Cardiovascular & Hematologic System

CARDIOLOGY NURSING

THE CARDIOVASCULAR SYSTEM

HEART’S 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 visceral pericardium

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 Cardiovascular System

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 the RIGHT 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 anterior wall of the LEFT ventricle, the anterior septum and the Apex of the left ventricle

The CIRCUMFLEX branch supplies the left atrium and the posterior LEFT ventricle

The CONDUCTING SYSTEM OF THE HEART

Consists of the

1. SA node- the pacemaker

2. AV node- slowest conduction

3. Bundle of His – branches into the Right and 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

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 blood away from the heart to the periphery

The veins are the vessels that carry blood to the 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 fluid from the tissues and returns it to the blood

Cardiac Assessment

Laboratory Test Rationale

1. To assist in diagnosing MI

2. 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

The Cardiovascular System LABORATORY PROCEDURES

CARDIAC Proteins and enzymes

CK- MB ( creatine kinase)

Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days

CK- MB ( creatine kinase)

Normal value is 0-7 U/L

Lactic Dehydrogenase (LDH)

Elevates in MI in 24 hours, peaks in 48-72 hours

Normally 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 hours

Returns to normal in a day

Myoglobin

Not used alone

Muscular and RENAL disease can have elevated myoglobin

Troponin I and T

Troponin 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 AVOID IM injections before obtaining blood sample!

Early and late diagnosis can be made!

SERUM LIPIDS

Lipid profile measures the serum cholesterol, triglycerides and lipoprotein levels

Cholesterol= 200 mg/dL

Triglycerides- 40- 150 mg/dL

SERUM LIPIDS

LDH- 130 mg/dL

HDL- 30-70- mg/dL

NPO post midnight (usually 12 hours)

ELECTROCARDIOGRAM (ECG)

A non-invasive procedure that evaluates the electrical activity of the heart

Electrodes and wires are attached to the patient

Holter Monitoring

A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours

Holter Monitoring

Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop

ECHOCARDIOGRAM

Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound

No special preparation is needed

Stress Test

A non-invasive test that studies the heart during activity and detects and evaluates CAD

Exercise test, pharmacologic test and emotional test

Stress Test

Treadmill testing is the most commonly used stress test

Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise

Stress Test

Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine

Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath . Instruct client to avoid taking a hot shower for 10-12 hours after the test

Pharmacological stress test

Use of dipyridamole

Maximally dilates coronary artery

Side-effect: flushing of face

Pharmacological stress test

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

Post test: report symptoms of chest pain

CARDIAC catheterization

Insertion of a catheter into the heart and surrounding vessels

Determines the structure and performance of the heart valves 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, blood tests and document the peripheral 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 the heart; inform the patient that a feeling of warmth and metallic taste may occur when dye is administered

Post-test: Monitor VS and cardiac rhythm

Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site

Maintain sandbag to the insertion site if required to maintain pressure

Monitor for bleeding and hematoma formation

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 vein is used

Monitor for dye allergy

CVP

The CVP is the pressure within the SVC

Reflects the pressure under which blood is returned to the SVC and right atrium

CVP

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

Elevated CVP indicates increase in blood volume, excessive IVF or heart/renal failure

Low CVP may indicated hypovolemia, hemorrhage and severe vasodilatation

Measuring CVP

1. Position the client supine with bed elevated at 45 degrees

2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4 th ICS

3. Instruct the client to be relaxed and avoid coughing and straining.

CARDIAC ASSESSMENT

ASSESSMENT

1. Health History

Obtain description of present illness 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 skin

