Assessing Clients with Cardiac Disorders

7/29/2019 Assessing Clients with Cardiac Disorders

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Assessing Clients with Cardiac Disorders

I. Background of Anatomy and PhysiologyA. Heart

1.Size of adults fist, weight < 1 pound2. Located in mediastinum, between vertebral

column and sternum

3.2/3 of heart mass is left of sternum; upper base

is beneath second rib; pointed apex liesapproximately with fifth intercostal space,mid-clavicular

B. Pericardium

1. Covering of double layered fibroserousmembrane, forming pericardial sac

2.Layers of pericardiuma. Parietal pericardium: outermost layer

b. Visceral pericardium (epicardium)

adheres to heart surface3. Small space between layers is pericardial

cavity which contains small amount of serous

lubricating fluid that cushions heart as it beats

C. Layers of Heart Wall1. Epicardium: same as visceral pericardium2. Myocardium: specialized cardiac muscle cells

provide bulk of contractile heart muscle

3. Endocardium: sheath of endothelium that islining inside hearts chambers and great

vessels


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D. Chambers and Valves

1.Four hollow chambers: two upper atria, twolower ventricles; separated lengthwise byinterventricular septum

a. Right atrium: receives deoxygenatedblood from veins of body

1.Superior vena cava: blood from body

above diaphragm

2.Inferior vena cava: blood from bodybelow diaphragm

3.Coronary sinus: blood from heartb. Left atrium: receives freshly oxygenated

blood from lungs via pulmonary veinsc. Right ventricle: receives deoxygenated

blood from right atrium and pumps it tolungs for oxygenation via pulmonaryartery

d.Left ventricle: receives freshlyoxygenated blood from left atrium and

pumps it to arterial circulation via aorta

2.Valves separate each chamber of heart

allowing unidirectional blood flowa. Atrioventricular (AV) valves: between

atrium and ventricle; Flaps of valvesanchored to papillary muscles of

ventricles by chordae tendineae1. Tricuspid: right side

2. Mitral (biscuspid): left side


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b. Semilunar valves: connect ventricles to

great vessels1.Pulmonary: right side; joins rightventricle and pulmonary artery

2.Aortic: left side; joins left ventricleand aorta

c. Heart sounds associated with closure of

valves

1. S1 (lub): first heart sound; closureof AV valves

2. S2 (dub): second heart sound;closure of semilunar valves at onset

of relaxationE.Systemic Circulation

1.Pulmonary circulation begins with right heart:deoxygenated blood from superior and inferiorvena cavae is transported to lungs via

pulmonary artery and branches2.In lungs, oxygen and carbon dioxide are

exchanged in capillaries of lungs, and blood

returns to left atrium through several

pulmonary veins3.Blood pumped out of left ventricle through

aorta and major branches to all body tissuesF.Coronary Circulation (Circulation for heart)

1.Left and right coronary arteries originate atbase of aorta and branch out to encircle

myocardium


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2. During ventricular relaxation coronary arteries

fill with oxygen-rich blood3. Blood perfuses heart muscle and cardiac veinsdrain blood into coronary sinus, which empties

into right atriumG. Cardiac Cycle and Cardiac Output

1. Cardiac cycle: one heartbeat involving

contraction and relaxation of heart

2. Systole: phase during which ventriclescontract and eject blood into pulmonary andsystemic circuits

3. Diastole: phase during which ventricles relax

and refill with blood; atria contract andmyocardium is perfused

4.Heart Rate (HR): number of cardiac cycles in aminute (normal 70 80)

5.Stroke Volume (SV): volume of blood ejected

with each contraction6. Ejection Fraction (EF): percentage of total

blood in ventricle at the end of diastole ejected

from heart with each beat; normal ejection

fraction is 50% 70%7.Cardiac Output (CO): amount of blood

pumped by ventricles into pulmonary andsystemic circulations in 1 minute

a. Formula (HR x SV =CO)b. Average cardiac output is 4 8 liters per

minute (L/min)


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c. Indicator of pump function of heart; if

heart is ineffective pump, then cardiacoutput and tissue perfusion are decreased;body tissues become ischemic (deprived

of oxygen)d.Cardiac output is influenced by

1. Activity level

2.Metabolic rate

3.Physiologic and psychologic stressresponses

4.Age5.Body size

e. Cardiac Reserve: ability of heart torespond to bodys changing need for

cardiac output8.Cardiac output is determined by interaction of

four factors

a. Heart rate: affected by direct and indirectautonomic nervous system stimulation

