Cardiovascular disorders

CARDIOVASCULAR DISORDERS

CYNTHIA R. ACOSTA, RN, MAN

LEARNING OBJECTIVES:LEARNING OBJECTIVES:

At the end of the lecture, the students will be able to:

1.Identify the major organs and structures of cardiovascular system

2.Discuss the risk factors associated in the development of cardiovascular disorder

3.Discuss the physical assessment that provide information about the functioning of the cardiovascular disorder



4.Describe common diagnostic tests and their nursing responsibilities

5.Discuss the pathophysiology of clients with cardiovascular disorder

6.Enumerate the different clinical manifestations associated with each illness of clients with cardiovascular disorder



7.Identify actual and at-risk nursing diagnosis8.Discuss medical and surgical interventions 9.Discuss the appropriate nursing

interventions with client/s and family for identified nursing interventions

10.Implement plan of care with clients and family

CARDIOVASCULAR SYSTEM

is a closed system consistingof the heart and blood vessels

- to supply body cells and tissues with

oxygen-rich blood and eliminate carbon

dioxide and cellular wastes

FUNCTIONFUNCTION

- a cone-shaped muscle with four

chambers; a double pump about the size

of a clenched fist

HEARTHEART

-pumps blood throughout circulatory system

RIGHT SIDERIGHT SIDE

- upper chamber of right heart- receives

unoxygenated blood from superior and inferior vena cava

RIGHT ATRIUM


-Right AV valve with three cusps (tricuspid)

-Valve between right atrium and right

ventricle

TRICUSPID VALVE


-lower chamber of right heart

-receives blood from right atrium and

pumps it into pulmonary circuit

RIGHT VENTRICLE


-composed of three cusps

-valve between right ventricle and main pulmonary artery

PULMONARY SEMILUNAR VALVE


-artery leading from right ventricle to lungs-divides into right and

left branches supplying respective lungs

-carries unoxygenated blood from right ventricle to lungs

MAIN PULMONARY ARTERY


-veins leading from lungs to left atrium-carry oxygenated blood to left atrium

PULMONARY VEINS

LEFT SIDELEFT SIDE

- upper chamber of left heart.- receives

oxygenated blood from lungs through pulmonary veins

LEFT ATRIUM

LEFT SIDELEFT SIDE

-AV valve with two cusps (bicuspid)

-valve between left atrium and left

ventricle

MITRAL VALVE

LEFT SIDELEFT SIDE

-lower chamber of left half of heart

- receives blood from left atrium and pumps

oxygenated blood through systemic

circulation

LEFT VENTRICLE

LEFT SIDELEFT SIDE

- composed of three cusps

- valve between left ventricle and aorta.

AORTIC VALVE

LEFT SIDELEFT SIDE

- wall between left and right ventricles.- vertically separates left and right sides of

heart

INTERVENTRICULAR SEPTUM

LAYERS OF THE HEARTLAYERS OF THE HEART

- inner layer of heart; a smooth,

thin layer of endothelium and

connective tissue. -smooth inner

lining of the heart

ENDOCARDIUM


- middle and thickest layer of heart; heart muscle.

-responsible for cardiac contraction

MYOCARDIUM

- the layer of serous pericardium on heart’s surface.

- contains main coronary blood vessels

EPICARDIUM


- Sac that surrounds the heart and roots of the great vessels.

-Composed of two layers: Fibrous pericardium (outer layer of

fibrous connective tissue) and serous pericardium

PERICARDIUM

SYSTEMIC AND SYSTEMIC AND PULMONARY PULMONARY CIRCULATIONCIRCULATION

LAYERS OF ARTERIES AND VEINSLAYERS OF ARTERIES AND VEINS

- blood vessels with three coats: tunica intima, tunica media, and tunica

adventitia.- carry oxygenated blood away from left heart and unoxygenated blood to

lungs via pulmonary arteries

ARTERIES


- Smallest arteries; contain large amount of smooth muscle cells that

can dilate and constrict.- Carry blood to capillaries and control

blood flow to capillaries throughdilation/constriction

ARTERIOLES


- Single layer of microscopic endothelial cells.

- Connect arterial and venous system for exchange of gases, fluids,

nutrients, and wastes.

CAPILLARIES


- Contain same three layers as arteries, but are thinner with less

elastic and collagenous tissue and smooth muscle.

- BP in venous system is low; veins have valves to prevent backflow.

VEINS

- VEINS carry unoxygenated blood back to

right heart, except for pulmonary

veins, which carry oxygenated blood from lungs to left

heart.

- HEART RATE fluctuates according to

stimulation from autonomic nervous

system, baroreceptors, and chemoreceptors

REGULATION OF HEART RATE

- AUTONOMIC NERVOUS SYSTEM

affects heart rate through sympathetic and parasympathetic

nervous system innervation

- SYMPATHETIC NERVE FIBERS, adrenergic neurotransmitters

(norepinephrine, epinephrine) excite SA and AV nodes in the conduction system,

thus INCREASING HEART RATE

- The same neurotransmitters also stimulate

BETA ADRENERGIC RECEPTORS in the atria ventricles, increasing force of

myocardial contraction

- Heart rate slows when parasympathetic nerve fibers from the cardiac branches of

the vagus nerve release the CHOLINERGIC neurotransmitter

ACETYLCHOLINE

CARDIAC OUTPUT – is the amount of

blood pumped out of the left ventricle

each minute

PROPERTIES OF CARDIAC CYCLE

AUTOMATICITY: Generates electrical impulse independently,

without involving the nervous system

EXCITABILITY: Responds to electrical stimulation

PROPERTIES OF CARDIAC CYCLE

CONDUCTIVITY: Passes or propagates electrical impulses from cell to cell

CONTRACTILITY: Shortens in response to electrical stimulation

ELECTRICAL CONDUCTION SYSTEM OF

THE HEART

Conduction System Structures and

Functions

ELECTRICAL CONDUCTION SYSTEM OF THE HEART

SINOATRIAL (SA) NODE: Dominant pacemaker of the heart, located in

upper portion of right atrium. Intrinsic rate

60–100 bpm.

SA NODE


INTERNODAL PATHWAYS: Direct electrical impulses

between SA and AVnodes.

