS*)S:are normal, lu-)du-

S;and S



Assessment

Cardiac 0utput 1lood pressure Peripheral pulse =uality +eart rate

>rine output

?ung Sounds# Coarse -reath sounds Pulmonary edema



Assessment

@eneral .ppearance Color of skin, lips, nail -eds Mucous mem-ranes 0-vious shortness of -reath

?evel of consciousness

Peripheral Pulses !ate, rhythm, strength *A to



Normal Lab Values

Serum Chemistries# Sodium *;)*



Lab Studies

EnJymes#"otal CK Creatine Kinase2)*I( u/l for males

;()*; u/l for females CKM1 (L of total CK ?D+ F():(( >/?

Muscle Proteins#"roponin *4 ng/ml



Lab Studies

?ipid ProBle#

Cholesterol *():(( mg/dl"riglycerides



Lab Studies

+ematology#

+ematocrit#



Lab Studies

Clotting ProBle# Prothrom-in time P"/5!2 *:)* sec/:4("herapeutic levels for

.)B- *4):4 DV"/PE :4();4(

Prosthetic valves :4);4

.ctivated Partial "hrom-oplastin "ime P""2 :);H sec4

"herapeutic is *4):4 times normal

Platelets *(,((()



Cardiac Angiography



PTCA

Percutaneous "ransluminal Coronary.ngioplasty P"C.2

"he physician inserts a -alloon)tipped

catheter through the femoral artery up to theheart4 0nce the -alloon)tipped catheter is atthe site of the -lockage, the -alloon at the tipof the catheter is in7ated, pushing the pla=ue

in the artery -ack against the &all of theartery4



Cardiac Stent

3irst performed in the mid)*FH(s and Brstapproved -y the 3D. in the mid *FF(s

. stent a small, expanda-le &ire mesh tu-e2 isinserted into a diseased artery to hold it open

Drug eluding stents are coated &ith a drug thatdramatically reduces any re-lockage of the stent-y inhi-iting scar tissue formation &ithin the stent

Currently, stenting is performed most often inconunction &ith other catheter)-ased procedures,such as P"C. and atherectomy


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Coronary Atherectomy

.therectomy is performed &ith a catheter thathas a -lade)like device on the end

"he coronary atherectomyactually cuts a&ay

or Nde-ulksN some of that pla=ue

. physician is more likely to chooseatherectomy over angioplasty/stenting &hen

the pla=ue is very hard due to calciBcation2or presents other challenges4


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Intervention


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Coronary Re-Stenosis

"o prevent restenosis, one of the follo&ingantiplatelet medications may -e administered priorto or during intervention and continue for up to *:hours after#

ntegrelin !eopro .ggrastat .ngiomax

Post)stent or P"C., patients usually take PlavixImg po =d for several months or for life to assist&ith antiplatelet activity and decrease risk of re)

stenosis


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Post-Intervention Care

EC@# for signs of a-rupt re)occlusion Pedal Pulses

1leeding at groin site/+ematoma formation

Coronary dissection

Postural or vasovagal syncope during sheathremoval2

Pseudoaneurysm formation auscultate sitefor a -ruit2

!etroperitoneal -leed


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Femoral Sheath Removal

0rders for type of removal# 3emostopManualVascular closure devices i4e4 Perclose,

Vasoseal, .ngioseal, Starclose2

0n hand items to include 7uids andatropine


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Femoral Sheath Removal

Consider pre)med &ith pain medicine prior tosheath removal Morphine systemically or?idocaine locally at the site2

P.!#

P $ Pressure

. $ .pplication of Pressure

! $ !elease slo&2 of Pressure


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Module II: Care of the Post-op

CABG PatientCare of the Post-op CABG and Valve Replacement

Patient


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CABG Care

Concerns in the early post)operative period# +emodynamics

1leeding +eart rhythm

>rine 0utput

?a-s !espiratory status

ncisions


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CABG Care

!ecord/Monitor +ourly# .rterial 1P, +!, !! = * min4

till patient is extu-ated2

P.P, CVP, EDV, !E3 C0/C

SV!

