Cardiovascular

sudden, rapid regular beating

Paroxysmal SVT

TABLE 16-5. Variations and Abnormalities of the Ventricular Impulses (p. 547)

Location: in the fourth or fifth left intercostal space, at the midclavicular line Diameter: discrete, or ≤2 cm Amplitude: brisk and tapping Duration: ≤2/3 of systole Hyperkinetic: The hyperkinetic ventricular impulse from transiently increased stroke volume—this change does not necessarily indicate heart disease. Sustained: The sustained ventricular impulse of ventricular hypertrophy from chronic pressure load, known as increased afterload (see p. 519). Diffuse: The diffuse ventricular impulse of ventricular dilation from chronic volume overload, or increased preload.

W/ carotid obstruction, kinking, or thrills

assess pulse in brachial artery

Absent a waves (JVP)

atrial fibrillation

Causes of Carotid Stenosis

Stenosis ( → ischemic CVA & CAD), tortuous carotid artery, external carotid artery disease, aortic stenosis, hypervascularity of hyperthyroidism, external compression from thoracic outlet syndrome

Sustained movement later in systole Use The diaphragm of stethoscope Extra systole sounds: systolic click of mitral valve prolapse murmur can radiate to axilla thru bone conduction Pansystolic or late systolic murmur

mitral regurgitation

Atrial or Nodal Premature Contractions (Supraventricular)

A beat of atrial or nodal origin comes earlier than the next expected normal beat. A pause follows, and then the rhythm resumes.

SPORADIC Ventricular Premature Contractions (Ventricular bigeminy or trigeminy)

A beat of ventricular origin comes earlier than the next expected normal beat. A pause follows, and the rhythm resumes. S1 &S2 are likely to be split.

Periorbital puffiness & tight rings

nephrotic syndrome

Bigeminal Pulse

normal beat alternating with a premature contraction. The stroke volume of the premature beat is diminished in relation to that of the normal beats, and the pulse varies in amplitude

S2

A2 (Closure of aortic valve) + P2 (Closure of pulmonic valve) A2 = normally louder & heard throughout precordium d/t high pressure in aorta P2 = soft & heard at 2nd & 3rd left intercostal spaces close to sternum d/t lower pressure in pulmo artery --> Listen here for S2 split Inspiration delays closure of P2 It is normally heard late in inspiration. Expiratory splitting suggests a valvular abnormality.

Sustained left parasternal movement beginning at S1

pressure overload from pulmo HTN and pulmonic stenosis or the chronic ventricular volume overload of an atrial septal defect

JVP

Atrial contraction (a wave) Carotid transmission (c wave at S1) Atrial relaxation (x descent) Right ventricular systole & venous filling of atria (v wave at S2) Blood passively empties from right atrium into RV (y descent)

S4 (Diastolic)

Atrial gallop just before S4 increased left ventricular end diastolic stiffness → decreases compliance Atrial contraction or ventricular stiffness d/t HTN & acute MI TEN-nes-see Normal in older adults, esp. after exercise, athletes

SPORADIC Sinus Arrhythmia

The heart varies cyclically, usually speeding up with inspiration and slowing down with expiration.

Screening for CV Risk Factors

Begin routine screening at 20 years and for any family history of premature heart disease (Less than 55 yo in 1st-degree male relatives & less than 65 yo in 1st-degree female relatives) Calculate 10-year & lifetime global CVD risk using a web-base calculator for ages 40-79 years

Elevated above normal: JVP > 3cm above sternal angle or > 8cm total distance

Causes: Acute & chronic heart failure, tricuspid stenosis, chronic pulmo HTN, SVC obstruction, cardiac tamponade, constrictive pericarditis > 95% specific for increased left ventricular end-diastolic pressure & low left ventricular EF Obstructive lung disease → JVP elevated w/ expiration & collapse on inspiration

decreased pulsations

Decreased SV from shock or MI & local atherosclerotic narrowing or occlusion

Split S1

Delayed closure of the tricuspid valve increases splitting of S1, best heard along the lower left sternal border where the tricuspid component, often too faint to be heard, becomes audible. A more prominent split S1 than normal occurs in right bundle branch block. This split may rarely be heard at the apex, but must be distinguished from an S4, an aortic ejection sound, and an early systolic click.

