NURS 202 - Heart & Neck Vessels

Precordium

Midthroacic cavity in the 2nd to 5th ICS, right sternal border to border to left MCL

Contains the heart & great vessels (aorta, pulmonary artery, inferior / superior vena cava)

Top

Apex is pointed and located at the bottom

5th ICS, 7 - 9 cm left of midsternal line (approximately at MCL)

Heart is rotated so that the right side is anterior & left side is poterior

• Cardiomyopathy
• Hypertrophy of heart muscle

• Pericardium
• Epicardium
• Myocardium
• Endocardium

Pericardium is the pericardial sac

It is attached to vessels, esophagus, sternum & pleura; anchored to the diaphragm

Epicardium

A lot of muscle on the left side pumps blood throughout the body compared to the right side that pumps blood to the lungs.

Endocardium

Unidirectional Valves

• Open & close passively hearts
• Greater the volume, greater the pressure.

• Left AV = Mitral (Bicuspid)
• Right AV = Tricuspid

Chordae tendinea attach the AV valves to papillary muscles & provide stability to valves during systole

Rupture of the chordae tendinea may be life threatening. When the chordae tendinea pulls away from the muscle, immediate death occurs.

• Right = Pulmonic
• Left = Aortic

Pulmonic Semilunar Valve (Right)

Aortic Semilunar Valve (Left)

Conduction System & Hemodynamic System

Conduction System

Hemodynamic System

Conduction

SA node

SA node

It works like a spark that starts the heart beat & then it is transmitted across atria to the AV node, then to the Bundle of His & finally to the Perkinje fibers in the ventricles.

True

Electrocardiogram (ECG)

P wave

P wave

SA node isn't firing properly or doesn't fire at all

60 - 100 beats per minute (bpm)

As the heartbeat is lower, the lower pacemakers (AV node / junctional node, which is 40 - 60 bpm) take over

SA node generates heartbeat.

It is the time from stimulation of atria to stimulation of ventricles.

Firing of the SA nodes

• 1. Depolarization of ventricles
• 2. Spread of stimuli through ventricles

• 1. Repolarization of ventricles.
• 2. Resting phase

• 1. Final ventricular repolarization
• 2. Not always seen on EKG

• Vessels
• - Venous blood
• - Arterial blood

Blood flows from higher to lower pressure gradients

Lower Body (abdomen, liver) -> Inferior Vena Cava -> Right Atrium

Head & neck -> superior vena cava drains venous blood -> Right Atrium

Right Atrium carries venous blood -> Tricuspid Valve -> Right Ventricle -> Pulmonary Semilunar Valve -> Pulmonary Arteries (unoxygenated blood) -> lungs / alveoli (oxygenate the blood) -> pulmonary veins (oxygenated blood) -> Left Atrium (arterial blood) -> Mitral Valve -> Left Ventricle -> Aortic Semilunar Valve -> Aorta -> Body

Blood moves by pressure gradients.

Backflow of blood is caused when atrial pressure are excessively high.

• 1. No valves between right atrium & vena cava
• 2. If pressure in the right atrium is greater than vena cava, then blood back flows to the veins of the neck & PV system & results in distended neck veins & peripheral edema - which can lead to right valve disease, lung disease, etc.

Swelling in feet and legs

• 1. No valves are between the left atrium & pulmonary veins
• 2. If pressure in the left atrium is greater than the pulmonary veins, then blood back flows to the lungs & results in pulmonary congestions (ex. crackles / rales) - which can lead to right valve disease, Hypertension (HTN), defective aortic valve etc.

crackles / rales

10 breaths / hour

Bronchia tubes

No function

CO = HR x SV

- increase heart rate leads to increase cardiac output

- Stroke Volume = amount of blood ejected w/ one heart beat (70 mL)

4 - 6 L / min

Left Ventricular End Diastolic Volume (LVEDV)

- Causes more stretch on the myocardial muscle fibers at the end of diastole

Greater the stretch of muscle fibers, stronger the contraction

- Give fluids until Stroke Volume starts to decrease

- If Cardiac Output is too low, give pt. diuretic

The goal is to maximize preload (volume) in order to maximize left ventricular contraction & cardiac output

Excessive preload leads to decreased Cardiac Output & heart failure

Plaque build-up which leads to not enough oxygen in blood & makes the muscle work harder

SVR

PVR

- Ventricles work harder & use more oxygen to pump but don't want to use more oxygen b/c can lead to myocardial infarction

- The opposing pressure in the ventricle must generate to open the aortic valve during systole, which increases SVR (afterload)

- Causes increased aortic pressures

Myocardial workload & oxygen consumption

May be caused by arteriosclerosis, HTN, sympathetic nervous system stimulation (stress - anything that causes stress on the sympathetic nervous system), excessive alcohol intake

Hardening of plaque in artery

Heart sounds are produced by closure of the valves

Louder on the left side (ex. mitral valve closure is louder than tricuspid & aortic valve closure is louder than pulmonic)

