cardio med-surg nursing

7/31/2019 Cardio MED-SURG NURSING

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Nursing Board Review

Cardiovascular System



The Cardiovascular System

Normal Anatomy

The heart is located in the LEFT side of the

mediastinumConsists of Three layers- epicardium,

myocardium and endocardium




The epicardium covers the outer surface of

the heart

The myocardium is the middle muscularlayer of the heart

The endocardium lines the chambers and

the valves




The layer that covers the heart is the

PERICARDIUM

There are two parts- parietal and visceralpericardium

The space between the two pericardial

layers is the pericardial space




The heart chambers are guarded by

valves

The atrio-ventricular valves-Tricuspid and bicuspid

The semi-lunar valves- Pulmonic and

aortic valves




The Blood supply of the heart comes from

the Coronary arteries

1. Right coronary artery supplies theRIGHT atrium and RIGHT ventricle,

inferior portion of the LEFT ventricle,

the POSTERIOR septal wall and the two

nodes- AV (90%) and SA node (55%)




2. Left coronary artery- branches into the

LAD and the circumflex branch

The LAD supplies blood to the anteriorwall of the LEFT ventricle, the anterior

septum and the Apex of the left ventricle

The CIRCUMFLEX branch supplies theleft atrium and the posterior LEFT

ventricle




The CONDUCTING SYSTEM OF THEHEART

Consists of the

1. SA node- the pacemaker

2. AV node- slowest conduction

3. Bundle of His – branches into the Rightand the Left bundle branch

4. Purkinje fibers- fastest conduction



The Heart sounds

1. S1- due to closure of the AV valves

2. S2- due to the closure of the semi-lunarvalves

3. S3- due to increased ventricular filling

4. S4- due to forceful atrial contraction





Heart rate

Normal range is 60-100 beats per minute

Tachycardia is greater than 100 bpmBradycardia is less than 60 bpm

Sympathetic system INCREASES HR

Parasympathetic system (Vagus)

DECREASES HR




Blood pressure

Cardiac output X peripheral resistance

Control is neural (central and peripheral)and hormonal

Baroreceptors in the carotid and aorta

Hormones- ADH, aldosterone,epinephrine can increase BP; ANF can

decrease BP




The vascular system consists of the arteries,veins and capillaries

The arteries are vessels that carry bloodaway from the heart to the periphery

The veins are the vessels that carry blood tothe heart

The capillaries are lined with squamos cells,they connect the veins and arteries




The lymphatic system also is part of the

vascular system and the function of this

system is to collect the extravasated fluidfrom the tissues and returns it to the blood




Cardiac Assessment




Laboratory Test Rationale

1. To assist in diagnosing MI2. To identify abnormalities

3. To assess inflammation




Laboratory Test Rationale

4. To determine baseline value

5. To monitor serum level of medications

6. To assess the effects of medications




LABORATORY PROCEDURES

CARDIAC Proteins andenzymes

CK- MB ( creatine kinase)

Elevates in MI within 4

hours, peaks in 18 hoursand then declines till 3 days






CK- MB ( creatinekinase)

Normal value is 0-7 U/L






Lactic Dehydrogenase (LDH)

Elevates in MI in 24 hours,

peaks in 48-72 hoursNormally LDH1 is greater

than LDH2






Lactic Dehydrogenase (LDH)

MI- LDH2 greater than

LDH1 (flipped LDH pattern)Normal value is 70-200 IU/L






Myoglobin

Rises within 1-3 hours

Peaks in 4-12 hoursReturns to normal in a day






Myoglobin

Not used alone

Muscular and RENAL diseasecan have elevated myoglobin

Th C di l S t





Troponin I and TTroponin I is usually utilized for

MI

Elevates within 3-4 hours, peaks

in 4-24 hours and persists for 7

days to 3 weeks!

Normal value for Troponin I is

less than 0.6 ng/mL





Troponin I and T

REMEMBER to AVOIDIM injections before

obtaining blood sample!

Early and late diagnosis can

be made!





SERUM LIPIDS

Lipid profile measures the

serum cholesterol,triglycerides and lipoprotein

levelsCholesterol= 200 mg/dL

Triglycerides- 40- 150 mg/dL





SERUM LIPIDS

LDH- 130 mg/dLHDL- 30-70- mg/dL

NPO post midnight (usually12 hours)





Holter Monitoring

A non-invasive test in

which the client wears aHolter monitor and an

ECG tracing recordedcontinuously over a periodof 24 hours





Holter Monitoring

Instruct the client to resumenormal activities and maintain

a diary of activities and anysymptoms that may develop





ECHOCARDIOGRAM

Non-invasive test that studies

the structural and functionalchanges of the heart with the

use of ultrasoundNo special preparation isneeded





Stress Test

A non-invasive test thatstudies the heart duringactivity and detects and

evaluates CADExercise test, pharmacologictest and emotional test





Stress Test

Pre-test: consent may berequired, adequate rest ,eat a light meal or fast for

4 hours and avoidsmoking, alcohol and

caffeine





Post-test: instruct client tonotify the physician if any

chest pain, dizziness orshortness of breath . Instruct

client to avoid taking a hotshower for 10-12 hours afterthe test





Pharmacological stress test

Use of dipyridamoleMaximally dilatescoronary artery

Side-effect: flushing of face





Post-test: instruct client tonotify the physician if any

chest pain, dizziness orshortness of breath . Instruct

client to avoid taking a hotshower for 10-12 hours afterthe test





Pharmacological stress test

Pre-test: 4 hours fasting,avoid alcohol, caffeine

Post test: reportsymptoms of chest pain





CARDIAC catheterization

Insertion of a catheter into

the heart and surroundingvessels

Determines the structure andperformance of the heartvalves and surrounding

vessels





CARDIAC catheterization

Used to diagnose CAD,

assess coronary atery

patency and determine

extent of atherosclerosis





Pretest: Ensure Consent,assess for allergy to

seafood and iodine, NPO,document weight and

height, baseline VS, bloodtests and document theperipheral pulses





Pretest: Fast for 8-12

hours, teachings,medications to allay

anxiety





Intra-test: inform patient of a fluttery feeling as the

catheter passes through theheart; inform the patient

that a feeling of warmth andmetallic taste may occurwhen dye is administered





Post-test: Monitor VS and cardiacrhythm

Monitor peripheral pulses, color andwarmth and sensation of theextremity distal to insertion site

