heart and vessels

8/8/2019 heart and vessels

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CARDIOCARDIO

VASCULARVASCULARSYSTEMSYSTEM


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THE HEARTTHE HEART

Anatomy and PhysiologyAnatomy and Physiology

Theheart compose of three layers

Endocardium: the inner layer ofendothelial

tissue

Myocardium: the middle layer of the muscle

fiber responsible for pumping action

Epicardium: the outer layer

it is encased in a thin fibrous sac epicardium


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THE HEARTTHE HEART

Anatomy and PhysiologyAnatomy and Physiology

Pericardium consists of Veseral, parital

pericardium layers and space in between,

pericardium space is filled with 30 ml of

lubricating fluid


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Heart ChampersHeart Champers

Right heart consists of Rt atrium, Rt ventricle,

distribute deoxygenated blood

Left heart consists of Lt atrium, Lt ventricle ,

distribute oxygenated blood

Varying thickness of a trial and ventricular wall

and left and right ventricles related to work load


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Heart ChampersHeart ChampersHEART VALVES:

Atrioventricular, separate atria fromventricles

Semilunar valves ( threehalf-moon

leaflet


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Coronary ArteriesCoronary Arteries

Theheart has large metabolic requirement, 70-

80% of delivered oxygen

Coronary arteries are perfused during diastole

Left coronary artery branches ( LAD & LCX )

Right coronary artery branch ( RCA )

Posterior wall received blood by ( PDCA )


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CONDUCTING SYSTEMCONDUCTING SYSTEM

cardiac electrical cell is characterized by

Atomicity: ability to initiateelectricalimpulses

Exitability: ability to respond to impulses

Conductivity: ability to transmit impulses( SA AV bundle ofhis bundle branch )


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CONDUCTING SYSTEMCONDUCTING SYSTEMPhysiology of cardiac conduction

Electrical activity (ions move acrosscell membrane)

Polarization, Depolarization,

electromechanical coupling andrepolarization


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contcont

Cardiac homodynamic

Cardiac cycle ( flow of blood )Cardiac output ( ejection of blood )

= stroke volume x heart rate

Heart Rate: affected by central

nervous system and baroreceptors


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cont.cont.

STROKE VOLUME : the amount of blood

ejected by Lt ventricle in each beat which is 70 ml

determined by preload, after load and contractility

EJECTION FRACTION: 42% for right heart

and 50% for the left heart


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ASSESSMENTASSESSMENT

Theextent of assessment is determined by:

Purpose of nursing assessment

Severity of pts condition

Practice setting of the nurse


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ASSESSMENTASSESSMENT Healthhistory and clinical manifestations

Acute symptoms: current medication,

allergies, general appearance,

homodynamic status

Stable patients: completehistory, spouse

or partner, demographic information


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ASSESSMENTASSESSMENTCardiac symptoms: pt will have one of

the followingShortness of breath, dizziness,

syncope, loss of consciousness,

edema and weight gain, fatigue,palpitation and chest discomfort


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NURSING DIAGNOSISNURSING DIAGNOSIS

Decrease cardiac output related to structural

disorders

Activity intolerance related to decrease cardiacoutput orexcessive fluid volume

Anxiety related to change in health status and

change in role functionCOLLABRATIVE PROBLEMS

Congestiveheart failure, ventricular

dysrhythmias, and atrial dysrhythmias


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PLANNING AND GOALSPLANNING AND GOALS

Improve and maintain cardiac output

Increase activity toleranceReduction of anxiety

Absence of complications


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NURSING IMPLEMENTATIONNURSING IMPLEMENTATION

Encourage rest, leaning back in a chair

Oxygen through nasal prongs

Careful monitoring to correlate intervention

with patients response to adjust treatment plan

Decrease sodium diet intake

Change position frequently


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PHYSICAL ASSESSMENTPHYSICAL ASSESSMENT

Performed to confirm the data in healthhistoryIt should include the following

Effectiveness ofheart as a pump, filling

volume and pressure, cardiac output,compensatory mechanisms


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PHYSICAL ASSESSMENTPHYSICAL ASSESSMENT

General appearance

Level of consciousness, thought

process, heart ability to perfuse brain

tissue, distress and anxiety


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Pulse pressure:

Difference between systolic and diastolic, 30-40mmhg, reflects strock volume & ejection velocity,

vascular resistance,

Less than 30 mmhg = serious reduction in output


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PHYSICAL ASSESSMENTPHYSICAL ASSESSMENT Postural hypotension

