Cardiovascular

Assessment &
Common Cardiac
Disorders
HEART
• Pericardium
• Cardiac Muscle
• Chambers and Valves
• Cardiac Blood Vessels
• Conduction System
 SYSTOLE

S1 S2
MITRAL, TRICUSPID AORTIC, PULMONIC
VALVES CLOSE VALVES CLOSE

DIASTOLE
LANDMARKS OF CARDIAC ASSESSMENT
• Sternum
• Clavicles
• Ribs
• Second through fifth
intercostal spaces
FOCUSED INTERVIEW
SPECIFIC QUESTIONS

 Illness  Age
 Symptoms  Gender
 Behaviors  Language
 Infants and Children  Culture (Privacy)
 Pregnant Female
 Older Adult
 Environment
PHYSICAL ASSESSMENT OF THE
CARDIOVASCULAR SYSTEM
TECHNIQUES
 Inspection
 Palpation
 Percussion
 Auscultation
SPECIFIC AREAS OF THE CARDIOVASCULAR
ASSESSMENT

 Inspection of the face and lips

 Inspection of the jugular veins
 Inspection of the carotid arteries
 Inspection of the hands and fingers
 Inspection of the chest, abdomen, legs and
skeletal structure
JUGULAR VENOUS PRESSURE (JVP) AND
PULSATIONS
 Recall that jugular veins reflect right atrial pressure
 Steps for examination
 Raise the head of the bed or examining table to 30
 Turn the patient’s head directly to the left
 Identify the topmost point of the flickering venous pulsations
 Place a centimeter ruler upright on the sternal angle
 Place a card or tongue blade horizontally from the top of the
JVP to the ruler, making a right angle
 Measure the distance above the sternal angle in centimeters: a
3- to 4- centimeter elevation is normal
SPLINTER HEMORRHAGE
PALPATING THE CAROTID
ARTERY
ASSESSING THE CAROTID PULSE

 Keep the patient’s head elevated to 30

 Place your index and middle fingers on the right then
the left carotid arteries, and palpate the carotid
upstroke
 Never palpate right and left carotid arteries
simultaneously
 Listen with the stethoscope for any bruits
PERCUSSING THE
CHEST
SPECIFIC AREAS OF THE CARDIOVASCULAR
ASSESSMENT
Auscultation of the chest using the diaphragm and bell in
various positions to include the following locations
• Aortic area at the right second intercostal space – S2 is
louder than S1
• Pulmonic area are the left second and intercostal space – S 2
is louder than S1
• Erb’s point at the left third intercostal space – S2 and S1 are
heard equally
SPECIFIC AREAS OF THE CARDIOVASCULAR
ASSESSMENT

Auscultation of the chest using the diaphragm and bell in

various positions to include the following locations
 Tricuspid area at the left fourth intercostal space-S1 is
louder than S2
 Apex at the left fifth intercostal space at the midclavicular
line-S1 is louder than S2
  Listen in all 5 listening areas for S1 and S2 using the
diaphragm of the stethoscope
 Then listen at the apex with the bell
 The diaphragm is best for detecting high-pitched sounds like
S1, S2, and also S4 and most murmurs
 The bell is best for detecting low-pitched sounds like S3 and
the rumble of mitral stenosis

Erb's point is the auscultation location for heart sounds and

heart murmurs located at the third intercostal space and the
left lower sternal border.
ABNORMAL FINDINGS IN THE
CARDIOVASCULAR SYSTEM

 Myocardial and pump

disorders
 Valvular disease
 Septal defects
 Congenital heart disease
 Electrical Rhythm
Disturbances
MYOCARDIAL AND PUMP DISORDERS

 Myocardial ischemia
 Myocardial infarction
 Congestive heart disease
 Ventricular hypertrophy
Myocardial
infarction
MYOCARDIAL INFARCTION
 Also known as "heart attack"
 Newest term: Acute Coronary Syndrome
 Leading cause of death in many countries
 Reduced blood flow through one of the coronaries results in
myocardial ischemia and necrosis
 Usually affects the LV - "workhorse" of the heart
 Good collateral circulation limits the size of an MI
MYOCARDIAL INFARCTION

 Death usually results from cardiac damage or complications

 Mortality is high when treatment is delayed
 Almost half of sudden deaths from MI occur before
hospitalization, within 1hr of the onset of symptoms
 Prognosis improves if vigorous tx begins immediately - early
recognition and aggressive treatment is vital
 Modifiable
 Non Modifiable
SIGNS AND SYMPTOMS
-Typical distribution of referred pain
Persistent, crushing/heavy/squeezing substernal
chest pain that may radiate to the L arm, jaw, neck,
or shoulder blades caused by reduced 02 supply to
the myocardial cells

Important!
Many older adults don't have CP but experience atypical
symptoms e.g. fatigue, dyspnea, falls, tingling of extremities,
nausea, vomiting, weakness, syncope and confusion
Cool extremities, perspiration, anxiety, and restlessness Fatigue and weakness
*due to catecholamine release *Reduced perfusion to skeletal muscles
BP and HR initially elevated Nausea and vomiting
* due to SNS activation *Reflex stimulation of vomiting centers by pain fibers or
Bradycardia from vasovagal reflexes
* due to conduction disturbance esp. if with damage to inferior wall OSOB and crackles
of the LV *Reflects heart failure
Reduced urine output Low-grade fever days after AMI
*Due to ⇓ renal perfusion and aldosterone and ADH *Due to inflammatory response
EFFECTS

 Scar tissue (necrotic area) inhibits contractility

(+) vasoconstriction, HR, Na and H2O retention to maintain C.O.

