RESPONSES TO ALTERD TISSUE PERFUSION
STRUCTURE OF THE HEART
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Endocardium (inner lining of heart chambers
and valves).
Myocardium (thickest part of the heart; consists
of cardiac muscle).
Epicardium (inner layer of a double walled sac
called the pericardium that surrounds the
heart).
Pericardium (protective covering
hollow muscular organ containing four
chambers:
Atria (upper chambers).
Ventricles (lower chambers/main pumping
forces).
Right atrium: receives deoxygenated blood from
systemic circulation via the vena cava
Right ventricle: pumps deoxygenated blood to
the pulmonary circulation via the pulmonary
artery
Left atrium: receives oxygenated blood from the
pulmonary circulation via the pulmonary vein
Left ventricle: pumps oxygenated blood to the
systemic circulation via the aorta
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Right side of heart—workload is light compared
to left side; pulmonary circulation
 Left side of heart—high pressure system,
systemic circulation
 FOURVALVES
 Apical pulse or mitral valve/bicuspid: located at
fifth intercostal space near left midclavicular
line
 Aortic valve: located at second intercostal space
on right of sternum
 Pulmonic valve: located at second intercostal
space on left of sternum
 Tricuspid valve: located at fifth intercostal space
on left of sternum
Heart sounds
 S1 (first sound “lub”) caused by closure of
mitral and tricuspid valves
 S2 (second sound “dub) caused by the
closure of aortic and pulmonic valves
 Splitting of S1 and S2 can be accentuated by
inspiration
 Gallops=S3 and S4
 S3 is ventricular gallop—normal in children.
In those over 35, indicates early heart
failure, VSD or decreased ventricular
compliance
 S4 is an atrial gallop—seen in hypertension,
anemia, aortic or pulmonic stenosis and
pulmonary emboli
Circulation of Blood
 Blood enters the heart through veins
and leaves the heart through arteries.
 Blood is distributed throughout the
body and returns to the right atrium of
the heart through the inferior and
superior vena cava.
Coronary Arteries
 Supply nutrients and oxygen to the
muscle tissue of the heart.
 The two coronary arteries are the right
coronary artery and the left coronary
artery, which branch off the aorta.
Conduction System
 consists of the sinoatrial node,
atrioventricular node, bundle of His, bundle
branches and Purkinje fibers
Arterioles and Arteries
 Arteries are thick-walled tubes that
vasoconstrict (decrease in diameter) or
vasodilate (increase in diameter).
 The arteries divide and branch into smaller
vessels called arterioles, or smaller arteries
Capillaries
 Very thin vessels that connect the smallest
arterioles with the smallest venules.
Venules and Veins
 Venules are small vessels that emerge from the
capillaries and gradually increase in size.
 As venules increase in size, they eventually form
veins.
UNIQUE CHARACTERISTICS
 Automaticity—intercalated discs
 Conductivity
 Contractility
 Excitability
CARDIAC OUTPUT
 Cardiac output (CO) (CO = heart rate × stroke
volume): volume of blood pumped per minute
by the ventricles; average for adult at rest is
approximately 5 L/min
SV CAN BE AFFECTED BY
 Preload
 afterload
 contractility
 heart rate
REGULATION OF CARDIAC OUTPUT
 STARLING’S LAW OF THE HEART- THE
HEART PUMPS IN PROPORTION TO
PERIPHERAL DEMAND
 AUTOREGULATION- VOLUME OF BLOOD
RETURNING TO THE HEART AND
SUBSEQUENTLY PUMPED BY THE HEART IS
DETERMINED BY THE TISSUES
 VENOUS RETURN- SUM OF ALL VOLUMES
OF BLOOD FLOWING THROUGH ALL
CAPILLARY BEDS OF THE BODY
 NERVOUS AND HORMONAL INFLUENCES
 NEURAL INFLUENCE ON VEINS
Regulatory Mechanisms Affecting Circulation
A. Autonomic nervous system
 Sympathetic nervous system: increases
heart rate and cardiac contractility,
dilates coronary and skeletal blood
vessels, and constricts blood vessels
supplying abdominal organs and skin
through stimulation of alpha- and betaadrenergic receptors by catecholamines
(epinephrine,
norepinephrine,
dopamine)
 Parasympathetic nervous system:
decreases heart rate and contractility,
and causes vasodilation through
cholinergic fibers; stimulation of vagus
nerve
initiates
parasympathetic
response
 Baroreceptors in the aortic arch and
carotid sinus respond to changes in BP
a. Increased arterial BP baroreceptors,
which
causes
parasympathetic
responses (vasodilation and decreased
heart rate and contractility)
b. Decreased arterial pressure inhibits
baroreceptors, which results in
increased
sympathetic
responses
(vasoconstriction and increased heart
rate and contractility)
 Chemoreceptors respond to changes in
levels of oxygen, carbon dioxide, and
blood pH by stimulating the autonomic
nervous system
B. Renin-angiotensin-aldosterone
mechanism:
when renal perfusion decreases, there is
retention of sodium and water, which increases
blood volume; vasoconstriction occurs, which
increases BP
C. Intrinsic circulatory regulation: increased BP
raises hydrostatic pressure of plasma, leading to
increased filtration of plasma from intravascular
to interstitial spaces, resulting in reduced
venous return, decreased cardiac output, and
decreased BP
History and Interview
Types of Dyspnea
 Exertional (when client participates in activity
and becomes short of breath).
