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175 Cards in this Set
- Front
- Back
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Precordium |
Area on the anterior chest overlying the heart and great vessels |
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Mediasinum |
Midthoracic cavity that contains the heart and great vessels 2nd to 5th ICSD right sternal border to left MCL |
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Base of heart |
Top |
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Apex of heart |
Bottom 5th ICS, 7 - 9 cm left of midsternal line (appx MCL) Heart is rotated so that the right side is anterior and the left side is posterior |
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Pericardium |
Fibrous outer sac Attached to vessels, esophagus, sternum, pleura Anchored to diaphragm |
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Pericardial Friction Rub |
Differentiate from pleural friction rub Does not disappear when pt holds breath Caused by inflammation of parietal and visceral surfaces High pitched grating/scratching heard through systole and diastole Common after MI, may cause bleeding into pericardial sac: tamponade, decreased CO May need to give anti-inflammatory drugs |
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Epicardium |
Outer muscle layer |
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Myocardium |
Thick muscular pump |
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Endocardium |
Lines the inside of the heart Contains electrical pathways |
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Valves |
Unidirectional to prevent backflow of blood Open and close passively, dependent on pressure changes |
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Atrioventricular valves |
Between atria and ventricles |
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Mitral valve |
Left atrioventricular valve Bicuspid |
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Tricuspid Valve |
Right atrioventricular valve Three leaflets |
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Chordae tendinae |
Attach the AV valves to papillary muscles and provide stability to valves during systole Rupture of the chordae may be life threatening Valve loses integrity and flaps loosely |
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Semilunar Valves |
Outlet from ventricles |
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Pulmonic Valve |
Right semilunar valve |
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Aortic Valve |
Left semilunar valve |
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Conduction system |
The electrical system that initiates and conducts the heart beat |
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Hemodynamic System |
Moves blood through the heart and vessels |
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SA Node |
Intrinsic pacemaker Spark that starts the heart beat that is transmitted across atria to AV node, Bundle of His, Perkinje fibers in the ventricles Fires at 60-100 bpm If another pacemaker takes over, rate will be slower |
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Electrocardiogram |
ECG Reflects the electrical conduction through the heart |
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P wave |
Depolarization of the atria Spread of stimuli through atria If SA node isn't firing properly or at all, P wave is abnormal or absent |
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PR interval |
Time from stimulation of atria to stimulation of ventricles |
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QRS |
Depolarization of the ventricles Spread of stimuli through ventricles |
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T Wave |
Repolarization of ventricles Resting phase |
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U Wave |
Final ventricular repolarization Not always seen on the ECK |
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Vessels |
Lie at base of the heart Venous blood on right side Arterial blood on left side |
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Flow of blood from body |
Blood flows from higher to lower pressure gradients Lower body to IVC to RA Head and neck to SVC to RA |
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Flow of blood through heart |
RA through tricuspid valve to RV to pulmonic valve to pulmonary arteries to lungs/alveoli Pulmonary veins to LA to mitral valve to LV to aortic valve to aorta and body |
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Backward flow |
Blood moves by pressure gradients Backflow when atrial pressures are excessively high |
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Right heart backflow |
No valves between right atrium and vena cava Pressure in RA is greater than the vena cava, blood backflows to veins of neck and PV system Distended neck veins and peripheral edema r/t valve disease, lung disease, hepatomegaly, etc. |
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Left heart backflow |
No valves between left atrium and pulmonary veins Pressure in LA is greater than the pulmonary veins, blood backflows into the lungs Pulmonary congestion, crackles, rales R/t valve disease, HTN, HF, etc. |
