NUR207 NURSING THERAPEUTICS I

LECTURE 3

NURSING CARE RELATED

TO CARDIOVASCULAR
DISORDERS

MR. ADAM WONG

Date: 7/1/2021
Learning objectives
After completion of this session, you will be able
to:
❑ explain common cardiovascular disorders and their
etiologies
❑ state the prevalence & incidence of illness
❑ describe the clinical manifestations, diagnostic tests
and treatment of common cardiovascular disorders
❑ discuss the appropriate nursing interventions for the
care of clients with cardiovascular disorders
Content
Disorders of Cardiac Function
❑ Arrhythmia

❑ Cardiac Arrest

❑ Pacemaker

❑ Coronary Artery Disease

❑ Heart Failure
Content
Disorders of Cardiac Structure
❑ Valvular Heart Disease

❑ Cardiomyopathy

Inflammatory Heart Disorders

❑ Carditis

❑ Endocarditis, Myocarditis, Pericarditis

Content
Disorders of Vascular system
❑ Hypertension

❑ Arterial disorders

❑ Aneurysms, Peripheral Artery Disease, Raynaud’s

Disease
❑ Venous disorders
❑ Deep Venous Thrombosis, Varicose Veins
❑ Lymphatic disorders
❑ Lymphedema
Disorders of Cardiac Function:
Arrhythmia
❑ aka dysrhythmia
❑ A group of conditions in which the heartbeat is
irregular, too fast, or too slow.
❑ Heart rate (HR) > 100 bpm, tachycardia
❑ HR < 60, bradycardia
Arrhythmia –
Cardiac conducting system

The ONLY
electrical connection
between atria and
ventricles
Arrhythmia –
Electrocardiogram (ECG/EKG)
❑ Gold standard as a non-invasive diagnostic method
of cardiac arrhythmias
❑ Graphic display of electrical activity of the heart

❑ Use
❑ Record changes due to myocardial disease, electrolyte
❑ imbalance, drug effects

❑ Evaluate functioning of implanted devices

Electrocardiogram – Types
❑ 12-lead ECG: record the electrical activities of cardiac cycle from 12
different angles
❑ Nursing care:
❑ accurate landmarks of leads
❑ ensure client is warm and relaxed
❑ shave the region if very hairy → ensure good contact
❑ thoroughly clean the area with dry gauze pad
❑ do not apply electrodes over bony areas, broken skin, joints, skin creases, scar tissue,
burns or rashes
❑ Holter monitor:
❑ continuous ECG monitor & recorder, usu. 24- 48hrs.
❑ Nursing care:
❑ accurate & secure placement of leads
❑ educate client to mark any cardiac symptoms on the log book
❑ avoid electric blankets, magnets & high voltage areas
❑ Stress test:
❑ If symptoms occur most often during exercise, doctor may ask client to walk on a
treadmill or ride a stationary bike during an ECG
Electrocardiogram – 12-lead ECG

Limb Leads Chest Leads/Precordial leads

Electrocardiogram – 12-lead ECG

Limb Leads Chest Leads

Long Lead II
Electrocardiogram – 12-lead ECG
❑ Time – horizontal axis of
ECG paper
❑ ECG paper records at a
constant speed of 25 mm/sec
❑ Each horizontal 1-mm box
represents 0.04 sec
❑ 1 large box = 0.04 X 5 =
0.20 sec
❑ Voltage – vertical axis of
ECG paper
❑ Measured in millivolts (mV)
❑ Amplitude of waves
measured in millimeters (mm)
❑ ECG machine calibration
❑ One small box = 1mm =
0.1mV
Electrocardiogram – Waveform
❑ P wave
❑ First deflection, small, smooth,
rounded
❑ QRS complex
❑ Sharp, pointed spiky deflection
❑ Consisting Q wave, R wave, and S
wave
❑ Sometimes Q and/or S waves may
be absent, it still refers to QRS
complex
❑ T wave
❑ Broad and slow upstroke
❑ Repolarization is slower than
depolarization
❑ U wave
❑ Small, following T wave, not always
seen
❑ Presence may indicate hypokalemia
Electrocardiogram – Waveform
❑ PR interval
❑ Time from the beginning of P
wave to the beginning of the
QRS complex
❑ Represent the time for atrial
depolarization, conduction
through the AV node, bundle of
His, bundle branches and the
Purkinje fibers
❑ Normal: 0.12-0.20 sec
❑ QRS interval
❑ Time it takes for ventricular
depolarization
❑ Normal: 0.06-0.10 sec
❑ Wide QRS (>0.12 sec)
❑ A beat initiated in the ventricle
Electrocardiogram – Waveform
❑ ST segment
❑ End of QRS complex to the
beginning of the T wave
❑ Represent the time interval
after ventricular
depolarization and before
repolarization has begun
❑ Normal: isoelectric (flat on
the baseline)
❑ Elevation
❑ Acute myocardial infarction
❑ Pericarditis
❑ Normal variant
❑ Depression
❑ Myocardial ischemia
Electrocardiogram – Waveform
❑ QT interval
❑ Measure from beginning
of QRS complex to the
end of T wave
❑ Normal: 0.36-0.44 sec

❑ Vary with heart rate,

needs formula correction
❑ Prolonged QT interval
❑ Lengthened relative
refractory period
❑ Prone to arrhythmia
Electrocardiogram – Interpretation
1. Is the rhythm regular?
❑ Compare P-P intervals (atrial rhythm) & R-R interval
(ventricular rhythm)
2. Is the PR interval normal (0.12-0.20 sec.)?
3. Is there a P wave associated with each QRS complex?
4. Is the QRS duration normal (0.06-0.1 sec.)?
5. Is the heart rate normal (60-100 bpm)?
6. Is the T wave normal (board and slow upstroke)?
7. Is the ST segment normal (isoelectric)?
Electrocardiogram – Heart Rate
❑ Look at long Lead II
❑ Regular Heart Rate (bpm):
60/ (R-R interval in sec) OR
300/ no. of BIG square between R-R interval OR
1500/ no. of SMALL square between R-R interval
❑ Heart rate:
60/0.4 or
300/2 or
1500/10
=150 bpm
Electrocardiogram – Heart Rate
❑ Look at long Lead II
❑ Irregular Heart Rate (bpm) = QRS complex no. x 6
❑ the ECG displays a period of 10 seconds
❑ 6 × 10 seconds = 60 seconds (1 minute)

❑ Heart rate:
QRS complex no. x 6
=15 x 6
=90 bpm
Electrocardiogram –
Normal Sinus Rhythm (NSR)
ECG Characteristics:
❑ ventricular rate: normal