 Orthopnea (difficulty breathing when lying
down).
 Paroxysmal nocturnal dyspnea (person
suddenly awakes, is sweating, and is having
difficulty breathing).
Homan’s sign
 Indicator of deep vein thrombosis (DVT).
 nurse dorsiflexes the client’s foot. If there is pain
in the calf or the leg or behind the knee, the
Homan’s sign is positive and may indicate the
presence of a venous clot
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Echocardiograms
EKG, ECG—Electrocardiogram
Cardiac Catheterization (CC
Hemodynamic Monitoring with Pulmonary
Artery Catheter
CORONARY ARTERIAL DISEASE/ISCHEMIC HEART
DISEASE
 the focal narrowing of the large and mediumsized coronary arteries due to deposition of
atheromatous plaque in the vessel wall
Stages of Development of Coronary Artery Disease
1. Myocardial Injury: Atherosclerosis
2. Myocardial Ischemia: Angina Pectoris
3. Myocardial Necrosis: Myocardial Infarction
ATHEROSCLEROSIS
PRESDISPOSING FACTORS
 Sex: male, Race black, Smoking, Obesity
Hyperlipidemia, Sedentary lifestyle, Diabetes
Mellitus, Hypothyroidism, Diet: increased
saturated fats & Type A personality
 SIGNS AND SYMPTOMS
1. Chest pain
2. Dyspnea
3. Tachycardia
4. Palpitations
5. Diaphoresis
TREATMENT
 Percutaneous Transluminal Coronary Angioplasty
and Intravascular Stenting
- Mechanical dilation of the coronary vessel
wall by compresing the atheromatous plaque.
 Objectives of CABG
- Revascularize myocardium
- To prevent angina
- Increase survival rate
- Done to single occluded vessels
- If there is 2 or more occluded blood vessels CABG is
done
Nursing Management:
 Nitroglycerine is the drug of choice for relief of
pain from acute ischemic attacks
- Instruct to avoid over fatigue
- Plan regular activity program
 Wear support stocking 4-6 week postop
- Apply pressure dressing or sand bag on the
site
- Keep leg elevated when sitting
 3 Complications of CABG
- Pneumonia: encourage to perform deep
breathing, coughing exercise and use of
incentive spirometer
- Shock
- Thrombophlebitis
ANGINA PECTORIS
 Transient paroxysmal chest pain produced by
insufficient blood flow to the myocardium
resulting to myocardial ischemia
Types of Angina Pectoris
 Stable Angina: pain less than 15 minutes,
recurrence is less frequent.
 Unstable Angina : pain is more than 15 mins.,but
not less than 30 minutes, recurrence is more
frequent and the intensity of pain increases.
 Variant Angina ( Prinzmetal’s Angina ): Chest
pain is on longer duration and may occur at
rest. Result from coronary vasospasm.
 Angina Decubitus: paroxysmal chest pain that
occur when the client sits or stand.