1.Sympathetic nervous system:

increases heart rate

2. Parasympathetic nervous system:decreases heart rate

3.Reflex regulation occurs in responseto systemic blood pressure through

activation of baroreceptors orpressure receptors (located in carotid


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sinus, aortic arch, venae cavae,

pulmonary veins)4.Very rapid heart rate decreasescardiac output and coronary artery

perfusion due to decreased fillingtime

5. Bradycardia decreases cardiac output

if stroke volume stays the same

b. Preload: amount of cardiac muscle fibertension or stretch at the end of diastole(right before contraction of ventricles)

1.Influenced by venous return and

ventricular compliance2.Starlings Law of the heart: Greater

the volume, the greater the stretch ofcardiac muscle fibers, and greater theforce with which fibers contract to

accomplish emptying3.Physiologic limit to Starlings Law:

overstretching of cardiac muscle

fibers results in ineffective

contractiona. Like continuous overstretching

of rubber bandb. Disorders which result in

increased preload:1. Congestive heart failure

2. Renal disease


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3. Vasoconstriction

c. Disorders which result indecreased preload:1.Decreased circulating blood

volume2.Hemorrhage3.Third-spacing

c. Afterload: force the ventricles must

overcome to eject their blood volume1.Pressure in arterial system ahead of

ventriclesa. Right ventricle: generates enough

tension to open pulmonary valve,eject its volume into low-

pressure pulmonary arteries:Pulmonary Vascular Resistance(PVR)

b. Left ventricle: ejects load byovercoming pressure behindaortic valve: systemic vascular

resistance (SVR); much greater

than right ventricle2.Alterations in vascular tone affect

afterload and ventricular worka. As PVR and SVR increase, work

of ventricles increases andconsumption of myocardial

oxygen increases


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b. Very low afterload decreases

forward flow of blood intosystemic and coronarycirculation

d. Contractility: inherent capability ofcardiac muscles fibers to shorten

1.Poor contractility

a. Reduces forward flow of blood

from heartb. Increases ventricular pressure

from accumulated blood volumec. Reduces cardiac output

2. Increased contractility: overtaxesheart

9.Conduction System of Hearta. Cardiac muscle cells have inherent

characteristic of self-excitation: can

initiate and transmit impulses independentof stimulus

b. Conduction system

1.Sinoatrial (SA) node: located junction

of superior vena cavae and rightatrium

a. Acts as normal pacemaker ofheart

b. Inherent rate: 60 100times/minute


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2.Impulse travels across atria via

internodal pathways toAtrioventricular (AV) node: locatedfloor of interatrial septum; fibers of

AV node slightly delay transmissionto ventricles

3.Impulse travels through bundle of His

at atrioventricular junction and down

interventricular septum through rightand left bundle branches out toPurkinje fibers in ventricular musclewalls

c. Path of electrical transmission producesseries of changes in ion concentration

across membrane of each cardiac musclecell

1. Electrical stimulus: increases

permeability of cell membrane,creates action (electrical) potential

2.Exchange of sodium, potassium, and

calcium ions across cell membrane;

intracellular electrical state: positivecharge; depolarization (myocardialcontraction)

3.Ion exchange reverses; cell returns to

resting state; electrical state: negative;repolarization (cardiac muscle

relaxes)


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10. Cardiac Index

a. Cardiac output adjusted for clients bodysize, which is the Body Surface Area(BSA)

b. More accurate indicator of ability of heartto effectively circulate blood

c. BSA is stated in square meters (m2);

Cardiac index calculated by dividing

cardiac output by BSA: CI = CO BSAd.Normal CI is 2.5 4.2 L/min/m

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II. Assessing Cardiac Function

A. Health assessment interview to collect subjectivedata

1. Explore clients chief complaint2. Description of clients symptoms regarding

a. Location

b. Quality or characterc. Timingd.Setting or precipitating factors

e. Severity

f. Aggravating and relieving factorsg. Associated symptoms

3.Explore client history fora. Heart disorders

1.Angina2.Myocardial infarction (Heart attack)

3.Congestive Heart Failure (CHF)


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4.Hypertension (HTN)

5.Valvular Diseaseb. Previous heart surgeries or relatedillnesses

1.Rheumatic fever2.Scarlet fever3. Recurrent streptococcal throat

infection

c. Pertinent other chronic illnesses1.Diabetes Mellitus2.Bleeding disorders3.Endocrine disorders

d. Client family history for specific heartconditions

1.Coronary artery disease (CAD)2.HTN3.Stroke

4.Hyperlipidemia5.Diabetes Mellitus6.Congenital heart disease

7. Sudden death

4.Past or present occurrence of cardiacsymptoms

a. Chest painb. Shortness of breath

c. Difficulty breathing, coughd.Palpitations

e. Fatigue


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f. Light-headedness or fainting

