PC 615 test 1 - Sheet1(1) Flashcards
Reasons to order an ECG
To provide support for a diagnosis. Questionable cardiovascular complaint, including chest pain, dyspnea, and dizziness, routine physical exams (to obtain a baseline), pre-op, and for individuals starting exercise programs. Quick and inexpensive, non-invasive.
Downfall of ECG
Can provide false positives and false negatives. Brief view of heart, not 100% specific, specific lead placement required, doesn’t specifically diagnose MI, many normal variations, difficult to interpret, and cannot replace thorough H&P.
Important information to gather along with the ECG
Complete history and complete physical exam
Information provided by the ECG
Rhythm disturbances, conduction abnormalities, electrolyte disturbances, medication/drug effects, chamber enlargement, ischemia, mass of cardiac muscle, and orientation of heart in the chest
What cardiac leads of an ECG do
Provide a view of the heart’s electrical activity between two points and each has a negative and positive pole.
Measurement of smallest boxes on ECG paper
1 mm
Measurement between heavy lines on ECG paper
5 small boxes
Time measurements of boxes on ECG
Large blocks = 3 seconds; 30 large blocks = 6 seconds
Wave forms on ECG
Represents the heart’s electrical activity that occurs in one cardiac cycle
P wave
First component of normal ECG and represents artial depolarization.
ECG indications of atrial hypertrophy - such as tricuspid valve stenosis or pulmonary hypertension
Peaked notched or inverted P waves
Indication of broad or bifid P waves
Anything that causes left atrium hypertrophy, such as mitral stenosis
ECG indications of retrograde conduction through AV junction
Inverted P wave
Indication if P wave does not precede the QRS
Heart block may be present
Indication of a prolonged PR interval
Conduction delay as with digoxin or heart block
QRS wave
Represents depolarization of the ventricles.
Indication of deep and wide Q wave
Possible MI and also buncle branch blocks
Pathological Q wave
Depth is greater than 33% of height of next R wave or if the Q wave is 0.04 seconds or more.
Indication of pathological Q wave
Dead non-conducting tissue
Indication of notched R wave
Possible bundle branch block
Indication of tall R wave
Left ventricular hypertrophy in V5 or V6
Indication of missing QRS
Possible AV block or ventricular standstill
What does the ST segment measure
The end of ventricular conduction and beginning of re-polarization
J joint
Located at the end of the QRS complex and the beginning of the ST segment
Indication of ST segment elevation
Small infarct, pericarditis, or ventricular aneurysm
Indication of ST segment depression
Partial thickness infarct or digitalis effect
T wave
Indicates ventricular repolarization
Indication of peaked T wave
Ventricular recovery and can be caused by hyperkalemia
Indication of bumpy T waves
May indicate a hidden P wave
Indication of tall or tented T waves
Possible MI or electrolyte imbalances such as hyperkalemia
Indication of MI looking at T wave deflection
Inversion in leads I, II, aVl, aVf, or V2 through V6
Indications of notched or pointed T waves
Possible pericarditis
When is T wave inversion normal
Common in blacks and with digoxin treatment.
Indication of T wave inversion in lateral leads
Left ventricular hypertrophy
Indication of sloping ST depression and T wave inversion
Indicates digoxin treatment
Indication of T wave flattening
Hypokalemia
What does the QT interval measure
The time needed for ventricular depolarization and repolarization.
Causes of prolonged QT intervals
Certain drugs and congenital cardiac anomalies
Causes of short QT intervals
Digoxin toxicity o electrolyte disturbances
Dangers of prolonged QT intervals
Can produce drug-induced ventricular tachycardia. This form of drug toxicity is called Torsades de Points.
What does the U wave measure
Re-polarization of the HIS Purkinje system. Not present on every ECG. Follows T wave and is usually upright.
Pathological U wave
Occurs if it follows a flat T wave
Indication of prominent U wave
May result from hypercalcemia, hypokalemia, or digoxin toxicity
S wave
Any deflection below the baseline following an R wave and is when the main muscle is depolarized
Indication of deep S wave in V1 or V2
Left ventricular hypertrophy
Is the rhythm regular or irregular?
Refers to the part of the heart that is controlling the activation sequence. For atrial rhythm, measure P-P interval. For ventricular rhythm, measure R-R intervals
System of examining a heart rhythm
Rate - rhythm - axis - description of QRS complexes - description of ST segments and T waves - look for hypertrophy - look for infarction
Are P waves present?
