Section 1

Cardiovascular Assessment

Cardiovascular Assessment
Objectives 1. Outline a systematic approach to cardiovascular assessment. 2. Differentiate normal from abnormal findings when assessing the cardiovascular system. 3. Relate the events of the cardiac cycle to auscultatory findings.

History and Subjective Data

Past medical history 1. Previus illness (CAD, Antina, MI, CHF, Murmurs, HTN, CVA, PVD) 2. Diagnostic/Interventional cardiac procedures (Stress test, cardiac cath, Echo, PTCA, Stent) 3. Hospitalizations 4. Surgeries (CABG, Valve repair, Vascular surgeries) 5. Allergies (Medications, food, contrast agents)

Self Assessment
Chief complaint Common signs and symptoms of cardiovascular disease
Use systematic approach to avoid omission of important data Onset, location, duration, characteristics, associated S/S, relief, treatment

Chest Pain
Severity rated on a scale of 0 10 (10 being worst pain imaginable) Angina pectoris (caused by ischemia)
Often described as pressure rather than pain Usually brought on by stress Risk factors: sedentary lifestyle, smoker, diabetic, hyperlipidemia, family history

Angina
Stable does not increase in severity and promptly relieved with rest and/or NTG Unstable (USA) progressively increases in severity, duration and quality *Can be increased by physical or emotional stress

Is It Cardiac?
Cardiac
Substernal Radiates (jaw, back, left shoulder) Relieved by NTG

Non-Cardiac
Pleuritic and positional Reproducible Relieved by GI Cocktail Constant

Chest Pain
Myocardial Infarction (MI)
15% of people deny symptoms

Women experience fewer symptoms. Typically SOB, weakness and indigestion

Think MONA (morphine, O2, NTG, ASA) Top 5 symptoms #1 Angina #2 Arrhythmias #3 Dizziness #4 SOB #5 Radiating Pain

Risk Factors
Non-modifiable risk factors
Age Sex Family history Race

Risk Factors
Modifiable risk factors
Cigarette smoking (causes increased HR & BP = vasoconstriction, decreased blood flow to heart, increases blood clot formation) Hypertension Hyperlipidemia Physical inactivity Diabetes Stress Obesity

Social History
Alcohol intake (high consumption predisposes to cardiomyopathy, withdrawal increases metabolic need for O2 b/c of increased HR & BP) Dietary pattern (fast food, caffeine, salt) Educational level (there is an inverse relationship between educational level and risk)

Medication History
Prescribed drugs Beta blockers, calcium channel blockers, digoxin, antiarrhythmics, antihypertensives, anticoagulants Over the counter (OTC) Many interact with cardicac meds (cold and sinus, headache preparations, laxatives, sleeping pills, diet pills)
Investigate the use of a single pharmacy The average CHF patient is on 6 or more

Physical Exam: Inspection

General appearance:
Is pt in acute distress? Observe for common S/S of CV disease (SOB, fatigue, edema, etc) Assess emotional status (calm, anxious) Note posture (Tripod position = heart failure, leaning forward = pericarditis, pulmonary edema, pulmonary disease) Mentation decreased O2 to brain alters LOC and quality of mentation (use family to determine/identify baseline and subtle changes)

Pericarditis
May mimic MI; described as sharp, stabbing Aggravated by movement and is constant Relieved by sitting up, leaning forward, shallow breathing Signs: friction rub squeaky leather, infection, ST elevation in all leads Could lead to cardiac tamponade! Treatment includes: antibiotic therapy, repeat echos and pericardial window.

