Assessing Clients with Cardiac Disorders I. Background of Anatomy and Physiology A. Heart 1.

Size of adults fist, weight < 1 pound 2. 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 lies approximately with fifth intercostal space, mid-clavicular B. Pericardium 1. Covering of double layered fibroserous membrane, forming pericardial sac 2. Layers of pericardium a. Parietal pericardium: outermost layer b. Visceral pericardium (epicardium) adheres to heart surface 3. 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 Wall 1. Epicardium: same as visceral pericardium 2. Myocardium: specialized cardiac muscle cells provide bulk of contractile heart muscle 3. Endocardium: sheath of endothelium that is lining inside hearts chambers and great vessels

D. Chambers and Valves 1. Four hollow chambers: two upper atria, two lower ventricles; separated lengthwise by interventricular septum a. Right atrium: receives deoxygenated blood from veins of body 1. Superior vena cava: blood from body above diaphragm 2. Inferior vena cava: blood from body below diaphragm 3. Coronary sinus: blood from heart b. Left atrium: receives freshly oxygenated blood from lungs via pulmonary veins c. Right ventricle: receives deoxygenated blood from right atrium and pumps it to lungs for oxygenation via pulmonary artery d. Left ventricle: receives freshly oxygenated blood from left atrium and pumps it to arterial circulation via aorta 2. Valves separate each chamber of heart allowing unidirectional blood flow a. Atrioventricular (AV) valves: between atrium and ventricle; Flaps of valves anchored to papillary muscles of ventricles by chordae tendineae 1. Tricuspid: right side 2. Mitral (biscuspid): left side

b. Semilunar valves: connect ventricles to great vessels 1. Pulmonary: right side; joins right ventricle and pulmonary artery 2. Aortic: left side; joins left ventricle and aorta c. Heart sounds associated with closure of valves 1. S1 (lub): first heart sound; closure of AV valves 2. S2 (dub): second heart sound; closure of semilunar valves at onset of relaxation E.Systemic Circulation 1. Pulmonary circulation begins with right heart: deoxygenated blood from superior and inferior vena cavae is transported to lungs via pulmonary artery and branches 2. In lungs, oxygen and carbon dioxide are exchanged in capillaries of lungs, and blood returns to left atrium through several pulmonary veins 3. Blood pumped out of left ventricle through aorta and major branches to all body tissues F.Coronary Circulation (Circulation for heart) 1. Left and right coronary arteries originate at base of aorta and branch out to encircle myocardium

2. During ventricular relaxation coronary arteries fill with oxygen-rich blood 3. Blood perfuses heart muscle and cardiac veins drain blood into coronary sinus, which empties into right atrium G. Cardiac Cycle and Cardiac Output 1. Cardiac cycle: one heartbeat involving contraction and relaxation of heart 2. Systole: phase during which ventricles contract and eject blood into pulmonary and systemic circuits 3. Diastole: phase during which ventricles relax and refill with blood; atria contract and myocardium is perfused 4. Heart Rate (HR): number of cardiac cycles in a minute (normal 70 80) 5. Stroke Volume (SV): volume of blood ejected with each contraction 6. 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 and systemic circulations in 1 minute a. Formula (HR x SV =CO) b. Average cardiac output is 4 8 liters per minute (L/min)

c. Indicator of pump function of heart; if heart is ineffective pump, then cardiac output 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 stress responses 4. Age 5. Body size e. Cardiac Reserve: ability of heart to respond to bodys changing need for cardiac output 8. Cardiac output is determined by interaction of four factors a. Heart rate: affected by direct and indirect autonomic nervous system stimulation 1. Sympathetic nervous system: increases heart rate 2. Parasympathetic nervous system: decreases heart rate 3. Reflex regulation occurs in response to systemic blood pressure through activation of baroreceptors or pressure receptors (located in carotid

sinus, aortic arch, venae cavae, pulmonary veins) 4. Very rapid heart rate decreases cardiac output and coronary artery perfusion due to decreased filling time 5. Bradycardia decreases cardiac output if stroke volume stays the same b. Preload: amount of cardiac muscle fiber tension or stretch at the end of diastole (right before contraction of ventricles) 1. Influenced by venous return and ventricular compliance 2. Starlings Law of the heart: Greater the volume, the greater the stretch of cardiac muscle fibers, and greater the force with which fibers contract to accomplish emptying 3. Physiologic limit to Starlings Law: overstretching of cardiac muscle fibers results in ineffective contraction a. Like continuous overstretching of rubber band b. Disorders which result in increased preload: 1. Congestive heart failure 2. Renal disease