INTERNODAL PATHWAYS


ATRIO VENTRICULAR (AV) NODE: Part of AV junctional tissue. Slows conduction, creating a

slight delay before impulses reach

ventricles. Intrinsic rate 40–60 bpm

AV NODE


BUNDLE OF HIS: Transmits impulses to

bundle branches.Located below AV

node

BUNDLE OF HIS


LEFT BUNDLE BRANCH: Conducts impulses that lead to

left ventricle

LEFT BUNDLE BRANCH


RIGHT BUNDLE BRANCH: Conducts impulses that lead to

right ventricle

RIGHT BUNDLE BRANCH


PURKENJE SYSTEM: Network of fibers that

spreads impulsesrapidly throughout ventricular walls.

Located at terminals of bundle branches.

Intrinsic rate 20–40 bpmPURKENJE FIBERS

ELECTROPHYSIOLOGY

DEPOLARIZATION: The electrical charge of a cell is altered by a shift of electrolytes on either side of the cell membrane. This

change stimulates muscle fiber to contract

ELECTROPHYSIOLOGY

REPOLARIZATION: Chemical pumps re-establish an internal negative charge

as the cells return to their resting state

Mechanical and electrical functions of the heart are influenced by proper

electrolyte balance. Important components of this balance

are sodium, calcium, potassium, andmagnesium

ASSESSMENT

CARDIOVASCULAR

PAST MEDICAL HISTORY

REVIEW OF ALLERGIES

MEDICATION HISTORY

FAMILY HISTORY

PERSONAL AND SOCIAL HISTORY

COMMON MANIFESTATIONS OF

HEART DISEASE

CHEST PAIN

OTHER MANIFESTATIONS:

•shortness of breath

•palpitations•weakness

•fatigue•dizziness•syncope

•GI complaints

PHYSICAL EXAMINATION

GENERAL APPEARANCE-non-verbal behavior and body position

(anxious, depressed, pain, uncomfortable)

PAIN -classic sign of

ischemia


VITAL SIGNS

TEMPERATURE-note presence of fever

PULSE RATE-note rate, rhythm and

quality


VITAL SIGNS

RESPIRATORY RATE-note if patient has labored breathing

BLOOD PRESSURE-take BP lying, sitting, & standing positions

(orthostatic VS)

CARDIAC RHYTHM

-electrical activity can be observed continuously with bedside CARDIAC

MONITOR

-electrodes are attached to the chest & connected to a machine that displays the

cardiac rhythm

HEART SOUNDS

“LUBLUB” – first heart sound – referred to S1,

is the closing of the mitral and tricuspid

valves

“DUBDUB” – referred to S2, is the closing of the aortic and pulmonic valves

ABNORMAL HEART SOUNDS

S3 HEART SOUND – or a ventricular gallop“LUB-DUB-DEELUB-DUB-DEE” or

“KEN-TUCK-Y”

Normal in children, but indication of heart failure in an adult

ABNORMAL HEART SOUNDS

S4 HEART SOUND – or a atrial gallop, an extra heart sound

before S1“LUB-LUB-DUBLUB-LUB-DUB” or “TEN-NES-SEE” –

- often associated with hypertensive heart disease

PERIPHERAL PULSES

-palpate the radial arteries and the major arteries of the leg bilaterally

-record the presence or

absence of pulses and strength

SKIN

-note changes in skin color (cyanosis, pallor)

-note if the skin is warm or cold, dry

or clammy

PERIPHERAL EDEMA

EDEMA occurs when blood is not pumped efficiently or plasma protein

levels are inadequate to maintain osmotic pressure

AREA: feet and anklesOTHER AREAS: fingers, hands, over the

sacrum

Evaluated on a scale of 1-4

PERIPHERAL EDEMAPITTING EDEMA – marks of the

fingers remain

1+ PITTING EDEMA – slight indentation (2mm), normal contours

2+ PITTING EDEMA – deeper pit after pressing (4mm), lasts longer than 1+

PERIPHERAL EDEMA

3+ PITTING EDEMA – deep pit (6mm), remains several seconds after pressing

4+ PITTING EDEMA – dip pit (8mm), remains prolonged time after pressing,

possibly minutes

WEIGHT GAIN-can indicate edema

JUGULAR VEINS-distention of this vein usually indicates

increased fluid volume and pressure in the right side of the heart

MENTAL STATUS-note if patient is alert and oriented,

confused and disoriented

CONFUSION and DISORIENTATION can

result from a decrease in the oxygen supply to the brain (cerebral ischemia) as a result of poor circulation

DIAGNOSTIC DIAGNOSTIC TESTSTESTS

LABORATORY LABORATORY STUDIESSTUDIES

Enzyme,

Isoenzyme,

and Biochemical Markers

ENZYMES

CREATINE KINASE (CK) - 98% sensitivity for AMI 72 hours after

infarction

-present in heart muscles, skeletal muscles, and brain tissue

ENZYMES

CK ISOENZYMES - more specific than CK

CK-MM – skeletal musclesCK-BB – appears primarily in the brain

and nerve tissueCK-MB – heart muscles

-generally, CK-MB levels rise 4-8hrs after the onset of AMI, peak after 20hrs, & may

remain elevated for up to 72hrs

ENZYMES

TROPONIN I and TROPONIN T - is a protein found in the skeletal and

cardiac musclesTROPONIN T – may also be found in

the skeletal muscleTROPONIN I – found only in the myocardium, (more specific to

myocardial damage)

TROPONIN LEVELS rises within 3-6hrs after myocardial damage.

Troponin I peaks in 12-24hrs, with a return to baseline in 5-7days

Troponin T peaks in 24hrs , with a return to baseline in 10-15days

ENZYMES

MYOGLOBIN - is a small, oxygen-binding protein found in cardiac and

skeletal muscles and is rapidly released into the bloodstream

ENZYMES

C-REACTIVE PROTEIN (CRP) - is an inflammatory marker that may be

an important risk factor for atherosclerosis and ischemic heart

disease

Elevated CRP is associated with AMI, stroke, and the progression of peripheral vascular disease

ENZYMES

LIPOPROTEIN - a molecule that is similar to low-density lipoprotein

cholesterol (LDL-C)

It increases cholesterol deposits in the arterial wall, enhances oxidation of LDL-C, and inhibits fibrinolysis, resulting in the formation of atherosclerotic plaque

and thrombosis

ENZYMES

FACTOR I or FIBRINOGEN - is directly linked to increased

cardiovascular risk

It is involved in the coagulation cascade (converting fibrinogen to

fibrin by thrombin)

HEMATOLOGIC STUDIES

CBC - indication of the type and number of formed elements in the

blood

HEMATOLOGIC STUDIES

HEMATOCRIT – expresses the relationship of the formed elements in

the blood to the total volume

LOWERED when blood volume increases as in CHF

RISES when blood volume is lost as in bleeding, shock and burns

HEMATOLOGIC STUDIES

PROTHROMBIN TIME - measures how long it takes for prothrombin to become active in clotting process