Pulse Pressure

Difference btw. SBP & DBP

Dyslipidemia Goals

Grade B Recommendation: Low to moderate dose statins for primary CVD prevention in adults aged 40-75 years who have one or more CVD risk factors and a 10-year calculated CVD event risk more than 10%. Measure lipid levels in adults aged 40-75 years w/o existing CVD every 5 years High-intensity therapy lowers LDL cholesterol by 50% Moderate-intensity therapy lowers LDL cholesterol by 30-50%

CO

HR x SV CO: volume of blood ejected in 1 minute SV: Volume of blood ejected w/ each contraction

Heart Failure Valsalva Maneuver

"Square wave" Response: BP remains elevated and there are Korotkoff sounds during strain phase, but not during phase 4 release Highly correlated with volume overload, elevated left ventricular end-diastolic pressure, pulmonary capillary wedge pressure

Varying S1

(1) in complete heart block, when atria and ventricles are beating independently of each other and (2) in any totally irregular rhythm (e.g., atrial fibrillation). In these situations, the mitral valve is in varying positions before being shut by ventricular contraction.

Accentuated S1

(1) tachycardia, rhythms with a short PR interval, and high cardiac output states (e.g., exercise, anemia, hyperthyroidism) and (2) mitral stenosis.

S1 diminished

1st-degree heart block, left bundle branch block, and myocardial infarction. Early mitral valve closure occurring before ventricular contraction also causes a soft S1, seen in severe aortic regurgitation.

PMI in xiphoid or epigastric area

COPD d/t right ventricular hypertrophy

right atrial pressure

CVP + right ventricular end-diastolic pressure

Midsystolic murmur

Can be functional murmurs Typically arise from blood flow across semilunar valves Short midsystolic murmurs decrease in intensity with maneuvers that reduce left ventricular volume, such as standing, sitting up, and straining during the Valsalva maneuver. Often heard in healthy patients and are not pathologic Begins after S1 and stops before S2. Brief gaps are audible between the murmur and the heart sounds. Listen carefully for the gap just before S2

Small Weak Pulses

Causes include (1) decreased stroke volume, as in heart failure, hypovolemia, and severe aortic stenosis; and (2) increased peripheral resistance, as in exposure to cold and severe heart failure.

Large Bounding Pulses

Causes include (1) increased stroke volume, decreased peripheral resistance, or both, as in fever, anemia, hyperthyroidism, aortic regurgitation, arteriovenous fistulas, and patent ductus arteriosus; (2) increased stroke volume because of slow heart rates, as in bradycardia and complete heart block; and (3) decreased compliance (increased stiffness) of the aortic walls, as in aging or atherosclerosis.

Continuous Murmurs

Congenital patent ductus arteriosus and AV fistulas

HTN Goals

For patients w/ existing CVD, target BP goal of 130/80 For CVA or TIA, target BP goal of 140/90

Hyperkinetic PMI

Forceful PMI that terminates quickly Caused by hypermetabolic states: Severe anemia, hyperthyroidism, volume overload of left ventricle from aortic regurgitation

Isometric Handgrip

Increases the systolic murmurs of mitral regurgitation, pulmonic stenosis, and ventricular septal defect Murmurs of mitral regurgitation & ventricular septal defect could be differentiated from other systolic murmurs by augmentation of their intensity with handgrip (68% sensitivity, 92% specificity) and during transient arterial occlusion (78% sensitivity, 100% specificity). Increases the diastolic murmurs of aortic regurgitation and mitral stenosis.