Maintain sandbag to the insertion siteif required to maintain pressure

Monitor for bleeding and hematomaformation

h C di l S





Maintain strict bed rest for 6-12 hours

Client may turn from side to side but bed

should not be elevated more than 30 degrees

and legs always straight

Encourage fluid intake to flush out the dye

Immobilize the arm if the antecubital veinis used

Monitor for dye allergy

Th C di l S





CVP

The CVP is the pressurewithin the SVC

Reflects the pressure under

which blood is returned tothe SVC and right atrium

Th C di l S





CVP

Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O

Elevated CVP indicates increasein blood volume, excessive IVF or

heart/renal failureLow CVP may indicatedhypovolemia, hemorrhage and

severe vasodilatation

Th C di l S





Measuring CVP

1. Position the client supine with bed

elevated at 45 degrees2. Position the zero point of the CVPline at the level of the right atrium.

Usually this is at the MAL, 4 th

ICS3. Instruct the client to be relaxedand avoid coughing and straining.



CARDIAC ASSESSMENT

ASSESSMENT

1. Health History

Obtain description of presentillness and the chief complaint

Chest pain, SOB, Edema, etc.

Assess risk factors



CARDIAC ASSESSMENT

2. Physical examinationVital signs- BP, PP, MAP

Inspection of the skinInspection of the thorax

Palpation of the PMI, pulses

Auscultation of the heartsounds



CARDIAC ASSESSMENT3. Laboratory and diagnostic studies

CBC

cardiac catheterization

Lipid profilearteriography

Cardiac enzymes and proteins

CXR

CVP

EEG

Holter monitoring

Exercise ECG

CARDIAC



CARDIAC

IMPLEMENTATION

1. Assess the cardio-pulmonary

status

VS, BP, Cardiac assessment

2. Enhance cardiac output

Establish IV line to administerfluids

CARDIAC



CARDIAC

IMPLEMENTATION

3. Promote gas exchange

Administer O2

Position client in SEMI-Fowler’s

Encourage coughing and deep

breathing exercises

CARDIAC



CARDIAC

IMPLEMENTATION

4. Increase client activity tolerance

Balance rest and activity periods

Assist in daily activities5. Promote client comfort

Assess the client’s description of

pain and chest discomfortAdminister medication asprescribed

CARDIAC



CARDIAC

IMPLEMENTATION

6. Promote adequate sleep

7. Prevent infection

Monitor skin integrity of lowerextremities

Assess skin site for edema, redness

and warmthMonitor for fever

Change position frequently

CARDIAC



CARDIAC

IMPLEMENTATION

8. Minimize patient anxiety

Encourage verbalization of feelings, fears and concerns

Answer client questions.Provide information aboutprocedures and medications



CARDIAC DISEASES

Coronary Artery Disease

Myocardial Infarction

Congestive Heart FailureInfective Endocarditis

Cardiac TamponadeCardiogenic Shock



VASCULAR DISEASES

Hypertension

Buerger’s disease

Varicose veins

Deep vein thrombosis

Aneurysm



CAD

CAD results from the focal

narrowing of the large andmedium-sized coronary

arteries due to deposition of atheromatous plaque in the

vessel wall



CADRISK FACTORS

1. Age above 45/55 and Sex- Males andpost-menopausal females

2. Family History

3. Hypertension

4. DM

5. Smoking

6. Obesity

7. Sedentary lifestyle

8. Hyperlipedimia



CADRISK FACTORS

Most important MODIFIABLE

factors:

Smoking

Hypertension

DiabetesCholesterol abnormalities



CAD

Pathophysiology

Fatty streak formation in the

vascular intima T-cells andmonocytes ingest lipids in the area

of deposition atheroma

narrowing of the arterial lumen reduced coronary blood flow

myocardial ischemia

CAD



CAD

Pathophysiology

There is decreased perfusion of myocardial tissue and inadequatemyocardial oxygen supply

If 50% of the left coronary arteriallumen is reduced or 75% of the othercoronary artery, this becomes

significantPotential for Thrombosis andembolism



Angina Pectoris

Chest pain resulting

from coronaryatherosclerosis or

myocardial ischemia

A i P t i Cli i l S d



Angina Pectoris: Clinical Syndromes

Three Common Types of ANGINA

1. STABLE ANGINA

The typical angina thatoccurs during exertion,relieved by rest and drugs

and the severity does not change






2. Unstable angina

Occurs unpredictably

during exertion andemotion, severity increaseswith time and pain may not

be relieved by rest and drug






3. Variant angina

Prinzmetal angina, results

from coronary arteryVASOSPASMS, may occur at rest



Angina Pectoris

ASSESSMENT FINDINGS

1. Chest pain- ANGINA

The most characteristic symptomPAIN is described as mild tosevere retrosternal pain, squeezing,

tightness or burning sensation Radiates to the jaw and left arm



Angina Pectoris

ASSESSMENT FINDINGS

1. Chest pain- ANGINA

Precipitated by Exercise, Eatingheavy meals, Emotions like

excitement and anxiety and

Extremes of temperature

Relieved by REST and Nitroglycerin



Angina Pectoris

ASSESSMENT FINDINGS

2. Diaphoresis

3. Nausea and vomiting4. Cold clammy skin

5. Sense of apprehension anddoom

6. Dizziness and syncope



Angina Pectoris

LABORATORY FINDINGS

1. ECG may show normal tracing if patient is pain-free. Ischemic changes

may show ST depression and T waveinversion

2. Cardiac catheterization

Provides the MOST DEFINITIVEsource of diagnosis by showing thepresence of the atherosclerotic lesions



Angina Pectoris

NURSING MANAGEMENT

1. Administer prescribed medications

Nitrates- to dilate the coronary arteriesAspirin- to prevent thrombusformation

Beta-blockers- to reduce BP and HRCalcium-channel blockers- to dilatecoronary artery and reduce vasospasm