PARTIAL THROMBOPLASTIN TIME - determine deficiencies in all

coagulation factors except factor VII

HEMATOLOGIC STUDIES

ERYTHROCYTE SEDIMENTATION RATE (ESR) - indicates the extent to which RBC settle to the bottom of the

test tube containing a sample of blood

ESR rises during the inflammatory processes such as rheumatic fever and MI

BLOOD CHEMISTRIES

SERUM CHOLESTEROL

SERUM TRIGLYCERIDES

GRAPHIC GRAPHIC RECORDING RECORDING

STUDIESSTUDIES

ECGHOLTER

MONITORING

GRAPHIC RECORDING STUDIES

ECG - graphically record electrical current generated by the heart

Helps identify primary conduction

abnormalities, arrhythmias, cardiac

hypertrophy, pericarditis, electrolyte imbalance,

and MI


EXERCISE ECG (Stress Test) - non invasive test that helps the doctor

assess cardiovascular response to an increased workload

Provides diagnostic information that can’t be obtained from a resting ECG


HOLTER MONITORING - records the heart’s electrical activity for 24 hours or longer as the patient performs his

usual activities and experiences normal physical and emotional stress

RADIOLOGY AND RADIOLOGY AND IMAGINGIMAGING

Chest X-rayMyocardial Imaging

RADIOLOGY AND IMAGING

CHEST X-RAY - a noninvasive tool used to visualize internal structures,

such as the heart, lungs, soft tissues, and bones


MYOCARDIAL IMAGING - with the use of radionuclides and scintillation cameras, radionuclide angiograms

can be used to assess left ventricular performance


ECHOCARDIOGRAPHY – a noninvasive imaging technique,

records the reflection of ultra-high frequency sound waves directed at

the patient’s heart


MRI (MAGNETIC RESONANCE IMAGING)– yields high-resolution,

tomographic, three dimensional images of body structures

Permits visualization of valve leaflets and structures, pericardial abnormalities and

processes, ventricular hypertrophy, cardiac neoplasm, infarcted tissue


ULTRAFAST CT SCAN – uses a scanner that takes images as fast speeds, resulting in high resolution

pictures

-can identify microcalcifications in the coronary arteries


ELECTRON BEAM COMPUTED TOMOGRAPHY – a radiologic test

that produces x-rays of the coronary arteries using electron beam

-can detect and quantify calcified plaque in the coronary arteries

RADIONUCLIDE RADIONUCLIDE IMAGING TESTSIMAGING TESTS

CARDIAC CATHETERIZATION

AND CORONARY ANGIOGRAPHY

RADIONUCLIDE IMAGING TESTS

CARDIAC CATHETERIZATION AND CORONARY ANGIOGRAPHY –

invasive tests, use a catheter threaded through an artery or vein into the heart

-to determine the size and location of a coronary lesion, evaluate ventricular

function, measure heart pressures and oxygen saturation


CORONARY FLOW AND PERFUSION EVALUATION – used to assess blood

flow through the coronary arteries, investigate myocardial anatomy and

perfusion, and determine the extent of lesions


DSA – combines angiography with computer processing to produce high-

resolution images of cardiovascular structures

-provides a clear view of arterial structures


VENOGRAM– Insertion of a dye into the vein for the purpose of outlining an

obstruction or lesion

TREATMENTSTREATMENTS

DRUG THERAPYDRUG THERAPY

ADRENERGICSANTIANGINALS

ANTIARRHYTHMICSANTIHYPERTENSIVES

ANTILIPEMICSANTIPLATELET AGENTS

DIURETICSINOTROPHIC AGENTS

THROMBOLYTICS

ANALGESIC

Antipyretic, Non-Steroidal Anti-inflammatory drugs, acetaminophen,

acetylsalicylic acid, ibuprofen

Relieves pain, fever, and inflammation

ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS

Captopril, Enalapril

Prevent angiotensin I from converting to angiotensin II, a potent

vasoconstrictor, thereby decreasinbg peripheral vascular resistance, blocks

the secretion of aldosterone from adrenal gland

ANGIOTENSIN II RECEPTOR ANTAGONISTS

LOSARTAN, VALSARTAN

Block angiotensin II at the receptor sites, thereby decreasing peripheral

vascular resistance

ANTIARRHYTHMICS

Lidocaine, propanolol, amiodarone

Reduce automaticity, slow conduction of electrical impulses through the heart,

and prolong the refractory period of myocardial cells

ANTIBIOTICS

Aminoglycocides (gentamycin, tobramycin), Amoxicillin, Erythromycin,

penicillin, tetracycline

Prevent or treat infections caused by pathogenic microorganism

ANTICHOLINERGICS

Atropine

Block effects of vagus nerve stimulation

ANTICOAGULANTS

IV Heparin, oral warfarin sodium

Prevent recurrence of emboli but have no effect on emboli that are

already present

ANTICOAGULANTS

Subcutaneous – low dose heparin (5,000 units)

Prophylactically prevent deep vein thrombosis, heparin activates

antithrombin III

ANTILIPEMIC AGENTS

Cholestyramine, clofibrate, colestipol, lovastatin

Lower the serum cholesterol level by binding bile salts in the bowel and

forming an insoluble complex that is excreted in the stool

ANTIPLATELET AGENTS

Aspirin, ticlopidine

Inhibit the aggregation of platelets to form a plug, platelets do not initiate thrombus formation as readily when

taking antiplatelets

BETA-ADRENERGIC BLOCKERS

Atenolol, metoprolol, propanolol

Decrease the heart rate and the force of contraction and reduce

vasoconstriction by antagonizing beta-receptors in the myocardium and

vasculature

BETA-ADRENERGICS

Beta only (dobutamine), beta or alpha plus beta – dopamine, epinephrine,

metaraminol

Increase myocardial contractility and heart rate, which in turn raises blood pressure, alpha plus beta-adrenergic