Do the P waves have normal configuration? Is ther a 1:1 ration between P waves and QRS complexes? Do all P waves have similiar shape and size? Is the PR interval constant?
Examining the QRS wave
Is the duration within normal limits? Are all the QRSs the same size and shape? Does a QRS come after each P wave?
Causes of abnormal cardiac rhythm
Flutter, fibrillation, heart block, escape rhythm
Axis
The direction of the movement of electrical depolarization as it spreads through the heart. Electrical impulses occur in 3 dimensions.
Normal axis measurement
30 to +90 degrees. Some books say 0 degrees to +90 degrees
Normal path of electrical currents of the heart
Normally from the right atrium through the left ventrical
Depolarization of the septum
Occurs left to right
Normal axis
0 to +90 degrees
Causes of right axis deviation
Normal variation, lateral wall MI, left posterior hemi-block, RBBB, emphysema, right ventricular hypertrophy, pulmonary hypertension, pulmonic stenosis. Mainly caused by pulmonary conditions and congenital disorders. Requires no treatment.
Axis deviation of infants and children
Normally have right axis deviation
Axis deviation of pregnant women
Normally have left axis deviation
Causes of left axis deviation
Caused by a conduction defect. Normal variation, inferior wall MI, left anterior hemi-block, Wolff Parkinson White syndrome, mechanical shifts (ascites, pregnancy, tumors), aortic stenosis, aging
Right atrium enlargement
Affects P wave and caused by COPD, tricuspid stenosis, tricuspid regurgitation, and PE. Caused by any severe lung disease.
Axis deviation in tall, thin individuals and short, fat individuals
Normal left deviation
ECG changes related to right atrium enlargement
Peaked P wave in lead II greater than 2.5 mm amplitude; V1 increasing in initial positive deflection
Left atrium enlargement
Causes delay in electric in left atrium, causing change in shape of P wave. Caused by mitral valve stenosis or insufficiency and left ventricular hypertrophy
ECG changes related to left atrium enlargement
P wave duration of 0.11 msec or longer; notching of P wave with peaks 1 mm apart, prominence of the terminal portion of P wave in V1
Right ventricular hypertrophy
Caused by right ventricular outflow obstruction, pulmonary disease, pulmonary HTN, pulmonary valve stenosis, tetratology of Fallot, and ventricular septal defect
ECG changes related to right ventricular hypertrophy
QRS complex: R wave getting progressively smaller from V1-V6, deep S wave in V5 or V6, slightly increased QRS duration, ST depression may occur, T wave inverted in V1 and V2, and may have right axis deviation
Causes of left ventricular hypertrophy
Mitral insufficiency, cardiac myopathy, aortic stenosis or insufficiency, HTN
ECG changes related to left ventricular hypertrophy
QRS prolonged with increased amplitude, increasing amplitude in R waes in I, aVl, V5, V6. S wave increasing in V1 and V2. Possible ST depression with T wave inversion. T wave may be inverted in V5 or V6. May have left axis deviation
Ischemia
Blood flow and O2 demands are out of sync, can be reversed. Indicated by ST depression on ECG
Injury
Ischemia prolonged and damage present. Indicated by ST depression on ECG
Infarction
Death of cells, damage irreversible. Indicated by ST segment elevation on ECG. Represents MI or pericarditis.
ECG changes of anterior MI
Q wave in V1 to V4 and ST elevation. V3 and V4
ECG changes of lateral MI
aVl and lead I, V5 and V6 with Q wave and ST elevation
ECG changes of inferior MI
Leads II and III, and aVF with Q wave and ST elevation
ECG changes of posterior MI
Oppositeo f anterior MI, with a larger R wave, and with ST wave depression
Diagnosing MI on ECG
Look for changes in 2 contiguous leads. Changes in more than 1 lead in a cluster or grouping is diagnostic. That means two leads are in diagnostic groupings.