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Cardiac Output |
CO = HR x SV Normal 4-6 L/min |
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Stroke volume |
Volume of blood per beat |
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Decreased CO |
Decreased HR (MI, block) Decreased SV (dehydration) Increased HR (decreased diastolic filling) |
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Preload |
Left ventricular end diastolic volume (LVEDV) Measured by PA wedge pressure |
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Increased Preload |
Increased LVEDV causes more stretch on the mycardial muscle fibers at end of diastole |
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Frank Starling Law |
The greater stretch of muscle fibers, the stronger the contraction...up until a point |
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Maximize preload |
Goal in order to maximize LV contraction and CO |
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Excessive preload |
Leads to decreased CO and heart failure Overstretch loses its ability to snap back |
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Afterload |
Systemic or peripheral vascular resistance Opposing pressure that the ventricle must generate to open the aortic valve during systole |
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Increased afterload |
Causes increased aortic pressures |
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Excessive afterload |
Increases myocardial workload and O2 consumption May be caused by arteriosclerosis, HTN, SNS stimulation (stress), excessive ETOH intake |
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Heart sounds |
Produced by closure of valves Valves sound louder on left side Mitral valve louder than tricuspid Aortic valve louder than pulmonic |
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Aortic Valve site |
2nd ICS, Rt sternal border |
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Pulmonic valve site |
2nd ICS, Lt sternal border |
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Tricuspid Valve site |
4th ICS, Lt sternal border |
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Mitral Valve site |
5th ICS, MCL |
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Erbs Point site |
3rd ICS, Lt sternal border Location for referred sounds |
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Listening to heart sounds |
Listen to all sites with diaphragm and bell
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Listening for aortic murmurs |
Sitting and leaning forward Brings heart closer to chest wall |
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Listening for extra heart sounds |
Left lateral decubitus position is best |
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S1 |
Loudest at Apex Mitral/Tricuspid valves close Aortic/Pulmonic valves open Ends diastole and begins systole |
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Diastole |
20% is Atrial contraction: Atrial kick 80% is Rapid filling phase - passive initial filling of ventricles |
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Systole |
Ventricle Contraction Ventricular pressure exceeds aortic pressure Ventricles contract and blood is ejected from ventricles into pulmonary artery and aorta |
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S2 |
Loudest at base Aortic and pulmonic valves close Mitral and tricuspid valves open Ends systole and begins diastole (ventriclar relaxation) |
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Atrial kick |
Atrial contraction ejects last 25% of SV into ventricles Lost with atrial fibrillation, decreased diastolic filling |
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S3 |
Extra heart sounds, gallops Ventricular gallop Early diastolic sound, immediately after S2 Best heard at apex with bell Ken....tucky Indicates ventricular resistance to early passive filling Stiff, non-compliant ventricles Caused by decreased ventricular compliance, early sign of HF, high output conditions, high LV preload, poor ejection of SV ie. hyperthyroidism, pregnancy |
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S4 |
Extra heart sounds, gallops Atrial gallop Best heard at apex with bell Tenness...ee Indicates ventricular resistnace to filling during atrial kick Occurs late in diastole, immediately before S1 Caused by HTN, elderly |
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Summation gallop |
S3 and S4 Both, difficult to distinguish Irratic sounds |
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Split sounds |
Asynchronous valve closures |
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Split S1 |
Mitral closing before tricuspid Higher pressures on left uncommon since closure of tricuspid is usually too faint to hear May be mistaken for an S4 |
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Split S2 |
Aortic valve closing before pulmonic during deep inspiration Very common Changes in intrathoracic pressure with deep inspiration causes asynchronous valve closure May be mistaken for S3, S3 not affected by breathing pattern Most prominent at 2nd ICS, lt Sternal border at peak inspiration, S3 best heart at apex |