Inspection of the thorax

Palpation of the PMI, pulses

Auscultation of the heart sounds

CARDIAC ASSESSMENT

3. Laboratory and diagnostic studies

CBC

cardiac catheterization

Lipid profile

arteriography

Cardiac enzymes and proteins

CXR

CVP

EEG

Holter monitoring

Exercise ECG

CARDIAC IMPLEMENTATION

Assess the cardio-pulmonary status

VS, BP, Cardiac assessment

2. Enhance cardiac output

Establish IV line to administer fluids

3. Promote gas exchange

Administer O2

Position client in SEMI-Fowler’s

Encourage coughing and deep breathing exercises

4. Increase client activity tolerance

Balance rest and activity periods

Assist in daily activities

5. Promote client comfort

Assess the client’s description of pain and chest discomfort

Administer medication as prescribed

6. Promote adequate sleep

7. Prevent infection

Monitor skin integrity of lower extremities

Assess skin site for edema, redness and warmth

Monitor for fever

Change position frequently

8. Minimize patient anxiety

Encourage verbalization of feelings, fears and concerns

Answer client questions. Provide information about procedures and medications

CARDIAC DISEASES

Coronary Artery Disease

Myocardial Infarction

Congestive Heart Failure

Infective Endocarditis

Cardiac Tamponade

Cardiogenic Shock

VASCULAR DISEASES

Hypertension

Buerger’s disease

Varicose veins

Deep vein thrombosis

Aneurysm

CAD

CAD results from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous plaque in the vessel wall

CAD

RISK FACTORS

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

2. Family History

3. Hypertension

4. DM

5. Smoking

6. Obesity

7. Sedentary lifestyle

8. Hyperlipedimia

CAD

RISK FACTORS

Most important MODIFIABLE factors:

Smoking

Hypertension

Diabetes

Cholesterol abnormalities

CAD

Pathophysiology

Fatty streak formation in the vascular intima  T-cells and monocytes ingest lipids in the area of deposition  atheroma  narrowing of the arterial lumen  reduced coronary blood flow  myocardial ischemia

CAD

Pathophysiology

There is decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply

If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, this becomes significant

Potential for Thrombosis and embolism

Angina Pectoris

Chest pain resulting from coronary atherosclerosis or myocardial ischemia

Angina Pectoris: Clinical Syndromes

Three Common Types of ANGINA

1. STABLE ANGINA

The typical angina that occurs during exertion, relieved by rest and drugs and the severity does not change

2. Unstable angina

Occurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and drug

3. Variant angina

Prinzmetal angina, results from coronary artery VASOSPASMS, may occur at rest

Angina Pectoris

ASSESSMENT FINDINGS

1. Chest pain- ANGINA

The most characteristic symptom

PAIN is described as mild to severe 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 and doom

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 wave inversion

2. Cardiac catheterization

Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions

Angina Pectoris

NURSING MANAGEMENT

1. Administer prescribed medications

Nitrates- to dilate the coronary arteries

Aspirin- to prevent thrombus formation

Beta-blockers- to reduce BP and HR

Calcium-channel blockers- to dilate coronary artery and reduce vasospasm

2. Teach the patient management of anginal attacks

Advise patient to stop all activities

Put one nitroglycerin tablet under the tongue

Wait for 5 minutes

If not relieved, take another tablet and wait for 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 rest

Administer O2 @ 3 lpm

Advise to avoid valsalva maneuvers

Provide laxatives or high fiber diet to lessen constipation

Encourage to avoid increased physical activities

Angina Pectoris

5. Assist in possible treatment modalities

PTCA- percutaneous transluminal coronary angioplasty

To compress the plaque against the vessel wall, increasing the arterial lumen

CABG- coronary artery bypass graft

To improve the blood flow to the myocardial tissue

Angina Pectoris

6. Provide information to family members to minimize anxiety and promote family cooperation

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 the heart with abrupt interruption of coronary blood supply

ETIOLOGY and Risk factors

1. CAD

2. Coronary vasospasm

3. Coronary artery occlusion by embolus and thrombus

4. Conditions that decrease perfusion- hemorrhage, shock

Risk factors

1. Hypercholesterolemia

2. Smoking

3. Hypertension

4. Obesity

5. Stress

PATHOPHYSIOLOGY

Interrupted coronary blood flow  myocardial ischemia  anaerobic myocardial metabolism for several hours  myocardial death  depressed cardiac function  triggers autonomic nervous system response  further imbalance of myocardial O2 demand and supply