Dyspnea
Subjective sensation of being unable to breath Cardiac cause due to pulmonary edema from LV failure
Ischemia, rheumatic disease, hypertension, congenital disease, or heart valve dysfunction

Fatigue/Weakness
Symptom of decreased CO (LV failure) Unusual fatigue at the end of a normal day Exertional fatigue is a sense of weakness or heaviness in extremities Assess meds that may produce fatigue
Diuretics: orthostatic hypotension and hypokalemia Beta blockers, calcium channel blockers, digoxin, & antihypertensives Cause alterations in cardiac function and reduced SVR

Fluid Retention
Fluid accumulation in tissues Common cardiac causes:
1. Heart failure secondary to sodium/water retention by kidneys - Wt gain of 2 lbs in 4 days or 3 5 lbs in month Constrictive pericarditis (CO) 1. Restrictive cardiomyopathies prevents adequate preload filling of heart (it cant pump normally)

Syncope/Pre-syncope
Temporary loss of consciousness, lightheadedness, dizziness Cardiac cause most commonly result of inadequate CO secondary to arrhythmias
Aortic stenosis, hypertrophic obstructive cardiomyopathy, cardiac tamponade, acute MI, vasovagal attacks and orthostatic hypotension are other cardiac causes If on beta blockers typically will have to wait b/f PPM is placed, may require temp pacer.

Palpitations
abnormal awareness of the beating heart
Sudden changes in rate & rhythm that increases stroke volume (SV) Associated with cardiac pathologies:
Tachycardia, bradycardia, complete heart block, atrial fibrillation, PVCs, aortic and mitral valve regurgitation

Other causes:
Overexertion, ETOH, nicotine, caffeine, drugs, anemia, thyroid dysfunction

Diagnosis of problem may include holter monitor, blood work and Echocardiogram.

Gastrointestinal Symptoms
Nausea, anorexia, vomiting that may be a result of RV failure, digitalis toxicity, inferior MI Indigestion or flu-like symptoms may be sole S/S of angina or MI, especially in elderly or diabetic patients

Decreased Urine Output and Nocturia

Decreased U/O is indicative of heart failure and hypovolemia Watch for weight gain if due to CHF Nocturia is a sign of heart failure Caused by increased preload to heart when pt is flat that improved CO and renal perfusion

Color
Cyanosis blue tint that occurs when at least 5 gm of hemoglobin not saturated
Presence of cyanosis depends on absolute amount of unoxygenated hemoglobin, not ratio of unoxygenated to oxygenated Almost impossible for an anemic pt to show cyanosis Easy for polycythemic pt to appear cyanotic when normal saturation is present

Central Cyanosis
Seen in buccal mucosa, conjunctiva Almost always indicated cardiopulmonary disease Related to decrease SaO2 usually <80% (congenital heart disease, PEW, decreased CO)

Peripheral Cyanosis
Indicates reduced blood flow to extremity Seen on tip of nose, ears, distal extremities Indicates exposure to cold, anxiety, decreased CO as in latent heart failure or shock

Jaundice/Pallor
Jaundice
Best seen in sclera, using natural light Seen in late heart failure caused by hepatic impairment.

Pallor
Indicates anemia or increased SVR Inspect palm of both hands (Palms become pale as hemoglobin decreases, but when severely anemic, only the creases become pale)

Jugular Vein Distention (JVD)

Reflects right heart function Estimates CVP or RA pressure Determined by measuring height of jugular vein
JVD > 10 cm indicates RV failure, tricuspid or pulmonic stenosis, cardiac tamponade, increased intrathoracic pressure, superior vena caval obstruction Decreased or flat neck veins in supine position indicate hypovolemia or dehydration

Check Circulation
Pulses
Location Strength
Present and equal bilaterally?

Capillary refill
<3 seconds
Is the pt dusky? Are they mottled? Is there any cyanosis?