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Murmurs |
Blowing/swooshing sound that occurs with turbulent flow through valves or great vessels |
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Causes of murmurs |
Increased velocity: exercise Decreased viscosity: thin Decreased volume: anemia Defective valves: forward/backward flow Septal defects: abnormal opening between chambers |
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Stenotic murmurs |
Occurs when a valve is open Prevents adequate forward flow through thick, stiff valves Causes harsh murmurs |
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Regurgitant Murmurs |
Occures when valve is closed Also referred to as insufficiency Backward flow r/t poor valve closure Causes turbulent sound |
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Systolic murmurs |
Heard in systole after S1 Aortic/pulmonic stenosis: when semilunar valves open Mitral/tricuspid insufficiency: when AV valves closed High pitched, use diaphragm |
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Diastolic murmurs |
Heard in diastole after S2 Mitral/Tricuspid Stenosis: when AV valves open Aortic/Pulmonic insufficiency: When semilunar valves closed Low pitched, use bell |
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Determine the murmur |
1. Know if you are in systole or diastole: palpate the carotid pulse while listening to heart sounds 2. Identify which valve site the murmur is loudest 3. Know which valves are open and closed to determine if it's a stenotic/regurgitant murmur |
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Characteristics of murmurs: timing |
Systolic vs diastolic Early, mid, late cycle Entire cycle: - Holodiastolic between S2 to S1 - Holosystolic between S1 to S2 |
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Characteristics of murmurs: intensity |
Graded 1 (soft) to 6 (loud) 1 - Barely audible 2 - Clearly audible but faint 3 - Moderately loud 4 - Loud with palpable thrill, chest wall 5 - Loud, heard with one side of diaphragm off chest wall 6 - Loud, heard with stethoscope off chest wall |
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Characteristics of murmurs: Location |
Valve site Where it's heard loudest |
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Characteristics of murmurs: Pattern |
Crescendo: increases in intensity Decrescendo: decreases with intensity Crescendo-decrescendo: increases then decreases Uniform: constant intensity |
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Innocent Murmur |
Functional murmur No valve, cardiac, or other palpation Common in childhood, usually r/t increased blood flow |
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Chest pain etiology |
May be life-threatening |
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Cardiac Chest pain |
Angina, Acute MI, mitral valve prolapse R/o ACS (Acute coronary syndrome) Coronary insufficiency Nonobstructive, nonspastic angina Dissection of aorta |
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CP in young adult |
HTN and tachycardia with CP, r/o cocaine abuse Trauma Exercise-induced asthma |
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Pulmonary CP |
PNA, pleurisy, embolism Pulmonary HTN Bronchial hyperractivity Tension Pneumothorax |
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Pericardial CP |
Pericarditis Common after MI Pneumothorax Mediastinal emphysema |
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Musculoskeletal/Chest wall CP |
Costochondritis: inflammation of joint between rib and cartilage Arthritis Hurts with palpation Cervical randiculopathy Shoulder disorder or dysfunction (bursitis, rotator cuff injury, biceps tendonitis, arthritis) Xiphodynia |
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Gastrointestinal CP |
May mimic MI Ulcer, hiatal hernia, esophagitis, indigestion Esophageal rupture or spasm Cholecystitis Peptic ulcer disease Pancreatitis |
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Neurotic CP |
Anxiety Panic attack Illicit drug use (cocaine) Herpes zoster: thoracic lesions |
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OLD CART CP |
Onset: at rest, with activity, after eating (GI), both at rest and activity (mycordial ischemia) Location: substernal, localized vs. radiating (jaw, arm) Duration Character: burning, sharp/stabbing, crushing, pressure (may not be diagnostic) |
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Angina |
Myocardial ischemia, chest discomfort with or without radiating, SOB Imbalance between O2 supply and demand More common with exercise, stop all activity and rest (could save their life) Should resolve in a couple of minutes with rest or treatment (NTG): may progress to MI if untreated Prolonged symptoms may indicate MI |
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Myocardial Infarction: heart attack |
Ischemia leading to necrosis Similar symptoms to angina, may be diaphoretic, n/v, palpitations, sense of impending doom, lasts longer and more severe than angina May not realize that CP/SOB is ischemic cardiac disease - ask about discomfort rather than pain Pts with DM may not have MI symptoms r/t neuropathy |