ECG changes hours following cardiac blood flow obstruction
May see ST depression
ECG changes hours to days following cardiac blood flow obstruction
May have Q wave, may have ST elevation, may have T wave inversion
ECG changes days to weeks following cardic blood flow obstruction
Q wave may be present, ST elevation decreasing, may have deepening T wave inversion
ECG changes weeks to months following cardiac blood flow obstruction
May have Q wave, ST elevation may resolve, and T wave my return to positive deflection
Depressed ST segments
In ischemia and with digoxin
Supraventricular rhythms tracings on ECG
Have narrow QRS complexes. Only exception are right or left BBB that will produce wide QRS complexes
Ventricular rhythm tracings on ECG
Have wide QRS complexes and a rate of 30 or less
Acute causes of chest pain
MI, PE, pneumothorax and other pleuritic disease, pericarditis, aortic dissection
Causes of intermittent chest pain
Angina, oseophageal pain, muscular pain, and nonspecific pain
Diseases associated with left ventricular hypertrophy
Aortic stenosis or regurgitation or mitral regurgitation
Diseases associated with right ventricular hypertrophy
Mitral stenosis, severe lung disease
Most common sustained cardiac rhythm disturbance
A fib. More common in men and increasing in prevalence with age
Mechanism for reentry
Involves the existence of two conduction pathways with different refractory periods
Symptoms of tachyarrhythmias
Usually asymptomatic, but when symptoms do occur, it is related to ventricular rate, extent of underlying heart disease, ventricular function, and associated precipitating factors. Palpitations are most common symptom
Adverse effects of tachyarrhythmias
Ventricular filling is compromised, causing hypotension, chest pain, heart failue, change in LOC, or even sudden cardiac death
Physical exam of patient experiencing tachyarrhythmias
Color, respiratory effort, anxiety, hydration status, evidence of dehydration and hypovolemia, mental status, auscultation of heart and lungs, JVD
ECG of sinus tachycardia
P wave for each QRS. Rhythm regular, P waves identical, QRS complexes are normal and narrow, rate is above 100
Paroxysmal supraventricular tachycardia (PSVT)
Rate 140-240, regular rhythm, P waves may appear different, QRS more narrow, P waves may be buried in previous beats
Atrial flutter
Rate between 250-350, Sawtooth appearance of P waves
Atrial fibrillation
Normal P wave replaced by F wave producing wavy baseline, rate 350-650, irregularly irregular ventricular response. More common in men
PVCs
Wide QRS complexes that interrupt the prevailing rhythm, P wave usually absent, beat often followed by a full compensatory pause
Indications of S3 sound
Occurs in early diastole at time of maximum ventricular filling. May commonly be heard in young fit adults and during pregnancy. Best heard with bell. May warn of impending heart failure and is a significant finding.
Drug of choice for treatment of PVCs
Beta blockers
Symptomatic bradycardia
A documented bradyarrhythmia that is directly responsible for the development of frank syncope or near-syncope, transient dizziness, or lightheadedness and confusional states resulting from cerebral hypoperfusion attributable to a slow ventricular rate
Characteristic symptoms of chronic stable angina
Symptoms occur with predictable frequency, severity, duration, and provocation, occur with exertion, relieved by rest and no more than one nitro tab, and generally last for 1-3 minutes
Levine’s sign
Patients who present with a clenched fist over their sternal area as a result of chest pain
Murmur
A relatively lengthy series of sounds produced by the turbulent flow of blood
Causes of murmurs
High rates of flow through a normal or abnormal valve; forward flow through a constricted or irregular valve or into a dilated vessel; or backward flow through a regurgitant valve, septal defect, or patent ductus arteriosus
Aortic stenosis
Harch, creschendo-decrescendo characteristic sound. Located right sternal border, but the click is loudest at apex. Valsalva maneuver decreases murmur. Patient presents with chest pain, syncope, exercise intolerance, and dyspnea. Left ventricular hypertrophy results
Mitral regurgitation
Pansystolic blowing characteristic sound. Located apex, radiation to axilla. Left ventricular hypertrophy results. May be asymptomatic for years then present with complaints of fatigue and dyspnea on exertion
Mitral valve prolapse
Mid to late systolic; occasionally honking; may have midsystolic click. Located lower left sternal border. ECG usually within normal limits. May be asymptomatic for years then present with chest discomfort, palpitation, mid dyspnea, fatigue, and anxiety. Most prevalent in women. Often seen in pectus excavatum and shallow AP diameter. Moves forward with position change to standing.
Heart blocks
Interference with the conduction process
First-degree heart block
Conduction delay along the bundle of His. PR interval is prolonged. May be a sign of CAD, acute rheumatic carditis, digoxin toxicity, or electrolyte disturbances. No specific actions
Second-degree heart block
Some conduction failes to pass through the AV node or the bundle of His. Usually indicates a heart disease, often seen in MI.
Mobitz type 2
There is an occassional atrial contraction without a subsequent ventricular contraction.
Wenchkebach
There is progression lengthening of the PR interval until a QRS is eventually dropped
2:1 or 3:1 conduction disorder
There are more atrial contraction or P waves than QRS complexes. May indicate a need for temporary or permanent pacing
Third-degree heart block
Atrial contractions are normal, but there is no connection to the ventricular contractions. Indicates conducting tissue disease.