ASSESSMENT findings

1. CHEST PAIN

Chest pain is described as severe, persistent, crushing substernal discomfort

Radiates to the neck, arm, jaw and back

ASSESSMENT findings

1. CHEST PAIN

Occurs without cause, primarily early 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 doom

7. 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- Exercise tolerance test, thallium scans, cardiac catheterization

Nursing Interventions

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

2. Administer medications

Morphine to relieve pain

nitrates, thrombolytics, aspirin and anticoagulants

Stool softener and hypolipidemics

3. Minimize patient anxiety

Provide information as to procedures and 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 modalities such as PTCA and CABG

8. Monitor for complications of MI- especially dysrhythmias, since ventricular tachycardia can happen in the first few hours after MI

9. Provide client teaching

MI

Medical Management

1. ANALGESIC

The choice is MORPHINE

It reduces pain and anxiety

Relaxes bronchioles to enhance oxygenation

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 INTERVENTIONS AFTER ACUTE EPISODE

1. Maintain bed rest for the first 3 days

2. Provide passive ROM exercises

3. Progress with dangling of the feet at side of bed

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

5. Proceed with ambulation in the room  toilet  hallway TID

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  decreased blood ejection  increased blood remaining in the ventricle  ventricular stretching and dilatation.

SYSTOLIC DYSFUNCTION

HYPERTROPHIC CARDIOMYOPATHY

Associated factors:

1. Genetic

2. 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 findings

1. PND

2. Orthopnea

3. Edema

4. Chest pain

5. Palpitations

6. dizziness

7. Syncope with exertion

CARDIOMYOPATHIES

Laboratory Findings

1. CXR- may reveal cardiomegaly

2. 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 about transplantations

Support family in anticipatory grieving

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 users

5. Valvular dysfunctions

Pathophysiology

Direct invasion of microbes  microbes adhere to damaged valve surface and proliferate  damage attracts platelets causing clot formation  erosion of valvular leaflets and vegetation can embolize

Assessment findings

1. Intermittent HIGH fever

2. anorexia, weight loss

3. cough, back pain and joint pain

4. splinter hemorrhages under nails

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 undergoing procedures 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 antibiotic therapy

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 by inadequate cardiac function and inadequate cardiac output to meet the metabolic demands of tissues

CHF

Inability of the heart to pump sufficiently

The heart is unable to maintain adequate circulation to meet the metabolic needs of the body

Classified according to the major ventricular dysfunction- Left or Right

CHF

Etiology of CHF

1. CAD

2. Valvular heart diseases

3. Hypertension

4. MI

5. Cardiomyopathy

6. Lung diseases

7. Post-partum

8. Pericarditis and cardiac tamponade

New York Heart Association

Class 1

Ordinary physical activity does NOT cause chest pain and fatigue

No pulmonary congestion

Asymptomatic

NO limitation of ADLs

Class 2

SLIGHT limitation of ADLs

NO symptom at rest

Symptom with INCREASED activity

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

PATHOPHYSIOLOGY

LEFT Ventricular pump failure  back up of blood into the pulmonary veins  increased pulmonary capillary pressure  pulmonary congestion

CHF

PATHOPHYSIOLOGY

LEFT ventricular failure  decreased cardiac output  decreased perfusion to the brain, kidney and other tissues  oliguria, dizziness

CHF

PATHOPHYSIOLOGY

RIGHT ventricular failure  blood pooling in the venous circulation  increased hydrostatic pressure  peripheral edema

CHF

PATHOPHYSIOLOGY

RIGHT ventricular failure  blood pooling  venous congestion in the kidney, liver and GIT

