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Nursing Board Review

Cardiovascular System



The Cardiovascular System

Normal Anatomy

The heart is located in the LEFT side of the

mediastinum

Consists of Three layers- epicardium,

myocardium and endocardium




The epicardium covers the outer surface of

the heart

The myocardium is the middle muscular layer 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 also has four chambers-

two atria and two ventricles

The Left atrium and the right

atrium

The left ventricle and the right

ventricle




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 twonodes- 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 THEHEAR T

Consists of the1. SA node- the pacemaker

2. AV node- slowest conduction

3. Bundle of H

is ± branches into t

he Rig

htand 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-lunar

valves

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 bpm

Bradycardia is less than 60 bpm

Sympathetic system INCREASES HR

Parasympathetic system (Vagus)

DECREASES HR



The Cardiovascular SystemBlood 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 value5. 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





CARDIAC Proteins and

enzymesCK- MB ( creatine

kinase)

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





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




LABORAT

ORY PROCEDURESTroponin I and T

REMEMBER to AVOIDIM injections before

obtaining blood sample!

Early and late diagnosis can

be made!




LABORAT

ORY PROCEDURESSERUM LIPIDS

Lipid profile measures theserum cholesterol,triglycerides and lipoprotein

levelsCholesterol= 200 mg/dL

Triglycerides- 40- 150 mg/dL




LABORAT

ORY PROCEDURESSERUM 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 studiesthe 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

Treadmill testing is the most

commonly used stress testUsed to determine CAD,

Chest pain causes, drugeffects and dysrhythmias inexercise





Post-test: instruct client tonotify the physician if anychest 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 anychest 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 toseafood 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 thecatheter 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





Maintain strict bed rest for 6-12 hours

Client may turn from side to side but bed

should not be elevated more than 30 degreesand legs always straight

Encourage fluid intake to flush out the dye

Immobilize the arm if the antecubital veinis used

Monitor for dye allergy





CVP

The CVP is the pressurewithin the SVC

Reflects the pressure under

which blood is returned tothe SVC and right atrium





CVP

Normal CVP is 0 to 8 mmHg/ 4-1

0 cm H2OElevated CVP indicates increasein blood volume, excessive IVF or

heart/renal failureLow CVP may indicatedhypovolemia, hemorrhage and

severe vasodilatation





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, 4th

ICS 3. 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 examination

Vital signs- BP, PP, MAP

Inspection of the skinInspection of the thorax

Palpation of the PMI, pulsesAuscultation of the heartsounds



CARDIAC ASSESSMENT3. r t r i stic st ies

c r i c c t eteriz ti

i i r filerteri r

r i c e z es r tei s

lter it ri

ercise



CARDIAC

IMPLEMENTATION

1. Assess the cardio-pulmonary

status

VS, BP, Cardiac assessment

2. Enhance cardiac output

Establish IV line to administerfluids



CARDIAC

IMPLEMENTATION

3. Promote gas exchange

Administer O2

Position client in SEMI -F owler¶s

Encourage coughing and deep

breathing exercises



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

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

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 Failure

Infective Endocarditis

Cardiac TamponadeCardiogenic Shock



VASCULAR DISEASES

Hypertension

Buerger¶s diseaseVaricose 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



CAD

RISK FACTORS1. 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



CAD

RISK FACTORSMost 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

PathophysiologyThere 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



Angina Pectoris: Clinical Syndromes

Three Common Types of ANGINA

1. STABLE ANGINA

The typical angina thatoccurs during exertion,relieved by rest and drugsand the severity does not change