Sa0:

, SV0:

/0# >rine, C", 9P


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Hemodynamic Monitoring

!eport C :, S1P F(

"reat 1P O*( mm+g

Maintain volume status#

CVP/PC%P *()*: EDV *G(

>0 O ;(ml/hr

9P/C" *(():(( ml/hr


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Hemodynamic Monitoring

!eport EK@ Changes#

PVCQs

P.CQs

.3i- 1radycardia


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Post-op Monitoring

Maintain Sa0:OF()F:L

Monitor C0: Maintain KAO


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Post-op Monitoring

Monitor incisions# !adial artery grafts

Sternotomy Vein grafts

Chest "u-es

Dressing Changes

Pain Control


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Post-Op Pulmonary Management

.ccurate R fre=uent physical assessment

.rterial -lood gas analysis

Continuous pulse oximetry

Pulmonary care including suctioning &hile pt4

is intu-ated, coughing R incentive spirometryafter extu-ation2

Early mo-iliJation

Control of pain and shivering


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Post-Op Pulmonary Management

Chest )ray to determine placement of E"",thermodilution catheter, and nasogastric tu-e,as &ell as information a-out the &idth of themediastinum, amount of atelectasis, presenceof hemothorax or pneumothorax, and siJe of

the heart4 .ssess patient for readiness for extu-ation Considered if pt4 is arousa-le, a-le to follo&

commands, hemodynamically sta-le, and

initiating spontaneous ventilations &ithoutexcessive respiratory eTort


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Extubation Weaning Parameters
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Post-Op Management of Hemodynamics

CuT 1P is taken to provide correlation of 1Pfrom arterial line

Monitor the interrelationship -et&een# +eart rhythm and rate Preload .fterload Contractility Myocardial compliance

Monitor volume &ithin the system# !.P, P.%P


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f 1P is too lo"here is either too little volume

preload2

0! the SV! is too lo& patientQs -loodvessels are dilated2 Volume is generally replaced &ith a

colloid such as .l-umin or +etastarch,

unless hematocrit is lo&, then volumemay -e replaced &ith P!1C


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f 1P and C0 are lo&, -ut the PC%P is high# Patient may -e experiencing decreased

contractility and inotropic support may -einstituted &ith an agent such as Dopamine orDo-utamine

f the 1P is lo& R the C0 is ade=uate orelevated# "he SV! may -e lo& R the patient may need a

constrictive agent, such as Phenylephrine


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?o& 1P can also -e temporarily increased -yturning oT PEEP to decrease intrathoracic pressureand augment preload2 nad -y position changes4

"he patient should -e put in the supine position&ith legs elevated to allo& the 1P to increase until

the cause of the lo& 1P can -e determined andcorrective measures are taken4

"rendelen-erg position not universally utiliJed2 canalso oTer symptomatic relief, -y shifting volume

from the legs to the chest R increasing preload4 Provide only temporary improvement in clinical picture


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f 1P -ecomes too high, esp4 in the early postop period, surgical anastomoses may -edisrupted Can cause signiBcant intrathoracic -leeding,

hemodynamic insta-ility, poor tisse perfusion, andnecessitate return to the operating room

!5 needs to =uickly intervene for high 1P perinstitution protocol or MD orders

5itroprusside vasodilator2 is often administered to

lo&er 1P to the ordered parameter


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5itroglycerine a nitrate2 is given to cause

vasodilation and lo&er 1P

"hese medications need to -e started slo&ly, sopatient response can -e evaluated4

Patients must -e monitored closely as the 1P may

drop as the patientQs -ody temperature increases4


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Rewarmpatientafter surgery ifhypothermia persists >se of &arm -lankets

%arm, humidiBedoxygen

Convective airmattresses

0ther individual

institutionalapproaches

Negativeefectsofhypothermia# Depression of the

myocardium

Ventriculardysrhythmias

Vasoconstriction

Depression of clotting

factors increasing therisk of -leeding postoperatively2


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Carefully monitor the P.Ps R the C0, as &ellas 1P &hen interventions are instituted toassess the eTect4

5eed to maintain eTective C0 after C.1@ to

provide ade=uate tissue perfusion 5eed to regularly perform neurovascular

assessments of the lo&er extremities toprovide information a-out the eTectiveness of

the C0


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Continuously monitor the cardiac rate andrhythm Ventricular dysrhythmias are common in the early

post op period and SV" are more likely :< hours to

days post operatively4

ncidence of . 3i- is from *( to GL depending on

patientQs history


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3actors in post op dysrhythmias# +ypothermia nhaled anesthetics Electrolyte distur-ances hypo)/hypercalcemia,

hypomagnesemia, hypokalemia2

Meta-olic distur-ances .cidosis2 Manual manipulation of the heart Myocardial ischemia ncrease in catecholamine levels due to pain,

anxiety, inade=uate sedation


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Management of dysrhythmias#"reat patient, not the monitor