PMI > 2.5 cm

Left ventricular hypertrophy (LVH) d/t HTN or dilated cardiomyopathy

Edema

Interstitial tissue can absorb up to 5 L → accommodates up to 10% of weight gain before pitting edema appears Rapid weight gain will occur before visible edema

PMI lateral to midclavicular line or > 10 cm lateral to midsternal line

LVH & ventricular dilatation d/t MI or HF

Orthopnea & PND

LVHF, mitral stenosis, obstructive lung disease

S3, opening snap, diastolic rumble w/ restricted leaflet motion Use The bell of stethoscope Late diastolic (presystolic) murmur

Mitral Stenosis

Palpitations Health History

Obtain EKG Fast or slow Regular or irregular Duration Episode of rapid HR? Gradual or sudden? Teach to take serial measurements of HR

A2 Decreased or Absent:

Occurs in calcific aortic stenosis due to valve immobility. If A2 is inaudible, no splitting is heard.

Sudden dyspnea

PE, spontaneous pneumothorax, anxiety

Left lateral decubitus position

PMI, S3 or S4

ACS: Women > 65 yo w/ atypical symptoms

Pain in upper back, neck, or jaw SOB PND N/V Fatigue

transient skips & flip-flops

Premature contractions

Early diastolic murmur

Pulmonic Regurgitation

Regular rhythm, force alternates from strong & weak → severe left ventricular dysfunction

Pulsus Alternans

greater than normal drop in SBP during inspiration Highest SBP during resp cycle - Lowest SBP throughout the cycle = Normal 3-4 mmHg Paradoxical pulse = SBP decreases ≥ 10-12 mmHg during inspiration Causes: Pericardial tamponade, acute asthma, obstructive pulmonary disease, constrictive pericarditis, acute PE Varies with respiration

Pulsus Paradoxus

Chest Pain Health History

Quantify patient's baseline activity Severity of symptoms Significance of symptoms Consider angina pectoris, MI, AAA dissection, or PE

gradual, rapid regular rate > 120 bpm

ST

Early diastolic murmur

Starts immediately after S2, without a discernible gap, then usually fades into silence before the next S1. Typically reflect regurgitant flow across incompetent semilunar valves.

Late Systolic Murmur

Starts in mid- or late systole & persists up to S2 Mitral valve prolapse often preceded by systolic click Mitral regurgitation murmur may also be late systolic

Late diastolic (presystolic) murmur

Starts late in diastole and typically continues up to S1 Middiastolic and presystolic murmurs reflect turbulent flow across the AV valves.

Pansystolic murmur

Starts with S1 and stops at S2, without a gap between murmur and heart sounds. Often occur with regurgitant (backward) flow across the AV valves

Healthy Patients Valsalva Maneuver

Strain phase is silent; Korotkoff sounds are heard after straining is released during phase 4

Heaves

Sustained impulses rhythmically lift fingers Caused by enlarged right or left ventricle & ventricular aneurysms

Measuring BP

Take BP after patient rests for at least 5 min, feet on floor, unclothed arm at heart level Inflate cuff to about 30 mmHg above the pressure at which the brachial or radial pulse disappears. Listen for Korotkoff sounds of at least two consecutive heartbeats = SBP Listen for disappearing point of heartbeats = DBP

IRREGULARLY IRREGULAR Atrial Fibrillation and Atrial Flutter with Varying AV Block

The ventricular rhythm is totally irregular, although short runs of the irregular ventricular rhythm may seem regular.

unilateral pulsatile bulge

Tortuous and kinked carotid artery

Transient Arterial Occlusion

Transient compression of both arms by bilateral blood pressure cuff inflation to 20 mm Hg greater than peak systolic blood pressure augments the murmurs of mitral regurgitation, aortic regurgitation, and ventricular septal defect.