2. Teach the patient management of anginalattacks

Advise patient to stop all activities

Put one nitroglycerin tablet under thetongue

Wait for 5 minutes

If not relieved, take another tablet and waitfor 5 minutes

Another tablet can be taken (third tablet)

If unrelieved after THREE tablets seekmedical attention



Angina Pectoris

3. Obtain a 12-lead ECG

4. Promote myocardial perfusion

Instruct patient to maintain bed rest

Administer O2 @ 3 lpm

Advise to avoid valsalva maneuvers

Provide laxatives or high fiber diet tolessen constipation

Encourage to avoid increased physicalactivities



Angina Pectoris

5. Assist in possible treatment modalities

PTCA- percutaneous transluminalcoronary angioplasty

To compress the plaque against thevessel wall, increasing the arteriallumen

CABG- coronary artery bypass graft

To improve the blood flow to themyocardial tissue



Angina Pectoris

6. Provide information to familymembers to minimize anxiety

and promote familycooperation

7. Assist client to identify riskfactors that can be modified

8. Refer patient to proper

agencies



Myocardial infarction

Death of myocardial

tissue in regions of the

heart with abrupt

interruption of coronary

blood supply




ETIOLOGY and Risk factors

1. CAD

2. Coronary vasospasm3. Coronary artery occlusion byembolus and thrombus

4. Conditions that decreaseperfusion- hemorrhage, shock




Risk factors

1. Hypercholesterolemia

2. Smoking3. Hypertension

4. Obesity

5. Stress





PATHOPHYSIOLOGY

Interrupted coronary blood flow

myocardial ischemia anaerobicmyocardial metabolism for severalhours myocardial death depressed cardiac function

triggers autonomic nervous systemresponse further imbalance of myocardial O2 demand and supply




ASSESSMENT findings

1. CHEST PAIN

Chest pain is described as severe,persistent, crushing substernaldiscomfort

Radiates to the neck, arm, jawand back




ASSESSMENT findings

1. CHEST PAIN

Occurs without cause, primarilyearly morning

NOT relieved by rest or

nitroglycerin

Lasts 30 minutes or longer




Assessment findings

2. Dyspnea

3. Diaphoresis

4. cold clammy skin

5. N/V

6. restlessness, sense of doom7. tachycardia or bradycardia

8. hypotension

9. S3 and dysrhythmias




Laboratory findings

1. ECG- the ST segment is ELEVATED.T wave inversion, presence of Q wave

2. Myocardial enzymes- elevated CK-MB, LDH and Troponin levels

3. CBC- may show elevated WBC count

4. Test after the acute stage- Exercisetolerance test, thallium scans, cardiaccatheterization



Myocardial infarctionNursing Interventions

1. Provide Oxygen at 2 lpm, Semi-fowler’s

2. Administer medications

Morphine to relieve pain

nitrates, thrombolytics, aspirin andanticoagulants

Stool softener and hypolipidemics

3. Minimize patient anxiety

Provide information as to proceduresand drug therapy





4. Provide adequate rest periods

5. Minimize metabolic demands

Provide soft dietProvide a low-sodium, low

cholesterol and low fat diet

6. Minimize anxiety

Reassure client and provide

information as needed




7. Assist in treatment modalitiessuch as PTCA and CABG

8. Monitor for complications of MI-especially dysrhythmias, sinceventricular tachycardia can

happen in the first few hours afterMI

9. Provide client teaching



MI

Medical Management

1. ANALGESIC

The choice is MORPHINE

It reduces pain and anxiety

Relaxes bronchioles to enhanceoxygenation



MI

Medical Management

2. ACE

Prevents formation of angiotensin

II

Limits the area of infarction



MI

Medical Management

3. Thrombolytics

Streptokinase, Alteplase

Dissolve clots in the coronary

artery allowing blood to flow




NURSING INTERVENTIONSAFTER ACUTE EPISODE

1. Maintain bed rest for the first3 days

2. Provide passive ROM

exercises3. Progress with dangling of thefeet at side of bed




NURSING INTERVENTIONSAFTER ACUTE EPISODE

4. Proceed with sitting out of bed, on the chair for 30 minutesTID

5. Proceed with ambulation inthe room toilet hallway TID




NURSING INTERVENTIONS AFTERACUTE EPISODE

Cardiac rehabilitation

To extend and improve quality of life

Physical conditioning

Patients who are able to walk 3-4 mph are usually ready to resume sexual activities



CARDIOMYOPATHIES

Heart muscle disease

associated with cardiac

dysfunction



CARDIOMYOPATHIES

1. Dilated Cardiomyopathy

2. Hypertrophic

Cardiomyopathy

3. Restrictive cardiomyopathy



DILATED CARDIOMYOPATHY

ASSOCIATED FACTORS

1. Heavy alcohol intake

2. Pregnancy

3. Viral infection

4. Idiopathic



DILATED CARDIOMYOPATHY

PATHOPHYSIOLOGY

Diminished contractile proteins

poor contraction decreasedblood ejection increased bloodremaining in the ventricle

ventricular stretching anddilatation.

SYSTOLIC DYSFUNCTION

HYPERTROPHIC



CARDIOMYOPATHY

Associated factors:

1. Genetic2. Idiopathic

HYPERTROPHIC



CARDIOMYOPATHY

Pathophysiology

Increased size of myocardium

reduced ventricular volume increased resistance to

ventricular filling diastolic

dysfunction

RESTRICTIVE



CARDIOMYOPATHY

Associated factors

1. Infiltrative diseases like

AMYLOIDOSIS

2. Idiopathic

RESTRICTIVE



CARDIOMYOPATHY

Pathophysiology

Rigid ventricular wall

impaired stretch and diastolic

filling decreased output

Diastolic dysfunction



CARDIOMYOPATHIES

Assessment findings1. PND

2. Orthopnea

3. Edema

4. Chest pain

5. Palpitations6. dizziness

7. Syncope with exertion



CARDIOMYOPATHIES

Laboratory Findings

1. CXR- may reveal

cardiomegaly2. ECHOCARDIOGRAM

3. ECG

4. Myocardial Biopsy

CA O O A S



CARDIOMYOPATHIES

Medical Management

1. Surgery

2. pacemaker insertion

3. Pharmacological drugs for

symptom relief

CARDIOMYOPATHIES



CARDIOMYOPATHIES

Nursing Management

1.Improve cardiac output

Adequate rest

Oxygen therapy

Low sodium diet

CARDIOMYOPATHIES



CARDIOMYOPATHIES

Nursing Management

2. Increase patient tolerance

Schedule activities with rest

periods in between

CARDIOMYOPATHIES



CARDIOMYOPATHIES

Nursing Management

3. Reduce patient anxiety

SupportOffer information abouttransplantations

Support family in anticipatorygrieving

I f i d di i



Infective endocarditis

Infection of the heart

valves and the endothelial

surface of the heart

Can be acute or chronic

I f i d di i




Etiologic factors

1. Bacteria- Organism

depends on several factors

2. Fungi

I f i d di i




Risk factors

1. Prosthetic valves

2. Congenital malformation3. Cardiomyopathy

4. IV drug users5. Valvular dysfunctions

I f i d di i




PathophysiologyDirect invasion of microbes microbes adhere to damagedvalve surface and proliferate damage attracts plateletscausing clot formation erosionof valvular leaflets andvegetation can embolize

I f ti d diti




Assessment findings1. Intermittent fever

2. anorexia, weight loss3. cough, back pain and jointpain

4. splinter hemorrhages undernails

I f ti d diti




Assessment findings

5. Osler’s nodes- painful

nodules on fingerpads6. Roth’s spots- pale

hemorrhages in the retina

I f ti d diti




Assessment findings

7. Heart murmurs

8. Heart failure

I f ti d diti




Prevention

Antibiotic prophylaxis if

patient is undergoingprocedures like dental

extractions, bronchoscopy,surgery, etc.

I f ti d diti




LABORATORY EXAM

Blood Cultures to determine

the exact organism

I f ti d diti




Nursing management

1. regular monitoring of

temperature, heart sounds2. manage infection

3. long-term antibiotictherapy

I f ti d diti




Medical management

1. Pharmacotherapy

IV antibiotic for 2-6 weeks

Antifungal agents are given –

amphotericin B





Medical management

2. Surgery

Valvular replacement

CHF



CHF

A syndrome of congestion of both pulmonary and systemic

circulation caused byinadequate cardiac functionand inadequate cardiac

output to meet the metabolicdemands of tissues

CHF



CHF

Inability of the heart to pumpsufficiently

The heart is unable to maintainadequate circulation to meet themetabolic needs of the body

Classified according to the majorventricular dysfunction- Left orRight



CHF



CHFEtiology of CHF

1. CAD

2. Valvular heart diseases

3. Hypertension4. MI

5. Cardiomyopathy

6. Lung diseases7. Post-partum

8. Pericarditis and cardiac tamponade

New York Heart Association




Class 1

Ordinary physical activity does

NOT cause chest pain andfatigue

No pulmonary congestion

Asymptomatic

NO limitation of ADLs





Class 2

SLIGHT limitation of ADLs

NO symptom at restSymptom with INCREASEDactivity

Basilar crackles and S3





Class 3

Markedly limitation on ADLs

Comfortable at rest BUT

symptoms present in LESS

than ordinary activity





Class 4

SYMPTOMS are present at

rest

CHF



CHF

PATHOPHYSIOLOGY

LEFT Ventricular pump

failure back up of bloodinto the pulmonary veins increased pulmonarycapillary pressure pulmonary congestion

CHF



CHF

PATHOPHYSIOLOGY

LEFT ventricular failure

decreased cardiac output decreased perfusion to thebrain, kidney and othertissues oliguria, dizziness

CHF



CHF

PATHOPHYSIOLOGY

RIGHT ventricular failure

blood pooling in thevenous circulation increased hydrostaticpressure peripheraledema

CHF



CHF

PATHOPHYSIOLOGY

RIGHT ventricular

failure blood pooling

venous congestion in the

kidney, liver and GIT

LEFT SIDED CHF

ASSESSMENT FINDINGS



ASSESSMENT FINDINGS

1. Dyspnea on exertion

2. PND

3. Orthopnea

4. Pulmonary crackles/rales

5. cough with Pinkish, frothysputum

6. Tachycardia

LEFT SIDED CHF

ASSESSMENT FINDINGS



ASSESSMENT FINDINGS

7. Cool extremities

8. Cyanosis

9. decreased peripheral pulses

10. Fatigue

11. Oliguria

12. signs of cerebral anoxia

RIGHT SIDED CHF

ASSESSMENT FINDINGS



ASSESSMENT FINDINGS

1. Peripheral dependent, pittingedema

2. Weight gain3. Distended neck vein

4. hepatomegaly

5. Ascites

RIGHT SIDED CHF

ASSESSMENT FINDINGS



ASSESSMENT FINDINGS

6. Body weakness

7. Anorexia, nausea8. Pulsus alternans

CHF



CHF

LABORATORY FINDINGS1. CXR may reveal

cardiomegaly2. ECG may identify Cardiachypertrophy

3. Echocardiogram may showhypokinetic heart

CHF



CHF

LABORATORY FINDINGS

4. ABG and Pulse oximetry may

show decreased O2 saturation

5. PCWP is increased in LEFT

sided CHF and CVP is increasedin RIGHT sided CHF

CHF



CHF

NURSING INTERVENTIONS

1. Assess patient's cardio-

pulmonary status

2. Assess VS, CVP and PCWP.

Weigh patient daily to monitorfluid retention

CHF



CHF


3. Administer medications-

usually cardiac glycosides aregiven- DIGOXIN or

DIGITOXIN, Diuretics,vasodilators and

hypolipidemics are prescribed

CHF



CHF


4. Provide a LOW sodium

diet. Limit fluid intake asnecessary

5. Provide adequate restperiods to prevent fatigue

CHF



CHF


6. Position on semi-fowler’s

to fowler’s for adequate chestexpansion

7. Prevent complications of immobility

CHF



CHF

NURSING INTERVENTION AFTERTHE ACUTE STAGE

1. Provide opportunities for

verbalization of feelings2. Instruct the patient about themedication regimen- digitalis,

vasodilators and diuretics3. Instruct to avoid OTC drugs,Stimulants, smoking and alcohol