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Silent MI |
Pts with diabetes No symptoms r/t neuropathy Discovered on routine EKGs |
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Atypical symptoms of CAD |
Especially in women SOB Sharp CP Fatigue Impending doom Chest/jaw discomfort Arm/back discomfort Trouble breathing Light headedness Palpitations Cold sweats N/V, fatigue, sick to stomach |
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Risk factors for CAD |
Age (>45 in males, >55 in women/postmenopausal) HTN or hypertensive treatment Smoking Hyperlipidemia DM (assume they have CAD) Family hx of premature CAD in 1st degree relative (Male<55, female <65) |
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Shortness of breath |
Dyspnea Dyspnea on exertion Paroxismal nocturnal dyspnea Orthopnea |
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Paroxismal Nocturnal dyspnea |
PND Awakens someone while sleeping R/t HF, lying down increases venous return and myocardial workload |
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Orthopnea |
Increasing HOB to breath Measured in angle of incline or pillows used for sleeping |
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Cough |
May occur with pulmonary congestion from HF |
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Fatigue |
Sudden vs gradual CHF may decrease skeletal muscle oxygentation |
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Syncope |
May be related to an arrhythmia Decreases cerebral perfusion |
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Palpitations |
May indicate an arrhythmia |
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Edema and Nucturia |
Seen in HF Dependent edema is worse in evening Nocturia: recumbent positioning increases venous return to heart, increases renal blood flow and increases UOP |
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Cardiac history |
Review cholesterol, murmurs, congenital heart disease, genetically transmitted disease, rheumatic fever, swollen joints, heart surgery, last ECG, stress test (ETT) results |
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Family cardiac history |
HTN, CAD, DM, obesity, congenital heart disease, genetically transmitted disease ie. hypertrophic CM |
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Hypertrophic Cardiomyopathy |
Leading cause of death in young athletes |
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Personal Habits affecting cardiac health |
Diet: high fat, sodium Smoking: vasoconstricts ETOH: increases afterload Exercise: increases HDL, myocardial muscle tone Medications: digitalis, diuretics, beta blockers, calcium channel blockers |
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Smoking |
Vasoconstricts Increases HR, myocardial workload, O2 consumption Increases afterload Watch for angina |
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ETOH |
Cardiac depressant causing sympathetic compensatory response Temporarily vasoconstricts and increases BP |
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NSAIDS |
Increases afterload and BP |
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Neck Vessels |
Carotid Arteries Jugular Veins |
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Carotid arteries |
Visualized at top of neck near mandible Palpate in lower 1/3 of neck, avoids carotid sinus that slows HR Palpate one artery at a time r/t risk for stroke Pulse strength 2+, diminished may mean decreased SV Auscultate for bruits, narrowing r/t atherosclerosis |
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Bruits in carotid arteries |
Carotid US for follow up Assess for internal carotid stenosis Increased risk for stroke |
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Jugular veins |
Indirect measurement of RA pressure Reflect changes in filling pressure since there are no valves between jugular veins and RA |
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External jugular vein |
Lies over SCM |
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Internal jugular vein |
Underneath and medial to SCM Directly attached to SVC More reliable than EJ for measuring RA pressure Can't see IJ, only see waves or fluctuations Rotate head slightly, note pulsations at right base of neck |
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Differentiate carotids from IJ |
IJ: pulsation visible by not palpable, two undulating waves or fluctuations Carotids Palpable pulsation, one brisk pulsation wave |
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Assess JVD |
Raise HOB to 30-45 degrees, locate IJ pulsation in right neck Normally 3-4 cm above sternal angle |
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Assess JVP |
Estimate of RA pressure JVD + 5 cm (distance of RA from sternal angle) Normally < 9cm H2O If JVD is up to jaw angle when HOB is 90 degrees, then RA pressure is probably > 15 cm H2O |
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Hepatojugular reflex |