LEFT SIDED CHF ASSESSMENT FINDINGS

1. Dyspnea on exertion

2. PND

3. Orthopnea

4. Pulmonary crackles/rales

5. cough with Pinkish, frothy sputum

6. Tachycardia

LEFT SIDED CHF 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

1. Peripheral dependent, pitting edema

2. Weight gain

3. Distended neck vein

4. hepatomegaly

5. Ascites

RIGHT SIDED CHF ASSESSMENT FINDINGS

6. Body weakness

7. Anorexia, nausea

8. Pulsus alternans

CHF

LABORATORY FINDINGS

1. CXR may reveal cardiomegaly

2. ECG may identify Cardiac hypertrophy

3. Echocardiogram may show hypokinetic heart

CHF

LABORATORY FINDINGS

4. ABG and Pulse oximetry may show decreased O2 saturation

5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF

CHF

NURSING INTERVENTIONS

1. Assess patient's cardio-pulmonary status

2. Assess VS, CVP and PCWP. Weigh patient daily to monitor fluid retention

CHF

3. Administer medications- usually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators and hypolipidemics are prescribed

CHF

4. Provide a LOW sodium diet. Limit fluid intake as necessary

5. Provide adequate rest periods to prevent fatigue

CHF

6. Position on semi-fowler’s to fowler’s for adequate chest expansion

7. Prevent complications of immobility

CHF

NURSING INTERVENTION AFTER THE ACUTE STAGE

1. Provide opportunities for verbalization of feelings

2. Instruct the patient about the medication regimen- digitalis, vasodilators and diuretics

3. Instruct to avoid OTC drugs, Stimulants, smoking and alcohol

CHF

4. Provide a LOW fat and LOW sodium diet

5. Provide potassium supplements

6. Instruct about fluid restriction

CHF

7. Provide adequate rest periods and schedule activities

8. Monitor daily weight and report signs of fluid retention

CARDIOGENIC SHOCK

Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion

ETIOLOGY

1. Massive MI

2. Severe CHF

3. Cardiomyopathy

4. Cardiac trauma

5. Cardiac tamponade

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

LABORATORY FINDINGS

Increased CVP

Normal is 4-10 cmH2O

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

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 and nitrates

CARDIAC TAMPONADE

A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion)

CARDIAC TAMPONADE

This condition restricts ventricular filling resulting to decreased cardiac output

Acute tamponade may happen when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac

CARDIAC TAMPONADE

Causative factors

1. Cardiac trauma

2. Complication of Myocardial infarction

3. Pericarditis

4. Cancer metastasis

CARDIAC TAMPONADE

ASSESSMENT FINDINGS

1. BECK’s Triad- Jugular vein distention, hypotension and distant/muffled heart sound

2. Pulsus paradoxus

3. Increased CVP

4. decreased cardiac output

CARDIAC TAMPONADE

ASSESSMENT FINDINGS

5. Syncope

6. anxiety

7. dyspnea

8. Percussion- Flatness across the anterior 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 degrees

Monitor 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 90 mmHg over a sustained period, based on two or more BP measurements .