PRESDISPOSING FACTORS
 Sex: male, Race: black , Smoking, Obesity,
Hyperlipidemia, Sedentary lifestyle ,
Diabetes Mellitus, Hypertension, CAD:
Atherosclerosis,
Thromboangiitis
Obliterans,
Severe Anemia, Aortic
Insufficiency: heart valve that fails to open
& close efficiently, Hypothyroidism, Diet:
increased saturated fats, Type A personality
PRESIPITATING FACTORS
4 E’s of Angina Pectoris
 Excessive physical exertion: heavy exercises,
sexual activity
 Exposure
to
cold
environment:
vasoconstriction
 Extreme emotional response: fear, anxiety,
excitement, strong emotions
 Excessive intake of foods or heavy meal
SIGNS AND SYMPTOMS
 Levine’s Sign: initial sign that shows the hand
clutching the chest
 Chest pain: characterized by sharp stabbing pain
located at sub sterna usually radiates from
neck, back, arms, shoulder and jaw muscles
usually
 Dyspnea
 Tachycardia
 Palpitation
 Diaphoresis
DIAGNOSTIC PROCEDURE
 History taking and physical exam
 ECG: may reveals ST segment depression &
T wave inversion during chest pain
 Stress test / treadmill test: reveal abnormal
ECG during exercise
 Increase serum lipid levels
 Serum cholesterol & uric acid is increased
MEDICAL MANAGEMENT
 Drug Therapy: if cholesterol is elevated
- Nitrates: Nitroglycerine (NTG)/ Betaadrenergic blocking agent: Propanolol
/Calcium-blocking agent: nefedipine/ACE
Inhibitor: Enapril
 Modification of diet & other risk factors
 Surgery: Coronary artery bypass surgery
 Percutaneuos
Transluminal
Coronary
Angioplasty (PTCA)
NURSING INTERVENTIONS
1. Enforce complete bed rest
2. Give prompt pain relievers with nitrates or
narcotic analgesic as ordered
3. Administer medications as ordered:
A. Nitroglycerine(NTG): when given in small doses will
act as venodilator, but in large doses will act as
vasodilator
 NTG Tablets(sublingual)
 NTG Nitrol or Transdermal patch
B. Beta-blockers: decreases myocardial oxygen demand
by decreasing heart rate, cardiac output and BP
 Propanolol
 Metropolol
 Pindolol
 Atenolol
C. Calcium – Channel Blockers: relaxes smooth
cardiac muscle, reduces coronary vasospasm
 Amlodipine ( norvasc )
 Nifedipine ( calcibloc )
 Diltiazem ( Cardizem
MYOCARDIAL INFARCTION
 Death of myocardial cells from inadequate
oxygenation, often caused by sudden complete
blockage of a coronary artery
 localized formation of necrosis (tissue
destruction) with subsequent healing by scar
formation & fibrosis
 Heart attack
 Terminal stage of coronary artery disease
Types of M.I
 Transmural Myocardial Infarction: most
dangerous type characterized by
occlusion of both right and left coronary
artery
 Subendocardial Myocardial Infarction:
characterized by occlusion of either
right or left coronary artery
PREDISPOSING FACTORS
 Sex: male, Race: black, Smoking,
Obesity, CAD: Atherosclerotic,
Thrombus Formation, Genetic
Predisposition,
Hyperlipidemia,
Sedentary
lifestyle,
Diabetes
Mellitus, Hypothyroidism, Diet:
increased saturated fats, Type A
personality
SIGNS AND SYMPTOMS
1. Chest pain
2. N/V
3. Dyspnea
4. Increase in blood pressure & pulse,
with gradual drop in blood pressure
(initial sign)
5. Hyperthermia: elevated temp
6. Skin: cool, clammy, ashen
7. Mild restlessness & apprehension
8. Occasional findings: Pericardial friction
rub/ Split S1& S2/ Rales or Crackles upon
auscultation/ S4 or atrial gallop
DIAGNOSTIC PROCEDURED
1. Cardiac Enzymes
 CPK-MB: elevated
 Creatinine
phosphokinase
(CPK):elevated
 Heart only, 12 – 24 hours
 Lactic acid dehydrogenase (LDH): is
increased
 Serum
glutamic
pyruvate
transaminase(SGPT): is increased
 Serum
glutamic
oxal-acetic
transaminase(SGOT): is increased
2. Troponin Test: is increased
3. ECG tracing reveals
 ST segment elevation
 T wave inversion
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Widening of QRS complexes:
indicates that there is arrhythmia
in MI
4. Serum Cholesterol & uric acid: are both
increased
5. CBC: increased WBC
NURSING INTERVENTIONS
Goal: Decrease myocardial oxygen demand
1. Decrease myocardial workload (rest heart)
Establish a patent IV line
Administer narcotic analgesic as ordered: Morphine
Sulfate IV
Antidote: Naloxone (Narcan)
2. Administer oxygen low flow 2-3 L / min: to prevent
respiratory arrest or dyspnea & prevent arrhythmias
3. Enforce CBR in semi-fowlers position without
bathroom privileges(use bedside commode): to
decrease cardiac workload
4. Instruct client to avoid forms of valsalva maneuver
5. Place client on semi fowler’s position
6. Monitor strictly V/S, I&O, ECG tracing &
hemodynamic procedures
7. Perform complete lung / cardiovascular assessment
8. Monitor urinary output & report output of less than
30 ml/hr: indicates decrease cardiac output
9. Provide a full liquid diet with gradual increase to soft
diet: low in saturated fats, Na & caffeine
10. Maintain quiet environment
11. Administer stool softeners as ordered: to facilitate
bowel evacuation & prevent straining
12. Relieve anxiety
13. Administer medication as ordered:
a.