Bundle branch blocks
Occurs with abnormal conduction with either BBB and causes a delay in ventricular depolarization resulting in wide QRS complex
Right bundle branch block
Often common in healthy people. Indicated by RSR1 wave in V1. Can be caused by PE
Left bundle branch block
Always indicates heart disease and prevents ECG interpretation. Lead V6 shows a letter “M”. May be asymptomatic, but may present with chest pain. May indicate MI.
Indications of PE on ECG
Peaked P waves, right axis deviation (S waves in lead I), tall R wave in V1, RBBB, inverted T in V1, V2, or V3
Lateral cardiac problems - ECG
Leads I, aVL, V5, and V6
Inferior cardiac problems - ECG
Leads II, III, and aVF
Septal cardiac problems - ECG
Leads V1 and V2, ST segment elevation
Posterior cardiac problems - ECG
Leads V1 to V2, V3. ST segment depression, tall upright R waves
Anterior cardiac problems - ECG
Leads V4 and V4
Types of bradycardias
Sinus brady, SA exit block, AV nodal block, first-degree AV block, second-degree AV block, third-degree AV block, bundle branch blocks
Types of narrow complex tachycardias
Sinus tach, atrial tach, a flutter, a fib, multifocal atrial tachycardias, paroysmal atrial tachycardia, AV nodal reentry tachycardia, AV reciprocating tachycardia, PACs, and PJC
Types of wide complex tachycardias
V tach, V fib
When is consultation most appropriate
Arrhythmia with hemodymanic decompensation - EMERGENCY!! Arrhythmias requiring non-pharmacologic agents - pacemaker, ablation, ICD implantation. New arrhythmias. Refractory to standard drug therapy - when pt on max doses. ECG changes. Co-mordibities - DM, HF, hyperlipidemia, PVD. Adventitious heart sounds, new murmurs, changes in heart sounds, arrhythmias
System of assessing cardiac sounds
First heart sound - second heart sound - sounds in systole - sounds in diastole - systolic murmurs - diastolic murmurs - sound/murmurs in systole AND diastole
Where to listen to diastolic murmurs
Best heard with patient sitting, leaning forward, and exhaling
Where to listen to aortic insufficiency murmurs
Best heard at upper right sternal border
When to use diaphragm of stethoscope
High frequency sounds of S1 and S2
When to use bell of stethoscope
Low frequency or low pitch sounds such as diastolic murmurs of mitral stenosis - listen to S3 and S4
S1
Closure of mitral and tricuspid valves
S2
Closure of aortic and pulmonic valves
Systolic murmurs
Pneumonic MRPASSMVP
Pneumonic MRPASSMVP
Mitral regurgitation, physiologic, aortic stenosis, systolic murmurs, mitral valve prolapse
Diastolic murmurs
Pneumonic MSARD
Pneumonic MSARD
Mitral stenosis, aortic regurgitation, diastolic murmur
Mitral stenosis
Always caused by rheumatic heart disease. May present with dyspnea and fatigue. Loud at S1. Low pitched diastolic rumble. Heard best at apex. Best heard in left lateral position. No radiation.
Physiological (innocent) heart murmurs
Not due to any pathologic obstruction to flow
Pathological heart murmur criteria
Murmurs that are due to an increased cardiac output are caused by excess flow across the outflow tract. May be caused by decreased mobility of aortic valves as a result of fibrosis and calcification. May be caused by atrial septal defect.
Atrial septal defect
Pathologic ejection murmur that mimic the flow murmur acorss the pulmonic valve. Common in individuals with pectus excavatum
Cardaic rubs
Rubbing together of inflamed membranes of the pericardium and often produces one systolic and two diastolic sounds. May occur in pericarditis or after an MI. Often mistaken for course crackles. Loudest at the left lower sternal border. Often transient and louder with inspiration or forced expiration with the patient leaning forward. Best heard with diaphragm and sounds high-pitched and scratchy, grating, or squeaking.
Characteristics of sinus arrhythmia
P waves with each QRS,, intervals ar normal, rhythm regular, and rate above 60
Common innocent murmurs in children and adults
Venous hum, pulmonary flow murmur, midsystolic murmur, innocent vibratory, mammary soufle, innocent pulmonary flow murmur
Venous hum
Common in kids ages 12 months to 6 years. May be present in fit young adults, pregnancy, and anemia. Low continuous hum loudest above the right clavicle, but may be heard in aortic and pulmonary areas. By changing position of pt’s head or by pressing in the area of the major neck veins, the flow may be changed and these murmurs will change or disappear. Having the child look down or to the side while listening will often make these murmurs or sounds disappear.