g. Heart murmurh.Blood clotsi. Swelling

5. Personal habits and nutritional historya. Body weight

b. Eating patterns: usual intake of fats, salt,

fluids

c. Restrictions, food intolerancesd.Use of alcohol and caffeine

6.Use of tobacco products, type, duration,amount, efforts to quit

7.Use of street drugs, type, efforts to quit8. Activity level and tolerance, recreation and

relaxation habits9. Sleep patterns; interruptions due to dyspnea,

cough, discomfort, urination, stress

10. Pillows used to sleep11. Psychosocial factors12. Personality type

13. Perception of health or illness, compliance

with treatmentB. Physical assessment to collect objective data

1. Apical impulse assessment with abnormalfindings

a. Positioning lateral to midclavicular line orbelow fifth left intercostals space:

enlarged or displaced heart


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b. Increased size, amplitude, duration of

point of maximal impulse (PMI)1.Left ventricular volume overload(increased preload): HTN, aortic

stenosis2.Pressure overload (increased

afterload): aortic or mitral

regurgitation

c. Increased amplitude alone: hyperkineticstates; anxiety, hyperthyroidism, anemia

d. Decreased amplitude: dilated heart incardiomyopathy

e. Displacement alone: dextrocardia,diaphragmatic hernia, gastric distention,

chronic lung diseasef. Thrill (palpable vibration over precordium

or artery): severe valve stenosis

g.Marked increase in amplitude of PMI atright ventricular area: right ventricularvolume overload in atrial septal defect

h.Increase in amplitude and duration with

right ventricular pressure overload (alsolift, heave): pulmonary stenosis,

pulmonary hypertension, chronic lungdisease

i. Palpable thrill: ventricular septal defect2.Subxiphoid area


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a. Downward pulsation: right ventricular

enlargementb. Accentuated pulsation at pulmonary area:hyperkinetic states

c. Prominent pulsation: increased flow ordilation of pulmonary artery

d. Thrill: aortic or pulmonary stenosis,

pulmonary HTN, atrial septal defect

e. Increased pulsation at aortic area: aorticaneurysm

f. Palpable second heart sound (S2):systemic HTN

3.Cardiac rate and rhythm with abnormalfindings

a. Heart rate > 100: tachycardiab. Heart rate< 60: bradycardiac. Pulse deficit (Radial pulse < than apical

when checked simultaneously): weakineffective contractions of left ventricle

d. Irregular rhythm: frequent ectopic beats

such as premature ventricular beats, atrial

fibrillatione. Gradual increase and decrease in heart

rate correlated with respirations: sinusarrhythmia

4. Heart sounds assessment with abnormalfindings

a. S1


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1. Accentuation: tachycardia, states of

high cardiac output such as fever,exercise, hyperthyroidism2. Diminishment: mitral regurgitation,

CHF, CAD, pulmonary or systemicHTN, obesity, emphysema,

pericardial effusion

3.Splitting: right bundle branch block,

premature ventricular contractionsb. S2

1.Accentuation: HTN, exercise,excitement, conditions of pulmonary

HTN (mitral stenosis, CHF, corpulmonale)

2. Diminishment: aortic stenosis, shock,pulmonary stenosis, increasedanterioposterior chest diameter

3.Splitting:a. Fixed: atrial septal defect, right

ventricular failure

b. Paradoxical: left bundle branch

blockc. Extra heart sounds in systole

1.Clicks: aortic and pulmonicstenosis

2. Midsystolic: mitral valveprolapse (MVP)


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d.Extra heart sounds in diastole:

Opening snap: opening sound ofa stenotic mitral valvee. S3 (ventricular gallop):

myocardial failure andventricular volume overload(CHF, mitral or tricuspid

regurgitation)

f. S4 (atrial gallop): increasedresistance to ventricular fillingafter atrial contraction (HTN,CAD, aortic stenosis,

cardiomyopathy)g. S4 (right-sided): less common,

occurs with pulmonary HTN andpulmonary stenosis

h.Combined S3 and S4 (summation

gallop): severe CHFi. Pericardial friction rub:

inflammation of pericardial sac

as with pericarditis

5. Murmur assessment with abnormal findingsa. Midsystolic murmurs: aortic and

pulmonic stenosis; hypertrophiccardiomyopathy

b. Pansystolic (holosystolic) murmurs:mitral and tricuspid regurgitation,

ventricular septal defect


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c. Late systolic murmur: MVP

d. Early diastolic murmur: aorticregurgitatione. Middiastolic and presystolic murmurs:

mitral stenosisf. Continuous murmurs throughout systole

and all or part of diastole: patent ductus

arteriosus

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Assessing Clients with Cardiac Disorders