Vasodilators:Nitroglycirine
(NTG),
Isosorbide
Dinitrate, Isodil (ISD): sublingual
b. Anti Arrythmic Agents: Lidocaine (Xylocane),
Brithylium Side Effects: confusion and dizziness
c. Beta-blockers: Propanolol (Inderal)
d. ACE Inhibitors: Captopril (Enalapril)
e. Calcium Antagonist: Nefedipine
f. Thrombolytics / Fibrinolytic Agents: Streptokinase,
Urokinase, Tissue Plasminogen Activating Factor (TIPAF)
 Heparin
Antidote: Protamine Sulfate
 Caumadin(Warfarin)
Antidote:Vitamin K
h. Anti Platelet: PASA (Aspirin): Anti thrombotic effect
14.Provide client health teaching & discharge planning
concerning
CONGESTIVE HEART FAILURE
 Inability of the heart to pump blood towards
systemic circulation
Etiology and pathophysiology
1. Inability of heart to meet oxygen demands of the
body
2. Pump failure may be caused by cardiac
abnormalities or conditions that place increased
demands on the heart
3. Heart failure may be classified as diastolic or
systolic; determined by ejection fraction
4. When one side of heart “fails,” there is buildup of
pressure in the vascular system feeding into
that side; signs of right ventricular failure are
first evident in the systemic circulation; those of
left ventricular failure are first evident in the
pulmonary system
5. Decreased cardiac output activates the
reninangiotensin
LEFT-SIDED HEART FAILURE
PREDISPOSING FACTOR
1. 90% - Mitral valve stenosis
 RHD
 Aging
2. MI
3. IHD
4. HPN
5. Aortic valve stenosis
SIGNS AND SYMPTOMS
1. Pulmonary edema/congestion
2. Pulsus alternans (A unique pattern during which
the amplitude of the pulse changes or alternates in
size with a stable heart rhythm.)This is common in
severe left ventricular dysfunction.)