Assessment of Extremities
Arterial insufficienty
Four Ps of blocked arteries
Pulseless, Pallor, Pain, Paralysis Acute changes in the 4 Ps are extremely important to note in patients undergoing femoral artery procedures (heart catheterization, IABP placement, history of PVD)

Assessment of Extremities
Color
Dusky when dependent Pale when elevated

Temperature/Moisture
Cool, moist skin results from increased catecholamines (sympathetic response) Indicate peripheral vasoconstriciton from stress or decreased CO (AMI, shock)

Arterial Pulses
Rate and Rhythm
If regular, count for 15 secs and multiply by 4 If irregular, count for an entire minute Rapid pulse suggests increased catecholamine levels (anxiety, exercise, heart failure, MI, arrhythmias) Slow pulse results from excessive vagal tone, athletic training, inferior MI, SA node disease Pulse deficit: occurs when apical rate exceeds radial rate (Premature beats & atrial fibrillation)

Pulse Examination
Radial, dorsalis pedis (DP), posterior tibial (PT) and carotid Pulse rating scale
0 Absent 1 Feeble, difficult to palpate, obliterated with pressure, fades in and out 2 Faint, easily obliterated 3 Normal, easily palpated, not easily obliterated 4 Bounding, strong, hyperactive, not obliterated D Doppler only

Extremity Pain
Intermittent claudication (pain with walking) indicates PVD due to decreased blood flow to muscles during time of increased demand. Ischemia from PVD is appreciated as pain or aching, especially in legs Associated with activity and relieved with rest

Arterial Insufficiency
Skin changes
Taut, scaly, atrophied Ulcerations common above lateral malleolus pale base, extremely painful Loss of hair especially feet and lower leg Nails
Deep transverse ridges in nails, thickened, clubbed nails may be seen chronic hypoxia.

Clubbing of Nails
Nail & nail base exceeds 180
Related to hypoxia Usually lung dx

Arterial Insufficiency
Delayed capillary refill
Provides estimate of peripheral blood flow Normal 2 seconds > 2 seconds indicates: decreased CO, decreased volume, and/or decreased SV

Diminished sensory/motor function

Inability to use limb Inability to feel/touch such as with diabetic neuropathy

S/S of Arterial Insufficiency

Color
Anemia will alter Dusky (rubor) when Pale when
4 Ps Pulseless Pallor Pain Paralysis

Pulses Temperature/Moisture
Cool, moist catecholamines (SNS response)

Skin changes
Taut, shinny, edema

Delayed cap refill Nails

Ridges, thickened, clubbed

Chronic Arterial Insufficiency

Pain Intermittent claudication, to pain @ rest Pulses - or absent Temp - cool Edema absent or mild, may develop if extremity

lowered Skin - s thin, shiny, atrophic, loss of hair, nails thickened & ridged Ulcer - usually toes, or points of truma

Gangrene - may develop

Treatments/Management
Keep extremity warm (rooke boot) Pain control Possible TPA infusion if clot present
Check PTT/Fibrinogen q6 hrs Monitor site for bleeding q1 hr pulse checks Typically on set dose of heparin

Venous Insufficiency
Pulses: normal Color: normal, cyanotic on dependency Edema: present Skin changes: brown pigmentation around ankles Ulcers found at side of ankle Should wear TED hose Muscles squeeze the veins to move blood back to the heart but sitting for long periods causes blood to pool leading to a DVT.

Chronic Venous Insufficiency

Pain none or aching on dependency Pulses WNL, difficult to find (edema) Color WNL, cyanotic with dependency, petechiae,
brown pigmentation

Temp WNL Edema present, marked Skin brown, stasis dermatitis, thickening of skin &
narrowing of leg as scarring develops

Thrombophlebitis
Due to vein inflammation related to a clot Inspect for pain, swelling, erythema Palpate for heat Calf enlargement Homans sign
Calf pain upon forceful dorsiflexion of foot

Palpation
Edema usually not detectable until interstitial fluid volume is 30% above normal Bilateral edema
Progression ascends to involve ankles, legs, thighs, genitals, and abdomen Indicative of heart failure or bilateral chronic venous insufficiency

Assess for Edema

Location
Extremities (i.e. arms, hands, thighs, shins, feet) Facial (orbital, sclera) Sacrum Generalized

Severity
24+ Weeping

Edema
Anasarca extreme edema
Generalized edema Seen in severe heart failure, hepatic cirrhosis, and nephrotic syndrome

Unilateral edema indicates venous thrombosis and lymphatic blockage of that extremity