Common pathologic murmurs in children and adults
Aortic stenosis, pulmonary stenosis, pansystolic murmurs, diastolic murmurs
Pulmonary stenosis
Heard upper left sternal edge over pulmonary area and is midsystolic. Loudest at times of high cardiac output, such as with febrile illness and pregnancy
Still’s murmurs
Innocent murmur that is low-pitched heart at the lower left sternal area. They are musical or have a relatively pure tone in quality or may be squeaky. Most common between age 3 and adolescence
Atrial septal defect
Hole in atrial septum and allows blood to flow from left to right atrium. During times of straining, blood is shunted right to left. Auscultation - normal S1, widely split S2. Loudest in the pulmonary area
Patent ductus arteriosus (PDA)
Normal fetal structure that should close at birth. Can be mistaken for venous hum and best heard at upper left sternal edge, under the clavicle. Occurs throughout systole into diastole. This is a continuous high pitched murmur in the pulmonary area.
Physiological split
Combined sound of aortic and pulmonary valves and S2 may sound like two separate and distinct sounds. Occurs during inspiration and best heard at left upper sternal border. Splitting heard at apex is almost always a sign of pulmonary hypertension.
Normal Sinus Rhythm
Atrial and ventricular rhythms are regular. Rate 60-100. P wave - normal and upright in lead II, similar shape and size, one for every QRS. PR interval - 0.12-0.20. QRS complex- 0.06-0.10. T wave - Normal shape, upright and rounded in lead II. QT interval - 0.46-0.44. No ectopic or aberrant beats
Sinus Brady
Rhythm - regular. Rate - less than 60. P wave - normal shape, upright in lead II, similar shape and size, one for every QRS. PR interval - 0.12-0.20. QRS complex - 0.06-0.10. T wave - normal shape, upright and rounded in lead II. QT interval - 0.36-0.44 or prolonged. No ectopic or aberrant beats.
Sinus Tachycardia
Rhythm - regular. Rate - greater than 100. P wave - Normal shape and upright in lead II, similar shape and size, one for every QRS, may increase in amplitude, may superimpose on T as rate increases. PR interval - 0.12-0.20. QRS - 0.06-0.10. T wave - normal shape, upright and rounded in lead II. QT interval - 0.36-0.44, possibly shortened. No ectopic or aberrant beats.
Paroxysmal atrial tachycardia (PAT)
Rhythm - regular. Rate - greater than 150. P wave - abnormal, may be hard to distinguish. PR interval - Usually within normal, but may be immeasurable. QRS - usually normal. T wave - usually distorted. QT - may be indistinguishable. Sudden onset, usually brought on by PAC
Hyperkalemia on ECG
Flattened P waves, QRS widens, peaked T waves
Hypokalemia on ECG
Flat T waves and U waves appear
Hypercalcemia on ECG
QT interval shortens
Hypocalcemia on ECG
QT interval prolonged
Digitalis effect on ECG
Can cause AV block
Effect of digitalis toxicity on ECG
Ventricular ectopy
Effect of quinidine on ECG
Widening of P wave, widening of QRS, ST depression, prolonged QT, presence of U wave
S3
An early diastolic sound usually caused by ventricular overload. Caused by left atrium pushing into an overfull ventricle during early diastolic filling. Can occur with heart failure. Best heard at apex 4th LICS MCL. Low pitch listen with bell. Can be normal in children and young adulte.
S4
Late diastolic or pre-systolic sound. Usually caused by poor diastolic function - inability of heart to relax during diastole. Caused by blood entering a stiff left ventricle during atrial contraction with uncontrolled hypertension and myocardial ischemia. Best heard at apex 4th LICS MCL. Best heard with bell.
Pathological or innocent and benign murmurs
Most innocent murmurs have these qualities - soft, relatively short systolic, medium pitch, vibratory, heard best at left lower sternal border, no radiation to apex, base, or back
Pathological murmurs
RED FLAGS. Accompanied by failure to thrive in infants. Accompanied by cyanosis. Diastolic only. Grave III/VI. Increases with standing.
Characteristics of physiological murmurs
Negative history. Less than grade 3. PMI is normal. Softens or disappears with standing
Characteristics for pathological murmurs
Symptomatic history. Grade 3 or higher. S1 and S2 obliterated. PMI displaced. Position change does not affect murmur or murmur becomes louder with standing.