CHF



CHF

NURSING INTERVENTIONAFTER THE ACUTE STAGE

4. Provide a LOW fat and LOWsodium diet

5. Provide potassium

supplements6. Instruct about fluid restriction

CHF



CHF

NURSING INTERVENTIONAFTER THE ACUTE STAGE

7. Provide adequate rest periodsand schedule activities

8. Monitor daily weight and

report signs of fluid retention

CARDIOGENIC SHOCK



CARDIOGENIC SHOCK

Heart fails to pump adequatelyresulting to a decreased cardiac outputand decreased tissue perfusion

ETIOLOGY1. Massive MI

2. Severe CHF

3. Cardiomyopathy4. Cardiac trauma

5. Cardiac tamponade

CARDIOGENIC SHOCK



CARDIOGENIC SHOCK

ASSESSMENT FINDINGS

1. HYPOTENSION

2. oliguria (less than 30 ml/hour)

3. tachycardia

4. narrow pulse pressure

5. weak peripheral pulses

6. cold clammy skin

7. changes in sensorium/LOC

8. pulmonary congestion

CARDIOGENIC SHOCK



CARDIOGENIC SHOCK

LABORATORY FINDINGS

Increased CVP

Normal is 4-10 cmH2O

CARDIOGENIC SHOCK



C OG N C S OC


1. Place patient in a modified

Trendelenburg (shock ) position

2. Administer IVF, vasopressors and

inotropics such as DOPAMINE and

DOBUTAMINE

3. Administer O2

4. Morphine is administered to decreased

pulmonary congestion and to relieve pain

CARDIOGENIC SHOCK



5. Assist in intubation, mechanical

ventilation, PTCA, CABG, insertion

of Swan-Ganz cath and IABP

6. Monitor urinary output, BP and

pulses

7. cautiously administer diuretics andnitrates

CARDIAC TAMPONADE



A condition where the heart

is unable to pump blood due

to accumulation of fluid inthe pericardial sac

(pericardial effusion)

CARDIAC TAMPONADE



This condition restrictsventricular filling resulting to

decreased cardiac outputAcute tamponade may happenwhen there is a sudden

accumulation of more than 50ml fluid in the pericardial sac

CARDIAC TAMPONADE



Causative factors

1. Cardiac trauma

2. Complication of Myocardialinfarction

3. Pericarditis4. Cancer metastasis

CARDIAC TAMPONADE



ASSESSMENT FINDINGS

1. BECK’s Triad- Jugular vein

distention, hypotension anddistant/muffled heart sound

2. Pulsus paradoxus

3. Increased CVP

4. decreased cardiac output

CARDIAC TAMPONADE



ASSESSMENT FINDINGS

5. Syncope

6. anxiety7. dyspnea

8. Percussion- Flatness across theanterior chest

CARDIAC TAMPONADE



Laboratory FINDINGS

1. Echocardiogram

2. Chest X-ray

CARDIAC TAMPONADE




1. Assist in PERICARDIOCENTESIS

2. Administer IVF

3. Monitor ECG, urine output and BP

4. Monitor for recurrence of tamponade

Pericardiocentesis



Patient is monitored by ECG

Maintain emergency equipments

Elevate head of bed 45-60 degreesMonitor for complications-

coronary artery rupture,

dysrhythmias, pleural laceration

and myocardial trauma

HYPERTENSION



A systolic BP greater than 140

mmHg and a diastolic

pressure greater than 90mmHg over a sustained

period, based on two or more

BP measurements.

HYPERTENSION



Types of Hypertension

1. Primary or ESSENTIAL

Most common type2. Secondary

Due to other conditions like

Pheochromocytoma, renovascularhypertension, Cushing’s, Conn’s ,

SIADH

HYPERTENSION



CLASSIFICATION OF

HYPERTENSION by JNC-

VII



HYPERTENSION

PATHOPHYSIOLOGY



PATHOPHYSIOLOGY

Multi-factorial etiology

BP= CO (SV X HR) x TPR

Any increase in the aboveparameters will increase BP

1. Increased sympathetic activity2. Increased absorption of Sodium,

and water in the kidney

HYPERTENSION

PATHOPHYSIOLOGY



PATHOPHYSIOLOGY

Multifactorial etiology

BP= CO (SV X HR) x TPR

Any increase in the above parameterswill increase BP

3. Increased activity of the RAAS

4. Increased vasoconstriction of theperipheral vessels

5. insulin resistance

HYPERTENSION



ASSESSMENT FINDINGS

1. Headache

2. Visual changes

3. chest pain

4. dizziness5. N/V

HYPERTENSION



Risk factors for CardiovascularProblems in Hypertensive patients

Major Risk factors

1. Smoking2. Hyperlipidemia

3. DM

4. Age older than 605. Gender- Male and post menopausal W

6. Family History

HYPERTENSION



DIAGNOSTIC STUDIES

1. Health history and PE

2. Routine laboratory- urinalysis,ECG, lipid profile, BUN, serum

creatinine , FBS

3. Other lab- CXR, creatinine

clearance, 24-huour urine protein

HYPERTENSION



MEDICAL

MANAGEMENT

1. Lifestyle modification

2. Drug therapy

3. Diet therapy

HYPERTENSION



MEDICAL MANAGEMENTDrug therapy

Diuretics

Beta blockersCalcium channel blockers

ACE inhibitors

A2 Receptor blockersVasodilators

HYPERTENSION



NURSING INTERVENTIONS1. Provide health teaching topatient

Teach about the disease process

Elaborate on lifestyle changes

Assist in meal planning to loseweight

HYPERTENSION



NURSING INTERVENTIONS1. Provide health teaching to thepatient

Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day

Limit alcohol intake to 30 ml/dayRegular aerobic exercise

Advise to completely Stop smoking

HYPERTENSION



Nursing Interventions2. Provide information about anti-hypertensive drugs

Instruct proper compliance and notabrupt cessation of drugs even if ptbecomes asymptomatic/ improvedcondition

Instruct to avoid over-the-counterdrugs that may interfere with thecurrent medication