❑ ventricular rhythm: regular

❑ P wave: precede every QRS, upright and uniform

❑ QRS complex: constant in shape

❑ PR interval: normal

❑ QRS complex: normal

Electrocardiogram – Arrhythmias
❑ Sinus bradycardia
❑ Sinus tachycardia
❑ Atrial flutter
❑ Atrial fibrillation (AF)
❑ Supraventricular tachycardia (SVT)
❑ Premature ventricular contractions (PVC)
❑ Ventricular tachycardia (VT)
❑ Ventricular fibrillation (VF)
Arrhythmia – Sinus Bradycardia
❑ ECG Characteristics:
❑ ventricular rate: <60 bpm
❑ ventricular rhythm: regular
❑ P wave: normal, precede every QRS complex
❑ QRS complex: constant in shape
❑ PR interval: normal
❑ QRS complex: normal
❑ Causes:
❑ Normal in athletes,
vagal stimulation, medication
❑ Clinical presentation:
❑ Dizziness, fatigue, syncope
❑ Treatment:
❑ Asymptomatic: no treatment
❑ Symptomatic (e.g. hypotension): e.g. Atropine 0.5/0.6 mg IV
❑ Withhold suspected medications
❑ Cardiac pacing
Arrhythmia – Sinus Tachycardia
❑ ECG Characteristics:
❑ ventricular rate: fast (>100/min, but rarely exceed 180/min)
❑ ventricular rhythm: regular
❑ PR interval: normal
❑ P wave: upright and uniform, every P wave is followed by a QRS
complex
❑ QRS complex: normal
❑ Causes:
❑ Exercise, anxiety, fever
❑ ↓ cardiac output (CO) – bleeding, shock
❑ Hypovolemia, anemia
❑ Acute myocardial infarction (MI)
❑ Medication effect: epinephrine, dopamine
❑ Treatment:
❑ Correct underlying disease
Arrhythmia – Atrial Flutter
Atrium extremely irritable, conduct at a rate too fast for the
ventricle to respond.
❑ ECG Characteristics:
❑ rate: atrial 240-360/min;
ventricular: variable (2:1, 3:1, 4:1)
❑ rhythm: regular/ irregular
❑ P wave: saw- toothed flutter wave
❑ PR interval: insignificant
❑ QRS complex: usually normal
❑ Clinical presentation:
❑ S/S depends on ventricular responses rate
❑ Treatment:
❑ Synchronized cardioversion
❑ Medication: beta blocker or calcium channel
blocker
Arrhythmia – Atrial Fibrillation
Atrium conducts extremely fast
❑ ECG Characteristics:
❑ atrial rate: 300-600 bpm
❑ rhythm: irregular
❑ P wave: fibrillation, no distinct
true P waves
❑ PR interval: none
❑ QRS complex: usually normal
❑ Clinical presentation:
❑ Shortness of breath
❑ Decreased CO
❑ Hypotension
❑ Fatigue
❑ Angina
Arrhythmia – Atrial Fibrillation
Management:
❑ Ventricular rate control
❑ Oral beta-blockers, calcium channel blockers, digoxin, amiodarone
❑ IV in acute setting
❑ Synchronized cardioversion for hemodynamically unstable patients
❑ AV nodal ablation with pacing when pharmacological therapy is
ineffective
❑ Rhythm control
❑ Electrical cardioversion (proper pre and post anti-coagulation)
❑ Pharmacological cardioversion
❑ Reducing stroke risk
❑ 5-fold increased ischemic stroke risk than people with normal rhythm
❑ 1 in 5 strokes occur due to AF
❑ Stroke risk assessment
❑ Antithrombotic therapy
❑ Anticoagulation therapy
Arrhythmia –
Supraventricular Tachycardia
Heart arrhythmias that originate above the ventricles (supraventricular)
in the atria or AV node (junctional)
❑ ECG Characteristics:
❑ ventricular rate: 150-250 bpm
❑ rhythm: regular
❑ P wave: not visible
❑ PR interval: not identifiable
❑ QRS complex: narrow (atrial and ventricular depolarization occur at the
same time)
❑ T wave: normal
❑ Etiology: atrial electrical conduction problem
❑ Treatment:
❑ Vagal maneuvers: vagal stimulation to decrease a rapid heart rate
❑ Medications: as an adjunct to keep the rate down or maintain the normal
rhythm (e.g. adenosine (ATP), amiodarone)
❑ Synchronized cardioversion
Arrhythmia –
Supraventricular Tachycardia
Vagal Maneuvers
❑ Valsalva maneuver
❑ breathe out forcibly while mouth & nose are firmly closed
❑ creates pressure in chest
❑ sitting or squatting may help
❑ try for 10 seconds
❑ Cold water treatment (Diver’s Reflex)
❑ put plastic bag of ice on face for 15 seconds or
❑ dunking face in ice water for few seconds
❑ Coughing
❑ Carotid sinus massage (or carotid massage)
❑ perform by physician
❑ neck extended, head turned away from the side being massaged
❑ put pressure on carotid sinus in a gentle circular motion for ~ 10 sec
Arrhythmia –
Premature Ventricular Contraction
❑ ECG Characteristics:
❑ ventricular rate: 60 -100 bpm
❑ ventricular rhythm: regular except the early beat(s)
❑ P wave: regular except with early beat(s)
❑ PR interval: regular except with the early beats
❑ QRS: regular except early beats with widened QRS
❑ T wave: normal except early beats

❑ Etiology: hypokalemia, acidosis etc.

❑ Perceived as a “skipped beats"
or felt as palpitations in the chest
❑ Treatment: correct underlying
cause
Arrhythmia – Ventricular Tachycardia
❑ ECG Characteristics:
❑ ventricular rate : >100 bpm
❑ rhythm: regular
❑ P wave: disassociated with QRS → no P wave
❑ PR Interval: not measurable
❑ QRS complex: > 0.12 sec, wide & bizarre (ventricular in origin)
❑ T wave: not identifiable
❑ Etiology: MI, cardiomyopathy, myocarditis, heart failure, etc.
❑ Treatment:
❑ Pulseless VT
❖ MEDICAL EMERGENCY!
❑ refer to ACLS guidelines: early defibrillation
❑ With pulse & sustained
❑ Synchronized cardioversion
Arrhythmia – Ventricular Fibrillation
❑ ECG Characteristics:
❑ ventricular rate : undetermined
❑ ventricular rhythm : irregular
❑ P wave: not seen
❑ PR interval: none
❑ QRS complex: not formed
❑ T wave : not seen
❑ chaotic undulations of varying amplitudes

❑ Etiology: MI, CAD, hypo/hyperkalemia, etc.

❑ Treatment:
❖ MEDICAL EMERGENCY!
❑ refer to ACLS guidelines: early defibrillation
Electrocardiogram –
Pulseless Electrical Activity (PEA)
Unresponsiveness and the lack of a palpable
pulse in the presence of organized cardiac
electrical activity
❑ Common during arrest situations

❑ ECG appears normal, but the client will have

no palpable pulse
❑ Treatment:

❑ Much like asystole!

❑ Refer to ACLS guidelines
Cardiac arrest – Asystole
Cardiac arrest rhythm in which there is no
discernible electrical activity
❑ ECG Characteristics
❑ ventricular rate: none
❑ ventricular rhythm: none
❑ P wave: not seen
❑ PR interval: none
❑ QRS complex: none

❑ No pulse
❑ Start cardiopulmonary resuscitation (CPR)
❑ Etiology: MI, cardiac tamponade, etc.
Basic Life
Support (BLS)
Basic Life Support
High-quality CPR
❑ Ensure proper hand placement on lower half of sternum

❑ Chest compressions of adequate rate (100-120

compressions/min)
❑ Chest compressions of adequate depth (at least one
third of the anterior-posterior diameter of the chest or
at least 2 inches depth or at least 5 cm depth)
❑ Complete recoil of the chest after each compression

❑ Minimal interruption in compressions

(Resume CPR immediately after shock)
❑ Avoid excessive ventilation

❑ Ratio: 30 compressions : 2 breaths

Advanced Cardiac
Life Support (ACLS)
ACLS algorithm is designed to
simplify the process for the
management and treatment of
patients experiencing a
cardiovascular emergency or
progressing toward a
cardiovascular emergency.
1) Cardiac Arrest
2) Bradycardia
3) Tachycardia
4) Acute Coronary Syndrome
(ACS)
5) Suspected Stroke
Intraosseous (IO): injecting directly
into the marrow of a bone
ACLS – Defibrillation
Non-synchronized shock in
cardiac cycle
❑ Delivers electrical current
from two paddles/pads
through myocardium in one
direction (monophasic) or
bidirection (biphasic)
❑ Depolarizes the myocardial
cells and terminates all
electrical activity
❑ Allows the sinus node to
resume normal pacemaker
activity
ACLS – Shockable Rhythm
Management: Early defibrillation
❑ Pulseless ventricular tachycardia (pVT)

❑ Ventricular fibrillation (VF)

Management: Synchronized Cardioversion

❑ Unstable supraventricular tachycardia

❑ Unstable ventricular tachycardia with pulse

❑ Unstable atrial flutter

❑ Unstable atrial fibrillation

ACLS – Synchronized Cardioversion
❑ Deliver a low energy
shock that is synchronized
with the peak of the QRS
complex
❑ Avoids the delivery of the
shock during cardiac
repolarization (t-wave)
❑ MUST choose “sync”
option of the defibrillator
❑ There will be a delay in
the shock after pressing
“shock” button
 ACLS – Medications

Drug Indication Action Dosage

Epinephrine - Cardiac arrest - - Stimulate adrenergic receptors Adrenaline 1:10000 (10 ml) 1mg
Symptomatic produce every 3 to 5 minutes IV/IO
bradycardia vasoconstriction
- Severe hypotension - - - Optimize cardiac
Anaphylaxis output and blood pressure
Lidocaine - VF or pulseless VT - Inhibit sodium ions Initial dose:
movement 1- 1.5mg/kg IV/IO
- Reduce depolarization of For refractory VF,
ventricles during diastole additional 0.5-0.75 mg/kg push,
repeat 5-10 minutes maximum 3
doses
Magnesium - Life threatening - Block neuromuscular 1-2g diluted in 10 ml D5 or NS
sulphate ventricular arrhythmia transmission IV/IO
due to digitalis toxicity - Prevent ventricular arrhythmias
- Torsades de pointes
 ACLS – Medications
Drug Indications Action Dose

Adenosine - SVT - Terminate reentry 6 mg in rapid injection

(ATP) conduction involving AV followed by 20 ml NS bolus then
node and SA node elevate the injection site
Amiodarone - VF/ pulseless VT - Prolong the repolarization First dose: 300 mg IV/IO push
unresponsive to shock period **must dilute in 20ml D5**
delivery, CPR and - Decrease automaticity and Second dose: 150 mg IV/IO
vasopressor conductivity of heart
- Recurrent, hemodynamically
unstable VT
Atropine - Symptomatic sinus An anticholinergic agent 0.5mg IV every 3 to 5minutes
sulfate bradycardia blocks the muscarinic Maximum dose:3mg
receptors in the heart and
abolishes bradycardia vagal
activity.