Edema Scale
Evaluated by pressing thumb for 5 seconds 0 = absent +1 = slight indentation, disappears rapidly +2 = indentation readily noticeable; disappears within 10-15 seconds +3 = deep indentation; disappears in 1-2 minutes +4 = marked, deep indentation; may be visible > 5 minutes

Skin Turgor
Assessed by lifting fold of skin between thumb and forefinger and releasing it. Decreased turgor is caused by dehydration
Skin fold returns slowly to original position Might be normal in an elderly patient Hypovolemia due to diuretic therapy Look for associated decreased BP and increased HR

Auscultation of BP
Overall reflection of LV function
Systolic = force of ventricular contraction Diastolic = vascular resistance (afterload) Pulse pressure is difference between Systolic & Diastolic
Reflects SV, SVR, vessel distensibility Increased pulse pressure occurs with bradycardias, anxiety, exercise, fever, aortic regurgitation, atherosclerosis Decreased pulse pressure occurs with heart failure, shock, hypovolemia, vasoconstrictive drugs

Orthostatic Hypotension
Position change from lying to sitting or sitting to standing causes > 10 mmHg drop in diastolic Indicates hypovolemia or disturbed vasopressor reflexes Caused by prolonged bed rest or medications Assessed on patients experiencing dizziness, bleeding, hypovolemia, vasodilators

Examination of Chest
Best sites for inspection, palpation and auscultation 1. Aortic area: 2nd ICS, right sternal border (RSB) 2. Pulmonic area: 2nd ICS, LSB 3. Tricuspid area: 5th ICS, LSB 4. Mitral or Apical area: 5th ICA, mid clavicular line 5. Erbs point: 3rd ICS, LSB where selected abnormalities in aortic and pulmonic detected. 6. Epigastric: over xyphoid process where selected aortic and right ventricular pulsations may be detected.

Palpation of Chest
Apical pulse (Point of Maximal Impulse)
Most lateral, inferior point where cardiac impulse can be seen or felt Indicator of heart size and activity Should feel like a short tap If prolonged it could indicate LV hypertrophy

Palpation of Chest
Thrill
Abnormal turbulent blood flow Associated with severe mitral regurgitation, ruptured ventricular septum

Right ventricular heave (lift)

Diffuse, lifting impulse seen/felt along LSB or RSB Caused by pulmonary hypertension, acute RV failure, atrial septal defect, valvular diseases

Heart Sounds
Where do I listen? Lub Dub Are there any extra sounds? Do they sound distant? Does the patient have a murmur, click, or rub? What does it mean?

Auscultation
Normal first and second heart sounds: S1 & S2 Sounds of valves closing S1
Lub Heard loudest at mitral and tricuspid areas (5th ICS) Closure of mitral and tricuspid valves Usually lower-pitched and longer than S2

Ausculation
S2
Dub Closure of aortic valve and pulmonic valves Best heard in aortic and pulmonic areas (2nd ICS) Usually higher-pitched and shorter than S1

Auscultation
S3 (Ventricular gallop)
Heard in early systole, just after S2 Lub-dub-ta Occurs as blood rapidly flows into a ventricle that is not completely emptied Heard best in mitral area if produced by left side of heart and sternal border if produced by right heart.

Auscultation
S4 (Atrial Gallop)
Heard in late diastole, just before S1 ta-lub-DUB Results from increased ventricular resistance to atrial filling (due to decreased ventricular compliance) or increased ventricular volume Seen in: ventricular hypertrophy, ischemic heart disease, MI, hypertension, mitral regurgitation

Auscultation
Murmurs produced by increased or turbulent blood flow
Often implies significant disease of heart valves, great vessels, or septal defects

Pericardial Friction Rub

Caused by inflammation of pericardium Associated with fever, sharp CP, elevated WBC Rough, scratching, squeaking sound

Cardiovascular Assessment: Rhythm and Vital Signs

What is the rhythm? Watch PR and QRS intervals Are there any ST changes? What are the Vital Signs Heart rate, Blood pressure, Respiratory rate, O2 Saturation, Temperature

Reading your Rhythm

Had a pic of the PQRSTU indicating each segment/interval And a pic of the big/small boxes on the paper indicating time and voltage

How Do I Read This Strip?