3. Anorexia and general body malaise
4. PMI displaced laterally, cardiomegaly
5. S3 (ventricular gallop
DIAGNOSTICS
1. CXR – cardiomegaly
2. PAP – pulmonary arterial pressure
 Measures pressure in right ventricle
 Reveals cardiac status
3. PCWP – pulmonary capillary wedge pressure
 Measures end-systolic and end-diastolic pressure
(elevated
 Done
through
cardiac
catheterization
(SwanGanz)
4. Echocardiograph – reveals enlarged heart chamber
5. ABG analysis reveals elevated PCO2 and decreased
PO2 (respiratory acidosis) hypoxemia and cyanosis
RIGHT SIDED HEART FAILURE
PREDISPOSING FACTORS
1. Tricuspid valve stenosis
2. COPD
3. Pulmonary embolism (char by chest pain and
dyspnea)
4. Pulmonic stenosis
5. Left sided heart failure
SIGNS AND SYMPTOMS (Venous congestion)
 Jugular vein distention, Pitting edema, Ascites,
Weight gain, Hepatosplenomegaly, Jaundice,
Pruritus/ urticarial, Esophageal varices,
Anorexia, Generalized body malaise
DIAGNOSTICS
1. CXR – cardiomegaly
2. CVP – measures pressure in right atrium; N = 4- 10cc
H2O
 Hypovolemia – fluid challenge
 Hypervolemia – diuretics (loop)
3. Echocardiography – reveals enlarged heart chamber
 Muffled heart sounds , cardiomyopathy
 Cyanotic heart diseases
4. Liver enzymes
 SGPT up
 SGOT up
NURSING MANAGEMENT
Normal CO is 3-6L/min; N stroke volume is 60-70ml/h2o
1. Administer medications as ordered
 Cardiac glycoside
 Digoxin (N=.5-1.5, tox=2
 Tox: Anorexia, N&V; A: Digibind
 Digitoxin – given if (+) ARF; metabolized in liver
and not in kidneys
 Loop diuretics
 Lasix – IV push, mornings
 Bronchodilators
 Aminophylline (theophylline)
 Tachycardia, palpitations
 CNS hyperactivity, agitation
 Narcotic analgesics
 Morphine sulfate – induces vasodilation
 Vasodilator
 NTG and ISDN
 Anti-arrhythmic agents
 Lidocaine (SE: dizziness and confusion)
 Bretyllium
 YOU DON’T GIVE BETA-BLOCKERS TO THESE
PATIENTS
2. Administer O2 inhalation at 3-4 L/minute via NC
as ordered will lead to high flow
3. High fowler’s, 2-3 Pillows
4. Restrict Na and fluids
5. Monitor strictly VS and IO and Breath Sounds
6. Weigh pt daily and assess for pitting edema
7. abdominal girth daily and notify MD
8. provide meticulous skin care
9. provide a dietary intake which is low in saturated
fats and caffeine
10. Institute bloodless phlebotomy
11. Health teaching and discharge planning
Aminophylline to reduce bronchospasm
caused by severe congestion.
Vasodilators to reduce venous return
Diuretics to decrease circulating volume
Cardiogenic shock
 POWER/PUMP FAILURE
 shock state which result from profound left
ventricular failure usually from massive MI
 result to low cardiac output, thereby
systemic hypoperfusion
SIGNS AND SYMPTOMS
1. Decrease systolic BP
2. Oliguria
3. Cold, clammy skin
4. Weak pulse
5. Cyanosis
6. Mental lethargy
7. Confusion
MEDICAL MANAGEMENT
 Counterpulsation - ( mechanical cardiac
assistance / diastolic augmentation )
NURSING INTERVENTIONS
 Provide psychosocial support
 Decrease pulmonary edema
 Auscultate lung fields for crackles and
wheezes
 Note for dyspnea, cough , hemoptysis and
orthopnea
 Monitor ABG for hypoxia and metabolic
acidosis
 Place in fowler’s position to reduce venous
return
 Administer during therapy as ordered:
Morphine sulfate to reduce venous return.
Hypertensive crisis
 situation that requires immediate blood
pressure lowering 240mmHg / 120
mmHg
 In hypertension, vasoconstriction –
vasospasm – increases PVR – decrease
blood flow to the organ
 Target Organs:
- Heart : MI, CHF, Dysrhythmias
- Eyes: blurred / impaired vision,
retinopathy, cataract.
- Brain: CVA, encephalopathy
- Kidneys : renal insufficiency, RF
- Peripheral Bloods Vessels –
aneurysm, gangrene
TYPES OF HYPERTENSIVE CRISES
 Hypertensive emergency is defined as a severe
elevation of BP–usually 220/130 mm Hg or
higher–with acute and ongoing target organ
damage to the kidneys, heart, vascular system,
brain, or eyes.
- requires the initiation of BP reduction
within minutes to hours to prevent
further progression of target organ
damage. BP should not be lowered to
less than 140/90 mm Hg
 Hypertensive urgency is defined as an elevation
of BP–usually 180/110 mm Hg or higher–
without target organ damage. BP should be
lowered gradually over12 to 24 hours, but not
to a normal level (target level, approximately
160/110 mm Hg)
Interpreting Test Results
 There may be no other test than an elevated
blood pressure that shows HTN.
 EKG may show left-ventricular hypertrophy if the
HTN is long standing.