Consider eTectiveness of 1P R C0 &henevaluating dysrhythmias

Cardiac surgeons place epicardial &ires on theatrium and/or ventricles during surgery

"emporary pacing can -e instituted to overrideslo&, rhythmic rhythm to maintain 1P and C

.tropine may -e given to increase the +! in thea-sence of epicardial pacing &ires

"achydysrhythmias can -e controlledpharmacologically depending on physicianQs ordersand hospital protocols


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Post-Op Management of Bleeding

Monitor patient for signs of -leeding from thechest tu-es and surgical sites, as &ell as clinicalsigns of hypovolemia related to -lood loss

++ should -e monitored at regular intervalsduring post op period according to hospitalprotocol

5urse must -e cogniJant of the potential forcardiactamponade, -lood could accumulatein the pericardiumSigns# ?ack of C" drainage, decreased 1P,

narro&ed pulse pressure, and muUed heartsounds


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Post-Op Management of Bleeding

f -leeding is an issue# Protamine sulfate may -e given to reverse the

eTects of heparin

0r antiB-rinolytic agents DD.VP2 may -e ordered

1lood products such as 33P and platelets may also-e ordered


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Post-Op Neurologic Management

Pupils should -e assessed initially 5ormal siJe R reactivity may not return until agents

utiliJed intraoperatively have -een meta-oliJed4

0ver the *stfe& hours, the results of neuroassessments should improve gradually

1y the time patient is ready for extu-ation, pt4should follo& commands R have e=ual movementand strength of the extremities

5euro status cannot -e completely assessed until

patient is fully a&ake R extu-ated Continue neurologic assessments on a regular

-asis


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Post-Op Renal Management

Monitor urinary output, at least, hourly

.ssess urine for color R characteristics, as&ell as amount

Potassium level should -e monitored every 5 and Creatinine


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Post-Op GI Management

Monitor the patient for -o&el sounds,a-dominal distention, and nausea andvomiting

ntu-ated patient &ill have nasogastric tu-e tolo& intermittent suction

Placement R patency should -e assessed, as&ell as amout, color, and characteristics of thedrainage4

.ntiemetic agents should -e administered for

nausea


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Post-Op Pain Management

3actors contri-uting to pain Median sternotomy incision, leg incisions

Manipulattion of chest cavity

>se of retractors during surgery

Electrocautery Positioning in the operating room ta-le

?ength of time of the surgery


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Poorly controlled pain can stimulate thesympathetic nervous system R lead to CVconse=uences

"he +! and 1P can increase and the -loodvessels can constrict Causes increase in cardiac &orkload and

myocardial oxygen demand

5urses must individualiJe pain assessmentand control for each patient as responses vary

among individuals


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0pioid analgesics, positioning, mo-iliJation,distraction, and relaxation techni=ues areamong some methods of pain control4

Ketoralac is an nonsteroidal anti)in7ammatoryagent, can -e administered V in the early postop period 5eed to monitor renal status of patients taking

Ketoralac Discontinued if creatinine level is elevated

"each client to splint incision &hen coughing Rmoving improves pain control


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Treatment Hemodynamic Changes
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Beta Blockers

Decreases myocardial &orkloadand myocardial oxygen demand-y decreasing +! and contractility

!hotral, Sectral

"enormin

e-eta, Monocor

1revi-loc ?opressor also -eta): at high doses2


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Ace Inhibitors

%ork -y suppressing the renin)angiotensin)aldosterone system, &hich results in 7uid lossand 1P

May get C0

%hen .CE inhi-itors are started, it may take&eeks to achieve optimal results

.CE inhi-itors &ork &ell &ith diuretics to 1Pand may &ork &ell for some heart failure

patients


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Renin-Angiotensin-

Aldosterone System


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So what happens

if you suppress the action

of the angiotensin- converting

enzyme?

You prevent the production

of angiotensin II which then

blocks the production of

Aldosterone and therefore

decreases the preload and

the afterload important inpatients with !"#$


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Ace Inhibitors

Examples# ?otensin

Capoten

Vasotec

Monopril

Prinivil

estril .ccupril

.ltace


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Calcium Channel Blockers

Calcium Channel 1lockers inhi-it thein7ux of CaAAthrough the cellmem-rane resulting in depression ofautomaticity and muscle contraction

ndications#

+ypertension

.ngina from vasospasm Dysrhythmias


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Angiotensin Receptor Blocker (ARB)

.ct -y -locking the angiotensinreceptor, &hich controls thephysiologic eTects of angiotensin on-lood pressure

ndications#

+ypertension+eart 3ailure


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So what happens if you

suppress angiotensin II?