Dopamine Second line drug for stimulates both 5-10 mcg/kg per minute
symptomatic bradycardia dopaminergic and β1-
For hypotension with signs of adrenergic receptors
shock producing cardiac stimulation
ACLS –
Reversible Causes of Cardiac Arrest

5H’s 5T’s
Hypovolemia Toxins
Hypoxia Tamponade (cardiac)
Hydrogen ion (acidosis) Tension pneumothorax
Hyper-/hypokalemia Thrombosis (coronary)
Hypothermia Thrombosis (pulmonary)
Hypoglycemia and Trauma should be considered during resuscitation
ACLS –
Return of Spontaneous Circulation
Resumption of sustained perfusing cardiac activity
associated with significant respiratory effort after
cardiac arrest.
❑ Manifestations:

❑ Cardiac: Pulse and blood pressure restored

❑ Resp.:Signs of breathing, coughing

❑ Others: Consciousness, movement of body
ACLS –
Post Cardiac Arrest Care
❑ Optimize ventilation and oxygenation
❑ maintain oxygen saturation ≥94%
❑ consider advance airway and waveform capnography

❑ Treat hypotension
❑ IV/IObolus
❑ Vasopressor infusion

❑ Consider treatable causes

❑ Obtain 12-lead ECG
❑ Initiate target temperature management between
32-36°C
❑ Arrange advanced critical care
Cardiac Arrest – Resuscitation Record
Cardiac Arrest – Extracorporeal
Cardiopulmonary Resuscitation (ECPR)
❑ Implantation of veno-
arterial extracorporeal
membrane oxygenation
(VA‐ECMO) in patients
with cardiac arrest.
Arrhythmia – Heart Block (HB)
Heart Block aka Atrioventricular block (AV block)
❑ First Degree Heart Block

❑ Second Degree Heart Block

❑ Mobitz Type I (aka Wenckebach Phenomenon)

❑ Mobitz Type II

❑ Third Degree Heart Block

❑ aka Complete Heart Block (CHB)
❑ Bundle Branch Block
❑ LeftBundle Branch Block (LBBB)
❑ Right Bundle Branch Block (RBBB)
Heart Block
Manifestations
❑ Fainting (syncope)
❑ Dizziness, lightheadedness
❑ Shortness of breath
❑ Decline in exercise capacity

Risk factors
❑ Heart failure
❑ Prior heart attack
❑ Heart valve abnormalities
❑ Heart valve surgery
❑ Congenital heart diseases
❑ Aging
Heart Block – 1st Degree HB
Electrical impulses slowed as they pass through the conduction
system, but successfully reach the ventricles
❑ Well-trained athletes may have

❑ Rarely causes S/S

❑ Causes: injury or infarct of AV node

❑ Characteristics of ECG:
❑ ventricular rate: normal
❑ ventricular rhythm: regular
❑ P wave: normal
❑ PR interval: prolonged > 0.2 sec.
❑ QRS complex : normal
❑ “R” is far from “P” (prolonged PR
interval)
❑ No treatment is generally needed
Heart Block –
2nd Degree HB: Mobitz Type I
Repeating pattern of increasing AV conduction delays until an impulse fails to conduct to the
ventricles
❑ Rarely causes S/S
❑ Characteristics of ECG :
❑ ventricular rate: normal or slow, irregular
❑ regular P waves but irregular QRS complex
❑ P waves: normal
❑ PR interval: progressive prolongation until one P wave fails to produce a QRS complex (dropped
beat)
❑ QRS complex: normal
❑ ‘Blocked’ P wave/ ‘Dropped’ QRS complex
❑ longer, longer, longer PR intervals
❑ Keep close observation
Heart Block –
2nd Degree HB: Mobitz Type II
Some atrial electrical signals cannot reach the ventricle
❑ Less common than Type I but more serious

❑ Frequently progresses to third degree heart block

❑ Non-conducted P waves

❑ Characteristics of ECG:
❑ ventricular rate: less than
atrial rate 3:1 block
❑ ventricular rhythm: R-R irregular
❑ P wave: normal
❑ PR interval: fixed and normal
❑ QRS complex: occasionally widened (> 2.5 small squares)
❑ sometimes “P” not followed with QRS
❖ Need medical treatment → pacing if hemodynamic
unsteady
Heart Block – 3rd Degree HB
Atrial impulse completely blocked at AV node and failed to reach the
ventricle
❑ When the ventricles do not receive electrical impulses from the atria

❑ Generate some impulses on their own (junctional or ventricular

escape beats), i.e. ventricular escape beats, usually very slow
❑ S/S: fatigue, lightheadedness, and decreased stamina

❑ Characteristics of ECG:
❑ ventricular rate: slow, 30 - 40 bpm (from ventricles)
❑ ventricular rhythm: regular
❑ P wave: regular
❑ PR interval: variable
❑ QRS complex: widened
❑ disassociation of “P” & “QRS”
❑ Atrioventricular (AV) dissociation (i.e. P-P regular, R-R regular, but P-
R irregular) → ↓CO
❑ Require medical treatment: Pacing
Heart Block – Bundle Branch Block
❑ Electrical impulses are slowed or blocked as they
travel through the specialized conducting tissue in
one of the two ventricles
❑ The pathway includes a bundle with two branches:
left and right
❑ If one of these is damaged,
ventricles don’t beat in
coordination with each other

❑ Characteristics of ECG:
❑ QRS complex: wide (≥ 0.12s)
Heart Block – Bundle Branch Block
❑ RBBB ❑ LBBB
❑ RSR’ pattern in V1-3 ❑ Dominant S wave in V1
❑ Wide slurred S wave ❑ Broad monophasic R
in lateral leads (I, aVL, wave in lateral leads
V5, V6) ❑ M-shape QRS complex
in V5,V6
Pacemaker
A electrical device to:
❑ keep track of client’s heart beat

❑ deliver an electrical current to the heart & initiate depolarization

❑ pacing rhythm consists of beats & rhythm produced by cardiac

pacemaker
❑ NO electrical shock delivered

Types
❑ Temporary pacing
❑ Indications
❑ Awaiting for permanent pacing
❑ Reversible conditions requesting short-term support, e.g. inferior AMI
❑ Modality
❑ Use external power sources
❑ Transvenous (more comfortable, durable)/ epicardial (post-cardiac surgery)/
transcutaneous (most rapid)
Pacemaker – Types
Permanent pacemaker
❑ Indications

❑ SA node dysfunction
❑ AV block

❑ After AMI with irreversible damage to conduction

system
❑ Congenital heart disease

❑ Modality
❑ Use internal power source
❑ Transvenous or epicardial approach
Pacemaker – Types

Temporary Pacemaker Permanent Pacemaker

Pacemaker – Mode
❑ Asynchronous pacing
❑ Pacemaker delivers a pacing stimulus at a set rate
regardless of intrinsic cardiac activity
❑ Risk
of developing arrhythmia
❑ Demand pacing
❑ Pacemaker delivers a pacing stimulus only when the
intrinsic rate falls below the pacemaker’s base rate
❑ Dual-chamber pacing
❑ Allows both the atria and the ventricles to be paced
❑ Most frequent used permanent pacing mode
Pacemaker – Nursing Interventions
Preparation for pacemaker implantation
❑ consent

❑ NPO/ NPO except medications for 6-8 hours

❑ ensure clotting profile result is available & report any

abnormalities
❑ withhold the anti-coagulants (warfarin: 2-3 days)

❑ ensure IV access is available

❑ skin preparation: bathing +/- shaving

❑ administer prophylactic antibiotics to prevent wound

infection as prescribed
❑ latest vital signs

❑ ECG strips / records

Pacemaker – Nursing Interventions
Post-operative care
❑ monitor client’s vital signs & ECG

❑ detect & inform doctor if any abnormalities in ECG as early as

possible
❑ educate client not to raise arm for 1 month

❑ remain bed rest for 1 day

❑ CXR : confirm the placement of pacemaker & its leads, any

pneumothorax
Pacemaker – Nursing Interventions
Post-operative care
❑ Wound care
❑ keep pressure dressing for 1-2 days
❑ keep sterile strips for ~ 7 days
❑ observe for any oozing, S/S of infections at the access
site
❑ Precautions of medical procedures
❑ notrecommend to have radiotherapy, electro-surgery
or MRI (unless with MRI compatible pacemaker)
❑ be careful when performing defibrillation (6 inches
apart)
Pacemaker – Nursing Interventions
Health education
❑ no heavy lifting or hand raising for 1 month
❑ operate electrical devices at least few inches away
❑ stay away from theft detection system & airport security full
body scanner
❑ keep ~30cm distance between mobile phone & pacemaker
❑ hold mobile phone to the ear on opposite side of pacemaker
❑ avoid working in areas near transmitting towers / antennas
❑ wear a medical alert bracelet / pacemaker ID card
❑ check pulse regularly & report any dizziness, generalized
malaise
❑ for non-MRI compatible pacemaker, patient need to inform
doctor for MRI procedure
❑ regular medical follow-up
Disorders of Cardiac Function:
Coronary Artery Disease (CAD)
❑ aka coronary heart disease (CHD), ischemic heart
disease (IHD)
❑ Impaired blood flow to the myocardium due to
accumulation of atherosclerotic plague in coronary
arteries (atherosclerosis)
Coronary Artery Disease –
Arteriosclerosis / Atherosclerosis
Arteriosclerosis
❑ occurs when arteries become thick and stiff →
restricting blood flow to organs and tissues