3. Vasoconstriction c. Disorders which result in decreased preload: 1. Decreased circulating blood volume 2. Hemorrhage 3. Third-spacing c. Afterload: force the ventricles must overcome to eject their blood volume 1. Pressure in arterial system ahead of ventricles a. Right ventricle: generates enough tension to open pulmonary valve, eject its volume into lowpressure pulmonary arteries: Pulmonary Vascular Resistance (PVR) b. Left ventricle: ejects load by overcoming pressure behind aortic valve: systemic vascular resistance (SVR); much greater than right ventricle 2. Alterations in vascular tone affect afterload and ventricular work a. As PVR and SVR increase, work of ventricles increases and consumption of myocardial oxygen increases

b. Very low afterload decreases forward flow of blood into systemic and coronary circulation d. Contractility: inherent capability of cardiac muscles fibers to shorten 1. Poor contractility a. Reduces forward flow of blood from heart b. Increases ventricular pressure from accumulated blood volume c. Reduces cardiac output 2. Increased contractility: overtaxes heart 9. Conduction System of Heart a. Cardiac muscle cells have inherent characteristic of self-excitation: can initiate and transmit impulses independent of stimulus b. Conduction system 1. Sinoatrial (SA) node: located junction of superior vena cavae and right atrium a. Acts as normal pacemaker of heart b. Inherent rate: 60 100 times/minute

2. Impulse travels across atria via internodal pathways to Atrioventricular (AV) node: located floor of interatrial septum; fibers of AV node slightly delay transmission to ventricles 3. Impulse travels through bundle of His at atrioventricular junction and down interventricular septum through right and left bundle branches out to Purkinje fibers in ventricular muscle walls c. Path of electrical transmission produces series of changes in ion concentration across membrane of each cardiac muscle cell 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: positive charge; depolarization (myocardial contraction) 3. Ion exchange reverses; cell returns to resting state; electrical state: negative; repolarization (cardiac muscle relaxes)

10. Cardiac Index a. Cardiac output adjusted for clients body size, which is the Body Surface Area (BSA) b. More accurate indicator of ability of heart to effectively circulate blood c. BSA is stated in square meters (m2); Cardiac index calculated by dividing cardiac output by BSA: CI = CO BSA d. Normal CI is 2.5 4.2 L/min/m2 II. Assessing Cardiac Function A. Health assessment interview to collect subjective data 1. Explore clients chief complaint 2. Description of clients symptoms regarding a. Location b. Quality or character c. Timing d. Setting or precipitating factors e. Severity f. Aggravating and relieving factors g. Associated symptoms 3. Explore client history for a. Heart disorders 1. Angina 2. Myocardial infarction (Heart attack) 3. Congestive Heart Failure (CHF)

4. Hypertension (HTN) 5. Valvular Disease b. Previous heart surgeries or related illnesses 1. Rheumatic fever 2. Scarlet fever 3. Recurrent streptococcal throat infection c. Pertinent other chronic illnesses 1. Diabetes Mellitus 2. Bleeding disorders 3. Endocrine disorders d. Client family history for specific heart conditions 1. Coronary artery disease (CAD) 2. HTN 3. Stroke 4. Hyperlipidemia 5. Diabetes Mellitus 6. Congenital heart disease 7. Sudden death 4. Past or present occurrence of cardiac symptoms a. Chest pain b. Shortness of breath c. Difficulty breathing, cough d. Palpitations e. Fatigue