 Ventricular dilation may occur - through a process called remodeling

 Functionally, MI may cause reduced contractility with abnormal wall

motion, altered LV compliance, ⇓ stroke volume, ⇓ EF, and 1 LVEDP
DIAGNOSIS
 Serial 12-Lead ECG
Identifies location and extent of MI

 Serial cardiac enzymes - serum cardiac markers

myoglobin, CK-MB
Troponin I and Troponin T

 Labs
CBC - elevated white cell count
Increased ESR - inflammation
Increased glucose - release of catecholamines
DIAGNOSIS
 Echocardiography
May show ventricular wall motion abnormalities
May detect septal or papillary muscle rupture

 Nuclear Imaging
To detect areas of infarction as well as viable muscle cells

 Coronary angiography
To identify the involved coronaries as well as provide info on
ventricular function, pressures and volumes within the heart.
IMMEDIATE GOALS OF TX

 Relieve chest pain

 Reduce the extent of myocardial damage

 Maintain cardiovascular stability

 Decrease cardiac workload

 Rapid defibrillation when fibrillation is

present
TREATMENT
Heparin Thrombolytic therapy
To increase the chances of patency in the Most effective within the first 3 hrs after onset
affected coronary of symptoms
Coronary angioplasty
(PTCA/PCI) M = Morphine or Meperidine
Because pain stimulates SNS
Limitation of physical activity O = Oxygen
for the first 12hrs N = Nitrates
Do not give for BP <90mmHg
Early IV beta adrenergic blockers with an systolic/HR<50/HR>100
evolving MI, followed by oral therapy A = Aspirin
Reduces myocardial 02 requirements Daily. To inhibit platelet aggregation.
NURSING CARE

 Establish an IV line.
 VS/Hemodynamic/Cardiac monitoring!!!
 NPO except sips of water until stable.
 Diet: Low salt, low fat
 CBR. Bedside commode and light activity
once stable.
 Oxygen: 2-3LPM via nasal cannula until
stable
 Stool softener as prescribed.
CARDIAC TAMPONADE

 A rapid, unchecked increase in pressure in the

pericardial sac that compresses the heart, impairs
diastolic filling, and reduces C.O.
 Usually results from blood or fluid accumulating in the
pericardial sac
 Rapid collection of fluid in the pericardial sac interferes
with ventricular filling and pumping, critically reducing
C.O.

Considered a medical emergency - Therefore, must be

aggressively treated to preserve life.
CAUSES
 Idiopathic
 Effusion - from CA, bacterial infections, TB, Rh fever
 Hemorrhage - from traumatic causes
 Hemorrhage - from non-traumatic causes e.g.
anticoagulant therapy
 Viral or post irradiation pericarditis
 CRF requiring dialysis
 Drug reaction
 Connective tissue disorders
 AMI
PROGNOSIS

Depends on the rate of fluid accumulation

 Rapid - requires emergency lifesaving measures

Even a small amount of fluid (50-100ml) can cause serious
tamponade if it occurs rapidly
 Slow - may not produce immediate symptoms because the
fibrous wall of the pericardial sac can gradually stretch to
accommodate as much as 1L to 2L of fluid
LAYERS OF THE HEART

 Endocardium
 Myocardium
 Pericardium - outermost layer
 Visceral pericardium
 Parietal pericardium
 Pericardial fluid
30-50ml separates the layers
PATHOPHYSIOLOGY
 Progressive accumulation of fluid in
the pericardial sac causes
compression of the heart chambers
 Compression obstructs blood flow
into the ventricles and reduces the
amount of blood that can be
pumped out of the heart with each
contraction
 Each time the heart contracts, more
fluid accumulates in the pericardial
sac further limiting the amount of
blood that can fill the ventricles
during the next cardiac cycle
SIGNS AND SYMPTOMS
• Elevated CVP with JVD • Anxiety, restlessness, and syncope
Caused by JVP Caused by a drop in C.O.

• Muffled heart sounds • Cyanosis

Caused by fluid in the peric. Sac Caused by reduced oxygenation of the tissues

• Diaphoresis and cool, clammy skin • Weak, rapid pulse

Caused by C.O. In response to a drop in C.O.