Atherosclerosis
❑ specific type of arteriosclerosis

❑ sometimes used interchangeably

❑ buildup of fats, cholesterol and other substances in

and on artery walls (plaque) → restrict blood flow

Atherosclerosis – Pathophysiology
❑ Unknown precipitating factors that cause lipoproteins and
fibrous tissue to accumulate in the arterial wall
❑ May start with damage or injury, to the inner layer of an
artery, that may be caused by:
❑ High blood pressure
❑ High cholesterol
❑ High triglycerides
❑ Smoking and other sources of tobacco
❑ Insulin resistance, obesity or diabetes
❑ Inflammation from diseases (e.g. arthritis)
❑ Blood cells and other substances often clump at the injury
site and build up in the inner lining of the artery
❑ Fatty deposits (plaque) made of cholesterol and other
cellular products also build up → harden, narrowing
arteries
Atherosclerosis – Pathophysiology
Coronary Artery Disease –
Medications
❑ Anti-hypertensive drugs
❑ Angiotensin-converting enzyme inhibitor and
angiotensin II receptor blocker
❑ Beta blockers

❑ Calcium channel blockers

❑ Nitroglycerin, e.g. TNG – initiates relaxation of

smooth muscle cells in blood vessels
❑ Antiplatelet, e.g. aspirin, Plavix
❑ prevent formation of blood clots
❑ Cholesterol-modifying medications, e.g. statin
Coronary Artery Disease – Risk Factors

❑ Gender & Age

❑ Male > 45 yrs old; Female > 55 yrs old
❑ Family history of heart disease
❑ Smoking
❑ High LDL cholesterol; Low HDL cholesterol; high
triglyceride
❑ Physical inactivity
❑ Being overweight or obese
❑ Hypertension
❑ Diabetes mellitus
Coronary Artery Disease

Coronary artery disease

Stable angina/ Acute coronary syndrome (ACS)

Angina pectoris

- Unstable angina (UA) ST elevation myocardial

- Non ST elevation myocardial infarction (STEMI)
infraction (NSTEMI)
Coronary Artery Disease –
Stable Angina
❑ aka angina pectoris
❑ Angina is a type of chest pain that results from reduced
blood flow to the heart
❑ Characteristics of the pain:
❑ Pressure or fullness in the center of the chest
❑ Feel like a vice squeezing your chest or like a heavy weight
resting on your chest
❑ May radiate to the neck, arms, and shoulders
❑ Predictable pattern of chest pain
❑ Provoked by increased level of activities or stress
❑ Other S/S includes SOB, nausea, fatigue, dizziness,
sweating, anxiety
❑ Tends to be temporary, lasting up to 15 minutes in most
cases, relieved by rest
Coronary Artery Disease –
Acute Coronary Syndrome
❑ Includes unstable angina and acute myocardial ischemia
(AMI) with or without significant injury of myocardial tissue

Precipitating factors
❑ rupture or erosion of atherosclerotic plaque with formation
of a blood clot that does not fully occlude the vessel
❑ coronary artery spasm

❑ progressive vessel obstruction by atherosclerotic plaque or

restenosis following a percutaneous coronary intervention
(PCI)
❑ inflammation of a coronary artery

❑ increased myocardial oxygen demand and/or decreased

supply (e.g. acute blood loss or anemia)
Acute Coronary Syndrome –
Unstable Angina
❑ Chest pain occurs with increasing frequency,
severity, and duration
❑ Pattern is unpredictable
❑ Occurs with decreasing levels of activities or stress,
even at rest
❑ Increased risk for MI
Acute Coronary Syndrome –
Acute Myocardial Infarction (AMI)
❑ Heart attack
❑ Obstruction of coronary artery(-ies) by
plague → necrosis of myocardium
❑ Life-threatening condition

❑ Clinical Manifestations
❑ Chest pain/discomfort (maybe absent)
❑ Radiation to jaws, back, arms or
shoulder
❑ SOB
❑ Nausea & vomiting
❑ Cold sweating
❑ Lightheadedness
Acute Myocardial Infarction

❑ STEMI
❑ caused by a complete blockage
in a coronary artery

❑ NSTEMI
❑ artery is partially blocked and
severely reduces blood flow
STEMI

Acute Inferior and lateral MI

Inferior leads: II, III, aVF
Lateral leads: V5, V6
 STEMI

RCA: Right coronary artery

LAD: Left anterior descending artery
LCx: left circumflex artery
Acute Coronary Syndrome –
Diagnostic Tests
❑ Physical exam
❑ Blood test
❑ Complete blood picture (CBP)
❑ Renal/Liver function test (R/LFT)
❑ Cardiac enzymes (CK, CK-MB, TnT/TnI)
❑ C-reactive protein (CRP)
❑ clotting profile (PT, APTT, INR)

Creatine Creatine kinase- Troponin T (TnT),

kinase (CK) myoglobin Troponin I (TnI)
(CK-MB) (highly sensitive)

onset 4-8 hr 3-12 hr 3-12 hr

peak 10-24 hr 15-24 hr 24-48 hr
 Acute Coronary Syndrome –
Diagnostic Tests
Unstable NSTEMI STEMI
angina
ECG No changes/ No changes/ ST elevation
ST depression ST depression

Cardiac enzyme No change Increase Increase

e.g. Troponin I ,
Troponin T ,
Creatinine kinase-
myocardial
muscle (CK- MB)
Acute Coronary Syndrome –
Diagnostic Tests
❑ ECG
❑ Echocardiogram
❑ Stress test (Treadmill)
❑ Computed tomography (CT) angiography
❑ Cardiac magnetic resonance imaging (MRI)
❑ Holter: 24 hrs ECG monitoring
❑ Chest X-ray (CXR)
Acute Myocardial Infarction –
Management
❑ Monitor vital signs and oxygen saturation
❑ Establish IV access
❑ Perform brief physical exam and history taking
❑ Obtain initial cardiac marker level, electrolytes and
coagulation studies
❑ Portable CXR
❑ ECG
Acute Myocardial Infarction –
Management
❑ For STEMI onset ≤ 12 hrs
❑ Reperfusion
❑ Door to balloon inflation (PCI) with goal of 90 mins
❑ Door to needle (fibrinolysis) with goal of 30 mins

❑ For NSTEMI and STEMI onset >12 hrs

❑ Consider early invasion strategy if
❑ Refractory ischemic chest discomfort
❑ Recurrent/ persistent ST deviation
❑ Ventricular tachycardia
❑ Hemodynamic instability
❑ Signs of heart failure
STEMI – Thrombolytic Therapy
Use thrombolytic agents to break down fibrin in blood
clots
❑ Restore blood flow to ischemic cardiac muscle

❑ Prevent permanent damage

❑ Thrombolytic agents
❑ Streptokinase (Streptase)
❑ Recombinant tissue plasminogen activator (rtPA)

❑ Assess and monitor

❑ S/S of bleeding tendency
❑ condition of IV site
STEMI – Thrombolytic Therapy
Contraindications
❑ Bleeding disorders

❑ History of cerebral vascular disease

❑ Uncontrolled hypertension

❑ Pregnancy

❑ Recent trauma

❑ Surgery to the head and spine

Acute Coronary Syndrome –
Treatments
Revascularization procedures
❑ Cardiac catheterization:

❑ Coronary angiogram (Coro) +/- percutaneous coronary

intervention (PCI)

Open Heart Surgery

❑ Coronary artery bypass graft (CABG)
Acute Coronary Syndrome –
Coronary Angiogram
❑ Invasive, non-surgical procedure
❑ study coronary arteries
❑ assess the function of the pumping
chamber of heart & patency of
coronary arteries
❑ By using X-ray with contrast
❑ Catheter introduced into the
arterial circulation into the opening
of the narrowed coronary artery
Acute Coronary Syndrome –
Percutaneous Coronary Intervention
❑ Unblocks narrowed coronary arteries without surgery
❑ Indication :
❑ Moderately severe, chronic stable angina unrelieved by
medical therapy
❑ Unstable angina
❑ AMI
❑ Significant stenosis of the left anterior descending coronary
artery
❑ Stenosis of a coronary artery bypass graft
❑ During PCI, cardiologist determines the best treatment
for client
❑ Percutaneous transluminal coronary angioplasty (PTCA)
❑ Balloon angioplasty
❑ Metal stent, drug-eluting stent, bio-absorbable stent
Acute Coronary Syndrome –
Percutaneous Coronary Intervention
Coro +/- PCI – Nursing Interventions
Preparation
 consent

 NPO / NPO except medications for 8 hours

 blood test results (CBC, R/LFT, clotting profile)

 withhold antiplatelet, anticoagulants (e.g. warfarin) (~5-7 days) &

metformin as prescribed
 check allergic history (drug, seafood, contrast)

 educate patient & family about the procedure

 skin preparation (femoral or radial area)

 mark baseline peripheral pulses

 administer pre-medications

 steroid cover for allergic patients e.g. IV hydrocortisone

 wear OT gown & cap

 remove all jewelry & dentures

 ensure bladder empty (+/- urethral catheterization)