Normal: when pressure applied to liver border, the Right jugular vein distends momentarily and returns to normal Abnormal: jugular veins remain elevated as long as pressure is applied, suggests CHF |
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Precordium assessment |
Inspect/palpate apical impulse/PMI Heaves/lifts Thrill |
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PMI |
Apical impulse Located at 4th or 5th ICS, left MCL Palpable in 1/2 adults - decreased with obesity and thick chest walls If shifted further left, may indicate cardiomegaly |
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Heaves/lifts |
Sustained forceful thrusting of ventricle during systole Visualized and palpated at apex May indicate myocardial hypertrophy |
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Thrill |
Palpable vibrations Associated with loud harsh murmurs Palpate across precordium Feels like a purring cat |
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Auscultate Precordium |
Rate: 60-100 Rhythm: regular, regularly irregular, irregular Heart sounds: listen to each valve with diaphragm and bell |
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Listening to S1 |
Loudest at apex Closure of AV valves Corresponds with R wave on ECG Diminished sounds: pericardial effusion, obesity, emphysema |
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Listening to S2 |
Loudest at base Closure of semilunar valves Aortic valve sounds are best heard when pt is sitting and leaning forward |
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Listening for gallops |
Turn pt on left side More pronounced over apex S3 and S4 normal in kids |
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Listening for murmurs |
Listen over site and note any radiation across precordium |
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Assess for AS |
Aortic stenosis Assess pt sitting and leaning forward Ask pt to exhale completely and hold breath Auscultate over 2nd ICS right sternal border and asses for radiation of murmur into neck and down left sternal border to apex |
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Dextrocardia |
Heart on the right side of body |
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Situs Inversus |
Organs reversed Heart and stomach on right Liver on left Many problems, murmurs, etc |
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Differential diagnosisL Cardiac CP |
Presence of cardiac risk factors Specifically noted time of onset r/t physical effort or emotion Disappears if stimulating cause can be terminated Commonly forces pt to stop effort May awaken pt Relief from NTG Pain in early am, after washing or eating More likely in cold weather |
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Differential diagnosis: Musculoskeletal CP |
History of trauma Vague onset r/t physical effort Continues after cessation of effort Pt often can continue activity Delays falling asleep Relief at times with heat, NSAIDS, rest Worse in evening after physical effort Likely in cold, damp weather |
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Differential diagnosis: GI CP |
History of indigestion Vague onset r/t food consumption or psychosocial stress May go on for several hrs, unrelated to effort Pt often can continue activity May awaken pt from sleep, particularly early am Relief at times with antacids No particular relationship to time of day, r/t more to food and tension |
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Light exercise |
wakling 10-15 steps, prepating simple meal for one, retrieving newspaper, pulling down bedspread, brushing teeth |
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Moderate exercise |
Making the bed, dusting and sweeping, walking a level short block, office filing |
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Moderately heavy exercise |
Climbing 1-2 flights of stairs, lifting full cartons, long walks, sexual intercourse |
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Heavy exercise |
Jogging, vigorous athletics of any kind, cleaning the entire house in less than a day, raking a large number of leaves, mowing a large lawn with a hand mower, shoveling deep snow |
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Thrill examination |
Level IV murmur can be felt |
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Systolic thrill: suprasternal notch or 2nd and 3rd right ICS |
Aortic stenosis |
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Systolic thrill: suprasternal notch or 2nd and 3rd left ICS |
Pulmonic stenosis |
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Systolic thrill: 4th left ICS |
Ventricular septal defect |
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Systolic thrill: apex |
Mitral regurge |
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Systolic thrill: left lower sternal border |
Tetrology of Fallot |
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Systolic thrill: left upper sternal border, with radiation |
Patent ductus arteriosus |
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Diastolic thrill: Right sternal border |
Aortic regurge Ascending aortic aneurysm |