Aldosterone production

is reduced andtherefore preload and

afterload are reduced.


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ARBs

Examples of .!1Qs#.tacand.vapro

1enicarCoJaarDiovan

Micardis"eveten


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Anticoagulants

+eparin or ?o& Molecular %eight +eparin?M%+2

Coumadin 3or patients &ith high risk for systemic em-oli

?arge anterior M .trial B-rillation

?V throm-us

Valve replacement

>se &ith B-rinolytics P"C. or C.1@ surgery


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Thrombolytics

ndications# S" segment elevation O* mm in t&o related leads

Chest Pain &ith ne& onset, ?111

Clinical suspicion of acute M even if chest pain is

a-sent .M Core Measures recommends throm-olytics -e

given &ithin ;( min of arrival to hospital4

t)P., .ctivase, !etivase Plasminogen activator causes transient, systemic

B-rinogen depletion

%eight -ased dosing see Policy and standingorders2) administered in the E!


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Contraindications for Thrombolytics

Hemorrhagic stroke

Intracranial neoplasm

Active internal bleeding

Pregnancy

Suspected aortic dissection


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Complications from Thrombolytics

1leeding#Cere-ral

hemorrhage

@ -leedEpitaxis+ematuria

Puncture sitesDysrhythmias+ypotension


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Other Interventions

Electrophysiology Studies EPStudy2#

. procedure in &hich a thin tu-e catheter

is inserted into a vein or artery e4g4, in thegroin2 and guided to the heart, &here itcan perform speciBc, essentialmeasurements of the heartQs electricalactivity and path&ays

"hese measurements are particularlyhelpful in the diagnosis of the origin oftachycardias, or -radycardias


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Other Interventions

.-lation is a procedure in &hich a physician

destroys very small, carefully selected parts ofthe heart that are causing tachycardia

.llo&s the heart to -eat more slo&ly and

normally

>sually used for .)3i-, .)7utter, %P%, .", SV",unctional tachycardia, and ventricular

tachycardia


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Cardiovascular System: Mitral Valve Stenosis

The mitral valve is located between the left

atrium and left ventricle and is also referred toas the atrioventricular valve

Mitral valve stenosis is the obstruction of bloodflow from the left atrium into the left ventricle most often caused by Rheumatic Endocarditis


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Pathophysiology: Since the left atrium has difficulty moving blood into theleft ventricle, the blood backs up into the pulmonary veins,overloading the pulmonary circulation.

The right ventricle must contract against a very highpulmonary arterial pressure causing strain and eventualfailure of the right ventricle.


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Clinicalmanifestations

dyspnea fatigue

hemoptysis

cough

repeated respiratoryinfections

Diagnosticsweak, often irregular

pulse diastolic murmur

EKG

cardiac catheterization


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Medical Management antibiotic prophylaxis treat Congestive Heart Failure anticoagulants treat anemia surgical intervention

valvuloplasty mitral valve replacement

Nursing Care same as post-op needs as other patients experiencingcardiac surgery


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Cardiovascular System:Mitral Valve Prolapse

Definition mitral valve prolapse is deformity that usually has no signsand symptoms

although rare, it can progress and lead to sudden death

occurs more frequently in women


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Pathophysiology:

a portion of the mitral valve leaflet balloons back intothe atrium during systole

occasionally the valve does not stay closed duringsystole, blood then backs into the left atrium from the

left ventricle


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ClinicalManifestations

many are asymptomatic others will have:dyspnea, fatigue, light-headedness,palpitations, dizziness,

syncope, chest pain andanxiety

Diagnostics Mitral click

murmur of mitral valveregurgitation

Rarely patient will havesigns and symptoms ofheart failure


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Medical Management

eliminate caffeine, avoid alcohol, smoking, oxygen,antiarrhythmic medications, diuretics, Angiotensin-Converting Enzyme Inhibitors, Angiotensin II ReceptorBlockers, Hydralazine and Isosorbide Dinitrate, BetaBlockers and Calcium Channel Blockers

Surgical intervention: mitral valve repair orreplacement


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Nursing Management Education

diagnosis, hereditary condition

prophylactic antibiotics

dietary and lifestyle changes


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Cardiovascular System:Rheumatic Endocarditis

Rheumatic Endocarditis is a potential sequel

seen in patients who have had Rheumatic Fever.Rheumatic Fever occurs most often in children

who have had a case of group A beta hemolyticstreptococcal pharyngitis (strep throat). With

prompt treatment with antibiotics the numbersof people afflicted with Rheumatic Fever hasdeclined in the United States.


