1 NCLEX RN Preparation Program Cardiovascular Disorders Module 5, Part 2 of 3.

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NCLEX RN Preparation Program

Cardiovascular DisordersModule 5, Part 2 of 3

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Cardiovascular System

IntroductionThe heart and the circulatory

system comprise one

of the most essential

parts of the body.

Failure to function

results in death of

the organism.Photo Source: National Heart, Lung and Blood Institute (NHLBI) http://www.nhlbi.nih.gov/health/dci/Diseases/arr/arr_howheartwork.html

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Gross Structure of the Heart

Layers: Pericardium

Fibrous Serous Pericardium

Epicardium Myocardium Endocardium

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Chambers of the Heart Heart, a muscular organ

divided by a septum into two halves. Right or venous chamber and left or arterial chamber.

Right Chambers Right Atrium Right Ventricle

Left Chambers Left Atrium Left Ventricle

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Coronary Blood Supply Right Coronary

Artery Left Coronary

Artery Left anterior

descending Circumflex

Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program

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Valves of the Heart Valves are strong membranous openings that provide

one-way flow of blood. Atrioventricular valves – prevent backflow of blood

from ventricles to atria during systole. Tricuspid Mitral

Semilunar valves – prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. Pulmonic Aortic

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Valves of the Heart

Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program

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Conduction system Specialized tissue that allows rapid

transmission of electrical impulses through the myocardium

Sinoatrial node – main pacemaker of heart. Normal rhythmic, self-excitatory impulse is generated.

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Conduction system

Photo Source: St. Francis Hospitals & Health Centers, http://www.stfrancishospitals.org/DesktopDefault.aspx?tabid=72&Class=Test&pageid=P07973

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Gross Structure of Vasculature Arteries: transport blood under high

pressure to body tissues Precapillary sphincters Arteriovenous shunts

Capillaries – exchanging fluid and nutrients between blood and interstitial space.

Veins: acts as conduits for transport of the blood from tissues back to heart

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Physiology of the Heart Contraction – shortening or increase in

muscle tension. Utilizes chemical energy to do the work of contraction

Cardiac Muscle Principle: Frank Starling Law: the greater the heart is

filled during diastole, within physiological limits, the greater the quantity of blood pumped into the aorta and pulmonary artery.

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Autonomic Nervous System Control

Cardiac Muscle Sympathetic (Adrenergic) Parasympathetic (Cholinergic)

Systemic blood Vessels Sympathetic – vasoconstriction Parasympathetic – vasodilation

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Baroreceptor Reflex (Pressoreceptors)

Located in the walls of large systemic arteries Rise in pressure results in baroreceptors

transmitting signals to CNS (Central Nervous System) to inhibit sympathetic action

Other signals, in turn, sent to circulatory system to reduce pressure back to normal.

Result: decreased heart rate, vasodilation, decreased BP.

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Other Chemical Controls of Blood Pressure

Kidney Adrenal cortex - aldosterone Renin-angiotensin system

Antidiuretic hormone (vasopressin)

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System AssessmentEvaluate Patient’s History

Pain Dyspnea Cyanosis Fatigue Palpitations Syncope Hemoptysis

Edema Condition of

Extremities

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Evaluate veins and arterial pulses through inspection/palpation

Veins Neck veins Arm and hand veins Leg and foot veins

Arteries Central Peripheral pulses

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Auscultate lung sounds

Lungs Listen for bibasilar crackles – if present,

suspect Congestive Heart Failure (CHF)

Photo Source, Wikimedia Commons, Creative Commons, http://commons.wikimedia.org/wiki/Image:X-ray_lung_consolidation.jpg

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Auscultate heart sounds Heart sounds – frequency, pitch, intensity,

duration Murmurs

Systolic Diastolic

Pericardial friction rubs

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Other parameters to assess

Arterial pressure Carotid blood vessels for bruit Palpate and percuss thorax Evaluate chest x-rays Assess lung sounds

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Diagnostic Tests & Procedures

Laboratory Studies Cardiac Enzymes

CK-MB LDH Troponin Myoglobin BNP

CBC Blood coagulation factors Serum lipids Electrolytes

K, Na

Calcium Phosphorus Magnesium BUN Blood glucose

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Diagnostic Procedures Electrocardiogram Central Venous Monitoring Cardiac Catheterization Echocardiography Angiography Chest x-rays