HYPERTENSION



Nursing Intervention

3. Promote Home care management

Instruct regular monitoring of BPInvolve family members in care

Instruct regular follow-up

4. Manage hypertensive emergency

and urgency properly

Vascular Diseases



ANEURYSM



Dilation involving an artery formed at aweak point in the vessel wall

ANEURYSM



Saccular= when one side of the vessel isaffected

Fusiform= when the entire segment

becomes dilated

ANEURYSM



RISK FACTORS

1. Atherosclerosis

2. Infection= syphilis

3. Connective tissue disorder

4. Genetic disorder= Marfan’s Syndrome

ANEURYSM



PATHOPHYSIOLOGY

Damage to the intima and media

weakness outpouching

Dissecting aneurysm tear in the intima and

media with dissection of blood through

the layers

ANEURYSM



ASSESSMENT

1. Asymptomatic

2. Pulsatile sensation on the abdomen

3. Palpable bruit

ANEURYSM



LABORATORY:

• CT scan

• Ultrasound

• X-ray

• Aortography

ANEURYSM



Medical Management:

• Anti-hypertensives

• Synthetic graft

ANEURYSM



Nursing Management:

• Administer medications

• Emphasize the need to avoid increased

abdominal pressure

• No deep abdominal palpation

• Remind patient the need for serial

ultrasound to detect diameter changes

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Refers to arterial insufficiency of the extremities usually secondary

to peripheral atherosclerosis.

Usually found in males age 50 and

above

The legs are most often affected

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Risk factors for PeripheralArterial occlusive disease

Non-Modifiable1. Age

2. gender

3. family predisposition

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Risk factors for Peripheral Arterialocclusive disease

Modifiable

1. Smoking2. HPN

3. Obesity


5. DM

6. Stress

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



ASSESSMENT FINDINGS1. INTERMITTENT CLAUDICATION- the hallmark of

PAOD

This is PAIN described as aching,cramping or fatiguing discomfortconsistently reproduced with thesame degree of exercise or activity

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



ASSESSMENT FINDINGS1. INTERMITTENTCLAUDICATION- the hallmarkof PAOD

This pain is RELIEVED by REST

This commonly affects the musclegroup below the arterial occlusion

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Assessment Findings2. Progressive pain on theextremity as the disease advances

3. Sensation of cold andnumbness of the extremities

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Assessment Findings4. Skin is pale when elevated andcyanotic/ruddy when placed on adependent position

5. Muscle atrophy, leg ulceration

and gangrene

PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Diagnostic Findings

1. Unequal pulses between the

extremities2. Duplex ultrasonography

3. Doppler flow studies



PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE



Nursing Interventions

1. Maintain Circulation to the

extremity

Evaluate regularly peripheral pulses,

temperature, sensation, motor

function and capillary refill time

Administer post-operative care to

patient who underwent surgery



PERIPHERAL ARTERIAL

OCCLUSIVE DISEASE




3. Promote Home management

Encourage lifestyle changes

Instruct to AVOID smoking

Instruct to avoid leg crossing

BUERGER’S DISEASE



Thromboangiitis obliterans

A disease characterized by

recurring inflammation of themedium and small arteries and

veins of the lower extremities

Occurs in MEN ages 20-35RISK FACTOR: SMOKING!

BUERGER’S DISEASE



PATHOPHYSIOLOGY

Cause is UNKNOWNProbably an Autoimmune disease

Inflammation of the arteries

thrombus formation occlusion of

the vessels

BUERGER’S DISEASE



ASSESSMENT FINDINGS

1. Leg PAIN

Foot cramps in the arch (instep

claudication) after exercise

Relieved by rest

Aggravated by smoking, emotional

disturbance and cold chilling

2. Digital rest pain not changed by activity

or rest

BUERGER’S DISEASE



ASSESSMENT FINDINGS

3. Intense RUBOR (reddish-blue

discoloration), progresses toCYANOSIS as disease advances

4. Paresthesia

BUERGER’S DISEASE



Diagnostic Studies

1. Duplex ultrasonography

2. Contrast angiography

BUERGER’S DISEASE




1. Assist in the medical and surgical

management

Bypass graft

amputation

2. Strongly advise to AVOID smoking3. Manage complications appropriately

BUERGER’S DISEASE



Nursing InterventionsPost-operative care: after amputation

Elevate stump for the FIRST 24 HOURS

to minimize edema and promote venousreturn

Place patient on PRONE position after 24

hoursAssess skin for bleeding and hematoma

Wrap the extremity with elastic bandage

RAYNAUD’S DISEASE



A form of intermittent arteriolarVASOCONSTRICTION that resultsin coldness, pain and pallor of the

fingertips or toes

Cause : UNKNOWN

Most commonly affects WOMEN, 16-40 years old

RAYNAUD’S DISEASE



ASSESSMENT FINDINGS1. Raynaud’s phenomenon

A localized episode of vasoconstriction of the smallarteries of the hands and feet

that causes color andtemperature changes

RAYNAUD’S DISEASE



W-B-RPallor- due to vasoconstriction,then

Blue- due to pooling of Deoxygenated blood

Red- due to exaggeratedreflow/hyperemia

RAYNAUD’S DISEASE



ASSESSMENT FINDINGS2. tingling sensation

3. Burning pain on the hands andfeet

RAYNAUD’S DISEASE



Medical management

Drug therapy with the use of

CALCIUM channel blockersTo prevent vasospasms

RAYNAUD’S DISEASE



Nursing Interventions1. instruct patient to avoid situationsthat may be stressful

2. instruct to avoid exposure to coldand remain indoors when the climateis cold

3. instruct to avoid all kinds of nicotine4. instruct about safety. Carefulhandling of sharp objects



Venous diseases

VARICOSE VEINS



THESE are dilated veinsusually in the lower

extremities

VARICOSE VEINS



Predisposing FactorsPregnancy

Prolonged standing or sitting

Constipation (forhemorrhoids)