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PathophysiologyThe damage to the heart is not directly related to thestreptococci but to the leukocytes that accumulate inthe tissue which leads to the formation of scar tissue.

Initially tiny translucent growths are seen on the valveflaps. Over time the valve leaflets thicken, preventing

them from closing completely


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Pathophysiologycont.The myocardium can compensate for quite a while, buteventually the condition will lead to heart failure

It is the mitral valve that is most often affected

The severity of symptoms is directly related to the locationand size of the lesion


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Assessment murmur, shortness of breath, crackles and wheezes to lungfields

there may also be emboli phenomena to the lung, kidney,heart, spleen or brain

* the key is prevention


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Medical Management eradicate the cause

antibiotic therapy risk for embolitic event

Nursing Management teaching: medications,

symptom monitoring &management

lifestyle changes:

diet

activity

CPR

birth control (female)


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Cardiovascular System:Infective Endocarditis

Definition

Infection of the valves and endothelial surface of theheart, especially seen in people with valve disorders more common in the elderly

high incidence among IV drug users

others at risk

invasive procedures can cause a bacteremia which leads toInfective Endocarditis


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Pathophysiology

caused by direct invasion of the endocardium by amicrobe, fungi or rickettsiae

leads to deformity of the valve leaflets, can also affectother structures, such as: chordae tendineae


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Assessment malaise anorexiaweight loss cough feverjoint pain

Oslers nodes Roths spots petechiae murmurs emboli

Diagnostics microorganism isidentified in 2 separateblood cultures

echocardiogram revealsa moving mass on the

heart valves orsupporting structures


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Medical Management

prevention antibiotic therapy

complications heart failure, cerebral vascular, other organ complicationsrelated to septic or non septic emboli

treatment Long-term antibiotics

surgical management: to replace severely damaged valves


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Nursing Management

monitor the patients temperature assess for new murmurs

assess for signs and symptoms of organ damage

education: antibiotics for treatment & prophylactic

emotional

post-op care if indicated

M ocarditis


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Myocarditis

Etiology#n7ammation of myocardiumas a response to invading organisms,chemicals or drugs

Causes# Viral, -acterial, fungal,protoJoal, autoimmune, toxins

ETects# Decreased contractility,decreased cardiac output, anddecreased ?V function leading to failure

C d l S


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Cardiovascular System:Pericarditis

Definition: an inflammation of the pericardium, the membranoussac enveloping the heart

may be a primary illness, or develop during the courseof another medical or surgical disorder

it may be classified by what accumulates in the sac:

blood, purulent drainage, clotting proteins

Pericarditis


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Pericarditis

6n7ammation of the pericardium8

Chronic vs4 .cute

Pericardial ETusion Cardiac "amponade

Constrictive Chronic scarring

StiT pericardium


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Pathophysiology

there are many underlying causes associated withpericarditis

leads to a buildup of fluid in the pericardium which cancause cardiac tamponade

can lead to thickening & decreased elasticity preventing

the heart to fill properly can become calcified further restricting ventricularexpansion during diastole

leads to decreased cardiac output, heart failure andhepatic failure

C di l S t d


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Pericarditis


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Pericarditis

Patient presents &ith chest pressure and

shortness of -reath that is &orse &hen lyingdo&n

Symptoms are some&hat relieved &hensitting upright and for&ard

>sually follo&s a -acterial or viral infection oracute M : &eeks later

*: ?ead EK@ follo&s no consistent ischemia

pattern Commonly have S" elevation in multiple leads

C di l S t P i diti


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Assessment pericardial rub

chest pain

fever

Diagnostics echocardiogram

CXR

12 lead ECG: STchanges

WBC

ESR

C di l S t P i diti


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Medical Management

determine cause administer therapy:

NSAIDs, corticosteroids, Colchicine

Pericardiocentesis

Pericardectomy

Pericarditis


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Pericarditis

"reatment# 5S.Ds Steroids Pericardial Drain

Potential Complications Development of pericardial eTusion +emodynamic insta-ility