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Acute Coronary Syndromes

Coronary Artery Disease (CAD) Narrowing or obstruction

of one or more coronary

arteries as a result of

atherosclerosis, an

accumulation of

lipid-containing plaque

in the arteries. Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html

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Pathophysiology Atherosclerosis - fat deposited in intima of arterial

wall Inflammatory response begins Macrophages inflitrate area to ingest lipids, then

die Smooth muscles cells within the blood vessel

cover the area with fiber and plaque is formed. If the plaque is thin, the lipid center may grow,

rupture, become a thrombus

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Myocardial Ischemia / Angina Pectoris

Decreased oxygen to heart Exercise-induced chest pain Unstable angina Other risk factors

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Coronary Artery DiseaseMyocardial ischemia

CLINICAL MANIFESTATIONS: May be asymptomatic unless ischemia occurs Chest pains or pressure, may radiate to jaw,

back, shoulder Palpitations, weakness Dyspnea Syncope Nausea Excessive fatigue EKG changes (T wave inversion)

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Coronary Ischemia/Angina

Silent angina - no

symptoms, but

EKG changes.

Often occurs in

diabetic

patients with CAD.

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Teaching for Angina

Rest at onset of chest pain Take one nitroglycerin, repeat 2 more

prn No relief by 3rd, call 911 Previous angina with particular activity,

take nitroglycerin prior to activity

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Unstable Angina Oxygen: 2-4L nasal cannula Nitroglycerin Morphine Aspirin Baseline vital signs 12 lead EKG Monitor for dysrhythmias, heart failure

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Myocardial Infarction

Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html

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MI: Signs and Symptoms Pain Nausea Impending doom Diaphoresis Dyspnea Dysrhythmias

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12-lead EKG Normal Ischemia Injury

Acute infarct

Old infarct

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LABS Myoglobin – non specific Troponin CK-MB BNP = CHF

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Collaborative Management Immediate assessment

Vital signs with oxygen saturation 12-lead EKG Cardiac enzymes Chest x-ray Electrolytes – K+ & Mg++

Immediate treatment – “MONA” Beta blockers?

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MONA

Acronym from Advanced Cardiac Life Support (ACLS) though order is ONMA.

O = Oxygen 2-4 liters per nasal cannula N = Nitroglycerin (if not already tried outside

hospital); relieves pain M= Morphine relieves pain, decreases

anxiety, increases venous pooling (to reduce cardiac workload)

A = Aspirin prevents platelet aggregation at the site of obstruction

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Reperfusion Strategies

Thrombolytics Percutaneous

Transluminal Coronary Angioplasty (PTCA)

Stent Procedure

Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html

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Post-PCTA Care Monitor V/S Assess distal pulses Bed rest with limb straight for 6 – 8 hours Anticoagulants/antiplatelet agents – prevent

thrombus formation Monitor IV nitroglycerin – prevent coronary

artery spasms ASA once a day permanently Assist planning lifestyle modification

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Acute Myocardial Infarction

Bed rest for 24 to 36 hrs

Pain control

Monitor rhythm

Assess for new murmurs

Monitor potassium, magnesium

Monitor for heart failure

Gradual increase of activities

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Rehabilitation Diet Progressive exercise Change modifiable risk factors

Weight loss Stress reduction Lipid-lowering drugs Anti-hypertensives Aspirin

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Coronary Artery Bypass Graft (CABG)

Bypass grafts sewn from aorta to below area of blockage

Fluid overload Pacemaker? Bleeding Atrial fibrillation

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Nursing Management

Control pain

Early ambulation

Incentive spirometer

Change dressings: watch for infection

Monitor: VS, lungs, heart, weight, I&O, labs, EKG

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Complications Stroke Tamponade: pulsus paradoxus Bleeding Dysrhythmias Post-cardiotomy syndrome

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Cardiac Dysrhythmias

Normal Sinus Rhythm/Regular Sinus Rhythm Rhythm originates from the SA node Atrial and ventricular rhythms are regular Rates are : 60- 100 beats per minute.

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Cardiac Dysrhythmias Sinus bradycardia

Atrial and ventricular rates below 60 beats per minute

Treatment may be necessary if symptomatic Note: low rates may be normal for some

patients.

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A-V block: 2nd Degree Mobitz I

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AV Block: 2nd Degree Mobitz II

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A-V Block: 3rd Degree

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Supraventricular Tachycardia

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Atrial Fibrillation

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Premature Ventricular Contractions (PVCs)

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Ventricular Tachycardia

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Ventricular Fibrillation

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Defibrillation Options

Paddles AED ICD

Photo Source: Wikimedia Commons (Creative Commons), http://commons.wikimedia.org/wiki/Image:Defibrillator_Monitor.jpg

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Asystole/PEA

CPR, epinephrine, vasopressin, atropine Consider 6 H’s, 5 T’s below:

Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypoglycemia, Hypothermia

Toxins, Tamponade (cardiac); Tension pneumothorax; Thrombosis (coronary or pulmonary); Trauma

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Cardiac Pacemaker

Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the patient’s intrinsic pacemaker fails to provide a perfusing rhythm.