HYPERTENSION

Types of Hypertension

1. Primary or ESSENTIAL

Most common type

2. Secondary

Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushing’s, Conn’s , SIADH

HYPERTENSION

CLASSIFICATION OF HYPERTENSION by JNC-VII

HYPERTENSION

PATHOPHYSIOLOGY

Multi-factorial etiology

BP= CO (SV X HR) x TPR

Any increase in the above parameters will increase BP

1. Increased sympathetic activity

2. Increased absorption of Sodium, and water in the kidney

HYPERTENSION

PATHOPHYSIOLOGY

Multifactorial etiology

BP= CO (SV X HR) x TPR

Any increase in the above parameters will increase BP

3. Increased activity of the RAAS

4. Increased vasoconstriction of the peripheral vessels

5. insulin resistance

HYPERTENSION

ASSESSMENT FINDINGS

1. Headache

2. Visual changes

3. chest pain

4. dizziness

5. N/V

HYPERTENSION

Risk factors for Cardiovascular Problems in Hypertensive patients

Major Risk factors

1. Smoking

2. Hyperlipidemia

3. DM

4. Age older than 60

5. 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 MANAGEMENT

Drug therapy

Diuretics

Beta blockers

Calcium channel blockers

ACE inhibitors

A2 Receptor blockers

Vasodilators

HYPERTENSION

1. Provide health teaching to patient

Teach about the disease process

Elaborate on lifestyle changes

Assist in meal planning to lose weight

HYPERTENSION

1. Provide health teaching to the patient

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

Limit alcohol intake to 30 ml/day

Regular aerobic exercise

Advise to completely Stop smoking

HYPERTENSION

2. Provide information about anti-hypertensive drugs

Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition

Instruct to avoid over-the-counter drugs that may interfere with the current medication

HYPERTENSION

Nursing Intervention

3. Promote Home care management

Instruct regular monitoring of BP

Involve family members in care

Instruct regular follow-up

4. Manage hypertensive emergency and urgency properly

Vascular Diseases

ANEURYSM

Dilation involving an artery formed at a weak point in the vessel wall

ANEURYSM

Saccular= when one side of the vessel is affected

Fusiform= when the entire segment becomes dilated

ANEURYSM

RISK FACTORS

Atherosclerosis

Infection= syphilis

Connective tissue disorder

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

Asymptomatic

Pulsatile sensation on the abdomen

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

Risk factors for Peripheral Arterial occlusive disease

Non-Modifiable

1. Age

2. gender

3. family predisposition

Risk factors for Peripheral Arterial occlusive disease

Modifiable

1. Smoking

2. HPN

3. Obesity

5. DM

6. Stress

ASSESSMENT FINDINGS

1. INTERMITTENT CLAUDICATION- the hallmark of PAOD

This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of exercise or activity

ASSESSMENT FINDINGS

1. INTERMITTENT CLAUDICATION- the hallmark of PAOD

This pain is RELIEVED by REST

This commonly affects the muscle group below the arterial occlusion

Assessment Findings

2. Progressive pain on the extremity as the disease advances

3. Sensation of cold and numbness of the extremities

Assessment Findings

4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position

5. Muscle atrophy, leg ulceration and gangrene

Diagnostic Findings

1. Unequal pulses between the extremities

2. Duplex ultrasonography

3. Doppler flow studies

PAOD

Medical Management

1. Drug therapy

Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles

Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation

2. Surgery- Bypass graft and anastomoses

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

2. Monitor and manage complications

Note for bleeding, hematoma, decreased urine output

Elevate the legs to diminish edema

Encourage exercise of the extremity while on bed

Teach patient to avoid leg-crossing

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 the medium and small arteries and veins of the lower extremities

Occurs in MEN ages 20-35

RISK FACTOR: SMOKING!

BUERGER’S DISEASE

PATHOPHYSIOLOGY

Cause is UNKNOWN

Probably 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 to CYANOSIS 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 smoking

3. Manage complications appropriately

Medical Management

1. Drug therapy

Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles

Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation

2. Surgery- Bypass graft and anastomoses

BUERGER’S DISEASE

Post-operative care: after amputation

Elevate stump for the FIRST 24 HOURS to minimize edema and promote venous return

Place patient on PRONE position after 24 hours

Assess skin for bleeding and hematoma

Wrap the extremity with elastic bandage

RAYNAUD’S DISEASE

A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain and pallor of the fingertips or toes

Cause : UNKNOWN

Most commonly affects WOMEN, 16- 40 years old

RAYNAUD’S DISEASE

ASSESSMENT FINDINGS

1. Raynaud’s phenomenon

A localized episode of vasoconstriction of the small arteries of the hands and feet that causes color and temperature changes