activity

CALCIUM CHANNEL BLOCKERS

Nifedipine, Verapamil

Inhibit calcium ions from crossing myocardial and vascular smooth

muscle, thereby producing vasodilation and decreased myocardial contractility

CARDIAC GLYCOSIDES

Digoxin

Increase the force of myocardial contractions and slow heart rate and

conduction through the atrioventricular node and bundle of His

CORTICOSTEROIDS

Oral hydrocortisone, oral methylprednisolone, oral prednisone

Strengthen the biologic membrane, which inhibits capillary permeability and

prevents leakage of fluid into the injured area and development of

edema

DIURETICS

Loop diuretics – furosemide, potassium sparing diuretic – spironolactone,

thiazide diuretic

Decrease blood volume, which decreases the workload of the heart

OPIOD ANALGESICS

Codeine, morpine, hydromorphone

Release moderate to severe pain by reducing pain sensation, producing

sedation, and decreasing the emotional upset often associated with pain

NITRATES

Isosorbide dinitrate, nitroglycerine – sublingual, topical, patch, tablet, IV

Reduce myocardial oxygen demand by promoting vasodilation and by

increasing oxygen supply to myocardial tissue

STOOL SOFTENERS

Docusate calcium, docusate sodium

Decrease the surface tension of the fecal mass to allow water to penetrate into the stool; prevents the client from

straining from defecation

THROMBOLYTIC AGENTS

Streptokinase, urokinase

Dissolve thrombus or emboli in the coronary arteries

VASODILATORS

Hydralazine, nitroprusside sodium

Decrease preload (venous dilators) and afterload (arterial dilators); act directly on blood vessels to cause dilation and decrease peripheral

vascular resistance

AUTONOMIC NERVOUS SYSTEM

DIVISIONS:

SYMPATHETIC NERVOUS SYSTEM

PARASYMPATHETIC NERVOUS SYSTEM

-generally function antagonistically toward each other

- critical to the stability of our internal environment (homeostasis)


- regulates the expenditure of energy

- Neurotransmitter are known as CATECHOLAMINES – epinephrine, norepinephrine, and dopamine

- controls “fight-or-flight responses”


ENZYMES: Monoamine oxidase (MAO) & Catechol-O-methyltransferase

(COMT)

4 TYPES OF RECEPTORS:alpha1, alpha2, beta1, beta2


-Works to conserve body energy and is partly responsible for slowing heart rate, digesting food, and eliminating

body wastes

- “rest and digest”

-Neurotransmitter: ACETYLCHOLINE


ENZYME: Acetylcholinesterase

2 TYPES OF RECEPTORS:Nicotinic, Muscarinic (both are

alkaloids)

CHOLINERGIC FIBERSCHOLINERGIC FIBERS – are NERVE ENDINGS that liberate

ACETYLCHOLINE

ADRENERGIC FIBERSADRENERGIC FIBERS – are NERVE ENDINGS that secrete

NOREPINEPHRINE

- They produce opposite responses

EXAMPLE:

HEART ADRENERGIC AGENTS

increase the heart rate

CHOLINERGIC AGENTS slow the heart rate

RESPONSES TO SYMPATHETIC

ACTIVATION

RESPONSES TO PARASYMPATHETIC

ACTIVATION

CARDIAC CARDIAC PACINGPACING

CARDIAC PACEMAKER

- is an electronic device that delivers direct

electrical stimulation to stimulate the

myocardium to depolarize, initiating a

mechanical contraction

The PACEMAKER initiates and maintains the heart rate when the

heart's natural pacemaker is unable to do so

PACEMAKERS can be used to correct bradycardias, tachycardias, sick sinus syndrome, and second-

and third-degree heart blocks, and for prophylaxis

Pacing may be accomplished through a permanent implantable

system, a temporary system with an external

pulse generator and percutaneously threaded

leads, or a transcutaneous external system with

electrode pads placed over the chest

CARDIAC PACEMAKER

INDICATIONSINDICATIONS

1. Symptomatic bradydysrhythmias2. Symptomatic heart block

a. Mobitz II second-degree heart blockb. Complete heart blockc. Bifascicular and trifascicular bundle

branch blocks

CARDIAC PACEMAKER


3. Prophylaxisa. After acute MI: dysrhythmia and

conduction defectsb. Before or after cardiac surgeryc. During diagnostic testing

CARDIAC PACEMAKER


4. Tachydysrhythmias; to break rapid rhythm disturbances

a. Supraventricular tachycardiab. Ventricular tachycardia

CARDIAC PACEMAKER

TYPESTYPES

PERMANENT PACEMAKERS•Used to treat chronic heart conditions; surgically placed, utilizing a local anesthetic, the leads are placed transvenously in the appropriate chamber of the heart and then anchored to the endocardium

CARDIAC PACEMAKER

TYPESTYPES

PERMANENT PACEMAKERS

• The pulse generator is placed in a surgically made pocket in subcutaneous tissue under the clavicle.

• Once placed and programmed it can be adjusted externally as needed.

CARDIAC PACEMAKER

TYPESTYPES

TEMPORARY PACEMAKERS

• are usually placed during an emergency, such as when a patient demonstrates signs of decreased CO until the temporary condition is resolved

CARDIAC PACEMAKER

TYPESTYPES

TEMPORARY PACEMAKERS

• Indicated for patients with high-grade AV blocks, bradycardia, or low CO

Temporary transvenous

pacer wire with external pulse

generator

SURGERYSURGERY

CORONARY ARTERY BYPASS GRAFTING

• CABG circumvents an occluded coronary artery with an autogenous

graft (usually a segment of saphenous vein or internal mammary artery, thereby restoring blood flow to

the myocardium

Coronary artery bypass graft

surgery is done primarily to

alleviate anginal symptoms as well

as improve survival

CORONARY ARTERY BYPASS GRAFTING

CANDIDATES FOR CABG- Severe angina from atherosclerosis

- CAD with high risk of MI

TRANSMYOCARDIAL REVASCULARIZATION

• TMR is a relatively new procedure.• Can provide relief for sever angina

when medical therapy fails or the patient isn’t a candidate for

angioplasty or by-pass surgery• Is performed through an incision on

the left side of the chest

TRANSMYOCARDIAL REVASCULARIZATION

POTENTIAL COMPLICATIONS:

- Arrhythmias, bleeding, damage to the great vessels, valves, and coronary

arteries

MINIMALLY INVASIVE CORONARY ARTERY BYPASS

• is CABG surgery done through a left anterior small thoracotomy (LAST)

• a short parasternal incision, or small incisions using port access and video-

assisted technology

Minimally invasive direct grafting of left

internal mammary

bypass graft to left anterior descending

coronary artery (LAD).