• Pulsus paradoxus - caused by impaired diastolic filling
Classic manifestation of cardiac tamponade
An inspiratory decrease in systemic BP greater than
15mmHg
• Cough, dyspnea, orthopnea, and
tachypnea
Caused by lung compression by an
expanding pericardial sac and the inability to
move blood from the pulmonary vasculature
into the compromised LV
DIAGNOSIS
CXR
Shows a slightly widened mediastinum and
possible cardiomegaly

ECG
May show a low-amplitude QRS complex and
electrical alternans (an alternating beat-to- beat
change in amplitude of the PQRST). Generalized
ST segment elevation is noted in all leads.

PA catheterization
Detects ↑ RAP, RVDP, and CVP

Echocardiography
May reveal pericardial effusion with signs of RV
and RA compression
SAMPLE CXR
NURSING CARE

1. Collaborative management
2. Report significant changes or trends in hemodynamic parameters and
dysrhythmias. Stay alert!
3. Maintain at least 1 patent IV access site.
4. Prepare for emergency pericardiocentesis and/or surgery as necessary
5. Later on, have a 'progressive activity' plan.
6. Support client towards independence.
TREATMENT
NSAIDS
to help reduce fever, inflammation, and pericardial
pain

Pericardial window
(surgical creation of an opening)
to remove accumulated fluid in the pericardial sac

Pericardiocentesis
(needle aspiration of peric. cavity)
to reduce fluid in the pericardial sac and improve
systemic arterial pressure and C.O.
ga
TREATMENT
Pericardiectomy (surgical resection of a portion, or all)
to allow full communication with the pleura, if repeated pericardiocentesis fails to
prevent recurrence

Blood transfusion

Thoracotomy
to drain re-accumulating fluid or to repair bleeding sites - may be necessary in cases
of traumatic injury

Administration of heparin antagonist (protamine)

to stop bleeding in heparin-induced tamponade

Use of Vit. K - in warfarin-induced tamponade

HEART FAILURE

 A syndrome rather than a disease

 Occurs when the heart can't pump enough
blood to meet the body's metabolic needs
 Results in intravascular and interstitial
volume overload + poor tissue perfusion
 Most common cause is CAD
 Also occurs in infants, children and adults
with congenital and acquired heart defects
INCIDENCE

 Rises with age

 1% of age >50 y/o experience heart
failure, majority are over 60 y/o
 10% of age >80 y/o have heart failure
 Nearly 50% die within 5 years post
diagnosis
 Mortality is greater for males, blacks,
and the elderly
PROGNOSIS

▪ Advances in diagnostic and therapeutic techniques have greatly

improved the outlook for patients Prognosis still depends on the
underlying cause and its response to treatment

Effects
• Reduced exercise tolerance
• Reduced quality of life
• Shortened life span
CAUSES

Pump Failure
• Cardiomyopathy, MI
• Valvular Stenosis
• COPD
• HPN
• Pericarditis
• AF
TWO TYPES
ASSESSMENT - LSHF

Early Manifestations of LSHF

• Dyspnea, orthopnea, PND
• Non-productive cough
• Fatigue

Later Manifestations of LSHF

• Crackles
• Hemoptysis
• Displaced PMI
 Tachycardia
 S3, S4
 Cool, pale skin
 Cyanosis
 Restlessness and confusion
ASSESSMENT - RSHF

Clinical Manifestations of RSHF

 Elevated JVD
 (+) hepatojugular reflux
 Hepatomegaly
 RUQ pain
 Anorexia, fullness, nausea
 Nocturia
 Wt. gain
 Edema
 Ascites, anasarca
TREATMENT & CARE
I. LSHF
ACE inhibitors (Captopril, Enalapril)
• Reduces preload and afterload
Digoxin
• Increases myocardial contractility
• Improves C.O.
• Reduces volume in LV
• Decreases ventricular stretch
Diuretics (furosemide, spironolactone,
etc.)
• Reduce fluid volume overload
• Reduce venous return
• Reduce preload
Beta-adrenergic Blockers (propranolol,
etc.)

Oxygen
TREATMENT & CARE

II. RSHF

• Diuretics (reduces preload)

• Nitrates (vasodilation, reduces preload)
• Morphine (calming effect, vasodilation)
• Oxygen
• I. ACUTE
• Pulmonary Edema
• Acute Renal Failure
• Arrhythmias

• II. CHRONIC
• Activity intolerance
• Renal Impairment
• Cardiac cachexia
• Metabolic impairment
• Thromboembolism
PATIENT TEACHING
• Avoid foods high in sodium to curb fluid
overload.
• Instruct pt how to replace K+ lost through
diuresis.
• Encourage pt to weigh self daily and maintain a
record.
Advise to report a wt gain or wt loss of 1kg or more in 3-4 days.
• Stress the importance of taking medications as
prescribed.
Watch for and immediately report signs of toxicity e.g. anorexia, vomiting,
confusion, slow or irregular HR and, in elderly, flu-like symptoms.
• Tell pt to check his own pulse and report if
<60/min.
• esp. for those taking Digitalis