RAYNAUD’S DISEASE

W-B-R

Pallor- due to vasoconstriction, then

Blue- due to pooling of Deoxygenated blood

Red- due to exaggerated reflow/hyperemia

RAYNAUD’S DISEASE

ASSESSMENT FINDINGS 2. tingling sensation

3. Burning pain on the hands and feet

RAYNAUD’S DISEASE

Medical management

Drug therapy with the use of CALCIUM channel blockers

To prevent vasospasms

RAYNAUD’S DISEASE

1. instruct patient to avoid situations that may be stressful

2. instruct to avoid exposure to cold and remain indoors when the climate is cold

3. instruct to avoid all kinds of nicotine

4. instruct about safety. Careful handling of sharp objects

Venous diseases

VARICOSE VEINS

THESE are dilated veins usually in the lower extremities

VARICOSE VEINS

Predisposing Factors

Pregnancy

Prolonged standing or sitting

Constipation (for hemorrhoids)

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

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

3. Provide high-fiber foods to prevent constipation

4. Teach simple exercise to promote venous return

VARICOSE VEINS

Nursing management

5. Caution patient to avoid knee-length stockings and constrictive clothings

VARICOSE VEINS

Nursing management

6. Apply anti-embolic stockings as directed

7. Avoid massage on the affected area

DVT- Deep Vein Thrombosis

Inflammation of the deep veins of the lower extremities and the pelvic veins

The inflammation results to formation of blood clots in the area

Predisposing factors

Prolonged immobility

Varicosities

Traumatic procedures

Complication

PULMONARY thromboembolism

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-embolic stockings

Nursing management

4. Administer anticoagulants as prescribed

5. Monitor for signs of pulmonary embolism

Blood disorders

Anemia

Nutritional anemia

Hemolytic anemia

Aplastic anemia

Sickle cell anemia

ANEMIA

A condition in which the hemoglobin concentration is lower than normal

ANEMIA

Three broad categories

1. 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 iron is inadequate to produce hemoglobin

Etiologic Factors

1. Bleeding- the most common cause

2. Mal-absorption

3. Malnutrition

4. Alcoholism

Pathophysiology

The body stores of iron decrease, leading to depletion of hemoglobin synthesis

Pathophysiology

The oxygen carrying capacity of hemoglobin is reduced  tissue hypoxia

Assessment Findings

1. Pallor of the skin and mucous membrane

2. Weakness and fatigue

3. General malaise

4. Pica

Assessment Findings

5. Brittle nails

6. Smooth and sore tongue

7. Angular cheilosis

Laboratory findings

1. CBC- Low levels of Hct, Hgb and RBC count

2. low serum iron, low ferritin

3. Bone marrow aspiration- MOST definitive

Medical management

1. Hematinics

2. Blood transfusion

Nursing Management

1. Provide iron rich-foods

Organ meats (liver)

Beans

Leafy green vegetables

Raisins and molasses

Nursing Management

2. Administer iron

Oral preparations tablets- Fe fumarate, sulfate and gluconate

Advise to take iron ONE hour before meals

Take it with vitamin C

Continue taking it for several months

Nursing Management

2. Administer iron

Oral preparations- liquid

It stains teeth

Drink it with a straw

Stool may turn blackish- dark in color

Advise to eat high-fiber diet to counteract constipation

Nursing Management

2. Administer iron

IM preparation

Administer DEEP IM using the Z-track method

Avoid vigorous rubbing

Can cause local pain and staining

APLASTIC ANEMIA

A condition characterized by decreased number of RBC as well as WBC and platelets

APLASTIC ANEMIA

CAUSATIVE FACTORS

1. Environmental toxins- pesticides, benzene

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

3. Heavy metals

4. Radiation

APLASTIC ANEMIA

Pathophysiology

Toxins cause a direct bone marrow depression  acellualr bone marrow  decreased production of blood elements