Three Common Types of ANGINA2. Unstable angina

Occurs unpredictably

during exertion andemotion, severity increaseswith time and pain may not

be relieved by rest and drug




Three Common Types of ANGINA3. Variant angina

Prinzmetal angina, results

from coronary arteryVASOSPASMS, may occur at rest



Angina Pectoris

ASSESSMENT FINDINGS

1. Chest pain- ANGINA

The most characteristic symptom

PAIN 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 E xercise, E ating

heavy meals, E motions like

excitement and anxiety and

E xtremes of temperature

Relieved by REST and Nitroglycerin



Angina Pectoris

ASSESSMENT FINDINGS

2. Diaphoresis

3. Nausea and vomiting

4. 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 changesmay 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 HR Calcium-channel blockers- to dilatecoronary artery and reduce vasospasm



2. Teach the patient management of anginal

attacksAdvise 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 seek medical attention



Angina Pectoris

3. Obtain a 12-lead ECG

4. Promote myocardial perfusion

Instruct patient to maintain bed restAdminister 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 transluminal

coronary angioplastyTo 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 risk factors that can be modified

8. Refer patient to proper

agencies



Myocardial infarction

Death of myocardial

tissue in regions of theheart with abrupt

interruption of coronary

blood supply




ETIOLOGY and Risk factors

1. CAD

2. Coronary vasospasm

3. 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 triggersautonomic nervous system response further imbalance of myocardialO2 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

N OT relieved by rest or

nitroglycerin

Lasts 30 minutes or longer




Assessment findings

2. Dyspnea

3. Diaphoresis4. 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




Nursing Interventions1. Provide Oxygen at 2 lpm, Semi-fowler¶s

2. Administer medications

Morphine to relieve painnitrates, 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 diet

Provide 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 MORPHI N E

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

exercises

3. 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 AFTER ACUTE EPISODE

Cardiac rehabilitationTo extend and improve quality of life

Physical conditioning

Patients who are able to walk 3-4 mphare 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 decreased bloodejection increased bloodremaining in the ventricle

ventricular stretching anddilatation.

SYSTOLIC DYSFUNCTION

HYPERTROPHIC



HYPER TROPHIC

CARDIOMYOPATHY

Associated factors:

1. Genetic2. Idiopathic

HYPERTROPHIC



HYPER TROPHIC

CARDIOMYOPATHY

Pathophysiology

Increased size of myocardium

reduced ventricular volumeincreased resistance to

ventricular filling diastolic

dysfunction

RESTRICTIVE



RESTRICTIVE

CARDIOMYOPATHY

Associated factors

1. Infiltrative diseases like

AMYLOIDOSIS

2. Idiopathic

RESTRICTIVE



ST CT V

CARDIOMYOPATHY

Pathophysiology

Rigid ventricular wall

impaired stretch and diastolic

filling decreased output

Diastolic dysfunction



CARDIOMYOPATHIESAssessment findings

1. 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



CARDIOMYOPATHIES

Medical Management

1. Surgery

2. pacemaker insertion

3. Pharmacological drugs for

symptom relief



CARDIOMYOPATHIES

Nursing Management

1.Improve cardiac output

Adequate rest

Oxygen therapy

Low sodium diet



CARDIOMYOPATHIES

Nursing Management

2. Increase patient tolerance

Schedule activities with rest

periods in between



CARDIOMYOPATHIES

Nursing Management

3. Reduce patient anxiety

Support

Offer information abouttransplantations

Support family in anticipatorygrieving



Infective endocarditis

Infection of the heart

valves and the endothelial

surface of the heart

Can be acute or chronic




Etiologic factors

1. Bacteria- Organism

depends on several factors

2. Fungi




Risk factors

1. Prosthetic valves

2. Congenital malformation

3. Cardiomyopathy

4. IV drug users5. Valvular dysfunctions




Pathophysiology

Direct invasion of microbes

microbes adhere to damagedvalve surface and proliferatedamage attracts platelets

causing clot formation

erosionof valvular leaflets andvegetation can embolize




Assessment findings

1. Intermittent fever

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

4. splinter hemorrhages undernails




Assessment findings

5. Osler¶s nodes- painful

nodules on fingerpads

6. Roth¶s spots- pale

hemorrhages in the retina




Assessment findings

7. Heart murmurs

8. Heart failure




Prevention

Antibiotic prophylaxis if

patient is undergoingprocedures like dental

extractions, bronchoscopy,surgery, etc.