Coro +/- PCI – Nursing Interventions
Post procedure care
❑ monitor vital signs & ECG pattern closely
❑ e.g. Q15min.x 4, Q1H x 4, Q4H till stable
❑ monitor & evaluate client’s chest pain level
❑ observe the wound (femoral / radial access site) for any bleeding,
oozing & bruises
❑ observe & monitor the peripheral circulation (limb of insertion site)
❑ i.e. skin color, circulation (pulses), movement & sensation
❑ bed rest in supine position ≥ 8 hrs
❑ resume diet when client is stable & according to physician’s order
❑ encourage early mobilization on the day after bed rest if condition
allows
❑ remind client to bring the reminder card in medical follow-up
Coro +/- PCI – Complications
❑ Hematoma at the catheter insertion site
❑ Pseudoaneurysm
❑ Embolism
❑ Hypersensitivity to contrast dye
❑ Bleeding
❑ Vessel perforation
❑ Restenosis
❑ Reocclusion of the treated vessel
❑ Stroke
❖ Post PCI medication: antiplatelet (e.g. Plavix)
Coronary Artery Bypass Graft
❑ Using a section of a vein and an artery to create a
connection between aorta and coronary artery beyond the
obstruction
❑ Cardiothoracic surgery: under general anesthesia using a
section of a vein (saphenous vein) or internal mammary
artery to create a
connection (bypass)
between aorta & a
site beyond the
obstructed coronary
artery
Coronary Artery Bypass Graft –
Nursing Interventions
Preparation
❑ consent

❑ withhold antiplatelet, anticoagulant according to physician’s

prescription (usually 5-7 days)
❑ assess any allergy history & lab. results
❑ cross match (type & screen)
❑ CBP
❑ R/LFT
❑ clotting profile
❑ ensure blood product(s) is/are reserved if necessary
❑ educate client & family about the procedure, deep
breathing ex. & the expected post-operative condition
❑ NPO ≥ 8 hours
❑ gain IV access +/- IV therapy
Coronary Artery Bypass Graft –
Nursing Interventions
Post operation care (CCU/ICU initially)
❑ Monitor client’s vital signs closely

❑ Monitor client’s ECG during & after the procedure

❑ Inform abnormalities immediately
❑ Wound care & drain care (patency & characteristics of drainage)
❑ Assess client’s bowel movement & return of gag reflex
❑ Resume diet as prescribed (NPO → sips of water → DAT)
❑ Encourage early mobilization
❑ Care of clients with ventilator if indicated

❑ Risk of hypothermia (Post cardiopulmonary bypass)

❑ Monitor core temperature
❑ Institute rewarming measure
➢ warm IV fluid or blood transfusion
➢ warm blanket
➢ radiant heat lamps
Coronary Artery Bypass Graft –
Nursing Interventions
❑ Risk for decreased cardiac output
❑ Monitor the vital signs & ECG closely
❑ Auscultate heart and breath sounds
❑ Muffled heart sound: early indication of cardiac tamponade

❑ Pain management
❑ Report & provide treatment to any arrhythmia &
hypotension promptly
❑ Avoid postural hypotension
❑ encourage client to change body positions slowly
❑ Monitor client’s peripheral circulation
❑ Monitor client’s intake & output
Cardiac Rehabilitation
❑ Long term program of medical evaluation, exercise, risk factors
modification, education and counselling

❑ Aims:
❑ improve client’s quality of life
❑ limit the physical and psychologic effects of cardiac illness

❑ Phase 1 : inpatient
❑ Assess client’s history, current status, risk factors and motivation
❑ Activities progress from bed rest to independent performance of ADLs
❑ Phase 2: immediate outpatient cardiac rehabilitation (within 3 weeks)
❑ Increase activity level, participation and capacity
❑ Improve psychological status
❑ Provide education and support
❑ Phase 3:
❑ Providing transition to independent exercise and exercise maintenance
❑ Follow up to evaluate the risk factors, quality of life and exercise habits
Disorders of Cardiac Function:
Heart Failure (HF)
❑ The most common cardiac disorder
❑ Heart is unable to pump effectively to meet the
body’s need to provide blood and oxygen to the
tissues

❑ Classifications
❑ Left-sidedvs Right-sided
❑ Congestive heart failure (CHF)
Heart Failure – Causes
❑ Coronary artery disease
❑ Hypertension
❑ Valvular heart disease
❑ Cardiomyopathy
❑ Carditis
❑ Congenital heart defects
❑ Arrhythmias
❑ Other diseases:
❑ DM
❑ HIV
❑ Viral attack
❑ Severe infections
Heart Failure – Risk Factors
❑ Causative diseases
❑ Virus
❑ Alcohol use
❑ Tobacco use
❑ Obesity
❑ Certain medications
Heart Failure – Left-sided HF
❑ Common causes: coronary heart disease, hypertension
❑ Can lead to right-sided HF (pressure in the pulmonary
vascular system increase)

❑ Manifestations
❑ Fatigue
❑ Activity intolerance
❑ Dizziness
❑ Syncope
❑ Pulmonary congestion
❑ dyspnea
❑ shortness
of breath
❑ orthopnea
Heart Failure – Right-sided HF
❑ Most common cause: left-sided HF
❑ Isolated right-sided HF is rare, causes include
❑ Acute RV infarction, pulmonary embolism, severe pulmonary
hypertension, conditions that restrict blood flow to the lungs

❑ Manifestations
❑ Weight gain
❑ ↑Abdominal girth
❑ Anorexia and nausea (due to congestion of GI tract vessels)
❑ Edema in the feet and legs
❑ Right upper quadrant pain (due to congestion of liver)
❑ Fatigue
Heart Failure – Congestive HF
❑ Impaired heart function
❑ Structural & functional impairment of ventricular filling
or ejection of blood
❑ Cardiac output decrease

❑ Clinical Manifestations
❑ dyspnea on exertion
❑ shortness of breath
❑ orthopnea
❑ paroxysmal nocturnal dyspnea
❑ nocturnal cough & increase nocturnal urination
❑ Weight gain and peripheral edema (esp. dependent areas)
Heart Failure – Diagnostic Tests
❑ CXR: assess any cardiac hypertrophy (cardiomegaly)
❑ ECG: sinus tachycardia, atrial arrhythmia with rapid
ventricular response
❑ Echocardiography: assess heart muscle thickness, heart
function, ejection fraction (normal 50-70%)
❑ Laboratory testing
❑ B-type natriuretic peptide (BNP): elevated for client with HF
❑ serum electrolytes
❑ blood urea nitrogen
❑ thyroid function test
❑ liver / renal function tests (L/RFT)
❑ blood urea nitrogen (BUN)/serum creatinine
❑ arterial blood gas (ABG)
Heart Failure – Complications
❑ Congestive hepatomegaly
❑ Splenomegaly
❑ Ascites
❑ Arrhythmia
❑ Cardiogenic shock
❑ Acute pulmonary edema (APO)
❑ Manifestation:
❑ Resp.:tachypnea, dyspnea, orthopnea, cough with frothy & pink
sputum, lung sounds with crackles
❑ CVS: tachycardia, hypotension, cyanosis, hypoxemia

❑ Managements include ventilation support & fluid removal

Heart Failure – Treatments
❑ Angiotensin-converting enzyme inhibitor/Angiotensin
II receptor blocker
❑ relaxing and opening up the blood vessels
❑ Beta-blocker
❑ ↓HR to reduce oxygen consumption and protecting the
heart from the effects of adrenaline and noradrenaline
❑ Diuretic
❑ ↓fluid retention → ↓blood volume
❑ Digoxin
❑ ↑myocardial contractility and ↓HR
❑ avoid first line using as its toxicity
Heart Failure – Treatments
❑ Coronary bypass surgery
❑ Heart valve repair or replacement
❑ Pacemaker
❑ Cardiac resynchronization therapy (CRT)
❑ Implantable cardioverter-defibrillator (ICD)
❑ Ventricular assist device (VAD)
❑ Heart transplant
Heart Failure – Treatments
❑ Cardiac resynchronization therapy
❑ a special type of pacemaker that can make the walls of the
both ventricle contract at the same time

❑ Implantable cardioverter defibrillator

❑ automatic defibrillation when fatal arrhythmia sensed
❑ ↓Sudden cardiac death
❑ correct fatal arrhythmia, but not altering the heart function

❑ CRT-D
❑ Devices that combine cardiac resynchronization and
defibrillation are implanted into patients who need both.
Heart Failure – Treatments
❑ Ventricular assist device
❑ mechanical circulatory support device used to partially
or completely replace the function of a failing heart
❑ powered by an electricity source from outside the body

❑ implantable mechanical pump

❑ implanted into abdomen or chest and attached to a

weakened heart to help it pump blood to the rest of
body
❑ to help keep heart transplant needed clients alive while
waiting for a donor heart
❑ may also be used as an alternative to transplantation
Heart Failure – Treatments
Implantable Cardioverter
Defibrillator Ventricular Assist Device
Heart Failure – Nursing Interventions
For acute exacerbation,
❑ Monitor vital signs (BP/P, RR, oxygen saturation)

❑ Administer supplemental oxygen for hypoxemia (SpO2

<90%)
❑ Monitor and keep accurate intake and output records

❑ Monitor client’s central venous pressure if indicated

❑ Monitoring of body weight (daily)