CardiovascularSystem:P i diti


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Nursing Management monitor for cardiac tamponade

pain management activity restriction

emotional support

monitor for heart failure

Endocarditis


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Endocarditis

6.cute or chronic infection of theendocardium, including valves, chordaetendinae, and septum48

>sually -acterial

3orms vegetations that destroy valve tissue,mainly tricuspid and pulmonic

0rganisms lead to -acteremia/sepsis

Can lead to cardiac failure

Endocarditis


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Endocarditis

"reatment#@enerally long term V anti-iotics Possi-le need to remove infected

valve and replace &ith ne& valveafter infection under control

Potential complications#Migration of vegetation to -rain or

other parts of -ody0ver&helming sepsis

Cardiomyopathy


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Cardiomyopathy

6Chronic or su-acute disorder ofthe heart muscle8

Dilated+ypertrophic!estrictive

Dilated


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Hypertrophic

Restrictive

DilatedCardiomyopathy


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Dilated Cardiomyopathy

Dilated Ventricle &ithout +ypertrophy

Etiology# viral, idiopathic, alcoholism

Clinical 3indings#

!ight and left heart failure Ventricular arrhythmias

Murmur

End-stage dilated Cardiomyopathy is the #1indication for heart transplant.



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Chamber Enlargement

Impaired Systolic and

Diastolic Dysfunction

Heart ailure

Refractory to

!reatment

Death



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"reatment#

3luid !estriction

.CE nhi-itors1eta)-lockersDiuretics

.ntidysrhythmics

CD

HypertropicCardiomyopathy


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Hypertropic Cardiomyopathy

SigniBcant increase in myocardialmass &ith decreased cham-er siJe

Diastolic dysfunction results

May -e related to genetics

Clinical Bndings#

Malignant ventricular dysrhythmias

Systemic em-oliJation and stroke

RestrictiveCardiomyopathy


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Restrictive Cardiomyopathy

?east common formDecreased cham-er siJe, rigid

ventricle, and right and left sidefailure, decreased cardiac output

Etiology#

!adiation

Sarcoidosis diopathic

Cardiomyopathy


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Cardiomyopathy

Shock


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Shock

.n acute, &idespread process ofimpaired tissue perfusion resulting incellular, meta-olic and hemodynamicderangements

+ypovolemic# 0ccurs from inade=uate 7uidvolume in intravascular space

Cardiogenic# !esult of failure of heart to pump

-lood for&ard eTectively Septic# 0ver&helming infection of usually

-acterial origin

CardiovascularSystem:CardiogenicShock


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Cardiovascular System:Cardiogenic Shock

Definition:

Occurs when the heart cant pump enough blood tosupply the amount of oxygen needed by the tissues

Occurs when: >40% of the myocardium is necrotic, dueto a ruptured ventricle, valve dysfunction, trauma to

the myocardium, end stage of heart failure, pulmonaryemboli, cardiac tamponade, cardiomyopathy anddysrhythmias



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Pathophysiology

cardiogenic shock is circular in nature. The degree ofshock is related to the amount of left ventriculardysfunction

damage to the myocardium results in a decreased CO2

which reduces arterial B/P and tissue perfusion to vitalorgans



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Pathophysiologycont..

As the flow to the coronary arteries is decreased, thereis less O2 to the myocardium increasing ischemia andreducing the hearts ability to pump

inadequate emptying of ventricles causes pulmonary

edema, making the hypoxia and tissue perfusion evenworse



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Assessment: tissue hypo-perfusion low B/P rapid, weak pulse cold, clammy skin respiratory crackles decreased urinaryoutput

hypoactive bowelsounds

respiratory alkalosis

Diagnostics pulmonary arterycatheter to measure leftventricular pressureand cardiac output

continued centralvenous oximetry

blood lactic acid levels



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Medical Management correct underlying problem restore tissue perfusion prevent further damage pharmacologic therapy:vasopressors, diuretics,vasodilators, positive inotropic medications

other treatments: intra aorticballoonpump {IABP}-decreases the workload of the heart by inflating duringdiastole and deflating just before systole


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y g

Nursing ManagementAssessment

cardiac rhythm hemodynamic parameters: tissue perfusion

intake & output

reduce anxiety of patient & family

safety due to confusion, anxiety


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Cardiovascular:Cardiac Tamponade