Orthostatic hypotension, may indicates low

intravascular volume, inadequate vaso

constrictor mechanism or autonomic

insufficiency

Arterial pressure Rate, rhythm, quality, volume, configration (

contor)


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PHYSICAL ASSESSMENTPHYSICAL ASSESSMENT Jugular venous pressure

Reflects Rt heart function, provideestimation

of CVP, increase incase of HF decrease in FVD

Heart

Inspection, palpation, percussion , auscultation,

S1 S2


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PHYSICAL ASSESSMENT

Inspection of Extremities

Capillary refill time (CHF, hypertension ),

hematoma (surgery & cath ), vascular changes,peripheral edema, lowerextremeties ulcer

Lungs

Tachypnea ( HF, pain, anxiety ), chynestokesbreathing ( pulmonary edema ), dry cough, crackles

and whezes


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PHYSICAL ASSESSMENTPHYSICAL ASSESSMENT Abdomen

Hepatojugular reflux, bladder distention

RISK FACTORS

Nonmodifiable: age, positive family history,

race &gender

Modifiable: hyperglycemia, hyperlipidemia,hypertension, inactivity, smoking, obesity &

type A personality


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DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION

Laboratory tests

Cardiac enzymes

Released from injured cells when ruptured

the membrane

Most of them are not specific for one type

of cell

Iso enzymes are more specific, createninekinase ( CK ) and its iso enzyme( CK-MB ),

lactic dehydrogenase (LDH) , troponin I


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DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION Blood chemistry

Lipid profile

A- cholesterol (less than 200 mg / dl ),required forhormonal synthesis, found

mainly in brain tissue and liver

B- triglycerides ( 40 150 mg / dl )

source ofenergy, cell wall, store in adipose tissue


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DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION C- LDL ( less than 130 mg / dl ) transportcholesterol from blood to peripheral

tissues, synthesized from VLDL

D- HDL ( 35 65 mg / dl M, 35 85 mg/ dl F ) transport cholesterol from

peripheral tissues to the liver, cardio

protectiveeffect, increase withexercise

and decrease with smoking DM and

obesity


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Serum electrolytes

K, Na, Ca and otherelectrolytes can reflect theheart

function as well as fluid & electrolyte disturbances

BUN

May indicates impaired renal function and impaired

cardiac output


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DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION Coagulation studies

Partial ThromboplastineTime ( PTT ) 25 40 sec, used

to regulateheparin dosage, 1.5 2.5 is the theraputicrange

Prothrombin Time ( PT ) less than 13 sec, used to

regulate warfarin, 1.5 2.5 times ofPT is the theraputic

range

International Normalized Ratio ( INR ) standarized

method for reporting PT level, used for regulating

warfarin dosage


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Chest X-Ray ( CXR )Assess size, position of theheart,

cardiothoracic ratio ( CTR ), position of central

lines

Electrocardiography ( ECG )

Can beeither on bed side or from a distance,

12 leads ECG, continuous monitoring,

telemetry monitoring 2 or 3 leads monitoring )


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DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION Cardiac Stress Test

During time of increased demand, abnormalities

in cardiovascular functions are more likely tobe detected, used to evaluate theheart function,

coronary arteries as well as the cause of chest

pain


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Con.

Exercise stress test: pt walk on a treadmill or

pedals (stationary bicycle), the goal is toincrease HR and monitored for ECH changes,

arrhythmias, hypotension, pain, dyspnea and

dizziness.P

t fast 4 hours before test, nurseneeds to instruct pt about the test


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DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION Echocardiography: a non invasive ultrasound used

to examine size shape and cardiac motion, used

also to evaluateheart function, valves andperipheral effusion

Pharmacologic stress test: used for pts

unable to achieve target HR, Dipyridamole,

Adenosine & dobutamine are used for this

purpose


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Cardiac catheterizationInvasive diagnostic procedure involves introduction

of specific catheter into Rt & Lt side blood vessels

under fluoroscopy. Its used to evaluate coronary

arteries patency, heart function as a pump, vascularsystem and heart structure

Its considered as a highly critical procedure

Take in consideration: monitoring IV line, BP

, ECG

,LOC, well prepared staff to provide ACLS, revission

of lab tests


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CORONARYCORONARYVASCULARVASCULAR

DISORDERSDISORDERS


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ATHEROSCLEROSISATHEROSCLEROSIS