• 1. Aortic Valve - 2nd ICS, right sternal border
• 2. Pulmonic Valve - 2nd ICS, left sternal border
• 3. Erbs Point - 3rd ICS, left sternal border (good location for referred sounds, place where murmurs radiate to)
• 4. Tricuspid Valve - 4th IC, left sternal border
• 5. Mitral Valve - 5th ICS, MCL

• - Listen to all sites w/ diaphragm & bell of stethoscope
• - Listen for aortic murmurs (sitting & leaning forward is best)
• - Listen for extra heart sounds (left lateral decubitus position is best)

• - Mitral / tricuspid valves closes -> creates S1
• - Aortic / pulmonic valves open (when ventricular pressure exceeds aortic) -> ventricles contract & blood is ejected from ventricles
• - Ends diastole; begins systole

• - Aortic / pulmonic valves (semilunar) close -> creates S2
• - Mitral / tricuspid valves open
• - Rapid filling phase (passive initial filling of ventricles)
• - Atrial kick (atrial contraction ejects last 25% of SV into ventricles). AK is normal, but not the S4
• - End systole; begins diastole. Diastolic filling

• S1 ------- S2, S3
• "Ken ------- tucky"

• - Extra Heart Sounds (Gallops) - diastolic sounds
• - Heart Failure
• - Non-compliant Ventricle
• - Early diastole
• - Indicates ventricular resistance to early passive filling
• - Occurs in early diastole (immediately after S2)

• - Decreased ventricular compliance (early sign of HF)
• - High output conditions such as hyperthyroid, pregnancy, etc.

Blood flows in freely

• S4, S1 ------- S2
• "Tenness ------- ee"

• - Extra Heart Sounds (Gallops) - diastolic sounds
• - Heart Failure
• - Indicates ventricular resistance to filing during the atrial kick
• - Occurs in late diastole (immediately before S1)

Hypertension

S3 & S4

• - Mitral valve closing before tricuspid valve due to higher pressures on the left
• - Uncommon since closure of tricuspid is usually too faint to hear
• - May be mistaken for S4

• - Common
• - Can be re-created
• - Aortic valve closing before pulmonic during deep inspiration
• - Changes in intrathoracic pressure w/ deep inspiration causes asynchronous valve closure
• - May be mistaken for S3 although S3 isn't affected by breathing patterns
• - Most prominent at 2nd ICS, left sternal border at peak inspiration (in contrast to S3 which is best heard at the apex)

Blowing / swooshing sound that occurs w/ turbulent flow through valves or great vessels

• - Increased velocity (exercise)
• - Decreased viscosity (thin)
• - Decreased volume (anemia)
• - Defective valves (forward or backward flow)
• - Septal defects (ABN openings between chambers)

• - Stenotic - narrow vessels / narrow valves
• - Blood flows through the narrow
• - Occurs when a valve is open
• - Prevents adequate forward flow through thick, stiff valves
• - Causes harsh murmurs

• - Regurgitant - blood goes the wrong way
• - Murmurs of insufficiency
• - Occurs when a valve is closed or not tightly closed
• - Also referred to as insufficiency
• - Results in backward flow due to poor valve closure
• - Causes turbulent sound

• - Heard in systole after S1
• - Aortic / pulmonic stenosis - when semilunar valves are open
• - Mitral / tricuspid insufficiency (regurgitant) - when A/V valves are closed

• - Heard in diastole after S2
• - Mitral / tricuspid stenosis - when A/V valves are open
• - Aortic / pulmonic insufficiency (regurgitant) - when semilunar valves are closed

• 1. Know if you are in systole or diastole
• - One way to tell if you are in systole or diastole is to palpate the carotid pulse while listening to the heart sounds; if you feel the pulse immediately after you hear the heart sound, then you are in systole.
• 2. Identify at which valve site the murmur is the loudest
• 3. Know which valves are open & closed to determine if it's stenotic or regurgitant murmur

• - Timing
• - Systolic vs Diastolic
• - Early, mid, or late cycle
• - Entire cycle
• - Holodiastolic (between S2 & S1)
• - Holosystolic (between S1 & S2)
• - Intensity (graded 1 [soft] through 6 [loud])
• - Location (valve site)

• - Functional murmur
• - No valve, cardiac or other pathology
• - Common in childhood (usually due to increased blood flow)

• - Cardiac (angina, MI, mitral valve prolapse)
• - Acute Coronary Syndrom until diagnosis w/ heart attack
• - Pulmonary (pneumonia, pleurisy, embolis)
• - Pericardial (pericarditis - pain with each heart beat after myocardial infarcation)
• - Musculoskeletal / chest wall (costochondritis, arthritis) - hurts w/ palpation
• - Gastrointestinal (may mimic MI) - ulcer, hiatal hernia, esophagitis, indigestion
• - Neurotic - anxiety

• - Onset (at rest, with activity, after eating, etc).
• - Location (substernal, localized vs radiating)
• - Duration
• - Character (burning, sharp / stabbing, crushing, pressure, etc)