Incompetent venous valves

VARICOSE VEINS



Pathophysiology

Factors venous stasis

increased hydrostaticpressure edema

VARICOSE VEINS



Assessment findings

Tortuous superficial veins

on the legs

Leg pain and Heaviness

Dependent edema

VARICOSE VEINS



Laboratory findings

Venography

Duplex scan

pletysmography

VARICOSE VEINS



Medical management

Pharmacological therapy

Leg vein stripping

Anti-embolic stockings

VARICOSE VEINS



Nursing management

1. Advise patient to elevate

the legs

2. Caution patient to avoid

prolonged standing or sitting



VARICOSE VEINS



Nursing management

5. Caution patient to

avoid knee-length

stockings and constrictive

clothings

VARICOSE VEINS



Nursing management6. Apply anti-embolic

stockings as directed7. Avoid massage on the

affected area



DVT- Deep Vein Thrombosis



Predisposing factors

Prolonged immobility

Varicosities

Traumatic procedures




Complication

PULMONARYthromboembolism



Laboratory findings

Venography

Duplex scan




Medical management

Antiplatelets

Anticoagulants

Vein stripping and

grafting

Anti-embolic stockings




Nursing management

1. Provide measures to avoid

prolonged immobilityRepositioning Q2

Provide passive ROM

Early ambulation




Nursing management

2. Provide skin care to

prevent the complication of leg ulcers

3. Provide anti-embolicstockings




Nursing management

4. Administer anticoagulants

as prescribed5. Monitor for signs of

pulmonary embolism



Blood disorders



AnemiaNutritional anemia

Hemolytic anemia Aplastic anemia

Sickle cell anemia

ANEMIA



A condition in whichthe hemoglobin

concentration islower than normal

ANEMIA



Three broad categories1. Loss of RBC- occurs with

bleeding

2. Decreased RBC production

3. Increased RBC destruction

Hypoproliferative Anemia



Iron Deficiency Anemia –Results when the

dietary intake of ironis inadequate to

produce hemoglobin




Iron Deficiency Anemia –Etiologic Factors –1. Bleeding- the most

common cause –2. Mal-absorption –3. Malnutrition

–4. Alcoholism




Iron Deficiency AnemiaPathophysiology

–The body stores of irondecrease, leading todepletion of hemoglobinsynthesis


fi i i



Iron Deficiency AnemiaPathophysiology

–The oxygen carryingcapacity of hemoglobin

is reduced tissuehypoxia




fi i i



Iron Deficiency Anemia Assessment Findings

5. Brittle nails6. Smooth and sore

tongue7. Angular cheilosis




I D fi i A i



Iron Deficiency AnemiaMedical management

1. Hematinics

2. Blood transfusion




Nursing Management

2 Ad i i t i



2. Administer ironOral preparations- liquid It stains teeth

Drink it with a strawStool may turn blackish- dark in

color

Advise to eat high-fiber diet tocounteract constipation


Nursing Management

2 Ad i i t i



2. Administer iron IM preparation Administer DEEP IM using the Z-

track method Avoid vigorous rubbingCan cause local pain and staining

APLASTIC ANEMIA

A diti



A conditioncharacterized by

decreased number of RBC as well as WBC

and platelets

APLASTIC ANEMIA

CAUSATIVE FACTORS



CAUSATIVE FACTORS1. Environmental toxins-

pesticides, benzene

2. Certain drugs-Chemotherapeutic agents,chloramphenicol,phenothiazines, Sulfonamides

3. Heavy metals4. Radiation

APLASTIC ANEMIA

P th h i l



PathophysiologyToxins cause a direct bonemarrow depression acellualrbone marrow decreasedproduction of blood elements

APLASTIC ANEMIA

ASSESSMENT FINDINGS



ASSESSMENT FINDINGS1. fatigue2. pallor

3. dyspnea4. bruising5. splenomegaly6. retinal hemorrhages

APLASTIC ANEMIA

LABORATORY FINDINGS



LABORATORY FINDINGS1. CBC- decreased blood cell

numbers

2. Bone marrow aspirationconfirms the anemia-hypoplastic or acellularmarrow replaced by fats

APLASTIC ANEMIA

M di l M t



Medical Management1. Bone marrowtransplantation2. Immunosupressantdrugs3. Rarely, steroids4. Blood transfusion

APLASTIC ANEMIA

N i t



Nursing management1. Assess for signs of bleeding and infection2. Instruct to avoidexposure to offending

agents

Megaloblastic Anemias

A i h t i d b



Anemias characterized byabnormally large RBCsecondary to impairedDNA synthesis due todeficiency of Folic acid

and/or vitamin B12


Folic Acid deficienc



Folic Acid deficiencyCausative factors

1. Alcoholism2. Mal-absorption

3. Diet deficient inuncooked vegetables


Pathophysiology of Folic acid

deficiency



deficiencyDecreased folic acid impaired

DNA synthesis in the bone

marrow impaired RBCdevelopment, impaired nuclearmaturation but CYTOplasmicmaturation continues largesize


Vitamin B12 deficiency



Vitamin B12 deficiencyCausative factors

1. Strict vegetarian diet

2. Gastrointestinalmalabsorption

3. Crohn's disease

4. gastrectomy






Pernicious Anemia

Due to the absence of intrinsicfactor secreted by the parietalcells

Intrinsic factor binds with Vit.B12 to promote absorption


Assessment findings



Assessment findings1. weakness

2. fatigue

3. listless

4. neurologic manifestations are

present only in Vit. B12deficiency


Assessment findings



Assessment findingsPernicious Anemia

–Beefy, red, swollen tongue

–Mild diarrhea

–Extreme pallor

–Paresthesias in the extremities


Laboratory findings



Laboratory findings1. Peripheral blood smear- shows

giant RBCs, WBCs with giant

hypersegmented nuclei2. Very high MCV

3. Schilling’s test

4. Intrinsic factor antibody test


Medical Management



Medical Management1. Vitamin supplementation

–Folic acid 1 mg daily

2. Diet supplementation – Vegetarians should have vitamin

intake

3. Lifetime monthly injection of IM Vit B12


Nursing Management



Nursing Management1. Monitor patient

2. Provide assistance in

ambulation3. Oral care for tongue sore

4. Explain the need for lifetimeIM injection of vit B12

Hemolytic Anemia: Sickle Cell

A severe chronic



A severe chronicincurable hemolytic

anemia that resultsfrom heritance of the

sickle hemoglobingene.


