CARDIOVASCULAR DISEASES

REVIEW

How many chambers are in the heart?

How does the blood flow through the heart?

What vessels take blood AWAY from the heart?

What vessels take blood TO the heart?

What is Pulse Pressure? What is Cardiac Output? What is Stroke Volume?

Terms associated with Stroke Volume

Preload – degree of stretch of the cardiac muscle fibers at the end of diastole Direct effect on stroke volume: more blood

then causes more effective contraction Afterload – pressure the ventricle

myocardium must overcome to eject blood during systole

Systemic vascular resistance - resistance of the systemic pressure to the left ventricle ejection

Pulmonary vascular resistance - resistance of the pulmonary pressure to the right ventricle ejection

Ejection fraction – percentage of the end – diastole volume that is ejected with each stroke (42 – 50%) (used to assess contractility)

Contractility – the force generated by the contracting myocardium under any given condition Increased contractility leads to increased stroke

volume

Effects of Aging

Aging heart muscle can provide adequate CO until emotional /physiological stress

Less activity can lead to left ventricular atrophy

Decreased elasticity and widening of the aorta

Thickening & rigidity of the cardiac valves Increased connective tissue in the SA & AV

nodes LEADS to decreased contractility, increased

left ventricular ejection, & delayed conduction

Differences in Males & Females

WOMAN HEART Smaller in size Smaller coronary arteries ▪ Occlude easier with atherosclorosis▪ Makes angioplasty more difficult

Higher stroke volume, ejection fraction, resting HR

Shorter SA to AV node conduction

Differences continued

Female hormones such as estrogen protect women from developing coronary artery disease (CAD)

Estrogen affects cholesterol levelReduce LDLIncreases HDLImprove blood flow

Menopause – decreased estrogen causes women to be at equal risk for CAD with men

Signs & Symptoms to evaluate Chest discomfort

Angina Pectoris MI

SOB Left ventricular failure; CHF

Edema/weight gain Rt ventricular failure; CHF

Palpitations Dysrhythmias; valvular disease; ventricular aneurysm;

electrolyte imbalance Fatigue

Associated with numerous heart conditions Dizziness

Postural hypotension; dysrhythmias; vasovagal effect; cerebrovascular disorders

Activity & Exercise on Heart disease

Decreases in activity tolerance are usually gradual

Easily Fatigued after activity is an early indication of progressing disease

After activity, patients may experience chest pain, SOB, palpitations

Sleep & Rest

Progressing disease has symptoms when the patient is at rest

Increasing the number of pillows to sleep

Awakening due to SOB (paroxysmal noturnal dyspnea)

Awakening chest discomfort

Pulse Pressure

Systole – Diastole= Pulse Pressure Normal: 30 – 50 mmHg Increases in conditions that increase stroke

volume Anxiety Exercise bradycardia

Decreases in abnormal conditions Shock Heart failure hypovolemia

Postural (orthostatic) pressure When BP drops significantly after the

patient assumes the upright position Symptoms

Dizziness Lightheadedness syncope

Causes Hypovolemia Inadequate vasoconstrictor mechanisms Insufficient autonomic effect on vascular

constriction

Assessing Orthostatic hypotension

Have the patient lie supine & flat as symptoms permit for 10 minutes before taking BP & HR

Check supine before doing upright measurement

Check & compare supine, sitting, & standing pressures & HR

Wait 1 – 3 minutes after each postural change before measuring BP

NORMAL findings

LYING to sitting/standing HR increases 5 – 20 beats above resting Systole is the same or slightly decreases

(w/in 10 mm Hg) Slight increase in diastole (5 mm Hg)