❑ Restrict fluid as prescribed, provide ice cubes, hard

candies and mouth care (relief of dry mouth and thirst)
❑ Restrict dietary sodium intake

❑ Keep bed resting with head of bed elevated

❑ Provide emotional support

Heart Failure – Nursing Interventions
Patient education
❑ Symptom management and self-care
❑ Monitor and recognize condition changes
❑ Flexible diuretic regimen
❑ Pharmacological treatment
❑ Understand the indications, dosing and side effects of drugs
❑ Recognize the benefits of taking medications as prescribed
❑ Implanted devices
❑ Understand the indications/benefits/complications of the
devices
❑ Immunization
❑ Receive immunization against influenza and pneumococcal
disease
Heart Failure – Nursing Interventions
Patient education
❑ Diet and alcohol
❑ Avoid excessive fluid intake (1.5 – 2.0 L/day as prescribed)
❑ Monitor body weight
❑ Avoid excessive salt intake (>6g/day)
❑ Abstain from alcohol intake
❑ Smoking cessation
❑ Regular exercise
❑ Sexual activity
❑ Be reassured about engaging in sex
❑ provided sexual activity does not provoke undue symptoms
❑ recognize problems with sexual activity (e.g. erectile
dysfunction)
Disorders of Cardiac Structure:
Valvular Heart Disease
Damage or defect in
one of the four heart
valves: the mitral,
aortic, tricuspid or
pulmonary.
❑ Stenosis

❑ Regurgitation, aka

insufficiency
Valvular Heart Disease: Causes
❑ Valvular Stenosis
❑ tissues
forming the valve leaflets become stiffer
❑ narrow valve opening

❑ impede forward flow → ↓ cardiac output

❑ caused by scarring of the valves and calcium deposits

❑ Valvular Regurgitation (insufficiency)

❑ leafletsdo not close completely → backflow of blood
❑ caused by deformity or erosion of valve cusps induced
by infective endocarditis, MI, cardiac dilation
Mitral Stenosis
❑ Narrowing MV → ↓blood volume to LV & CO
❑ ↑pressure in LA → LA hypertrophy & pulmonary
congestion
❑ ↑pressure in pulmonary vessels → RA+RV hypertrophy

❑ Causes:
❑ rheumatic heart disease, bacterial
endocarditis
❑ Complication:
❑ atrial fibrillation
❑ pulmonary hypertension/edema
❑ heart failure
Mitral Regurgitation
❑ Incomplete closure of MV during systole → backflow of
blood → ↓CO → to compensate, LV hypertrophy
❑ ↑LA pressure → LA hypertrophy & pulmonary congestion
❑ ↑pressure in pulmonary vessels → slightly enlargement of
RV

❑ Causes:
❑ mitral valve prolapse, rheumatic heart
disease, damaged tissue cords,
cardiomyopathy, endocarditis
❑ Complications
❑ pulmonary hypertension/edema
❑ heart failure
Aortic Stenosis
❑ ↓ EF during systole & CO → LV hypertrophy
❑ Incomplete emptying of LA → pulmonary
congestion

❑ Causes:
❑ idiopathic
❑ congenital heart defect
❑ aging as calcium or scarring
damages the valve
❑ Complication:
❑ pulmonary hypertension/edema
❑ heart failure
Valvular Heart Disease: Manifestations
❑ Can be asymptomatic
❑ S/S depends on severity
❑ Dyspnea on exertion
❑ Fatigue & weakness
❑ Exercise intolerance
❑ Murmur during auscultation (high pitched, rumbling, loud)
❑ Heart palpitations
❑ Swollen feet or ankles
❑ Orthopnea
❑ Hemoptysis
❑ Dizziness
❑ Angina
❑ Syncope on exertion (exercise or strong emotion)
Valvular Heart Disease: Diagnostic
Tests
❑ Electrocardiography
❑ Echocardiography

❑ Chest X-ray

❑ Cardiac CT/MRI

❑ Stress test

❑ Cardiac catheterization
Valvular Heart Disease: Treatments
❑ Medication
❑ Anticoagulants
❑ Anti-arrhythmic drugs
❑ Diuretics
❑ ACEI
❑ Vasodilators
❑ Beta-blockers
❑ Antibiotic

❑ Surgical treatment
❑ valve repair surgery
❑ valve replacement
 Valvular Heart Disease: Treatments
Types Materials Advantages Disadvantages Selection

Mechanica Strong materials Long term • Lift time anti- <65 yrs old
l e.g. titanium durability Coagulation
carbon • Audible click
• Risk of
thromboembolism

Biological Biological tissues Low incidence of • Prone to >65 yrs old

e.g. pig thromboembolism Deterioration
-quiet • Less durable
(~15 yrs)
Valvular Heart Disease:
Nursing Interventions
❑ Monitor vital signs & ECG patterns
❑ note for decreased systolic BP & tachycardia → signs of ↓
cardiac output
❑ Restrict fluid & salt intake as prescribed
❑ reduce cardiac workload due to fluid overload
❑ monitor I&O, body weight QD, monitor signs of fluid retention
❑ educate the fluid restriction (1 - 1.2L/day) & low salt diet (<
2g/day)
❑ Monitor oxygen saturation & arterial blood gas (ABG)
❑ elevate head of bed +/- oxygen therapy → improve tissue
perfusion
❑ Provide psychological care
Disorders of Cardiac Structure:
Cardiomyopathy
❑ Dilated & Hypertrophic Cardiomyopathy
Cardiomyopathy

Dilated Cardiomyopathy Hypertrophic Cardiomyopathy

❑ Most common ❑ Causes: Hereditary, may

be 2nd to chronic
❑ Causes: Idiopathic, may hypertension
be 2nd to alcoholism or ❑ Manifestations: Dyspnea,
myocarditis angina, syncope, LV
hypertrophy, arrhythmias,
❑ Manifestations: HF, sudden death
cardiomegaly, ❑ Managements:
arrhythmias Medications, ICD, cardiac
pacing, surgical excision
❑ Managements: As HF, of part of the ventricular
ICD, cardiac transplant septum
Cardiomyopathy
Restrictive Cardiomyopathy
❑ Less common

❑ Causes

❑ Secondary to amyloidosis, radiation or myocardial

fibrosis
❑ Manifestations
❑ Dyspnea, fatigue, HF
❑ Managements
❑ As HF, exercise restriction
❑ Poor prognosis
Inflammatory Heart Disorders:
Carditis
❑ Pericarditis
❑ the inflammation of
the pericardium
❑ Myocarditis
❑ the inflammation of
the heart muscle
❑ Endocarditis
❑ the inflammation of
the endocardium
Pericarditis – Causes
❑ Infectious
❑ Viruses, bacteria, tuberculosis, syphilis, parasites

❑ Noninfectious
❑ myocardial and pericardial injury
❑ rheumatic fever

❑ autoimmune disorders

❑ exposure to radiation

❑ connective tissue diseases

Pericarditis – Manifestations
❑ Pleuritic chest pain (due to inflammation of nerve
fibers)
❑ rapid onset, sharp, persistent or intermittent
❑ may radiate to neck or back

❑ commonly substernal, left anterior chest or epigastrium

❑ aggravated by respiratory movements

❑ relieved by sitting up and worsened by lying down

❑ Other signs & symptoms

❑ dyspnea, cough, fever, tachycardia
❑ pericardial friction rub (by auscultation)
Pericarditis – Diagnostic Tests
❑ CXR: cardiac enlargement in pericardial effusion
❑ ECG: diffuse ST segment elevation in all leads
❑ Echocardiogram: assess heart function, check for
fluid or pericardial effusion
❑ Classic signs: stiff or thick pericardium that constricts the
heart’s normal movement
❑ Cardiac CT or MRI: identify pericardial effusion or
constrictive pericarditis
Pericarditis – Diagnostic Tests
❑ Cardiac catheterization: assess the filling pressures
in the heart to confirm a diagnosis of constrictive
pericarditis
❑ Blood tests: rule out MI, culture of pericardial fluid
❑ Inflammation markers
❑ Erythrocyte sedimentation rate (ESR)
❑ C-reactive protein (CRP)

❑ CBP – WBC

❑ Autoimmune disease marker like lupus and rheumatoid

arthritis
Pericarditis – Complications
❑ Pericardial effusion
❑ Abnormal collection of fluid between pericardial layers
❑ Can lead to cardiac tamponade

❑ Constrictive pericarditis
❑ Chronic inflammation → scar tissue formation between
pericardial layers
❑ Scar tissue contracts → restrict diastolic filling →
elevated venous pressure
❑ Manifestation:

➢ Progressive dyspnea, fatigue and weakness

➢ Ascites is common
Pericarditis – Complications
❑ Cardiac tamponade
❑ Acute accumulation of fluid (>200ml) in the pericardial
sac → increased pressure on the myocardium
❑ Manifestation: Beck’s triad

➢ hypotension (due to excessive fluid exerting pressure on

the myocardium, limiting proper ventricular filling)
➢ distended jugular veins (due to poor right ventricular
filling)
➢ distant & muffled heart sounds
Pericarditis – Treatments
❑ Medication
❑ Antibiotic or antifungal medication
❑ Anti-inflammatory drug
❑ Colchicine: help control the inflammation and prevent
recurrence
❑ Analgesics
❑ Nonsteroidal anti-inflammatory drug (NSAID)
❑ Corticosteroid if responds poorly to NSAID