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Pacemakers

Types of Pacemakers Temporary Transvenous invasive temporary pacing Epicardial invasive temporary Permanent

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Patient Education Programmed rate When to notify MD:

Dizziness, weakness, sudden weight gain of 3-5 pounds overnight, persistent hiccups. Check pulse daily, report sudden slowing or increasing of pulse.

Signs/symptoms to report:Fever, redness, swelling, drainage from insertion site, dizziness, fatigue, shortness of breath, chest pains, swelling of ankles/legs

Pacemaker identification, medic alert Measure pulse daily, keep record

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Patient Education(continued)

Wear loose-fitting clothing Avoid contact sports Inform all health care providers of pacemaker Most electrical appliances can be used

without any interference with the functioning of the pacemaker.

If any unusual feelings occur when near any electrical devices, move 5 to 10 feet away and check pulse.

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Congestive Heart Failure Inability of the heart to maintain adequate

circulation to meet the metabolic needs of the body because of impaired pumping actions.

Cardiac output diminished and peripheral tissue not adequately perfused

Congestion of the lungs and periphery may occur.

Classification: Acute and Chronic Types: Right-sided/left-sided heart failures

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Congestive Heart Failure Clinical manifestations

Weight gain, I & 0, edema, if severe: ascites Crackles in lungs (especially bibasilar) Dyspnea, orthopnea, urinary frequency, murmurs (if valve problem) S3 heart sound - sign heart beginning to fail & increased

blood volume remains in heart after each beat BNP lab test - the higher the number, the worse the CHF

is. Can monitor severity of CHF, improvement due to treatment regimen, timely diagnosing of CHF

Jugular vein distension, LOC, pulse oximetry.

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CHF: Collaborative Mgmt

Vasodilators: Nitrates Positive inotropes: increase contraction

Digoxin (Lanoxin) Beta blockers (though some

contractility & are contraindicated) ACE inhibitors

Diuretics

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CHF: Nursing Management Elevate head of bed Give oxygen Decrease oxygen demand Exacerbation? Identify precipitating factors Teach: low-salt diet, medications and their

rationale, weigh daily, exercise but pace activities. Wait 90 min. after meals to exercise. Avoid extremes in weather when exercising.

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Cardiac Valve Disorders

Mitral stenosis

Mitral prolapse

Aortic stenosis

Aortic regurgitation

Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html

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Cardiac Valve Disorders

Clinical Manifestations: Heart murmur Left ventricular hypertrophy seen on EKG

Congestive Heart Failure

Photo Source: Lippincott, Williams, & Wilkins Connection Image Bank, http://connection.lww.com/products/smeltzer9e/imagebank.asp

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Congestive Heart Failure Collaborative Management

Digoxin (inotropic) Diuretics (lasix, aldactone) Coreg - beta blocker shown to improve

cardiac function in CHF patient Ace inhibitor - shown to improve cardiac

function in CHF patient Oxygen, cardiac rehab

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CHF Management (continued)

Treat heart failure if present Atrial fibrillation? Antibiotic prophylaxis Weigh daily

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Pericarditis

Inflammation of pericardial sac. Can be caused by viral infection, complicaton after cardiac surgery 10 days to 2 months, or after MI

Idiopathic cause, or disorder of connective tissue (lupus), cancer, radiation therapy, etc

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Pericarditis: Manifestations

Chest pain on inspiration, worse when patient leans forward, lying down or turning

Pericardial friction rub Symptoms of right-sided heart failure Mild fever, elevated WBC, ESR Atrial fibrillation common 12 lead EKG may have elevation in ALL leads Can worsen to cardiac tamponade

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Pericarditis Collaborative Management

NSAIDs or corticosteroids Pericardiocentesis or surgical pericardial

window

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Pericarditis: Nursing Mgmt Position for comfort Monitor for cardiac tamponade (fluid between

heart and pericardial sac) that causes heart to be compressed inside the sac leading to decreased blood pressure and shock, distant heart sounds

Teach: gradual increases of activity Teach: avoid aspirin, anticoagulants

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Infective Endocarditis Valves infected, spreads to endothelium Leaflets deform, leak High risk: elderly, prosthetic valves, IV

drug abusers, immunosuppressed

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Manifestations Slow onset

Flu-like symptoms, anorexia, weight loss, joint & back pain, fever, splinter hemorrhages undernails, petechiae, murmur, headache?