Pansystolic murmur

Tricuspid Regurgitation

Late diastolic (presystolic) murmur

Tricuspid Stenosis

DM Goals & American College of Cardiology/American Heart Association cholesterol guideline

Week 3 Bates' Notes Figure 16-33, p. 537

TABLE 16-1. Selected Heart Rates and Rhythms

Week 3 Bates' Notes p. 540

S3 (Systolic)

abrupt deceleration of inflow across mitral valve Normal in children & young adults, athletes Abnormal S3 in older adults = ventricular gallop Ken-tucky-Y

Bounding carotid, radial, and femoral pulses Sit up, lean forward, & exhale to assess Soft decrescendo higher-pitched diastolic murmur Use The diaphragm of stethoscope Early diastolic murmur "medium-pitched, grade 2/4, blowing decrescendo diastolic murmur, best heard in the fourth left intercostal space, with radiation to the apex" soft S1

aortic regurgitation

Carotid thrills, delayed upstrokes, S2 diminished Murmurs radiate to neck, esp. Right side Midsystolic murmur. sluggish pulses

aortic stenosis

Wide S2 Split during expiration

caused by delayed closure of the pulmonic valve (as in pulmonic stenosis or right bundle branch block) or early closure of the aortic valve (mitral regurgitation). Right bundle branch block is illustrated here.

Abnormally prominent cannon a waves (JVP)

d/t increased resistance to right atrial contraction

Increased RV preload w/ increased venous return to right heart

d/t inspiration, exercising muscles, or dilated RV in HF

Fixed S2 Split

does not vary with respiration, often due to prolonged right ventricular systole, seen in atrial septal defect.

Increased v waves

tricuspid regurgitation, atrial septal defects & constrictive pericarditis

"The JVP is 5 cm above the sternal angle with the head of bed elevated to 50°. Carotid upstrokes are brisk; a bruit is heard over the left carotid artery. The PMI is diffuse, 3 cm in diameter, palpated at the anterior axillary line in the fifth and sixth intercostal spaces. S1 and S2 are soft. S3 is present at the apex. High-pitched harsh 2/6 holosystolic murmur best heard at the apex, radiating to the axilla."

heart failure with volume overload with possible left carotid occlusion and mitral regurgitation

P2 Decreased or Absent

increased AP diameter of the chest associated with aging. It can also result from pulmonic stenosis.

Bisferiens Pulse

increased arterial pulse with a double systolic peak, detected during moderate compression of the artery. Causes include pure aortic regurgitation, combined aortic stenosis and regurgitation, and hypertrophic cardiomyopathy.

increase w/ expiration

left-sided murmurs

Hypertrophic cardiomyopathy murmur

only systolic murmur that increases during the "strain phase" of the Valsalva maneuver d/t increased outflow tract obstruction increase in intensity during squatting-to-standing action (95% sensitivity, 84% specificity) and by a decrease in intensity during standing-to-squatting action (95% sensitivity, 85% specificity)

TABLE 16-3. Syncope and Similar Disorders

p. 542

TABLE 16-8. Extra Heart Sounds in Systole

p. 550

TABLE 16-9. Extra Heart Sounds in Diastole

p. 551

TABLE 16-10. Midsystolic Murmurs

p. 552

TABLE 16-11. Pansystolic (Holosystolic) Murmurs

p. 554

TABLE 16-12. Diastolic Murmurs

p. 555

TABLE 16-13. Cardiovascular Sounds with Both Systolic and Diastolic Components

p. 556

listen at the lower right sternal border, often accentuated with inspiration

right-sided murmurs

Anasarca

severe generalized edema extending to sacrum & abdomen

Tricuspid Valve

softer, heard best at lower left sternal border Listen here for S1 split

S2 Paradoxical or reversed splitting

splitting that appears on expiration and disappears on inspiration. Closure of the aortic valve is abnormally delayed so that A2 follows P2 in expiration. Normal inspiratory delay of P2 makes the split disappear. The most common cause is left bundle branch block

P2 with Increased Intensity

suspect pulmonary hypertension. Other causes include a dilated pulmonary artery and an atrial septal defect.

A2 with Increased Intensity

systemic hypertension because of the increased pressure load. Increased intensity also occurs when the aortic root is dilated, attributed to the increased proximity of the aortic valve to the chest wall.

Edema Causes

ventricular dysfunction, obstructive lung disease, hypoalbuminemia, positional

Metabolic Syndrome Diagnosis

w/ ⅗ risk factors present: Elevated waist circumference Elevated trigs Reduced HDL Elevated BP Elevated fasting plasma glucose