The P wave represents atrial activation PR interval is the time from onset of atrial activation to onset of ventricular activation
Normal is .12 - .20

QRS complex = ventricular activation QRS interval is the duration of ventricular activation
Normal is 0.06

How Do I Read This Strip?

ST-T wave represents ventricular repolarization The QT interval is the duration of ventricular activation and recovery U wave represents after depolarization in the ventricles

What to document
Is there a P wave? Length of PR interval Length of QRS interval Rate Rhythm Signature

What if its abnormal?

Something is causing a change in the conduction process
Damage or ischemia Electrolyte imbalances Valvular disease or backflow Fluid overload Overdose on cardiac medications

SIGNS OF ISCHEMIA
T Wave Changes: symmetrical, tall peaked or inverted = ischemia ST Segment: depression or elevation may be seen in acute injury

Do they have a Pacemaker?

Is it a temporary or permanent pacer? What is the patients underlying rhythm? Is it working couldnt see thru pic What are the s. Couldnt see thru pic.

Pacing
Electrode is looped or sutured to the myocardium Lead is attached to pacemaker generator Generator senses and sends electrical stimulus as needed to initiate depolarization of myocardium

Temporary Pacemakers
Temporary pacemakers are placed for a short period of time Used in patients with heart blocks, bradycardia, and AMI Placed at bedside or in the Cath Lab Threaded through a central venous catheter called a cordis

Care of a Temporary Pacer

Ensure leads are plugged into generator Verify pacer is sensing and capturing appropriately Unplug leads once per shift to check underlying rhythm (Notify MT before doing this!) If patient needs pacer as a back-up set at a low rate to pace only when necessary

Nursing Precautions
Insulate unused epicardial pacemaker wires Continuous EKG monitoring Consider immobilizing extremity of insertion site

Nursing Responsibilities
Assess, monitor, & record cardiac rhythm Monitor & document pacemaker settings Monitor & care for insertion sites Patient education

Possible Complications
Pacemaker malfunction Pneumothorax, hemothorax Lead perforation Air embolus Arrhythmias Infection Endocarditis Venous thrombosis

Permanent Pacemakers (PPM)

Placed in the cath lab using sterile technique Placed in patients chest in Subclavian vein Looks like a box under patients skin Different types of pacemakers and different modes PPM Paces patient when needed AICD Automatic Internal Coronary Defibrillator Some patients have a PPM with AICD

Care of Permanent Pacemakers

PPM nneds dressing changes every 24 hours (dont remove steri-strips) Pt will wear arm sling on affected side for 1-2 days to avoid pulling on incision site Watch that pacemaker is sensing and capturing Call physician if there is a problem with PPM If defibrillator is shocking patient at inappropriate times, place magnet on pacer

Failure to Pace
Pacemaker doesnt fire when HR goes below set rate Watch for:
Bradycardia Hypotension Cardiac arrest

Absent pacer spikes on rhythm strip

Failure to Capture
Watch for
Bradycardia Hypotension Cardiac arrest

Pacer spikes that are not followed by a P, QRS, T complex

Failure to Sense
Fires when it shouldnt or too close to QRS Can stimulate a lethal arrhythmia Under sensing pacer spikes anywhere on the P, QRS, T Over sensing pacer senses extraneous electrical signal & fires inappropriately

Group Questions
1. List differences between cardiac and noncardiac symptoms. 2. What is usually the cause of dyspnea related to cardiac problems? 3. The most common cause of cardiac syncope is ____________.

Group Questions
4. List the 4 Ps of acute arterial obstruction. 5. S2 is best heard where? 6. Fluid retention is best assessed with what intervention? 7. List 4 modifiable risk factors for CV disease.

End of Section 1

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