 BUN and creatinine may be elevated if renal
damage has occurred
Hallmark Signs and Symptoms
 an acute hypertensive crisis the patient may
present with one or more of the following
symptoms: changes in neurological status
like changes in the level of responsiveness,
headache, visual disturbances, nausea,
and/or vomiting, chest pain, and shortness
of breath
Treatment
 the patient’s BP needs to be brought down
slowly but steadily
 Start at least one peripheral IV and begin an
infusion of nitroprusside (Nipride) at 0.1
μg/kg per minute to lower the mean arterial
blood pressure (MAP) at least 25% below
the MAP
 IV labetalol (Normodyne, Trandate),
nitroglycerin (Nitropaste), or a calcium
channel blocker like nicardipine (Cardene)
infusion; hydralazine (in eclampsia); or
furosemide (Lasix)
 For a hypertensive urgency, a loop diuretic
and an antihypertensive medication like a
beta-adrenergic blocker, calcium channel
blocker, or an ACE inhibitor may be
prescribed with a follow-up appointment
with a clinic or primary physician to occur
within 24 to 48 hours
Nursing Interventions
 Monitor the patient’s BP until stable; this may
include intraarterial monitoring to see if therapy
is effective in lowering the BP 25% within 2
hours.
 Monitor for signs/symptoms of stroke
(numbness/tingling in extremities, paralysis or
weakness, change in ability to talk). Stroke is a
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major complication of acute hypertensive
emergencies.
Initiate and monitor the effects of BP lowering
medications to see if therapy is effective.
Assess patient’s financial status, as money to buy
medications is a big issue in today’s economic
crisis.
Teach the patient the importance of taking
medications even if he or she feels well. The
patient may have high BP and not feel ill.
Teach the patient ways to modify risk factors to
help lower the BP and give a sense of control.
Cardiomyopathy
 heart muscle disease associated with cardiac
dysfunction. It is classified according to the
structural and functional abnormalities of the
heart muscle
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ASSESSMENT FINDINGS
stable and asymptomatic
signs and symptoms of Heart Failure
PND
orthopnea
fluid retention
peripheral edema
nausea
chest pain
palpitations
dizziness
syncope with exertion
sudden death with HCM
Tachycardia and extra heart sounds
2D Echo and ECG
 CXR
 Cardiac Cath to rule out coronary artery disease
as a cause
 Endomyocardial biopsy
Medical management:
1. Treat the underlying cause
2. Low Na diet
3. Exercise Rest Regimen
4. Control dysrhythmias with medications
5. If there are symptoms of CHF limit fluid intake into 2
L/day
6. Pacemaker
Surgical Management
1. Heart Transplantation
2. LVAD
3. Left Ventricular Outflow Tract Surgery
Nursing Management
1. Improve CO
2. Increase activity tolerance
3. Reduce anxiety
4. Decrease the sense of powerlessness
5. Promote Self-Care
6. Promote Home and Community-Based care
7. Continuing Care
Arrhythmias
 cardiac
arrhythmia,
abnormal
electrical
conduction or automaticity changes heart rate
and rhythm
 Arrhythmias vary in severity, from mild and
asymptomatic ones that require no treatment
(such as sinus arrhythmia, in which heart rate
increases and decreases with respirations) to
catastrophic ventricular fibrillation, which
necessitates immediate resuscitation
 Arrhythmias are generally classified according to
their origin (atrial or ventricular); their effect on
cardiac output and blood pressure, partially
influenced by the site of origin, determines their
clinical significance
 Causes of arrhythmias include congenital heart
disease, degeneration of the conduction
system, drug effects or toxicity, heart disease,
myocardial ischemia, stress, alcohol, electrolyte
imbalance, acid-base imbalances, cellular
hypoxia, and conditions such as anemia,
anorexia,
thyroid
dysfunction,
insufficiency, and pulmonary disease
adrenal
ARRHYTHMIAS
Signs and symptoms
◆The patient with an arrhythmia may be asymptomatic
or may report palpitations, chest pain, dizziness,
weakness, fatigue, and feelings of impending doom
◆Other signs and symptoms include an irregular heart
rhythm, bradycardia or tachycardia, hypotension,
syncope, reduced level of consciousness, diaphoresis,
pallor, nausea, vomiting, and cold, clammy skin
◆ Life-threatening arrhythmias may result in
pulselessness, absence of respirations, and no palpable