Surgery is performed on the beating heart. To allow suturing of the graft anastomosis

to the beating heart, pharmacologic measures such as adenosine and beta-blockers are used to slow or temporarily

stop the heart

PORT ACCESS CARDIAC SURGERY

• is another minimally invasive surgical technique that uses femorofemoral bypass through a small incision with

aid of videoscopes.• is performed using a small anterior thoracotomy and several small “port”

chest incisions

VASCULAR REPAIR

• may treat:- Vessels damaged by arteriosclerotic or

thromboembolic disorders (such as aortic aneurysm or arterial occlusive

disease), trauma, infections, or congenital defects

- Vascular obstructions that severely compromise circulation

VASCULAR REPAIR

• may treat:- Vascular disease that doesn’t repsond

to drug therapy- Life-threatening dissecting or ruptured

aortic aneurysm

VASCULAR REPAIR

• includes aneurysm resection, grafting, embolectomy, vena caval filtering, and

vein stripping

VASCULAR REPAIR

TYPES:

AORTIC ANEURYSM REPAIR- Removes an aneurysmal segment of the

aorta

VEIN STRIPPING- Removes the saphenous vein and it's branches to treat varicosities

VASCULAR REPAIR

TYPES:

VENA CAVAL FILTER INSERTION- Traps emboli in the vena cava,

preventing them from reaching the pulmonary vessels

EMBOLECTOMY- Removes an embolism from an artery

VASCULAR REPAIR

TYPES:

BYPASS GRAFTING- bypasses an arterial obstruction

resulting from arteriosclerosis

BALLOON CATHETER TREATMENTS

PERCUTANEOUS BALLOON VALVULOPLASTY

PERCUTANEOUS TRANSLUMINAL CORONARY

ANGIOPLASTY (PTCA)

PERCUTANEOUS BALLOON VALVULOPLASTY

-can be performed in the cardiac catheterization laboratory

- seeks to improve valvular function by enlarging the orifice of a stenotic heart

valve caused by congenital defect, calcification, rheumatic fever, or aging

PTCA

-offers a nonsurgical alternative to coronary artery bypass surgery

- uses a balloon-tipped catheter to dilate a coronary artery that has become

narrowed because of atherosclerotic plaque

-can open an occluded coronary artery without opening the chest

DISEASES OF DISEASES OF THE HEARTTHE HEART

Thrombus• A thrombus

– a blood clot that can develop anywhere in the vascular system

– causing the narrowing of a vessel.

– blood flow can be occluded (reduced or totally blocked)

Thrombus– develop from any injury to the vessel wall

• endothelial cell injury draws platelets and other mediators of inflammation to the area.

• substances stimulate clotting and activation of the coagulation cascade.

• formation can occur when blood flow through a vessel is sluggish,

• when blood flow is irregular or erratic

–during periods of irregular heartbeat or cardiac arrest

Thrombus

Embolus• Embolus

–a substance that travels in the bloodstream from a primary site to a secondary site

–becomes trapped in the vessels at the secondary site

–causes blood flow obstruction. –Most emboli are blood clots

(thromboemboli) • usually deep leg veins

–Other sources of emboli • fat

–released during the break of a long bone–produced in response to any physical

trauma, and amniotic fluid»which may enter maternal circulation

during the intense pressure gradients generated by labor contractions.

• Air and displaced tumor cells also may act as emboli to obstruct flow.

Embolus

CORONARY ARTERY DISEASECORONARY ARTERY DISEASE

-focal narrowing of the large and medium-sized coronary arteries

- due to deposition of atheromatous plaque in the vessel wall

- LIPID or FATTY Substance- FIBROUS TISSUE

ARTERIOSCLEROSIS – hardening of the arteries, which results in loss of

elasticity of intimal layer of the artery

ATHEROSCLEROSIS – accumulated fatty plaques made of lipids in the

arteries


RISK FACTORS

- Hereditary, including race- Age, Gender

- Cigarette Smoking- HTN- Elevated Serum Cholesterol Level- Diabetes Mellitus- Physical Inactivity- Obesity

- fatty, fibrous plaques

- occlude the coronary arteries

- reduce volume of blood flow leading to myocardial ischemia

Progression of atheromatous plaque from initial lesion to complex and ruptured plaque


SIGNS AND SYMPTOMS

ANGINAANGINA – classic symptom

occurs as burning, squeezing or crushing

tightness in the substernal or precordial chest

- may radiate to the left arm, neck, jaw or shoulder blade

4 MAJOR FORMS OF ANGINA

STABLE – pain that’s predictable in frequency and duration and can be

relieved with nitrates and rest

UNSTABLE – increased pain that’s easily induced

4 MAJOR FORMS OF ANGINA

PRINZMETAL’S or VARIANT – from unpredictable coronary artery spasm

MICROVASCULAR – impairment of vasodilator reserve, which causes

angina-like chest pain in a patient with normal coronary arteries


OTHER SIGNS AND SYMPTOMS

NauseaVomiting

WeaknessDiaphoresis

Cool extremities


DIAGNOSTICS

ECG – shows ischemiaExercise ECG – provoke chest pain

Coronary Angiography – reveals coronary artery stenosis or obstruction,

shows arteries beyond narrowing


DIAGNOSTICS

Laboratory evaluation– to eliminate a diagnosis of MI

Serum lipid studies – to detect hyperlipidemia


NURSING DIAGNOSIS

Acute PainDecreased Cardiac Output

Anxiety


TREATMENT

MEDICATIONS:Nitrates

AntiplateletsAntilipemics

Beta-adrenergic blockersCalcium channel blockers


NURSING MANAGEMENT

Provide care during an acute anginal attack

- Nitrates (SL)-stat 12-Lead ECG


NURSING MANAGEMENT

PROMOTE PAIN RELIEF-reduce activity to a point at which pain

does not occur-Position patient for comfort; Fowler's

position promotes ventilation-Administer oxygen if prescribed


NURSING MANAGEMENT

MAINTAIN CARDIAC OUTPUT-monitor vital signs, note changes in BP-note patient complaints of headache

(especially with use of nitrates)-evaluate for development of heart

failure


NURSING MANAGEMENT

DECREASING ANXIETY-Rule out physiologic etiologies for increasing or new onset of anxiety

-Explain to patient and family reasons for hospitalization

Encourage patient to verbalize fears and concerns


SURGERY

Obstructive lesions may necessitate CORONARY ARTERY BYPASS surgery

or PTCA


PREVENTION

Cessation of smokingControl of high BP

Diet low in saturated fat, cholesterolLimit alcohol intakePhysical exercise Weight control