Auscultation of the heart Aortic area – 2nd intercostal space Rt of

sternum Pulmonic area – 2nd intercostal space LT of

sternum Erb’s point – 3rd intercostal space to LT Right ventricular/tricuspid area – 4th & 5th IC

to left @ midclavicular line Left ventricular/apical area – 5th IC to left

sternum @ midclavicular line Epigastric area – below the xiphoid process

Heart Sounds

S1 – closing mitral /tricuspid valve Heard loudest at the apex

Systole S2 – closing aortic & pulmonic valves

Sometimes the pulmonic is slightly late causing a split S2

Heard loudest at the base of the heart Diastole

Gallop – blood filling the ventricles is impeded during diastole Sounds like a galloping horse During rapid ventricular filling CHF: myocardial disease; ventricles fail to

eject all blood during systoleSnaps & Clicks

Stenosis of the mitral valve Early in diastole that is high pitched best

heard at left sternal border

Murmurs – turbulent flow of blood\critically narrowed valve

Malfunctioning valve allowing regurgitant blood flow Defect of the ventricular wall Defect between the aorta & pulmonary artery

Friction Rub Pericarditis Grating sound heard in systole & diastole Abrasion of the pericardial surface during

cardiac cycle

Inspecting Extremities

Capillary Refill – slow peripheral flow rate

Vascular changes Hematoma Peripheral edema Clubbing Lower extremity ulcers – may be

present in arterial and/or venous insufficiency

Respiratory findings related to CV disease

Tachypnea – heart failure Cheyne – Stokes respirations –

Severe Left ventricular failure Dry, hacky cough – pulmonary

congestion r/t heart failure Crackles – heart failure Wheezes – pulmonary edema or SE

of beta blockers (heart medication)

Cardiac Enzymes

Are elevated during/after MI Released from injured cells when the cell

membranes rupture due to prolonged hypoxia Isoenzymes come only from cardiac cells Creatine Kinase (CK) & CK – MB are the most

specific for MI; they are the first to elevate lactic dehydrogenase & its isoenzyme elevate

2 – 3 days later Troponin I is a contractile protein only in

cardiac muscle. Elevates within 3 – 4 hours after insult

Cholesterol Levels & HDL, LDL Cholesterol should be less than 200 mg/dL

Used for what? Where is it found? Sources? Contributing factors: age, gender, diet, exercise, &

stress LDL – normal is less than 130 mg/dL

Primary transporter of cholesterol into cell HDL – normal MALE: 35 – 65 FEMALE: 35 – 85

Transport cholesterol away from the cell to the liver for excretion

Electrolytes

Sodium Fluid balance Hyponatremia – fluid excess Hypernatremia – fluid deficit

Magnesium – absorption of CA & maintains K+ stores; Hypomagnesemia – lengthens QT interval

Calcium Blood coagulability & neuromuscular activity Hypocalcemia/hypercalcemia – causes dysrhythmia

Potassium Affected b/ renal function Decreased by diuretic (used to treat CHF) Hypokalemia – cardiac irritability Hyperkalemia /hypokalemia – lead to ventricular fibrillation or

cardiac standstill

Coagulation studies

Formation of a thrombus is initiated by injury to a vessel wall or tissue

Partial thromboplastin time (PTT) Measure the activity of the intrinsic pathway Normal: 25 – 38 seconds

Prothrombin time (PT) Measures the extrinsic pathway activity & monitored during

anticoagulation therapy Normal: less than 13 seconds

International Normalized Ratio (INR) Provides a standard method for reporting PT Patient receiving anticoag therapy: 2.0 – 3.0

Heparin & Coumadin – drugs that provide anticoagulation therapy

ECG

Universal diagnostic tool 12 Lead shows the activity from 12

different views Used to diagnose dysrhythmias,

conduction abnormalities, enlarged heart chambers, myocardial ischemia/infarction

Hypo/hyper calcemia; hypo/hyper kalemia

Reading EKG’s

Waveform represents the functions of the heart’s conduction activity

Printed on graph paper Time & rate measured on horizontal

axis Amplitude or voltage is measured on

vertical axis Represented by P Q R S T

P wave – is the electrical impulse from the SA node through the atria (atrial depolarization) Normal: 2.5 mm or less in height and .11 second

duration QRS Complex – ventricular muscle

depolarization; less than .12 seconds in duration Depression after P wave is the Q wave that is .04

seconds Positive deflection after P wave is R wave Negative deflection after R is the S wave