LABORATORY EXAM

Blood Cultures to determine

the exact organism




Nursing management

1. regular monitoring of

temperature, heart sounds

2. manage infection

3. long-term antibiotictherapy




Medical management

1. Pharmacotherapy

IV antibiotic for 2-6 weeks

Antifungal agents are given ±

amphotericin B




Medical management

2. Surgery

Valvular replacement



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

Etiology of CHF1. CAD

2. Valvular heart diseases

3. Hypertension4. MI

5. Cardiomyopathy

6. Lung diseases

7. Post-partum

8. Pericarditis and cardiac tamponade



k A i i



New York Heart Association

Class 2

SLIGHT limitation of ADLs

NO symptom at restSymptom with INCREASEDactivity

Basilar crackles and S3

N Y k H A i i




Class 3

Markedly limitation on ADLs

Comfortable at rest BUT

symptoms present in LESS

than ordinary activity

N Y k H A i i




Class 4

SYMPTOMS are present at

rest

CHF



CHF

PATHOPHYSIOLOGY

LEFT Ventricular pump

failure back up of blood intothe pulmonary veinsincreased pulmonarycapillary pressurepulmonary congestion

CHF



CHF

PATHOPHYSIOLOGY

LEFT ventricular failure

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



CHF



CHF

PATHOPHYSIOLOGY

RIGHT ventricularfailure 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. Cyanosis9. 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 FINDINGS

1. 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 AFTER THE ACUTE STAGE

1. Provide opportunities forverbalization of feelings

2. 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

ETIOLOGY

1. 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



CARDIOGENIC SHOCK


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



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



CARDIAC TAMPONADE

A condition where the heart

is unable to pump blood due

to accumulation of fluid inthe pericardial sac

(pericardial effusion)

CARDIAC TAMPONADE



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



CARDIAC TAMPONADE

Causative factors

1. Cardiac trauma

2. Complication of Myocardial

infarction

3. Pericarditis4. Cancer metastasis

CARDIAC TAMPONADE



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



CARDIAC TAMPONADE

ASSESSMENT FINDINGS

5. Syncope

6. anxiety

7. dyspnea

8. Percussion- Flatness across theanterior chest

CARDIAC TAMPONADE



CARDIAC TAMPONADE

Laboratory FINDINGS

1. Echocardiogram

2. Chest X-ray

CARDIAC TAMPONADE



CARDIAC TAMPONADE

N R IN INTER ENTION

. Assist i PERI RDI E TES I S

2. A i ister I

3. M it r EC , ri e t t P

. M it r f r rec rre ce f t e

Pericardiocentesis



Pericardiocentesis

Patient is monitored by ECG

Maintain emergency equipments

Elevate head of bed 45-60 degrees

Monitor for complications-

coronary artery rupture,

dysrhythmias, pleural laceration

and myocardial trauma

HYPERTENSION



HYPER TENSION

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



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



HYPER TENSION

CLASSIFICATION OF

HYPERTENSION by JNC-

VII



HYPER TENSION



PATHOPHYSIOLOGYMultifactorial 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 the

peripheral vessels

5. insulin resistance

HYPERTENSION



HYPER TENSION

ASSESSMENT FINDINGS

1. Headache

2. Visual changes

3. chest pain

4. dizziness5. N/V

HYPER TENSION



NS ON

Risk factors for CardiovascularProblems in Hypertensive patients

Major Risk factors

1. Smoking

2. Hyperlipidemia

3. DM

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

6. Family History

HYPER TENSION



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

HYPER TENSION



MEDICAL

MANAGEMENT

1. Lifestyle modification

2. Drug therapy

3. Diet therapy

HYPER TENSION



MEDICAL MANAGEMENT

Drug therapy

Diuretics

Beta blockersCalcium channel blockers

ACE inhibitors

A2

Receptor blockersVasodilators

HYPER TENSION




1. Provide health teaching topatient

Teach about the disease process

Elaborate on lifestyle changes

Assist in meal planning to loseweight

HYPER TENSION




1. Provide health teaching to thepatient

Provide list of LOW fat , LOW sodium diet of less than 2-3 gramsof N a/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