Definition

An increase in the intra-pericardial pressure due to: fluid accumulation in the pericardial sac

direct or metastatic tumor invasion in the pericardial sac, or

fibrosis of the sac due to radiation therapy

Pericardial Tamponade


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p



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p

Risk Factors: Primary tumors of the heart

Metastatic tumors to the pericardium: Lung Breast Gastro-intestinal Leukemia

Hodgkins & Non-Hodgkins Lymphomas Sarcoma Melanoma

other


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Risk Factorscont

Patients who have received > 4000 cGy to a field whichincludes the heart

Patients with Acquired Immunodeficiency Syndrome(AIDS) related Karposis Sarcoma

Drug related


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Pathophysiology

As the intra-pericardial pressure increases: left ventricular filling decreases

the ability of the heart to pump decreases

cardiac output decreases

impaired systemic perfusion occurs


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Clinical Manifestations:

Small effusions do not usually cause any symptoms Large effusions especially with rapid accumulation offluid causes:epigastric or retro-sternal chest pain which isoften relieved when sitting or leaning forward

dysphagia, cough, dyspnea, hoarseness, increased JVD,muffled heart sounds, pericardial friction rub, tachycardia,

and pulsus paradoxus complications

Pericardial Tamponade


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Cardiac tamponade usually occurs &ithin the

Brst *: hours post)op -ut may occur up to ;&eeks post)op

Signs/Symptoms# 3ever

Pericardial friction ru- ?ethargy

0liguria

Epigastric or sternal pain

Pulsus Paradoxus Decreased chest tu-e output

Chest pain

Cardiac Tamponade


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+emodynamic mplications#

Early# 5ormal C0, +!, normal to lo& 1P Middle to ?ate#

C0, 1P, 9VD, +!, CVP/PC%P, >0

Diastolic pressure, 5arro&ed pulse pressure, pulsusparadoxus, &idened mediastinum

?ate# Shock, PE., death

Cardiac Tamponade


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Diagnostic 3indings C!# %idened mediastinum

Pulsus Paradoxus

3lattening of arterial &aveform -yO*(mm+g pressure on expiration

Pericardial 3riction !u-

Widened Mediastinum


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Medical Management: Diagnostics:

CXR, EKG, Echocardiogram, CT, MRI

Treatment: Symptom management

pericardiocentesis

sclerosing radiation Therapy

chemotherapy

corticosteroids

Cardiac Tamponade


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"reatment 3luid Challenge for lo& 1P or lo&

C0

notropic medications

!e)exploration of mediastinum


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Nursing Management

Supportive Strategies: emotional support

O2

repositioning to promote circulation

assist with activities

administer medications as prescribed


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Cardiovascular:Hypokalemia


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Potassium below 3.5 mEq/L

common electrolyte imbalance Related to: deficit in potassium stores

metabolic alkalosis

loss of intestinal contents prolonged intestinal suctioning

recent illeostomy

villous adenoma



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Causes of Hypokalemiacont

Hyperaldosteronism potassium wasting diuretics

medications: corticosteriods

PCN, Carbenicillin, Amphotericin B

patients with long term insulinsecretion

magnesium depletion



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ClinicalManifestations fatigue, muscleweakness, leg cramps,constipation, anorexia,nausea, vomiting,numbness, tingling,dysrhythmias

Diagnostics EKG changes

flat T waves, inverted Twaves, depressed STsegment, elevated Uwave

24 hour urine

potassium excretion



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Medical Management Oral / IV potassium

replacement Monitor EKG

Nursing Management monitor for s/s in

patients at risk administer medicationsas directed

diet

Cardiovascular:Hyperkalemia


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Potassium level over 5.5 mEq/L seen in patients with poor renal function LeukocytosisThrombocytosis False Hyperkalemia Medications: Potassium, Heparin, Ace inhibitors,Captopril, NSAIDS, potassium sparing diuretics

Acidosis: K+ move out of cells into ECF: tumor lysis syndrome extensive injury or burns



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Clinical

Manifestations peaked, narrow T waves,ST segment depression,shortened QT interval,disappearance of P waves

cardiac arrest

muscle weakness,paralysis, GI disturbances

Diagnostics

EKG changesArterial blood gases

potassium levels

C di l


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MedicalManagement

restrict dietarypotassium

kayexelate

calcium gluconate

Insulin

Beta 2 Antagonists

Dialysis

D/C potassiumsparing diuretics

NursingManagement

observe for muscleweakness anddysrhythmias

accurate bloodsample

teach aboutfoods/salts withpotassium

Cardiovascular:Calcium8.5-10.5 mg/dL


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99% in the skeletal system; 1% in blood stream