Definition: abnormal accumulation of lipid or

fatty substances and fibrous tissues in vessel wall

PathophysiologyIt begins as a fatty streak, this streak develop into

advanced lesion which involves inflammatory

response, T.lymphocytes and monocytes ingest the

lipid and form fibrous cap called Atheroma Plaque,

this protrude into the lumen of the vessel narrowing

and obstruct it


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ATHEROSCLEROSISATHEROSCLEROSIS Clinical manifestations

Acute onset chest pain, ECG changes,

dyarhythmias & death

Risk factors

Age, family history of non modifiable risk

factors, high cholestrol, cigarette smoking,hypertension & DM


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PREVENTION

Control cholestrol level, LDL less than normal

Dietary control decrease fat & increase fiber

Medication to decrease serum fat & cholesterolQuit smoking

Early detection & control hypertension

Control DMGender & estrogen level

Behavior pattern


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ANGINA PECTORISANGINA PECTORIS

Definition: its a clinical syndrome ch.ch

by episodes of pain or pressure in the

anterior chest

Pathophysiology

Caused by atherosclerotic disease,

associated with significant obstruction ofCA and any cause that increase demand

or decrease supply


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ANGINA PECTORISANGINA PECTORIS

Medical Management: the objectives are to

decrease the demand and increase blood supply to

theheart

Pharmacological therapy & control risk factorsNitroglycerides, beta blockers, Ca channel blockers &

antiplatlet agents ( aspirin heparin )

Revascularization procedures

Coronary artery bipass ABG

Percutaneus transluminal coronary angioplasy PTCA

O2 administration


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MYOCARDIAL INFARCTION MIMYOCARDIAL INFARCTION MI

Definition: death ofheart tissue caused by

ischemia, a process by whichareas of the

myocardial cells destroyedClinical manifestation

Sudden sever chest pain radiated to left arm

anxious & restlessness,cool pale moist skin, sweating

tachypnea & tachycardia


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Diagnostic findings and assessment

Pt history, ECG: T wave & STsegment changes echo & lab tests

Medical management: objectives are to

- minimize myocardial damage,

- preserve function & preventcomplications


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Emergent PTCA to open occluded

arteryPharmacologic therapy:

thrombolytic ( STK, TPA ),

Analgesics ACE inhibitors


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MITRAL STENOSISMITRAL STENOSIS

Definition: an obstruction of blood flowing from

the left atrium into the left ventricle, most often

caused by rheumatic endocarditis

Clinical manifestation

Progressive fatigue due to low cardiac output,

hemoptesis, dyspnea

cough & repeated respiratory infections


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MITRAL STENOSISMITRAL STENOSIS

ManagementAntibiotic

Valvuloplasty

medication in case of surgical failure PTCA may relieve symptoms


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MITRAL REGURGITATIONMITRAL REGURGITATION

Definition: blood flowing back from the leftventricle into the left atrium during systole, the

margins of the mitral valves cannot close during

systole


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MITRAL REGURGITATIONMITRAL REGURGITATIONClinical manifestation

Chronic often asymptomatic

Acute :severe congestiveheart failure,

dyspnea, palpitation, fatigue & weakness,

shortness of breath & cough from pulmonary

congestion

ManagementSurgical mitral valve replacement

Valvuloplasty


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AORTIC STENOSISAORTIC STENOSIS

Definition: narrowing of the orifice between the

left ventricle &the aorta, congenital malformation

Clinical manifestationMany pts are asymptomatic

Exertional dyspnea, dizziness, fainting,

angina pectoris, low pulse pressure ( 30 mmhgor less )


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AORTIC STENOSISAORTIC STENOSIS

Management

Prophylactic antibiotic to prevent

endocarditis

Medication as prescribed for

dysrhythmias

Surgical replacement for the aortic valve

One-or-two-balloon percotaneous

valvuplasty


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AORTIC REGURGITATIONAORTIC REGURGITATION

Definition: flow of blood back into the left

ventricle from the aorta during diastole,

congenital deformities, endocarditis, syphilis,

dissecting aneurysm


Force full heart beat ( head & neck ),

arterial pulsation

exertional dyspnea and fatigue, difficult

breaths specially at night


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AORTIC REGURGITATIONAORTIC REGURGITATION Management

Prophylactic antibiotic to prevent

endocarditis

Treatment ofheart failure and dysrhythmiasAortic valve replacement ( treatment of

choice )

Surgery is recommended for pt with Ltventricularhypertrophy regardless the

presence or absence of symptoms


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CARDIOMYOPATHIESCARDIOMYOPATHIES Clinical manifestations