Functional murmurs
Due to increased blood flow through the heart - anemia, fever, hyperthyroidism, pregnancy
Continuous murmur
Begins in systole and continues into diastole. Includes - PDA, fistulas or local arterial obstructions, venous hum, mannary souffle
Description of murmurs
Loudness (grade). Pitch (high, medium, or low). Pattern (crescendo, decrescendo, or crescendo-decrescendo). Quality (musical, blowing, harsh, or rumbling). Location of where best heard. Radiation. Posture (disappear or increased with change of position).
Systolic ejection (midsystolic) murmur
Builds in intensity and decreases in intensity before the S2. Crescendo-decrescento. Occurs with left ventricular outflow obstruction
Systolic regurgitant (holosystolic) murmur
Caused by flow from high pressure to low pressure (incompetent valves or VSD). Murmur begins as soon as pressure starts to increase and continues throughout systole. Lasts the entire S1, not S1 and S2
Aortic stenosis
Caused by rheumatic disease, congenital defect, or degeneration. If severe may produce chest pain, dyspnea, exertional angina, and syncope. Loud and harsh. Crescendo-descendo mid-systolic ejection murmur. Loudest at second right intercostal border. Radiates widely to side of neck, down left sternal border, or apex.
Pulmonic sternosis
Caused by calcification of pulmonic valve. Systolic medium pitch. Crescendo-decrescendo. Best heard at second left intracostal space. Radiates to left and neck.
Mitral regurgitation
Incompetent mitral valve. This allows blood to flow from a high pressure area back to a low pressure area. Holosystolic. Loud and blowing. Best heard at apex. Radiates well to left axilla.
Tricuspid regurgitation
Caused by back flow of blood through incompetent tricuspid valve into RA. May have engorged pulsating neck veins and liver enlargement. Lift at sternum and thrill at left lower sternal border. Soft and blowing, holosystolic. Best heard at left lower sternal border. Increases with inspiration.
Diastolic murmurs
Caused by regurgitation across either aortic or pulmonic valve or filling rumbles casued by flow across obstructed mitral or tricuspid valve. Loudest early diastole. Best heard with patient sitting, leaning forward, exhaling. Best heard with diaphram of stethoscope.
Tricuspid stenosis
Casued by calcification of tricuspid valve obstructs flow into right ventricle. Diastolic rumble. Best heard at lower left sternal border. Louder with inspiration.
Aortic regurgitation
Caused by an incompetent aortic valve allows blood to back flow into left ventricle during diastole. “Water hammer” pulses with wide pulse pressure. Begins with S2. Soft high pitched, blowing diastolic, de-crescendo. Best heard at 3rd left intercostal space. Best heard sitting up leaning forward. Radiates down.
Pulmonic regurgitation
Caused by incompetent pulmonic valve allows backflow of blood into right ventricle. Same timing and characteristics of aortic regurgitation so hard to tell difference on physical exam.
Considerations of newborn murmurs
Should be grade 1 or 2, systolic,, not accompanied by cyanosis or respiratory distress and disappear within 2-3 days
Workup of pediatric murmur
Pregnancy - infection (Rubella 1st trimester, herpes), drugs, illness, genetic (Downs), prematurity
Birth - cyanosis, resuscitation
Growth and development - failure to thrive, gain weight, feeding problems
Dyspnea, anoxic spells, squatting when tired, eyelid edema
ECGs
Venous hum
Caused by turbulent flow in jugular veins. No pathological significance. Continuous low pitched soft hum, heard throughout entire cycle and not affected by respiration. May be louder with standing.
Mammary souffle
Occurs in near term pregnancy and when lactating. Caused by increased flow through internal mammary artery.
Continuous and best heard in systole.
Split S2
Can hear closure of aortic and pulmonic valve. Normally heard on inspiration and goes away on expiration.
Sinus arrhythmia
Rhythm change with inspiration - increases at peak of inspiration and slowing with expiration.
Normal in young adults and children
Cardiac Rubs
Inflammation of pericordium. High pitched and scratchy. Best heard with diaphragm. Best heard in sitting position leaning forward with breath held during expiration.
Sounds like sand paper being rubbed together.
Often occurs post MI
Name two innocent continuous murmurs
Venous hum
Mammary souffle
Name two abnormal continuous heart sounds
PDA
Friction rub
Name two heart sounds affected by respiration
Sinus arrhythmia
Split S2
Tricuspid regurgitation