Level is controlled mainly by the parathyroid hormonewhich releases calcium from bone Regulates: muscle contractions transmitting of nerve impulsesblood coagulation

absorbed from the GI tract in the presence of gastric acidand Vitamin D

excreted mainly in feces; some in urine

Cardiovascular:Hypocalcemia


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Calcium level below 8.5 mg/dL Causes:

Osteoporosis immobility Hypoparathyroidism Pancreatitis Renal failure Hyperphosphatemia Inadequate Vit. D absorption Magnesium deficiency Low serum albumin

C di l H l i


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Causescont alkalosis

alcohol abuse

Medications: aluminum containing antacids,caffeine, Aminoglycosides, Cisplatin, Corticosteroids,Mithramycin, loop diuretics, Phosphates andIsoniazid



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Clinical

Manifestations tetany pain due to spasms

Trosseaus sign

Chvosteks sign

Seizures

EKG changes

Diagnostics low albumin

(corrected serumcalcium)

other lab values: magnesium,

phosphorous, PTH


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Medical Management IV or p.o. calcium

Vit. D

dietary supplements

Nursing Management safety precautions:

seizures, airway,confusion

Teaching

risk for falls

dietary intake ofcalcium

medications:Fosamax, Evista,Calcitonin

Cardiovascular:Hypercalcemia


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Calcium level greater than 10.5 mg/dL

mortality 50 % if not treated Malignancies

Hyperparathyroidism

Immobility

Thiazide diuretics

Vit. A or D intoxication

Lithium

Alkaline antacids

Excessive milk intake



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ClinicalManifestations

muscle weakness incoordination

anorexia

constipation

paralytic ileus

confusion

cardiac standstill

Diagnostics calcium level

albumin EKG

PTH Levels

xrays

Sulkowitch urine test:

measures amount ofcalcium in urine



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Medical Management

decrease calcium: Chemotherapy

partialparathyroidectomy dialysis

medications: Lasix, IV fluids: NS, IV phosphate, Calcitonin, Aredia,Didronel, Mithramycin, Neutra-phos



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Nursing Management

monitor for s/s of Hypercalcemia push oral fluids with sodium

safety

teaching

Cardiovascular:Sodium135-145 mEq/L


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Mostly located in the extracellular fluid

controls water distribution throughout the body functions muscle contraction

transmission of nerve impulses

Cardiovascular:Hyponatremia


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Sodium less than 135 mEq/L

ratio of body sodium to body water can be related to fluid volume excess or deficit sodium can be loss via:

vomiting, diarrhea, fistulas, sweating diuretics deficiency of aldosterone

types of Hyponatremia SIADH: Dilutional Hyponatremia

Cardiovascular: HyponatremiaClinical Manifestations


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depends on cause/rate of occurrence

dry mucosa decreased saliva

poor skin turgor

low B/P

nausea abdominal cramping

confusion

muscle twitching to seizures

hemiparesis

papilledema

Cardiovascular: Hyponatremia


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Diagnostics

sodium levels urine sodium

urine specific gravity

Cardiovascular:Hyponatremia


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Medical Management

careful administrationof sodium( no > 12mEq/L every 24 hours

SIADH- Lasix is added

restrict fluid

Nursing Management

monitor patients at risk monitor for s/s ofhyponatremia

teach: dietary restrictions

medications safety

Cardiovascular:Hypernatremia


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Sodium level greater than 145 mEq/L gain of sodium in excess of water or loss of water in excess of sodium

fluid deprivation hypertonic enteral feedings Diabetes Insipidus heat stroke

excess of sodium bicarbonate or a hypertonic saline near drowning in sea water malfunction of hemodialysis or peritoneal dialysis



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ClinicalManifestations neurologic

delusions,disorientation

flushed skin

dry, swollen tongue

increased muscle tone pulmonary edemapostural hypotension

Diagnostics sodium level > 145

osmolarity level urineosmolarity

urine specific gravity



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Medical Management

gradually administer ahypotonic or isotonicnonsaline solution toavoid cerebral edema

Diuretics

Desmopressin Acetate(DDAVP): treat: Diabetes

Nursing Management

strict I&O teach

diet

medications

monitor for s/s of

Hypernatremia

cardiac combined powerpoint

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