A symptomatic for many years

Shortness of breath, nocturnal dyspnea, cough,

chest pain, palpitation, dizziness & fatigue

Medical management

Mange precipitating cause, correct heart failure,

diet & exercise regimen, control dysrhythmias, Implanted electrical device

myomectomy & heart transplantation


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RHEUMATIC ENDOCARDITISRHEUMATIC ENDOCARDITIS

Definition: inflammation ofendocardium result from rheumaticfever caused by a group A streptococcal infection


Tiny translucent growth, pin-head size beats of the valve flaps, seriousdysrhythmias, pneumonia, valvular deformities, murmur, thrill &palpitation

Medical management

Eradicate organism & prevent complications

Penicillin as a drug of choice ( long term therapy )

Nursing management

Teach pt about disease, prevention & treatment

Instruct about long term therapy

Instruct for prophylactic therapy


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PERICARDITISPERICARDITIS

Definition: inflammation of the pricardium

Clinical manifestations

Pain over pericardium, clavicle, neck &scapula

friction rub, aggravated by breathing&turning in bed, relieved by sitting up

dyspnea, low cardiac output, increase WBC,pt appears extremely ill


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PERICARDITISPERICARDITIS Medical management

Determine& treat cause, bed rest,

analgesics NSAID, corticosteroidsprevent pericardial effusion

Nursing management

Medication as prescribed, gradualincrease in activity unless fever, pain and

friction rub reappear


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ACUTE PULMONARY EDEMAACUTE PULMONARY EDEMA

Definition: abnormal accumulation of fluids inthe lungs either in interstitial space or in alveoli

Clinical manifestationsRestlessness, confusion, breathlessness

sense of suffocation, rapid weak pulse

distended neck veins, cold hands, cyanosed nail

beds, gray skincough & decrease O2 saturation


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Medical management: to improve res.

Exchange

O2 therapy, medication and nursingsupport

Intubation and mechanical ventilator in

severe failurePEEP, oximetry ABGs

Morphine ( 2-5 mg ) to reduce anxiety


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0


Duretic therapy

To increase rate of urin production, decrease

ECF, thiazide & loopduretics ( dose depends onindication, clinical signs & renal function )

Medications to increase myocardial

contractility & cardiac output ( digitalis )


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1


Nursing management

Position pt to promote circulation

Psychological support

Monitor medication


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CARDIAC FAILURECARDIAC FAILURE

congestive heart failurecongestive heart failure

Definition: inability ofheart to pump sufficient blood

to meat needs of tissue for O2 & nutrient


In adequate tissue perfusion, dizziness, confusion,

fatigue, cool extremities,

exercise & heat intolerance

low urine output, high venous pressure,

pulmonary & peripheral edema, weight gain


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CARDIAC FAILURECARDIAC FAILURE

congestive heart failurecongestive heart failureNursing management

I&O, daily wt, daily auscultate lungsounds,jugular vein assessment,

edema, pulse rate, BP, skin turgur &

manage complications


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VASCULARVASCULARSYSTEMSYSTEM


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The vascular system consists of two interdependentsystems

Right side of theheart pump

Left side of theheart pump

BLOOD VESSELS

Arteries and arteriolsHigh-pressure system, thick wall, transport oxygenated blood

away from theheartLocated in protected areas away from skin surface

Wall of arteries and arteriols composed of 3 layersIntema: inner indothelial layer, contact with blood

Media: smmothelastic tissue, constrict & dilate vessels

Adventitia: connective tissue, anchors vessels to surroundingCapillaries

Single layer ofendothelial cells, permits rapid & effectivetransport of nutrients to the cells & removal of metabolic waste


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Veins and venulesLarger in diameter than arteries but the wall are

thinner because there is a less muscle & elastic tissue

in the tonic & media, this allow these vessels to

distend more than arteriesEquipped by one-way bicusped valves that prevent

blood to back flow

Valves composed ofendothelial leaflets

Transport deoxygenated blood from the body to the

heart

Health History and ClinicalHealth History and Clinical


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Health History and ClinicalHealth History and Clinical

ManifestationsManifestations

A muscular cramp-type pain in theextremitiesreproduce with the same degree ofexercise oractivity & relieved by rest is experienced bypatients with peripheral arterial insufficiency

Intermittent claudication: its due to inability ofarterial system to provide adequate blood flow tothe tissues in the face of increased demand for

nutrients during exerciseRest pain: worse at night & may interfere with sleep

As general role, the pain of intermittent claudicationoccurs onejoint level below the disease process