Major complication: embolus Diagnosis: blood culture, echocardiogram

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Management IV antimicrobials based on cultures Teach prevention Monitor: sepsis, new murmur, stroke,

meningitis, CHF

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Hypertension Pathophysiology

90-95% unknown cause 5-10% secondary causes Some genetic tendency, obesity, stress,

excess sodium intake Prolonged hypertension eventually damages

blood vessels, heart (LVH) and kidneys, eyes, brain.

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Hypertension Clinical manifestations

Usually asymptomatic “silent killer” Some report headache, especially early morning

Risk factors Family history Age Diabetes Obesity Heavy alcohol High sodium intake

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Hypertension Goals: reduce BP. Goal: 120/80 Ask for S/S indicative of HTN Obtain BP on both arms Family history, weight, dietary patterns Identify medication therapy Assess cardiac, neuro, renal, diagnostic

and lab studies.

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Hypertension Collaborative Management

Medications: diuretics, beta blockers, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, alpha blockers

Monitor and routine follow-up with EKG, lipid lower agents if needed

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Hypertension Nursing Management

TEACH: weight loss, stress management, rationale for medications prescribed & their importance. Low-sodium, low-fat, low-cholesterol diet. Stop smoking. Limit caffeine, alcohol. Teach how to modify risk factors.

Monitor for target-organ problems. Teach potential problems if hypertension untreated.

Many people undiagnosed. Promote screening for early detection.

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Classification

Category Systolic Diastolic

Normal <120 mmHg <80 mmHg

Pre-HTN 120-139 or 80-89

Stage 1 140-159 or 90-99

Stage 2 ≥ 160 or ≥ 100

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Hypertensive Crisis…Assessment

Diastolic pressure > 120 mm Hg. Headache Drowsiness Confusion Changes in LOC Tachycardia and tachypnea Dyspnea/cyanosis/seizure

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Hypertensive Crisis: Mgmt Lower BP slowly

IV nitrates (nitroglycerin) Nitroprusside (Nipride) Enalapril (Vasotec) Beta blockers Diuretics

Monitor rhythm, vital signs

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Peripheral Vascular Disease (PVD)

Pathophysiology Generalized atherosclerosis (plaque

development) or arteriosclerosis (hardening of the arteries)

Narrowing of lumen, obstruction by thrombosis

Bifurcation or branch areas higher risk of blockage.

If have PVD, at risk of having CAD as well

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Peripheral Arterial Disease

Stage I: Asymptomatic Stage II: Claudication Stage III: Rest pain Stage IV: Necrosis

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PVD: Management Medications Control hypertension Angioplasty, bypasses Exercises Position Vasodilation Avoid vasoconstriction

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Arterial Bypass

Monitor for graft occlusion Promote graft patency Monitor for compartment syndrome

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Peripheral Venous Insufficiency

Stasis dermatitis lower legs Edema Ulcers over malleoli Anterior leg ulcers if arterial flow

impaired

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Peripheral Vascular Disease Compression stockings Sequential compression pump Manage ulcers Elevate legs Avoid prolonged sitting or standing No compression of legs

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Abdominal Aortic Aneurysm

Localized dilatation of the wall of the abdominal aorta caused by congenital weakness, trauma, disease, atherosclerosis

Risk factors: smoking, hypertension Progressive weakening and enlarging of area of vessel If a tear develops - medical emergency (rupture)

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Aortic Aneurysms Goal of treatment:

limit progression of the condition by modifying risk factors, controlling BP, recognizing symptoms early, and preventing rupture

Photo Source: National Heart, Lung and Blood Institute (NHLBI), http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html

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Abdominal Aortic Aneurysm Clinical Manifestations:

Can palpate enlarged aorta, possible bruit ausculated

If rupture, sudden pain in back or abdomen

If tearing, pain in abdominal area or back; can be slowly progressive

If rupture-hemorrhage, shock, death unless emergent surgical intervention

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Manage Abdominal Aneurysm

Non-surgical:

Modify risk factors Monitor BP Regular exams for size, pulsation Report: chest/back pain, SOB, Difficulty

swallowing, hoarseness

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Thoracic Aortic Aneurysm

Pain: neck, shoulders, lower back or abdomen

Syncope Dyspnea Tachycardia Cyanosis Weakness

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Manage Thoracic Aneurysm Monitor V/S Assess for pain – abdominal or back

pains. Check peripheral pulses, including

temperature and color Observe for signs of rupture Note tenderness/distention of abdomen

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Photo Acknowledgement:All unmarked photos and clip art

contained in this module were obtained from the

2003 Microsoft Office Clip Art Gallery.