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Diastolic thrill: apex |
Mitral stenosis |
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Click |
Prosthetic valve, either aortic or mitral Not caused by pacemakers |
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Mitral Stenosis |
Narrowed valve restricts forward flow from LA to LV Often occurs with mitral regurge Caused by rheumatic fever or cardiac infection |
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Aortic Stenosis |
Calcification of valve cusps restricts forward flow from LV to aorta/systemic circulation Caused by congenital bicuspid (rather than usual tricuspid), rheumatic heart disease, atherosclerosis May be cause of sudden death, particularly in children and adolescents |
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Pulmonic Stenosis |
Valve restricts forward flow from RV to pulmonary circulation Almost always congenital cause |
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Tricuspid stenosis |
Calcification of valve cusps restricts forward flow from RA to RV Usually seen with mitral stenosis, rarely occurs alone Caused by rheumatic heart disease, congenital defect, endocardial fibroelastosis, right atrial myxoma |
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Mitral regurge |
Valve incompetence allows backflow from LV to LA Caused by rheumatic fever, MI, myxoma, rupture of chordae, endocarditis, annular calcification of MV, cardiomyopathy, ischemic heart disease, MV prolapse SOB, pulmonary edema, orthopnea, PND |
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Mitral valve prolapse |
Valve is competent early in systole, but prolapses into atrium later in systole Progressively more severe Holosystolic murmur Concurrent with pectus excavatum |
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Aortic regurge |
Valve incompetence allows backflow from aorta to LV Caused by rheumatic heart disease, endocarditis, aortic disease (Marfan's, medial necrosis), syphilis, ankylosing spondylitis, dissection, cardiac trauma |
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Pulmonic regurge |
Valve incompetence allows backflow of pulmonary artery to RV Secondary to pulmonary HTN or bacterial endocarditis |
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Tricuspid regurge |
Valve incompetence allows backflow from RV to RA Caused by congenital defects, bacterial endocarditis esp. in IV drug users, pulmonary HTN, cardiac trauma |
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Angina |
Pain caused by myocardial ischemia, when oxygen demand exceeds supply Can be recurrent or present as initial incidence Substernal pain, pressure radiateing to neck, jaw, arms, accompanied by SOB, fatigue, diaphoresis, faintness, syncope May be tachycardic, tachypenic, HTN, crackles r/t pulmonary edema |
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Bacterial endocarditis |
Bacterial infection of endothelial layer of heart and valves Seen in those with previous endocarditis or IVDA Fever, fatigue, sudden onset of CHF, murmur, neurologic dysfunction, janeway lesion, osler nodes |
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Janeway lesion |
Small erythematous or hemorrhagic macules appearing on palms and soles |
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Osler nodes |
Appear on tips of fingers or toes, caused by septic emboli |
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Congestive Heart failure: left sided |
Failure to propel blood forward with usual force Congestion of pulmonary circulation Fatigue, SOB, orthopnea, exercise intolerance, pulmonary edema, crackles on pulmonary exam Systolic CHF: narrow pulse pressure Diastolic CHF: wide pulse pressure |
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Causes of CHF |
LV hypertrophy - high BP leading to thickening of left heart muscle Cardiomyopathy - weakened heart muscle Amage to aortic or mitral valves Ischemic cardiomyopathy: from CAD Nonischemic cardiomyopathy Toxic exposures: ETOH, cocaine Viruses: coxsackie B |
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Diastolic CHF: left |
Result of advanced glucation cross-linking collagen and creating a stiff ventricle unable to dilate actively Occurs in older adults with DM whose tissue is exposed to glucose for long periods of time |
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Congestive heart failure: right-sided |
Heart fails to propel blood forward resulting in congestion in systemic circulation Decreased cardiac output causes decreased blood flow to the tissues Peripheral edema, esp after long day or prolonged sitting, JVD Weight gain |
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Pericarditis |
Inflammation of pericardium Sharp, stabbing CP - heart rubbing against pericardium Worse pain with coughing, swallowing, deep breaths, lying flate, movement Pain in back, neck, left shoulder Difficulty breathing when lying down, dry cough, anxiety or fatigue Friction rub |
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Causes of pericarditis |