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Changes in skin appearance and temperature

Inadequate blood flow cause cool & paleextremities

Redish-blue discoloration ofextremities (rubor)

Additional changes resulting from chronicallyreduced nutrients supply like: loss ofhair, brittle

nails, dry skin, atrophy, ulceration, gangrene bytraumatic events

Pulses

Determining the presence or absence as well as

quality of peripheral pulses to assess the status ofperipheral arterial circulation

Absence of pulse may indicates the size of stenosis(narrowing or constriction )


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Diagnostic EvaluationDiagnostic Evaluation

Doppler ultrasoundWhen pulses cannot be reliably palpated, use of a

microphne-likehand held doppler ultrasound device

(tranceducer or prob) may behelpful in detecting and

assessing peripheral flowProcedure

Exercise testing

Used to determinehow long can a pt walk &measure ankle systolic BP in response to walking

A normal response is little or no drop in systolic BP,

it drops in true claudication


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Angiography

Used to confirm the diagnosis of occlusive arterial disease

when considering surgery or interventionInjecting radiopaque contrast agent directly into vascular

system to visualize the vessels

Pts experience temporary warmth during injection, side

effects are local irritation, allergic reactions, dyspnea, N & V,sweating tachycardia, numbness

Additional risks: vessel injury, bleeding & strock

Contrast plebography ( venography )

Performed if pt is to undergo thrombolytic therapyContrast is injected via dorsal foot vein then X-ray image will

disclos an unfilled vein

Injection may cause brief painful inflammation of the vein


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Medical management

Modification of risk factors to improve circulationSurgical management

Radiologic intervention

PERIPHERAL ARTERIALPERIPHERAL ARTERIAL


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OCCLUSIVE DISEASEOCCLUSIVE DISEASE

Arterial Insufficiency ofextremities is usually found in older

than 50 yrs, most often in men, legs are most frequently affected

Distal occlusive disease frequently seen in pts with DM &elderly pts


Intermittent claudication described as aching, cramp, fatigue,

weakness in joint muscles below stenosis or occlusion area

Decrease ability to walk, increase pain with ambulation

Ischemic pain at rest & worse at night

Bruit sound on auscultation

Absence of peripheral pulse


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OCCLUSIVE DISEASEOCCLUSIVE DISEASE Medical management

Exercise program with weight reduction

Smoking cessationSurgical management

- Grafting

- Endarterectomy

Nursing ManagementNursing Management


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Nursing ManagementNursing Management

Maintaining circulation

Check pulses of affected extremities, note symmetry,

color, temp., capillary refill, sensory & motorhourly

Dopplerevaluation of vessels distal to bypass graftMonitoring & managing potential complications

Urine output, CVP, pulse, leak, hematoma & edema

Promoting home & community based careDischarge plan, pt education, assess ability to change

life style & self care

AORTIC ANEURYSMAORTIC ANEURYSM


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Its a localized sac or dilation involving an artery

formed at a weak point in vessel wall

THORASIC AORTIC ANEURYSM

Caused by atherosclerosis in men aged ( 40-70 yrs )

Most common is dissecting aneurysm, 1/3 of cases

die of rupture


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Pain in supine position, dyspnea, hoarseness or

aphonia ( complete loss of voice ), dysphagia

Medical management

Surgical repair, control BP, correcting risk

factors


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ABDOMINAL AORTIC ANEURYSM

most common cause is atherosclerosis, affect men

4 times than women, occur mostly below renal stenosis,

untreated outcome is rupture & death


Abdominal heart beat on lying position,

abdominal mass

thrombing


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ARTERIAL EMBOLISM

Its acute vascular occlusion due to an embolus or acutethrombosis

Causes

Iatrogenic injury ( insertion of catheters ), trauma

from fractures, crush injury, penetrating wound,

thrombi development in heart champers as a result of

(AF, MI, CHF)

Clinical manifestationsCessation of distal bld flow, gradual loss of sensory

& motor function, pain, pallor, cold, paresthesia,

pulse lessens & paralysis


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ARTERIAL EMBOLISMARTERIAL EMBOLISM

Medical management Surgery ( embolectomy ),

Medication ( heparin bolus5000-10000 then contentiousinfusion) Thrombolytic therapy (STK; streptokainase)