T wave – represents ventricular muscle repolarization (resting state); after QRS wave & usually in the same direction of the QRS complex

U wave – represents the repolarization of Purkinje fibers; may be seen in hypokalemia or HTN

PR interval – beginning of P wave to beginning of QRS complex. Time for SA node stimulation, atrial depolarization, &

conduction through the AV node Normal .12 - .20 seconds

ST segment – early ventricular repolarization; lasts for end of QRS to beginning of T wave Beginning of ST segment is identified by

a change in the thickness of the terminal portion of the complex

QT interval – total time for ventricular depolarization & repolarization ; beginning of QRS to end of T wave .32 - .40 seconds

Interpreting EKG

1 minute strip has 300 large squares & 1500 small squares

15 large boxes in 3 seconds; 5 lg boxes/1 sec

Calculate the HR: count the R peaks in 6 seconds & multiply by 10

If the R peaks are equal distance apart, then the rate is regular

Dysrhythmia disorders

Formation of new electrical activity or alteration in the electrical activity

Review of normal conduction What are the structures & the steps to

electrical activity?

Sinus Bradycardia SA node fires at a slower than normal

rate Slower metabolic needs, vagal

stimulation, medications, increased ICP, MI (inferior wall)

Sinus Tachycardia Faster than normal rate Blood loss, anemia, shock,

hypervolemia, hypovolemia, CHF, pain, fever, exercise

Sinus Arrhythmia SA nodes creates an irregular rhythm;

increases during inspiration & decreases during expiration

Causes: heart disease, valvular disease

Atrial dysrhythmia

Atrial Flutter Atrium beats 250 – 400 times/minute Too fast for the AV node to send all to

ventricles Atrial Fibrillation

Inflammatory Disorders

Endocarditis – inflammation of endocardium Bacterial – leaflets of the mitral valve erode due

to bacteria Libman – Sacks – found in patients with lupus

Myocarditis – inflammation of the muscle Acute (usually caused by a virus) Chronic

Pericarditis – inflammation of the sac/outer layer Acute Chronic

Valvular Disease

Mitral Valve Prolapse Usually benign Causes▪ Calium degeneration▪ Inflammatory endocarditis▪ MI

Complications▪ Arrhythmia▪ Cardiomyopathy▪ Heart failure

Mitral Valve Stenosis Hardening of the mitral valve caused by

calcification/fibrosis Narrowing of the valve opening Dialation of the left atrium S & S▪ Dyspnea on exertion▪ Paroxysmal nocturnal dyspnea/orthopnea▪ Fatigue/weakness▪ Right sided heart failure▪ crackles

Aortic Stenosis Congenital aortic valve defect Due to rheumatic fever Treatment▪ Digoxin Nitroglycerine▪ Diuretics

S & S▪ Exertional dyspnea▪ Syncope▪ Angina, palpitations▪ Left sided failure

Hypertension

Essential – progressive 90% cases

Could be from mechanisms that:▪ Control cardiac output▪ Systemic vascular resistance▪ Blood volume

Secondary Caused by another disorder Less than 10% cases

Silent Killer

Affects other organs in the body Brain▪ Narrowed blood vessels will have clotted blood

& cause strokes▪ Weakened blood vessel walls can lead to

hemorrhage Eyes▪ Increased BP cause hemorrhage in retina▪ Swelling of optic disc leads to blindness

Kidneys▪ Arterioles harden & restrict O2 to glomeruli

Different Drugs for HTN

Diuretics Beta Blockers ACE Inhibitors

Thiazide Diuretics

Generic: Hydrochlorothiazide Effective & most cost-efficient Usually tried first Increases excretion of water, sodium, chloride, &

potassium Treats: edema, uncomplicated HTN, prophylaxis of

kidney stones, electrolyte imbalance SE: Hypokalemia, hypochloremia, muscle weakness,

postural hypotention, vertigo, HA, fatigue, lethargy, hyperglycemia, elevated uric acid