❑ Other treatments
❑ Pericardiocentesis: drain extra fluid in the pericardium and
decompresses the heart under echocardiography
❑ Pericardiectomy: remove some pericardium in constrictive
pericarditis
Pericarditis – Pericardiocentesis
❑ To remove fluid from the pericardial sac
❑ for diagnostic and/or therapeutic purpose
❑ emergency procedure for cardiac tamponade

❑ Procedure
❑ consent
❑ positioning (supine/semi-fowler)
❑ continuous cardiac monitoring and apply local anesthesia
❑ insertion of a large-gauge needle to the left of xiphoid
process into the pericardial sac, withdraw excessive fluid
under ultrasound guidance
❑ send specimen for exam if needed
Pericarditis – Pericardiocentesis
❑ Nursing care
❑ assess and record vital signs (every 5 mins, BP/P)
❑ instruct client to remain still during the procedure

❑ monitor the ECG during and

after the procedure, inform
abnormalities to physician
immediately
Myocarditis – Causes
❑ Often, no specific cause is identified
❑ Other causes:
❑ virus(most common)
❑ bacterial

❑ parasites

❑ toxins or drugs (e.g. ethanol, cocaine)

❑ autoimmune disease
Myocarditis – Manifestations
❑ Asymptomatic but with ECG and/or echocardiogram
abnormalities
❑ Non-specific cardiac symptoms:
❑ Fatigue
❑ Dyspnea on exertion
❑ Arrhythmias
❑ Palpitations
❑ Chest pain at rest

❑ Fever, chills
❑ Cardiac dysfunction, heart failure
❑ Haemodynamic collapse
Myocarditis – Diagnostic Tests
❑ ECG: transient ST segment & T wave changes (most
common)
❑ Laboratory testing
❑ Cardiac enzyme: e.g. TnI (most specific), TnT, CK/CK-
MB
❑ Cardiac imaging
❑ Echocardiogram
❑ Cardiac MRI
❑ Endomyocardial biopsy
❑ Invasive
❑ Essential for diagnosing specific form of myocarditis
Myocarditis – Complications
❑ Heart failure
❑ can't pump blood effectively → may require ventricular
assist device or heart transplant
❑ Heart attack or stroke
❑ bloodpools in heart → form clots → block arteries
→ heart attack or stroke
❑ Arrhythmias
❑ Sudden cardiac arrest
Myocarditis – Treatments
For mild cases,
❑ Rest, avoid competitive sports (> 3-6 months)

❑ Medications

❑ Angiotensin-converting enzyme inhibitor or angiotensin

receptor blocker
❑ Beta blocker
❑ Diuretic
❑ Corticosteroid/other immunosuppressive agent
❑ Antimicrobial/antiviral therapy

❑ Management of heart failure

❑ Temporary pacing for dysrhythmia
Myocarditis – Treatments
For severe cases,
❑ Hemodynamic support
❑ Inotropic agents
❑ Intra-aortic balloon pump

❑ Ventricular assist device

❑ Heart transplantation
❑ Extra-corporeal membrane oxygenation

(ECMO): Mechanical circulatory support

Endocarditis
❑ Inflammation of the endocardium, usually involving
heart valves
❑ Usually caused by infection
❑ bacterial

❑ viral

❑ fungal

❑ parasite

❑ Caused by colonization or invasion by pathogen

❑ Also called Infective endocarditis (IE)
Endocarditis – Classifications

Acute infective endocarditis Subacute infective

endocarditis
Onset Sudden Gradual

Risk factors Previously normal heart, IV Occur in damaged heart,

drug
use, infected IV sites
Pathologic Rapid valve destruction
process
Presentation Abrupt onset with spiking
fever and chills
Symptoms of heart failure
dental
procedure, invasive procedure,
infections
Valve destruction leading to
regurgitation, embolization of
vegetation
Gradual onset of febrile illness
with cough, dyspnea, join pain,
abdominal pain
Endocarditis – Manifestations
❑ Chills and fever
❑ General malaise, fatigue
❑ Joint pain
❑ Cough
❑ Dyspnea
❑ Anorexia, abdominal pain
❑ Petechiae (bleeding under skin)
❑ Splinter hemorrhage (tiny blood clot)
❑ Splenomegaly
❑ Heart murmur
Endocarditis – Diagnostic Tests
❑ Medical history
❑ Dental procedure
❑ Invasive procedure
❑ Blood test
❑ Inflammatory markers
❑ Cardiac enzymes
❑ Culture & sensitivity test (C/ST) (≥2 blood samples draw from
different sites and/ or at different times)
❑ Immune markers
❑ Echocardiography (transthoracic or transesophageal)
❑ Visualize fibrin clots or scars
❑ CXR
❑ ECG
Endocarditis – Antibiotic Prophylaxis

❑ Indications
❑ Prostheticvalves, previous episode IE, congenital heart
disease, cardiac transplant
❑ High risk procedures
❑ Dental procedures when bleeding is likely
❑ Most surgeries

❑ Bronchoscopy/Cystoscopy

❑ Urinary catheterization when infection is present

❑ Incision & drainage of infected tissue

❑ Vaginal delivery if infection is present

Endocarditis – Treatments
❑ Medications
❑ Start antibiotic (2-8 weeks) after taking the blood
cultures → titrate antibiotics according to blood culture
results
❑ Initial regimen: penicillin, gentamicin, ampicillin

❑ If allergic to penicillin → ceftriaxone, cefazolin or

vancomycin
❑ Surgery
❑ Replace the severely damaged valves with prosthesis
❑ Remove large scars or clots that at risk for embolization
Hypertension (HT)
❑ Prevalence & incidence
❑ Estimated 1.13 billion worldwide (WHO, 2019)
❑ According to Hong Kong 2014/15 population Health
Survey:
• aged 15-84, total prevalence 27.7% (self-reported +
detected during health exam)
• 47.5% undiagnosed
• prevalence ↑ : 4.5% (aged 15-24) → 64.8% (aged 65-84)
Hypertension – Definition
WHO 2019,
❑ when it is measured on two different days,

❑ Systolic BP (SBP) readings on both days is ≥140 mmHg

and/or
❑ Diastolic BP (DBP) readings on both days is ≥90 mmHg

❑ Pre-hypertension
❑ SBP:120-139 mmHg or DBP: 80-89 mmHg
Hypertension – Definition
Hypertension – Types
❑ Primary = Essential
❑ No identifiable cause
❑ ~ 90- 95%

❑ Secondary
❑ Caused by another medical condition
❑ E.g. diabetes, renal disease, hyperthyroidism

❑ ~ 5-10%
Hypertension – Risk Factors
❑ Modifiable:
❑ unhealthy diets (↑ salt, ↑saturated fat & trans fats, ↓fruits &
vegetables)
❑ physical inactivity

❑ consumption of tobacco & alcohol (increase heart workload)

❑ overweight or obese

❑ stress

❑ Non-modifiable:
❑ family history
❑ >65 years old (BP ↑ with age & arteries lose elasticity)

❑ co-existing diseases e.g. diabetes or kidney disease

Hypertension – Manifestations
❑ Early stage
❑ can be asymptomatic
❑ early morning headaches, nosebleeds, irregular heart
rhythms, vision changes, buzzing in the ears

❑ Later stage, more severe

❑ fatigue, nausea, vomiting, confusion, anxiety, chest pain,
muscle tremors
Hypertension – Diagnostic Tests
❑ Ambulatory blood pressure monitoring
❑ reduce white coat hypertension
❑ wear device 24 or 48 hrs
❑ record BP periodically (usu. 15 or 30 mins interval)
❑ consider average SBP, DBP

❑ Other investigations
❑ Blood test: CBC, RFT (Na+, K+, urea, creatinine),
fasting blood glucose, lipid profile (cholesterol)
❑ ECG
❑ CXR
Hypertension – Complications
❑ Excessive pressure harden arteries → ↓blood flow
& oxygen to heart:
❑ Angina

❑ Heart attack: blood supply to heart blocked & heart

muscle cells died due to lack of oxygen
❑ Heart failure: heart can’t pump enough blood &
oxygen to other vital body organs
❑ Arrhythmia → sudden death
Hypertension – Complications
❑ Stroke: burst or block blood & oxygen supply to
brain
❑ Kidney damage → kidney failure
❑ Peripheral arterial disease
❑ Retinopathy
Hypertension – Lifestyle Modifications
❑ ↓weight for overweight or obese
❑ ↓Na+ intake ( <2g daily) or ↓ salt ( <5g daily)
❑ Healthy diet e.g. Dietary Approaches to Stop Hypertension
(DASH diet) – ↑ fruits, ↑vegetables, ↓ fat dairy products,
↓saturated & trans fat
❑ Physically active – ≥ 30mins moderate intensity, ≥ 3 days/
week
❑ Smoking cessation
❑ ↓ alcohol consumption: (1 drink = 360ml beer /300ml wine
/ 90ml whisky)
❑ M:≤ 2 drinks/day
❑ F:≤ 1 drink/day
❑ Relaxation techniques e.g. yoga, meditation
Hypertension – Medications
Anti-hypertensive drug classes:
❑ Alpha-adrenergic blocker