Nursing management

Pre-op. bed rest, warm at room temp. protection

from traumaPost-op. encourage movement & continue

anticoogulants

VENOUS DISORDERSVENOUS DISORDERS


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DVT, THROMBOPHLEBITIS and

PHLEBOTHROMBITIS

Clinical manifestationsMassive swelling, tenderness,

warmer affected extremity,

homans sign,heaviness & functional loss


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Medical management

Anti coagulants (heparin 5-7 days), lowmolecular-weight heparin, thrombolytic therapy

Surgical management: thromboectomy whenanti coagulant is contraindicated or danger of

pulmonary embolism is extreme

Nursing management

MonitorPT, PTT, Hb, platlets, report bleeding,assess anti coagulant therapy, monitor &manage complications, provide comfort &apply elastic pressure stockings.


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CHRONIC VENOUS INSUFFICIENCY

Obstruction of venous valves in the legs or a

reflux of blood back through the valves


Chronic venous stasis, altered pigmentation, pain,

stasis dermatitis, stasis ulceration, dry skin, cracks &itches


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LEG ULCERS

Its an excavation of the skin surface that occurswhen inflamed necrotic tissue sloughs off


Open inflamed sore, pain & edema, discharge maybe present, heaviness, itching, area may covered with

eschar, gangrene

Medical management

Pharmacologic therapy (antibiotics based on culture)

depridement, topical therapy, stimulated healing by

Epigram


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VARICOSE VEINS

Abnormally dilated torturous superficial veins

caused by incompetent venous valvesClinical manifestations

Dull aches, muscle cramps, increase muscle fatigue,

ankleedema, S&S of venous insufficiency if obstruct


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VARICOSE VEINSVARICOSE VEINS

Medical management

Surgery ( ligation ) & sclerotherapy

Nursing management

Bed rest 1st 24 hours & start walking at 2nd day

5-10 min /2 hours, elastic pressure stockings,

elevate foot, discourage standing & sitting,promote comfort (analgesia), home &

community based care

NURSING PROCESSNURSING PROCESS


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Assessment

Sub. (interview) & obj. (physical assessment)

Diagnosis

Alteration in peripheral tissue perfusion

Pain, risk for impaired skin integrity, knowledge

deficit regarding self care activities


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Implementation

Lower theextremity below level of theheart

Encourage moderate amount of walking

Maintain warm & discourage nicotine use

Administer prescribed vasodilators, adrenergic blockagents

Evaluation

Goal met evidenced by: extremities warm to touch,color improved, decrease muscle pain, tolerate

performing exercise 6 times / day

HYPERTENTIONHYPERTENTION


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Definition: its a raise of blood pressure above normal

range

systolic above 140 mmhg & diastolic above 90mmhg over sustained period

A multifactorial condition

A sign ,a risk factor , and a disease .


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HYPERTENTIONHYPERTENTION Types & causes

1- Primary (idiopathic essential ) hypertention

80-90% of cases are of unknown cause butpredisposed by: old age over 60 yrs, obesity,

black race, atherosclerosis Benign or chronic hypertention

Rise is usually slight to moderate & continueto rise slowly often asymptomatic ( silentkiller )

Malignant (accelerated) hypertention

BP very high & continue to raise rapidly,diastolic pressure in excess of 120 mmhg &theeffects arequickly apparent


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2- Secondary hypertention: Increase BP

from an identified cause resulting from

other disease Causes

Renal disease, endocrine disorders, age & sex,

stressful occupation & situation, familytendency, DM, dyslipidemia, smoking &

alcohol


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High blood pressure reading

Headache, epistaxis, angina,

dizziness, dyspnea, ringing in ears

Retinal changes may be papilledema

a common consequence M.I. & CAD


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Medical management

Treatment of underlying cause

Life stile modification :- Management of predisposing factors (

low salt diet, decease weight, stop

smoking, decrease stress level)Pharmacologic therapy (diuretics,

vasoconstrictive agents & agents todecrease cardiac output )

Nursing ProcessNursing Process


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Nursing ProcessNursing Process

Nursing Diagnosis

Knowledge deficit ( medication & disease process )

Non compliance with therapeutic regimen

E.O

Pt will understand disease process & its treatment

Pt will participate in self care program

Implementation

Allow pt to rest & relax, medication as prescribed, report sideeffects, educate pt about rebound hypertention that occurs if

therapy suddenly stoppedMeasure BP routinely, follow up appointments,

Educate pt about arthostatic hypotention so to stand gradually

Life style modification

heart and vessels

Documents

Transcript of heart and vessels