APLASTIC ANEMIA

ASSESSMENT FINDINGS

1. fatigue

2. pallor

3. dyspnea

4. bruising

5. splenomegaly

6. retinal hemorrhages

APLASTIC ANEMIA

LABORATORY FINDINGS

1. CBC- decreased blood cell numbers

2. Bone marrow aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats

APLASTIC ANEMIA

Medical Management

1. Bone marrow transplantation

2. Immunosupressant drugs

3. Rarely, steroids

4. Blood transfusion

APLASTIC ANEMIA

Nursing management

1. Assess for signs of bleeding and infection

2. Instruct to avoid exposure to offending agents

Megaloblastic Anemias

Anemias characterized by abnormally large RBC secondary to impaired DNA synthesis due to deficiency of Folic acid and/or vitamin B12

Folic Acid deficiency

Causative factors

1. Alcoholism

2. Mal-absorption

3. Diet deficient in uncooked vegetables

Pathophysiology of Folic acid deficiency

Decreased folic acid  impaired DNA synthesis in the bone marrow  impaired RBC development, impaired nuclear maturation but CYTOplasmic maturation continues  large size

Vitamin B12 deficiency

Causative factors

1. Strict vegetarian diet

2. Gastrointestinal malabsorption

3. Crohn's disease

4. gastrectomy

Vitamin B12 deficiency

Pernicious Anemia

Due to the absence of intrinsic factor secreted by the parietal cells

Intrinsic factor binds with Vit. B12 to promote absorption

Assessment findings

1. weakness

2. fatigue

3. listless

4. neurologic manifestations are present only in Vit. B12 deficiency

Assessment findings

Pernicious Anemia

Beefy, red, swollen tongue

Mild diarrhea

Extreme pallor

Paresthesias in the extremities

Laboratory findings

1. Peripheral blood smear- shows giant RBCs, WBCs with giant hypersegmented nuclei

2. Very high MCV

3. Schilling’s test

4. Intrinsic factor antibody test

Medical Management

1. 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

1. Monitor patient

2. Provide assistance in ambulation

3. Oral care for tongue sore

4. Explain the need for lifetime IM injection of vit B12

Hemolytic Anemia: Sickle Cell

A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene.

Causative factor

Genetic inheritance of the sickle gene- HbS gene

Pathophysiology

Decreased O2, Cold, Vasoconstriction can precipitate sickling process

Pathophysiology

Factors  cause defective hemoglobin to acquire a rigid, crystal-like C-shaped configuration  Sickled RBCs will adhere to endothelium  pile up and plug the vessels  ischemia results  pain, swelling and fever

Assessment Findings

1. jaundice

2. enlarged skull and facial bones

3. tachycardia, murmurs and cardiomegaly

Assessment Findings

Primary sites of thrombotic occlusion: spleen, lungs and CNS

Chest pain, dyspnea

Assessment Findings

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 in the CXR

Medical Management

1. Bone marrow transplant

2. Hydroxyurea

Increases the HbF

3. Long term RBC trnasfusion

Nursing Management

1. manage the pain

Support and elevate acutely inflamed joint

Relaxation techniques

analgesics

Nursing Management

2. Prevent and manage infection

Monitor status of patient

Initiate prompt antibiotic therapy

Nursing Management

3. Promote coping skills

Provide accurate information

Allow patient to verbalize her concerns about medication, prognosis and future pregnancy

Nursing Management

4. Monitor and prevent potential complications

Provide always adequate hydration

Avoid cold, temperature that may cause vasoconstriction

Nursing Management

Leg ulcer

Aseptic technique

Nursing Management

Priapism

Sudden painful erection

Instruct patient to empty bladder, then take a warm bath

Polycythemia

Refers to an INCREASE volume of RBCs

The hematocrit is ELEVATED to more than 55%

Clasified as Primary or Secondary

Polycythemia

POLYCYTHEMIA VERA

Primary Polycythemia

A proliferative disorder in which the myeloid stem cells become uncontrolled

Polycythemia

POLYCYTHEMIA VERA

Causative factor

unknown

Polycythemia

POLYCYTHEMIA VERA

Pathophysiology

The stem cells grow uncontrollably

The bone marrow becomes HYPERcellular and all the blood cells are increased in number