f. Light-headedness or fainting g. Heart murmur h. Blood clots i. Swelling 5. Personal habits and nutritional history a. Body weight b. Eating patterns: usual intake of fats, salt, fluids c. Restrictions, food intolerances d. Use of alcohol and caffeine 6. Use of tobacco products, type, duration, amount, efforts to quit 7. Use of street drugs, type, efforts to quit 8. Activity level and tolerance, recreation and relaxation habits 9. Sleep patterns; interruptions due to dyspnea, cough, discomfort, urination, stress 10. Pillows used to sleep 11. Psychosocial factors 12. Personality type 13. Perception of health or illness, compliance with treatment B. Physical assessment to collect objective data 1. Apical impulse assessment with abnormal findings a. Positioning lateral to midclavicular line or below fifth left intercostals space: enlarged or displaced heart

b. Increased size, amplitude, duration of point of maximal impulse (PMI) 1. Left ventricular volume overload (increased preload): HTN, aortic stenosis 2. Pressure overload (increased afterload): aortic or mitral regurgitation c. Increased amplitude alone: hyperkinetic states; anxiety, hyperthyroidism, anemia d. Decreased amplitude: dilated heart in cardiomyopathy e. Displacement alone: dextrocardia, diaphragmatic hernia, gastric distention, chronic lung disease f. Thrill (palpable vibration over precordium or artery): severe valve stenosis g. Marked increase in amplitude of PMI at right ventricular area: right ventricular volume overload in atrial septal defect h. Increase in amplitude and duration with right ventricular pressure overload (also lift, heave): pulmonary stenosis, pulmonary hypertension, chronic lung disease i. Palpable thrill: ventricular septal defect 2. Subxiphoid area

a. Downward pulsation: right ventricular enlargement b. Accentuated pulsation at pulmonary area: hyperkinetic states c. Prominent pulsation: increased flow or dilation of pulmonary artery d. Thrill: aortic or pulmonary stenosis, pulmonary HTN, atrial septal defect e. Increased pulsation at aortic area: aortic aneurysm f. Palpable second heart sound (S2 ): systemic HTN 3. Cardiac rate and rhythm with abnormal findings a. Heart rate > 100: tachycardia b. Heart rate< 60: bradycardia c. Pulse deficit (Radial pulse < than apical when checked simultaneously): weak ineffective contractions of left ventricle d. Irregular rhythm: frequent ectopic beats such as premature ventricular beats, atrial fibrillation e. Gradual increase and decrease in heart rate correlated with respirations: sinus arrhythmia 4. Heart sounds assessment with abnormal findings a. S1

1. Accentuation: tachycardia, states of high cardiac output such as fever, exercise, hyperthyroidism 2. Diminishment: mitral regurgitation, CHF, CAD, pulmonary or systemic HTN, obesity, emphysema, pericardial effusion 3. Splitting: right bundle branch block, premature ventricular contractions b. S2 1. Accentuation: HTN, exercise, excitement, conditions of pulmonary HTN (mitral stenosis, CHF, cor pulmonale) 2. Diminishment: aortic stenosis, shock, pulmonary stenosis, increased anterioposterior chest diameter 3. Splitting: a. Fixed: atrial septal defect, right ventricular failure b. Paradoxical: left bundle branch block c. Extra heart sounds in systole 1. Clicks: aortic and pulmonic stenosis 2. Midsystolic: mitral valve prolapse (MVP)

d. Extra heart sounds in diastole: Opening snap: opening sound of a stenotic mitral valve e. S3 (ventricular gallop): myocardial failure and ventricular volume overload (CHF, mitral or tricuspid regurgitation) f. S4 (atrial gallop): increased resistance to ventricular filling after atrial contraction (HTN, CAD, aortic stenosis, cardiomyopathy) g. S4 (right-sided): less common, occurs with pulmonary HTN and pulmonary stenosis h. Combined S3 and S4 (summation gallop): severe CHF i. Pericardial friction rub: inflammation of pericardial sac as with pericarditis 5. Murmur assessment with abnormal findings a. Midsystolic murmurs: aortic and pulmonic stenosis; hypertrophic cardiomyopathy b. Pansystolic (holosystolic) murmurs: mitral and tricuspid regurgitation, ventricular septal defect

c. Late systolic murmur: MVP d. Early diastolic murmur: aortic regurgitation e. Middiastolic and presystolic murmurs: mitral stenosis f. Continuous murmurs throughout systole and all or part of diastole: patent ductus arteriosus