Causative factor



Causative factor –Genetic inheritance of

the sickle gene- HbS gene


Pathophysiology



PathophysiologyDecreased O2, Cold,

Vasoconstriction canprecipitate sickling

process


Pathophysiology

Factors cause defective



Factors cause defectivehemoglobin to acquire arigid, crystal-like C-shaped

configuration Sickled RBCswill adhere to endothelium pile up and plug the vessels ischemia results pain,swelling and fever


Assessment Findings

1 j di



1. jaundice

2. enlarged skull andfacial bones

3. tachycardia, murmursand cardiomegaly


Assessment Findings



Assessment FindingsPrimary sites of

thrombotic occlusion:spleen, lungs and CNS

Chest pain, dyspnea


Assessment Findings

1 Sickle cell crises



1. Sickle cell crises –Results from tissue hypoxia

and necrosis

2. Acute chest syndrome –Manifested by a rapidly falling

hemoglobin level, tachycardia,fever and chest infiltrates inthe CXR


Medical Management

1 B



1. Bone marrowtransplant

2. Hydroxyurea

–Increases the HbF

3. Long term RBCtrnasfusion


Nursing Management



Nursing Management1. manage the pain

–Support and elevateacutely inflamed joint

–

Relaxation techniques –analgesics


Nursing Management



Nursing Management2. Prevent and manage

infection –Monitor status of patient

–Initiate prompt antibiotictherapy


Nursing Management

3 Promote coping skills



3. Promote coping skills

–Provide accurate

information – Allow patient to verbalize

her concerns aboutmedication, prognosis andfuture pregnancy


Nursing Management

4 Monitor and prevent



4. Monitor and preventpotential complications

–Provide always adequatehydration

–

Avoid cold, temperaturethat may causevasoconstriction


Nursing Management



Nursing Management4. Monitor and prevent

potential complications –Leg ulcer

Aseptic technique


Nursing Management

4 Monitor and prevent



4. Monitor and preventpotential complications

–PriapismSudden painful erection

Instruct patient to emptybladder, then take a warmbath



Polycythemia

POLYCYTHEMIA VERA



POLYCYTHEMIA VERA –Primary Polycythemia

–

A proliferative disorder inwhich the myeloid stemcells become uncontrolled

Polycythemia

POLYCYTHEMIA VERA



POLYCYTHEMIA VERACausative factor

–unknown

Polycythemia

POLYCYTHEMIA VERA

Pathophysiology



Pathophysiology –The stem cells grow

uncontrollably –The bone marrow becomes

HYPERcellular and all theblood cells are increased innumber

Polycythemia

POLYCYTHEMIA VERA

Pathophysiology



Pathophysiology

–The spleen resumes its

function of hematopoiesisand enlarges

–

Blood becomes thick andviscous causing sluggishcirculation

Polycythemia

POLYCYTHEMIA VERA

Pathophysiology



Pathophysiology

–Overtime, the bone marrow

becomes fibrotic

PolycythemiaPOLYCYTHEMIA VERA

Assessment findings



Assessment findings –1. Skin is ruddy

–2. Splenomegaly

–3. headache

–

4. dizziness, blurred vision –5. Angina, dyspnea and

thrombophlebitis


Laboratory findings



Laboratory findings –1. CBC- shows elevated RBC

mass –2. Normal oxygen saturation

–3 Elevated WBC andPlatelets


Complications



Complications –1. Increased risk for

thrombophlebitis, CVA andMI

–2. Bleeding due to

dysfunctional blood cells


Medical Management



Medical Management –1. To reduce the high blood

cell mass- PHLEBOTOMY –2. Allopurinol

–3. Dipyridamole

–4. Chemotherapy tosuppress bone marrow

Polycythemia Nursing Management

–1. Primary role of the nurse is

EDUCATOR



–2. Regularly asses for thedevelopment of complications

–3. Assist in weekly phlebotomy

–4. Advise to avoid alcohol andaspirin

–5. Advise tepid sponge bath or coolwater to manage pruritus

Leukemia

Malignant disorders of blood

forming cells characterized byUNCONTROLLED lif ti



forming cells characterized byUNCONTROLLED proliferationof WHITE BLOOD CELLS in

the bone marrow- replacingmarrow elements . The WBCcan also proliferate in theliver, spleen and lymphnodes.



Leukemia

The leukemias are namedalso according to the



The leukemias are namedalso according to thematuration of cells

ACUTE –The cells are primarily

immature

CHRONIC

–The cells are primarily mature



Leukemia

ETIOLOGIC FACTORSUNKNOWM



ETIOLOGIC FACTORS –UNKNOWM

–Probably exposure to radiation

–Chemical agents

–Infectious agents

–Genetic

Leukemia

–PATHOPHYSIOLOGY of ACUTELeukemia



Leukemia

Uncontrolled proliferation of

immature cells suppressesbone marrow function severeanemia, thrombocytopenia and

granulocytopenia

Leukemia

–PATHOPHYSIOLOGY of CHRONIC Leukemia



CHRONIC Leukemia

Uncontrolled proliferation of

DIFFERENTIATED cells slowsuppression of bone marrowfunction milder symptoms

Leukemia

ASSESSMENT FINDINGS

ACUTE LEUKEMIA



– Pallor

– Fatigue

–Dyspnea

– Hemorrhages

– Organomegaly

–Headache

– vomiting

Leukemia

ASSESSMENT FINDINGS

CHRONIC LEUKEMIA



CHRONIC LEUKEMIA

–Less severe symptoms

–organomegaly



Leukemia

Medical Management

1 Chemotherapy



1. Chemotherapy

2. Bone marrow transplantation

Leukemia

Nursing Management

1 Manage AND prevent infection



1. Manage AND prevent infection

– Monitor temperature

– Assess for signs of infection

– Be alert if the neutrophil countdrops below 1,000 cells/mm3

Leukemia

Nursing Management

2. Maintain skin integrity



g y

3. Provide pain relief

4. Provide information as to therapy-chemo and bone marrowtransplantation

cardio med-surg nursing

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