Myocardial ischemia

• - Imbalance between oxygen supply & demand (thus, more common w/ exercise)
• - Lack of oxygen to heart muscle lead to heart attack b/c muscle dies
• - Symptoms: chest discomfort w/ or w/o radiation, SOB
• - Should resolve in couple of minutes w/ rest and / or treatment (NTG - nitroglycerin) -> may progress to myocardial infarction if not treated
• - Prolonged symptoms may indicate myocardial infarction

Cocaine that leads to heart attacks

Myocardial Infarction

• - Similar to angina
• - May have diaphoresis
• - Nausea and Vomiting
• - Palpitations
• - Sense of impending doom

• - SOB
• - Sharp chest pain
• - Fatigue

• - Age (male > 45; female > 55, or postmenopausal)
• - HTN or hypertensive treatment
• - Smoking
• - Hyperlipidemia
• - Diabetes
• - Family history of premature CAD in 1st degree relative (male < 55; female < 65)

• - Dyspnea
• - DOE
• - PND
• - HF (lying down increases venous return & myocardial workload)
• - Orthopnea

Back fluid into alveoli

Sudden vs Gradual

Fainting w/ no or decrease blood flow to brain

Cardiac Arrythmia

• - Dependent edema
• - Nocturia (recumbent position increases venous return to heart -> increase renal blood flow -> increases urinary output)

• - Cholesterol level
• - Murmurs
• - Congenital heart disease
• - Rheumatic fever
• - Swollen joints
• - Heart surgery
• - Last EKG
• - Stress test (ETT results)
• - etc.

• - HTN, CAD, DM, obesity, congenital heart disease, genetically transmitted disease
• - Ex. Hypertrophic cardiomyopathy is the leading cause of death in young athletes

• - Diet (high fat, sodium)
• - Smoking (vasoconstricts - heart vessels & coronary arteries) - Increases heart rate, myocardial workload & oxygen consumption
• - ETOH (increases afterload) - cardiac depressant causing sympathetic compensatory response. Increase blood pressure.
• - Exercise (increases HDL, myocardial muscle tone) - Decrease plaque build-up
• - Medications (digitalis, diuretics, beta blockers, calcium channel blockers, etc.)

Assess for cyanosis or clubbing

• - Inspect
• - Palpate
• - Auscultate

• - Visualized at top of neck hear mandible
• - Palpate in lower 1/3 of neck between trachea & SCM muscle (avoids carotid sinus which slows HR)
• - Palpate one artery at a time
• - Pulse strength 2+ (diminished w/ decreased stroke volume)
• - Auscultate for bruits (coronary artery can be occluded) - over carotid w/ bell and makes swooshing sounds.

• - Indirect measure of RA pressure
• - Jugular veins reflect changes in filling pressures
• - No valves between jugular veins & right atrium
• - Increased right atrial pressure = increased JVD
• - External jugular vein (lies over SCM)
• - Internal jugular vein (IJV) - underneath & medial to SCM
• - More reliable than external jugular vein for measuring RA pressure (attached directly to SVC)
• - Can't see IJV (can only see waves or fluctuations)
• - Slightly rotate head to side (look for pulsations at the right base of the neck (caused by IJ moving SCM)

• Internal Jugular Veins
• - Pulsation visible but not palpable.
• - 2 undulating waves or fluctuations.

• Carotids
• - Palpable pulsation (one brisk pulsation wave)

Raise HOB 30 - 45 degrees & locate top of the internal jugular pulsation in the right neck

Less than 5 cm

Norms: 3-4 cm above sternal angle (measure with ruler)

- estimate of RA pressure

JVP = JVD + 5 cm (distance of right atrium from sternal angle)

• Norms: < 9 cm water
• More than 9 = more pressure on right side of the heart

Normal - when pressure is applied to liver border, jugular vein on right side of neck will distend for few seconds, then return to normal

Abnormal - jugular veins will remain elevated as long as pressure is applied to liver - suggestive of CHF

Positive HJR is sign of heart failure

• - Inspect
• - Palpate
• - Auscultate

• - Located at 4th or 5th ICS, left of MCL
• - Palpable in 1/2 of adults
• - Decreased w/ obesity & thick chest walls

- If shifted farther to the left, this may indicate cardiomegaly (enlarged heart)

• - Sign of myocardiohypertrophy (enlarged heart)
• - Sustained forceful thrusting of ventricle during systole
• - Visualized & palpated at the apex

• - Palpable vibrations
• - Purring cat
• - Associated with loud harsh murmurs
• - Palpate across precordium

• - Rate: norm 60-100
• - Rhythm: regular; regular - irregular; irregular)
• - Heart sounds: listen to each valve w/ the diaphragm & bell

• S1 (loudest at apex)
• - Corresponds w/ R wave on ECG
• - Diminished wounds (pericardial effusion, obesity, emphysema)

• S2 (loudest at base)
• - Aortic valve sounds are best heard w/ the patient sitting & leaning forward

Split Sounds

• Gallops (S3, S4)
• - Turn patient to left side, often more pronounced over apex by using bell

Rubs & clicks

• Murmurs
• - Listen over the valve sites & note any radiation across precordium

Point of maximum inspection