Polycythemia

POLYCYTHEMIA VERA

Pathophysiology

The spleen resumes its function of hematopoiesis and enlarges

Blood becomes thick and viscous causing sluggish circulation

Polycythemia

POLYCYTHEMIA VERA

Pathophysiology

Overtime, the bone marrow becomes fibrotic

Polycythemia

POLYCYTHEMIA VERA

Assessment findings

1. Skin is ruddy

2. Splenomegaly

3. headache

4. dizziness, blurred vision

5. Angina, dyspnea and thrombophlebitis

Polycythemia

POLYCYTHEMIA VERA

Laboratory findings

1. CBC- shows elevated RBC mass

2. Normal oxygen saturation

3 Elevated WBC and Platelets

Polycythemia

POLYCYTHEMIA VERA

Complications

1. Increased risk for thrombophlebitis, CVA and MI

2. Bleeding due to dysfunctional blood cells

Polycythemia

POLYCYTHEMIA VERA

Medical Management

1. To reduce the high blood cell mass- PHLEBOTOMY

2. Allopurinol

3. Dipyridamole

4. Chemotherapy to suppress bone marrow

Polycythemia

Nursing Management

1. Primary role of the nurse is EDUCATOR

2. Regularly asses for the development of complications

3. Assist in weekly phlebotomy

4. Advise to avoid alcohol and aspirin

5. Advise tepid sponge bath or cool water to manage pruritus

Leukemia

Malignant disorders of blood forming cells characterized by UNCONTROLLED proliferation of WHITE BLOOD CELLS in the bone marrow- replacing marrow elements . The WBC can also proliferate in the liver, spleen and lymph nodes.

Leukemia

The leukemias are named after the specific lines of blood cells afffected primarily

Myeloid

Lymphoid

Monocytic

Leukemia

The leukemias are named also according to the maturation of cells

ACUTE

The cells are primarily immature

CHRONIC

The cells are primarily mature or diferentiated

Leukemia

ACUTE myelocytic leukemia

ACUTE lymphocytic leukemia

CHRONIC myelocytic leukemia

CHRONIC lymphocytic leukemia

Leukemia

ETIOLOGIC FACTORS

UNKNOWM

Probably exposure to radiation

Chemical agents

Infectious agents

Genetic

Leukemia

PATHOPHYSIOLOGY of ACUTE Leukemia

Uncontrolled proliferation of immature cells  suppresses bone marrow function  severe anemia, thrombocytopenia and granulocytopenia

Leukemia

PATHOPHYSIOLOGY of CHRONIC Leukemia

Uncontrolled proliferation of DIFFERENTIATED cells  slow suppression of bone marrow function  milder symptoms

Leukemia

ASSESSMENT FINDINGS

ACUTE LEUKEMIA

Pallor

Fatigue

Dyspnea

Hemorrhages

Organomegaly

Headache

vomiting

Leukemia

ASSESSMENT FINDINGS

CHRONIC LEUKEMIA

Less severe symptoms

organomegaly

Leukemia

LABORATORY FINDINGS

Peripheral WBC count varies widely

Bone marrow aspiration biopsy reveals a large percentage of immature cells- BLASTS

Erythrocytes and platelets are decreased

Leukemia

Medical Management

Chemotherapy

Bone marrow transplantation

Leukemia

Nursing Management

1. Manage AND prevent infection

Monitor temperature

Assess for signs of infection

Be alert if the neutrophil count drops below 1,000 cells/mm3

Leukemia

Nursing Management

2. Maintain skin integrity

3. Provide pain relief

4. Provide information as to therapy- chemo and bone marrow transplantation

Cardiovascular & Hematologic System

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