CI: diabetes, gout, severe renal disease, impaired liver function

Interactions: NSAIDS, corticosteroids, digitalis

Beta-Adrenergic Blocker

Inderal (propranolol) & Tenormin (atenolol) Used in patients with angina, postmyocardial infarction SE: hypotension, vertigo, syncope, bradycardia,

irritability, confusion, insomnia, N & V, Brochospams (in asthma), hypoglycemia,

CI: Major surgery, diabetes, renal or liver impairment, bradycardia, asthma, COPD

Interactions: Antidepressants Potentiate the hypotensive effects in:

Diuretics Tranquilizers Tagamet Other cardiac drugs alcohol

Calcium – Channel blockers Cardizem (diltiazem) & Procardia (nifedipine) Used in patients with diabetes or high coronary

risk Suppress the Calcium in muscle contraction;

reducing excitability & dilates coronary arteries SE: hypotension, HA, vertigo, bradycardia,

edema, N, constipation, & abdominal discomfort

CI: heart block, heart failure, pregnancy, children

Interaction: lithium, diuretics, barbiturates

ACE Inhibitors

Angiotensin – converting enzyme inhibitors Catopril & enalapril Decreases vasoconstriction (no change in CO or

HR) Usually used with diuretic therapy Used in patients with heart disease, diabetes, renal

disease SE: rash, loss of taste perception, severe

hypotension, chronic dry cough, nasal congestion, hyperkalemia

CI: Lupus, heart failure, angioedema, pregnancy I: diuretics, vasodilators, K+ sparing diuretics,

NSAIDS

Heart Failure

Myocardium can’t pump effectively enough to meet the body’s needs

Possible Causes Increased pressure/volume resulting

myocardial function Left ventricular remodeling Altered hemodynamics to maintain CO Hormonal changes that accelerate HR &

increase EF

Classifications Right or Left sided▪ Right – result of ineffective Rt ventricular contraction due to

infarction, PE, back flow due to Lt side failure▪ Left – ineffective Lt ventricular contraction leading to pulmonary

congestion & decreased CO Systolic or diastolic▪ Systolic – LT ventricle can’t pump to body▪ Diastolic – left ventricle can’t relax & fill appropriately leading to

decreased SV Acute or chronic▪ Acute – the compensatory mechanisms kick in; fluid status is

normal▪ Chronic – S & S present for some time, compensatory

mechanisms kicked in & fluid overload is present

Signs & Symptoms

LEFT

Dyspnea Cough Tachycardia Fatigue Muscle weakness Edema Weight gain Crackles

RIGHT

Edema Jugular vein distention Hepatomegaly Generalized weight

gain

Cardiomyopathy

Refers to the disease of the heart muscle fibers

3 classes Dilated - affects systolic function Hypertrophic – primarily affects diastolic

function Restrictive – stiffness of the ventricle

caused by left ventricular hypertrophy or endocardial fibrosis

CAD (Coronary Artery Disease)

Progressive buildup of atherosclerotic plaque in the coronary arteries

Risk factors High LDL’s Uncontrolled HTN Sex (Men are more prone) Smoking Heredity

Angina

Usually upon exertion Abnormal stress test or

Echocardiogram findings Chest pain May show up as a reversible ST Progressively will become worse &

severity over time

Angina vs MI

Angina Pain is burning,

squeezing, substernal Lasts 5 – 15 minutes Usually related to

exertion, stress, cold, exercise

Relief: nitroglycerin, rest, oxygen

Hypotension/HTN, tachy or brady cardia

Cardiac enzymes WNL

MI Severe substernal pain,

chest, shoulders, hand Lasts greater than 15

minutes Occurs all of sudden May be preceded by

unstable angina Relief: MS, reperfusion of

cardiac tissue Hypo/hyper tension,

palpable precordial pulse, muffled heart sounds, arrhythmia

Cardiac markers: Elevated