Often from viral infection: echovirus, coxsackie B May also be seen in cancer, HIV and AIDS, hypothyroidism, kidney failure, rheumatic fever, TB, Kawasaki disease, MI, heart surgery or trauma to chest, meds (procainamide, hydralazine, phenytoin, isoniazid), radiation therapy to chest May cause pericardial effusion, leading to tamponade |
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Cardiac tamponade |
Excessive accumulation, effused fluids or blood between pericardium and heart Impairs blood return to right heart Cause: pericarditis, malignancy, aortic dissection, trauma Anxiety, restlessness, SOB, CP, sitting upright or forward, syncope, pale/gray/blue skin, palpitations, swelling of abd, arms, neck Beck triad: JVD, hypotension, muffled heart tones Paradoxic pulse |
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Cor Pulmonale |
Enlargement of RV r/t chronic lung disease Usually chronic (COPD, PAH), occasionally acute (massive PE, ARDS) Chronic: gradual hyertrophy leads to HF Acute: right heart dilated and fails Fatigue, tachypnea, exertional dyspnea, cough, hemoptysis, syncope, cyanosis, left parasternal systolic heave, loud S2, Right heart failure + lung disease |
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Myocardial infactions |
Myocardial necrosis r/t abrupt decrease in coronary blood flow Most commonly affects LV r/t arthrosclerosis, artherosclerotic plaque rupture forming a thrombus CP that radiates, n/v, fatigue, SOB, dysrhythmias, S4, distant heart tones, blowing apical murmur, thready ulse, BP variable (HTN in early phase) |
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Myocarditis |
Focal or diffuse inflammation of myocardium Vague symptoms initially, fatigue, dyspnea, fever, palpitations, hx of flu-like symptoms within 1-2 weeks (tonsillitis, pharyngitis, URI) Cardiac enlargement, murmurs and gallops, tachycardia, dysrhythmias, pulsus alernans |
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Pulsus Alternans |
Alternation of strong and weak arterial pulse r/t alternate strong and weak ventricular contractions |
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Causes of Myocarditis |
Viral: enterovirus, coxsackie B, CMV, influenza, adenovirus Bacterial: TB, strep Spirochetal: syphilis, Lyme disease Fungal: candidiasis, aspergillosis, cryptococcosis, histoplasmosis Protozoal: Chagas disease, toxoplasmosis, malaria Helminthic: trichinosis, schistosomiasis Bites/stings: scorpion, snake, black widow Chemotherapy Amphetamines, cocaine, catecholamines Physical agents Systemic inflammatory disease: giant cell myocarditis, sarcoidosis, Kawasaki disease, Crohn disease, lupus Perpartum cardiomyopathy |
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Tetrology of Fallot |
Congenital heart defects: ventricular septal defect, pulmonic stenosis, dextroposition of the aorta, RV hypertrophy RV outflow obstruction leads to Right to Left shunt Leads to cyanosis associated with agitation and crying Dyspnea, poor growth, exercise intolerance, paroxysmal dyspnea with loss of consciousness, central cyanosis (tet spells), parasternal heave, clubbing |
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Ventricular septal defect |
VSD, opening between left and right ventricles May close spontaneously in first 2 yrs of life Blood usually shunts left to right Recurrent resp infections, rapid breathing, poor growth, CHF symptoms, arterial pulse small, holosystolic murmur,left peristernal lift |
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Patent ductus arteriosus |
Failure to close at birth, communication between PA and aortic arch Blood flows through systole and diastole Increases pulmonary circulation pressure, workload of right heart Dyspnea on exertion, dilated neck vessels, wide pulse pressure, continuous murmur |
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Atrial Septal Defect |
ASD, congenital defect in septum dividing left and right atria Left to right shunting, may lead to right sided volume overloading May reverse shunt as right heart becomes enlarged and hypertrophic RHF seen as a result in adults Early diastolic murmur, split S2 |
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Acute rheumatic fever |
Systemic connective tissue disease occurring after strep throat or strep skin infection May result in cardiac valvular involvement (mitral and aortic) - stenosis or insufficiency Most common in 5-15 yr olds Fever, inflamed swollen joints, erythema marginatum, jerky movements, small nodules beneath skin, CP, palpiations, fatigue, SOB, murmurs of MR or AI, cardiomegaly, friction rub, CHF |
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Artherosclerotic heart disease |
CAD Narrowing of blood vessels that supply blood and O2 to heart Deposits of cholesterol and lipids by a complex inflammatory process Leads to vascular wall thickening May be symptomatic, angina pectoris, SOB, dyslipidemia, dysrhythmias, CHF Note family history of heart disease |
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Senile cardiac amyloidosis |
Fibrillar protein (r/t chronic infammation or neoplastic disease) deposited in the heart Reduced heart contractility, CHF Palpitations, lower extremity edema, fatigue, pleural effustion, arrhythmia, JVD, hepatomegaly, ascites, EKG changes |