blood pressure
Nursing interventions
◆ Monitor the pulse for an irregular pattern or an
abnormally rapid or slow rate; if the patient is receiving
continuous cardiac monitoring, observe him for
arrhythmias
◆ Assess the patient for signs and symptoms of
hemodynamic compromise
◆If the patient has an arrhythmia, promptly assess his
airway, breathing, and circulation
◆Initiate basic life support measures if indicated, until
other advanced cardiac life support measures are
available and successful
◆Perform defibrillation early for ventricular tachycardia
and ventricular fibrillation
◆ Administer medications as needed, and prepare for
medical procedures (for example, cardioversion or
pacemaker insertion) if indicated
◆ Monitor the patient for fluid and electrolyte
imbalance and signs of drug toxicity, especially digoxin;
correct the underlying cause and adjust medications as
needed
◆ Provide adequate oxygen and reduce the heart’s
workload, while carefully maintaining metabolic,
neurologic, respiratory, and hemodynamic status
◆Provide support to the patient and family
◆Tell the patient signs and symptoms of an arrhythmia
to report, and teach him how to take his pulse
◆Explain all procedures such as pacemaker insertion to
the patient
Normal electrical conduction
 The electrical impulse that stimulates and paces
the cardiac muscle normally originates in the
sinus node (SA node)
 Inherent Rate: 60-100 times/minute
 The electrical impulse quickly travels from the
sinus node through the atria to the
atrioventricular (AV) node. The electrical
stimulation of the muscle cells of the atria
causes them to contract.
 Inherent Rate: 40-60 times/minute
 The structure of the AV node slows the electrical
impulse, which allows time for the atria to
contract and fill the ventricles with blood before
the electrical impulse travels very quickly
through the bundle of His (40-60 times/minute)
to the right and left bundle branches (20440
times/minute) and the Purkinje fibers (20-40
times/minute), located in the ventricular
muscle. The electrical stimulation of the muscle
cells of the ventricles, in turn, causes the
mechanical contraction of the ventricles
(systole).
 The cells repolarize and the ventricles then relax
(diastole). The process from sinus node
electrical
impulse
generation
through
ventricular repolarization completes the
electromechanical circuit, and the cycle begins
again
 Sinus
rhythm
promotes
cardiovascular
circulation. The electrical impulse causes (and,
therefore, is followed by) the mechanical
contraction of the heart muscle.
 The electrical stimulation is called depolarization;
 Mechanical contraction is called systole.
 Electrical relaxation is called repolarization.
 Mechanical relaxation is called diastole.
Components of Cardiac Cycle
Cardiac Cycle
 One Heartbeat
 Electrical Representation
of
Contraction,
Relaxation of Atria/Ventricles
Electrocardiogram (ECG
 Shows Cardiac Electrical Activity
 12-lead ECG = 12 Different Views
 Waveforms Change Appearance in Different
Leads
 Continuous Monitoring Often in Lead II
 Waveforms Upright in Lead II
Normal Cardiac Waves Are Equal Distances Apart
ECG Electrode Placement
DETERMINING VENTRICULAR HEART RATE FROM THE
ELECTROCARDIOGRAM
 FOR REGULAR RHYTHM
A 1-minute strip contains 300 large boxes and 1500
small boxes. Therefore, an easy and accurate method of
determining heart rate with a regular rhythm is to count
the number of small boxes within an RR interval and
divide 1500 by that number. If, for example, there are
10 small boxes between two R waves, the heart rate is
1500 ÷ 10, or 150; if there are 25 small boxes, the heart
rate is 1500 ÷ 25, or 60
 FOR IRREGULAR RHYTHM
count the number of RR intervals in 6 seconds and
multiply that number by 10. The top of the ECG paper is
usually marked at 3-second intervals, which is 15 large
boxes horizontally. The RR intervals are counted, rather
than QRS complexes, because a computed heart rate
based on the latter might be inaccurately high. The
same methods may be used for determining atrial rate,
using the PP interval instead of the RR interval.
Normal Sinus Rhythm
Atrial Fibrillation
Sinus Bradycardia
Ventricular Tachycardia
Multifocal PVCs-Quadrigeminy
Ventricular Fibrillation
Sinus Tachycardia
Asystole
Sinus Arrhythmia
First-Degree AV Block
Premature Atrial Complexes
Second-Degree AV Block, Type 1
Atrial Flutter
Second-Degree AV Block, Type 2
Third-Degree AV Block