Control of diabetes mellitus

MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION

refers to a dynamic process by which one or more regions of the heart

experience a severe and prolonged decrease in oxygen supply because of

insufficient coronary blood flow; subsequently, necrosis or death to the

myocardial tissue occurs

Obstruction in a coronary artery resulting in necrosis

Due to: Atherosclerotic plaque

ThrombusEmbolism


CLINICAL MANIFESTATIONS


CHEST PAIN

Typically, persistent and crushing, located

substernally with radiation to the arm,

neck, jaw and unrelieved by rest or nitrates



CHEST PAIN

Occurs without cause, primarily early morning

NOT relieved by rest or nitroglycerinLasts 30 minutes or longer



Diaphoresis, cool clammy skin, facial pallor

Hypertension or hypotensionBradycardia or tachycardia

Premature ventricular and/or atrial beats

Palpitations, severe anxiety, dyspnea



Disorientation, confusion, restlessness

Fainting, marked weaknessNausea, vomiting, hiccups

Atypical symptoms: epigastric or abdominal distress, dull aching or

tingling sensations, shortness of breath, extreme fatigue

DIAGNOSTICS


•ST segment is ELEVATED.

T wave inversion, presence of Q

wave

- Elevated CK-MB, LDH and Troponin levelsCBC - Elevated WBC count

NURSING DIAGNOSIS


•Acute Pain•Anxiety related to chest pain, fear of

death, threatening environment•Decreased Cardiac Output related to

impaired contractility•Activity Intolerance

•Risk for Injury (bleeding) related to dissolution of protective clots

MANAGEMENT


M – Morphine sulfateO – O2 therapyN – NitratesA – Aspirin/Adequate rest

MANAGEMENT


O2 – to increase oxygenation of the bloodNITRATES – to relieve chestpainMORPHINE – for analgesiaASPIRIN – to inhibit platelet aggregation

MANAGEMENT


-Relieve pain-Stabilize heart rhythm -Revascularize the coronary artery-Reduce cardiac workload-PTCA

NURSING MANAGEMENT


Administer prescribed medications – morphine, nitrates, antilipemics,

thrombolytics, anticoagulants

Provide ongoing assessment-monitor cardiac enzymes

NURSING MANAGEMENT


Minimize anxiety

Minimize metabolic demands-institute a liquid diet, advance to a low

sodium, low cholesterol, low fat diet

NURSING MANAGEMENT


prepare the client for treatment, such as percutaneous transluminal coronary angioplasty and coronary artery bypass

grafting

HEART FAILUREHEART FAILURE

is a syndrome of pulmonary or systemic circulatory congestion caused by decreased myocardial contractility,

resulting in inadequate CO to meet oxygen requirements of tissues.

HEART FAILUREHEART FAILURE

CLASSIFICATION:

LEFT-SIDED (or left ventricular)

RIGHT-SIDED (or right ventricular)

HEART FAILUREHEART FAILURELEFT-SIDED - congestion occurs primarily in

the lungs from backup of blood into pulmonary veins and capillaries because of

left ventricular pump failure.

As blood backs up into the pulmonary bed, increased hydrostatic pressure causes fluid

accumulation in the lungs.

Blood flow is consequently decreased to the brain, kidneys, and other tissues

HEART FAILUREHEART FAILURERIGHT-SIDED - congestion in systemic

circulation results from right ventricular pump failure.

As blood backs up into the pulmonary bed, increased hydrostatic pressure produces peripheral and dependent pitting edema.

Venous congestion in the kidneys, liver, and GI tract also develops.

http://rds.yahoo.com/_ylt=A2KJkIdpq79NK1QAgqijzbkF/SIG=11tsvr6tb/EXP=1304435689/**http%3A//canineheartdisease.ca/images/1.jpg

HEART FAILUREHEART FAILURECAUSES:

-atherosclerotic heart disease-MI

-hypertension-Rheumatic heart disease-congenital heart disease-ischemic heart disease

-Arrhythmias

HEART FAILUREHEART FAILUREDIAGNOSTICS:

ECHOCARDIOGRAPHY - depressed cardiac output, evidence of

cardiomegalyCHEST X-RAY-reveals cardiomegaly

ABG-decreased partial pressure of arterial O2

HEART FAILUREHEART FAILURECLINICAL MANIFESTATIONSLEFT SIDED HEART FAILURE

-dyspnea on exertion, paroxysmal nocturnal dyspnea, or orthopnea

-crackles on lung auscultation-frothy blood-tinged sputum

-tachycardia with S3 heart sound-pale, cool extremities

-peripheral and central cyanosis

HEART FAILUREHEART FAILURECLINICAL MANIFESTATIONSLEFT SIDED HEART FAILURE

-decreased peripheral pulses and capillary refill

Decreased urinary output easy fatigability

Insomnia and restlessness

HEART FAILUREHEART FAILURECLINICAL MANIFESTATIONSRIGHT SIDED HEART FAILURE

•dependent pitting edema (peripheral and sacral)

•Weight gain•Nausea and anorexia•Jugular vein distention

•Liver congestion, ascites, weakness

HEART FAILUREHEART FAILURENURSING DIAGNOSIS:

Decreased CO related to an ineffective ventricular pump

HEART FAILUREHEART FAILUREPHARMACOLOGIC TREATMENT:

VasodilatorsDiureticsDigoxin

DobutamineBeta-adrenergic blocking agents

(metoprolol, carvedilol)

HEART FAILUREHEART FAILURENURSING MANAGEMENT:

Administer medications as ordered Provide ongoing assessment

-Monitor hemodynamic parameters, HR, rhythm,

-weigh OD Prevent complications of immobility

HEART FAILUREHEART FAILURENURSING MANAGEMENT:

Provide a low-sodium diet, as prescribed

provide client and family teaching

HYPERTENSIONHYPERTENSION

refers to an intermittent or sustained elevation in diastolic or systolic blood

pressure


TYPES:TYPES:ESSENTIAL (IDIOPATHIC) – most

common formSECONDARY – results from a number of disorders that impair blood pressure

regulationMALIGNANT HYPERTENSION –

severe, fulminant form of hypertension common to both types


CAUSES:CAUSES:ESSENTIAL (IDIOPATHIC) –associated

with risk factors such as genetic predisposition, stress, obesity, and a

high-sodium diet


CAUSES:CAUSES:SECONDARY – results from underlying

disorders that impair blood pressure regulation, particularly renal, endocrine,

vascular, and neurological disorders; hypertensive disease of pregnancy

(formerly known as toxemia); and use of estrogen-containing oral contraceptives


CAUSES:CAUSES:

MALIGNANT HYPERTENSION – not known, but it may be associated with

dilation of cerebral arteries and generalized arteriolar fibrinoid necrosis,

which increases intracerebralblood flow, resulting in encephalopathy

Guidelines for Determining Hypertension

Category Systolic Pressure Diastolic Pressure

Normal <120 mm Hg <80 mm Hg

Prehypertension 120-139 mm Hg 80-89 mm Hg

Stage 1 hypertension

140-159 mm H g 90-99 mm Hg

Stage 2 hypertension

>160 mm Hg >100 mm Hg


RISK FACTORSRISK FACTORS

Family history of hypertensionRace (more common in blacks)

GenderDiabetes mellitus

Stress Obesity


RISK FACTORSRISK FACTORS

High dietary intake of saturated fats or sodium

Tobacco use Hormonal contraceptive use

Sedentary lifestyleaging

HYPERTENSIONHYPERTENSIONSYMPTOMS:SYMPTOMS:

blood pressure measurements of more than 140/90mmHg

Throbbing occipital headaches upon waking

DrowsinessConfusion

vision problemsnausea


DIAGNOSTICS:DIAGNOSTICS:

BUN - May be elevatedSERUM CREATININE - determines if

renal dysfunction is present as a complication of hypertension

Total cholesterol, TriglyceridesElectrocardiogram


TREATMENT:TREATMENT:

SECONDARY HPN - correcting the underlying cause and controlling

hypertensive effects

LIFESTYLE MODIFICATIONS: change in diet, relaxation techniques,

exercise, smoking cessation, limited intake of alcohol



DRUG THERAPY

THIAZIDE – for uncomplicated HPNACE INHIBITOR

BETA-ADRENERGIC BLOCKER



DRUG THERAPY

Angiotensin II receptor blockersAlpha-receptor blockers

Calcium channel blockers


NURSING DIAGNOSIS:NURSING DIAGNOSIS:

Knowledge deficit related to chronic disease management

INTERVENTIONS: Health education; Teaching: Diet, Disease process, Health

behaviors, Medication, Prescribed activity, Treatment regimen

INFLAMMATORY INFLAMMATORY DISORDERS OF THE DISORDERS OF THE PERIPHERAL BLOOD PERIPHERAL BLOOD

VESSELSVESSELS

VARICOSE VEINS

• Permanently distended veins that develop from

loss of valvular competency

• Faulty valves elevate venous pressure

• Causes distension and tortuosity

Predisposing Factors

•Pregnancy

•Obesity

•Heart disease

Assessment Findings

•Aching, a feeling of heaviness in the legs

• Itching, moderate swelling

•Superficial inflammation

•Dilated tortuous skin veins

Diagnostic test

• Trendelenberg test:

• Doppler ultrasound– Decrease or no blood flow

heard after calf or thigh compression

Medical Management

THROMBOPHLEBITISTHROMBOPHLEBITIS

-is an inflammation of a vein accompanied by clot or thrombus

formation

DEEP VEIN THROMBOSIS –

veins that are deep in the lower

extremeties


-when inner lining of a vein is irritated or injured, platelets clump together, forming

a clot

Clot interferes with blood flow, causing congestion of venous blood


SIGNS AND SYMPTOMS

-complaints of discomfort in the affected extremity

-Calf pain (+Homan’s sign)-heat, redness, swelling on the affected

vein


DIAGNOSTICS

VENOGRAPHY – indicates a filling defect in the area

of the clot


MANAGEMENT

Complete rest of the affected partanticoagulant therapy (heparin)Continues warm, wet packs – to

improve circulation, ease pain, decrease inflammation

THROMBECTOMY- surgical removal of the clot

THROMBOANGITIS OBLITERANS THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)(BUERGER’S DISEASE)

Inflammatory, nonatheromatous occlusive condition that causes

segmental lesions and subsequent thrombus formation

- affects small arteries and veins of the legs


CAUSE: -unknown but definite link to smoking

CLINICAL MANIFESTATIONS:-Intermittent Claudication


- No specific treatment exist, except smoking cessation

- Amputation maybe necessary for patients with

gangrene formation

INFECTIOUS AND INFECTIOUS AND INFLAMMATORY INFLAMMATORY

DISORDERS OF THE DISORDERS OF THE HEARTHEART

RHEUMATIC FEVERRHEUMATIC FEVERis a systemic inflammatory disease

that sometimes follows a group A streptococcal infection of the throat

RHEUMATIC CARDITISRHEUMATIC CARDITISrefers to the inflammatory cardiac

manifestations of Rheumatic Fever in either the acute or later stage

RHEUMATIC FEVERRHEUMATIC FEVER

STRUCTURES AFFECTED:

heart valves, praticularly mitral valveendocardiummyocardiumpericardium

RHEUMATIC FEVERRHEUMATIC FEVERSTREPTOCOCCAL INFECTION

Antistreptococcal antibodies attack normal heart cells

� � � � � � � � � � � � � � � � � � � � � � � � � � � �

� � � � � �

Rheumatic carditis develops


SIGNS AND SYMPTOMS:

most common in children 2-3 weeks after a streptococcal infection

CARDITIS – inflammation of the layers of the heart


POLYARTHRITIS – inflammation of more than 1 joint

rash, subcutaneous nodules, chorea (characterized by involuntary

grimacing & an inability to use skeletal muscles in coordinated manner

RHEUMATIC FEVERRHEUMATIC FEVERSIGNS AND SYMPTOMS:

mild feverHeart rate (rapid, rhythm abnormal)Red, spotty rash (trunk, disappears

rapidly)Swollen, warm, red & painful joints


DIAGNOSTICS:

no specific laboratory testsASO titer

ESR, C-reactive protein – elevated,ECG, ECHOCARDIOGRAPHY – structural changes in the heart

RHEUMATIC FEVERRHEUMATIC FEVERMEDICAL MANAGEMENT:

IV ANTIBIOTICS:PENICILLIN – drug of choice

Others: AZYTHROMYCIN (ZYTHROMAX), CLINDAMYCIN,

VANCOMYCINCEPHALOSPORINS: Cephalexin, Cefadroxil


MEDICAL MANAGEMENT:

ASPIRIN – to control the formation of blood clots around heart valvesSTEROIDS – to suppress the

inflammatory responseBED REST


MEDICAL MANAGEMENT:

SURGERY may be required to treat constrictive pericarditis and damage to

heart valves


NURSING MANAGEMENT:

Administer prescribed drug therapy and monitor

for therapeutic and adverse effects

Plan diversional activities that require minimal activity

INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS

formerly called BACTERIAL ENDOCARDITIS

is inflammation of the inner layer of heart tissue as a result of an infectious

microorganism

MICROORGANISM – bacteria and fungiBACTERIA: Streptococcus viridans,

Staphylococcus aureus


SIGNS AND SYMPTOMS:

-can have an acute onset – less than one week

-fever, chills, muscle aches in the lower back and thighs, joint pain

ADVANCE: OSLER NODES - purplish, painful nodules, appear on the pads of the

fingers & toes


SIGNS AND SYMPTOMS:

-SPLINTER HEMORRHAGES – black longitudinal lines can be seen in the nails

-JANEWAY LESIONS – small, painless, red-blue macular lesions on the palms

and soles of the feet


SIGNS AND SYMPTOMS:

-ROTH’S SPOT – white areas in the retina surrounded by areas of

hemorrhage

-HEART MURMUR – may be present from malfunctioning valves


SIGNS AND SYMPTOMS:

-PETECHIAE – tiny red-dish hemorrhagic spots on the skin and

mucous membranes

-weakness, anorexia, weight loss


DIAGNOSTICS

-BLOOD CULTURE – to determine microorganism circulating in the blood

-ECG


MEDICAL MANAGEMENT

High doses of IV Antibiotics Antibiotic Therapy extends at least 2-

6 weeksBed rest

SURGERY – valve replacement if heart valve is severely damaged

INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITISNURSING MANAGEMENTRemind client to limit activity

Assess for changes in weight and pulse rate and rhythm

Administer prescribed antibiotics Inform client that periodic antibiotic

therapy is a lifelong necessity because they will be vulnerable to the disease for

the rest of their lives

MYOCARDITISMYOCARDITIS

is an inflammation of the myocardium (the muscle layer

of the heart)

CAUSES: Viral, bacterial, fungal, or parasitic infections

VIRAL AGENTS: coxsackie virus A & B, influenza A & B, measles, adenovirus,

mumps, rubeola, rubella


Inflammatory response causes the cardiac muscle to swell

Interferes with the myocardium’s ability to stretch and recoil

Cardiac output is reduced and blood

circulation is impaired, predisposing the client to CHF


CLINICAL MANIFESTATIONS:

-sharp stabbing pain or squeezing chest discomfort that resembles a MI (pain is

relieved by sitting up)-Low-grade fever, tachycardia,

dysrhythmias-Dyspnea, malaise, fatigue, anorexia

-Skin is pale and cyanotic


CLINICAL MANIFESTATIONS:

IF THERE’S IMPAIRED HEART’S PUMPING ACTIVITY:

-Neck vein distention, ascites, -Peripheral edema,

-crackles


DIAGNOSTICS:

-WBC – elevated-C-Reactive protein – elevated,

inflammatory conditions-CARDIAC ISOENZYMES-elevated

-CHEST X-RAY – heart enlargement, fluid infiltration in the lungs


MANAGEMENT

Treat underlying cause and prevent complications

ANTIBIOTICS if bacterialBed Rest

Sodium-restricted dietCardiotonic drugs – digitalis to prevent or

treat heart failure


MANAGEMENT

Heart transplant is necessary in severe cases of cardiomyopathy

MYOCARDITISMYOCARDITISNURSING MANAGEMENT

Monitor client’s cardiopulmonary status (daily weights, vital signs, I & O, heart &

lung sounds, edema)Maintain bed rest

Administer antipyretics if patient has feverElevate head of the bed for maximal

breathing potential

CARDIOMYOPATHYCARDIOMYOPATHY

is a chronic condition characterized by structural changes in the heart muscle

TYPES:DILATED CARDIOMYOPATHY

HYPERTROPHIC CARDIOMYOPATHYRESTRICTIVE CARDIOMYOPATHY

CARDIOMYOPATHYCARDIOMYOPATHYDILATED CARDIOMYOPATHY

-dyspnea on exertion & when lying down, fatigue, edema, palpitations, chestpain

HYPERTROPHIC CARDIOMYOPATHY

-syncope, fatigue, shortness of breath, chestpain

-some are asymptomatic

CARDIOMYOPATHYCARDIOMYOPATHYRESTRICTIVE CARDIOMYOPATHY

-exertional dyspnea, dependent edema in the legs, ascites, hepatomegaly

CARDIOMYOPATHYCARDIOMYOPATHYDILATED CARDIOMYOPATHY

-the cavity of the heart is stretched (dilated)

CAUSES: Viral myocarditis, Autoimmune response, chemicals (chronic alcohol ingestion)

TREATMENT: Drug Therapy to minimize symptoms & prevent complications,

abstinence from alcohol, salt restriction, weight loss, possible heart transplantation

CARDIOMYOPATHYCARDIOMYOPATHYHYPERTROPHIC CARDIOMYOPATHY

-the muscle of the left ventricle & septum thickens, causing heart enlargement)

CAUSES: hereditary, unknown

TREATMENT: Drug Therapy to reduce heart rate & force of contraction, antidysrhythmic

drugs, artificial pacemaker

CARDIOMYOPATHYCARDIOMYOPATHYRESTRICTIVE CARDIOMYOPATHY-heart muscle stiffens, which interferes with

its ability to stretch & fill with blood

CAUSES: deposits of amyloid, scleroderma,

TREATMENT: no specific treatment, drugs such as diuretics & antihypertensives used to

control symptoms

CARDIOMYOPATHYCARDIOMYOPATHYTREATMENT:

-DIURETICS-CARDIAC GLYCOSIDES

-ANTIHYPERTENSIVE

PERICARDITISPERICARDITIS

inflammation of the pericardium

PRIMARY – develops independently of any

other condition

SECONDARY – develops because of another condition


Usually secondary to endocarditis, myocarditis, chest trauma or MI

OTHER CAUSES: tuberculosis, malignant tumors, uremia


SIGNS AND SYMPTOMSFever and malaise

Dyspnea, or complaints of chest heaviness

PRECORDIAL PAIN (relieved by upright or leaning forward)


DIAGNOSTICSECG – ST segment elevation (cardiac

isoenzymes normal)ECHOCARDIOGRAPHYWBC & ESR - elevated


MANAGEMENTRest

DRUGS: Analgesics, antipyretics, NSAIDs, corticosteroids

PERICARDIOCENTESIS – needle aspiration of fluid from between the visceral and parietal pericardium

Health & Medicine

Cardiovascular disorders