HYPER TENSION



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



Vascular Diseases



ANEURYSM



Saccular= when one side of the vessel is

affected

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 AR TERIAL

OCCLUSIVE DISEASE



Risk factors for Peripheral Arterialocclusive disease

Modifiable

1. Smoking

2. HPN

3. Obesity


5. DM

6. Stress


OCCLUSIVE DISEASE



ASSESSMENT FINDINGS

1. I N TERMITTE N T CLAUDICATION - the hallmark of PAOD

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


OCCLUSIVE DISEASE



ASSESSMENT FINDINGS

1. INTERMITTENT

CLAUDICATION- the hallmark of PAOD

This pain is RELIEVED by REST

This commonly affects the musclegroup below the arterial occlusion


OCCLUSIVE DISEASE



Assessment Findings

2. Progressive pain on the

extremity as the disease advances3. Sensation of cold andnumbness of the extremities


OCCLUSIVE DISEASE



Assessment Findings

4. Skin is pale when elevated and

cyanotic/ruddy when placed on adependent position

5. Muscle atrophy, leg ulceration

and gangrene


OCCLUSIVE DISEASE



Diagnostic Findings

1. Unequal pulses between the

extremities2. Duplex ultrasonography

3. Doppler flow studies




OCCLUSIVE DISEASE



Nursing Interventions

1. Maintain Circulation to the

extremity

Evaluate regularly peripheral pulses,

temperature, sensation, motor

function and capillary refill timeAdminister post-operative care to

patient who underwent surgery


OCCLUSIVE DISEASE




2. Monitor and manage complications

Note for bleeding, hematoma,decreased urine output

Elevate the legs to diminish edema

Encourage exercise of the extremitywhile on bed

Teach patient to avoid leg-crossing


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 20-35

RISK 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




1. Assist in the medical and surgical

management

Bypass graft

amputation

2. Strongly advise to AVOID smoking3. Manage complications appropriately



RAYNAUD¶S DISEASE



W-B-R

Pallor- due to vasoconstriction,then

Blue- due to pooling of Deoxygenated blood

Red- due to exaggeratedreflow/hyperemia

RAYNAUD¶S DISEASE



ASSESSMENT FINDINGS

2. 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




1. 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 veins

usually in the lower

extremities

VARICOSE VEINS



Predisposing FactorsPregnancy

Prolonged standing or sittingConstipation (forhemorrhoids)

Incompetent venous valves

VARICOSE VEINS



Pathophysiology

Factors venous stasis

increased hydrostatic

pressure 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



Nursing management

1. Advise patient to elevate

the legs

2. Caution patient to avoid

prolonged standing or sitting

VARICOSE VEINS



Nursing management

3. Provide high-fiber foods

to prevent constipation

4. Teach simple exercise to

promote venous return



VARICOSE VEINS



Nursing management

6. Apply anti-embolic

stockings as directed7. Avoid massage on the

affected area

DVT- Deep Vein Thrombosis



Inflammation of the deep

veins of the lower extremities

and the pelvic veinsThe inflammation results to

formation of blood clots inthe area




Predisposing factors

Prolonged immobility

Varicosities

Traumatic procedures




Complication

PULMONARYthromboembolism




Assessment findings

Leg tenderness

Leg pain and edema

Positive HOMAN¶s SIGN




Laboratory findings

Venography

Duplex scan




Medical management

Antiplatelets

Anticoagulants

Vein stripping and

grafting

Anti-embolic stockings




Nursing management

1. Provide measures to avoid

prolonged immobility

Repositioning 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 prescribed

5. Monitor for signs of

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