❑ Angiotensin-converting enzyme inhibitor

❑ Angiotensin receptor blocker

❑ Beta-adrenergic blocker

❑ Calcium-channel blocker

❑ Diuretics

❑ Vasodilators
Hypertension – Medications
Alpha-adrenergic blocker (-blocker)
❑ Action : Block α-receptors in smooth muscle →

prevent vasoconstriction at vascular level

❖ May cause significant postural hypotension &
tachycardia following initial dose
❑ Nursing care:

❑ change body posture slowly

❑ give the initial dose at bedtime → ↓risk of fainting

❑ Closely monitor BP/P

❑ E.g. Prazosin, Terazocin

Hypertension – Medications
Angiotensin-converting enzyme inhibitor (ACEI) &
Angiotensin receptor blocker (ARB)
❑ Action:

❑ ACEI: inhibit conversion of angiotensin I to angiotensin II →

prevent vasoconstriction and sodium and water retention
❑ ARB: block the activation of angiotensin II receptors directly
❖ Same effect for ACEI & ARB, NOT prescribe together
❖ ACEI may cause persistent dry cough, taste disturbance,
renal impairment
❑ Consider use of ACEI first : cheap
❑ Examples
❑ ACEI: Lisinopril, Captopril
❑ ARB: Losartan, Valsartan
Hypertension – Medications
Beta-adrenergic blocker (-blocker)
❑ Action: prevent beta-receptor stimulation in heart

→ ↓ heart rate & ↓ cardiac output

❖ Avoid sudden discontinuation

❖ NOT for clients with asthma, bradycardia, heart

block
❑ Nursing care:

❑ Monitorbronchospasm
❑ Check BP & heart rate before administration

❑ E.g.: Propranolol, Metoprolol, Atenolol

Hypertension – Medications
Calcium-channel blocker (CCB)
❑ Action: block calcium entry into smooth muscle

❑→ vasodilation, ↓ peripheral vascular resistance,

❑ →↓ heart rate, ↓ventricular conduction

❑ Nursing care:
❑ monitor BP/ P, LFT, RFT, ECG, I/O & daily weight
❑ report signs of heart failure, bradycardia, prolonged
hypotension
❑ E.g. Amlodipine, Nifedipine, Diltiazem
Hypertension – Medications
Diuretic
❑ Action: ↓ tubular reabsorption of sodium &
water →↓ total blood volume → ↓ BP
❖ Administer last dose in early evening (~18:00)
to avoid nocturia
❑ Nursing care:
❑ monitor
BP, I&O, body weight, potassium level, S/S of
dehydration (thirsty, dizziness, dry mouth, dry skin,
decreased urinary output)
❑ E.g. Furosemide, Spironolactone
Hypertension – Medications
Vasodilator
❑ Action: relax vascular smooth muscle (especially

arterioles) → ↓ peripheral vascular resistance

❖ NOT for chronic HT management due to its toxic
effect
❑ Nursing care:

❑ check BP/ P before administration

❑ monitor peripheral edema, heart failure, postural BP

❑ advice clients change posture slowly

❑ E.g. Hydralazine
Hypertension – Nursing Interventions

Assessment
❑ History taking
❑ Risk factors
❑ Signs of target organ damage
❑ Physical examination
❑ BP: Both arms, sitting & supine positions
❑ Apical & peripheral pulses
❑ BMI
❑ Retinal fundus
❑ Laboratory results
Hypertension – Nursing Interventions

Increase knowledge & promote compliance

❑ Teach about disease process

❑ Education on medications
❑ Expected effect
❑ Side effects
❑ Rebound hypertension if discontinue suddenly
❑ Identify current behaviors contributing to
hypertension
❑ Develop a realistic health maintenance plan

❑ Self-monitoring
Arterial disorders:
Aneurysms
❑ Abnormal dilation of a blood vessel
❑ Affect the aorta and peripheral arteries

❑ Caused by:
❑ Arteriosclerosis/atherosclerosis
❑ Trauma

❑ Risk factors
❑ HT
❑ Hyperlipidemia
❑ Smoking
❑ Family history
Aortic Aneurysms – Manifestations
❑ May be asymptomatic until ruptures
❑ Different sites of aortic aneurysms

❑ Thoracic aortic aneurysm (TAA) – Pain (back, neck or

substernal), edema of face & neck, distended neck
veins
❑ Abdominal aortic aneurysm (AAA) – Pulsating abd
mass, pain (mid-abd, lumbar)
❑ Aortic dissection – Pain in area of aneurysms, weak or
absent pulses and BP in upper extremities, syncope
Aortic Aneurysms – Complications
❑ Rupture and haemorrhage – is a medical
emergency and life threatening
❑ Abdominal aortic aneurysm
❑ peripheral emboli to lower extremities
❑ Aortic dissection
❑ renal failure
❑ myocardial infarction
❑ heart failure
❑ cardiac tamponade
❑ sepsis
❑ weakness or paralysis
Aortic Aneurysms – Diagnostic Tests
❑ CXR – to visualize TAA
❑ Abdominal ultrasonography – to diagnose

AAA
❑ Transesophageal echocardiography – to

identify TAA and dissecting aneurysm

❑ Contrast enhanced CT or MRI – allow precise

measurements of aneurysm size

❑ Angiography- uses contrast solution to visualize
the precise size and location of the aneurysm
Aortic Aneurysms – Treatments
❑ Medication
❑ Beta-blocker

❑ Adjacent antihypertensive
❑ Anticoagulant after surgery to prevent formation of clot

❑ Surgery
❑ Operative repair of aortic aneurysm – aneurysm is
excised and replaced with a synthetic fabric graft
❑ Endovascular aortic repair (EVAR) – stent is placed
percutaneously via the femoral artery
Arterial disorders:
Peripheral Artery Disease (PAD)
❑ Causes:
❑ Atherosclerosis (most common)
❑ Injury, infection, irregular
anatomy of muscles or
ligaments
❑ Usually affects the legs

❑ Types:
❑ Acute – Formation of occlusive clots, e.g. thrombosis → impair
tissue perfusion
❑ Chronic – Structural defects of arterial walls or spasm of the
affected arteries → limit O2 & nutrients to tissues

❑ Complication:
❑ Gangrene (tissue death) → can lead to limb amputation
Peripheral Artery Disease –
Risk Factors
❑ >50 years old
❑ Male
❑ Overweight
❑ Kidney disease
❑ History of stroke
❑ DM
❑ HT
❑ Hyperlipidemia
❑ Smoking
❑ Physical inactivity
Peripheral Artery Disease –
Manifestations
❑ Painful cramping in one or both of your hips, thighs or calf
muscles after certain activities, such as walking or climbing
stairs (claudication)
❑ Leg numbness or weakness
❑ Coldness in your lower leg or foot, especially when
compared with the other side
❑ Sores on your toes, feet or legs that won't heal
❑ A change in the color of your legs
❑ Hair loss or slower hair growth on your feet and legs
❑ Slower growth of your toenails
❑ Shiny skin on your legs
❑ No pulse or a weak pulse in your legs or feet
❑ Erectile dysfunction in men
Peripheral Artery Disease –
Diagnostic Tests
❑ Ankle-brachial index (ABI)
❑ ratio of ankle systolic pressure to the
arm systolic pressure

❑ Doppler ultrasound flow studies

❑ Computerized tomography angiography (CTA)
❑ Magnetic resonance angiography (MRA)
Peripheral Artery Disease –Treatments

❑ Lifestyle modifications (similar to CAD)

❑ Medications
❑ Antiplatelet such as aspirin or clopidogrel (Plavix)
❑ Cilostazol – a platelet inhibitor with vasodilator
properties
❑ Revascularization (for severe cases)
❑ Percutaneous transluminal angioplasty (PTA) –
Nonsurgical methods of balloon angioplasty,
atherectomy, laser/thermal angioplasty + stent
❑ Endarterectomy – remove occlusive plaque from the
artery and bypass grafts
Peripheral Artery Disease – Foot Care

❑ keep lower limbs clean, dry & comfortable

❑ wash lower limbs daily with warm soap water (mild soap)
❑ pat dry with soft towel
❑ apply moisturizing cream to prevent dryness
❑ wear sock & comfortable shoes fit to the feet
❑ prevent accidents & injuries e.g. no barefoot
❑ inspect lower limbs daily
❑ do not cross legs
❑ do not swim in cold water
❑ report foot problems to health professionals
Arterial disorders:
Raynaud’s Disease
❑ aka Raynaud's phenomenon or Raynaud's syndrome
❑ Smaller arteries that supply blood flow to the skin
to narrow in response to cold or stress.
❑ Unknown cause
❑ The affected fingers and toes, might turn white or
blue, feel cold and numb until
circulation improves.
❑ Primarily affects young
women age 20-40
❑ Provokes by cold weather or
stress
Raynaud’s Disease – Treatments
❑ Supportive treatment
❑ Avoidprovoking factors
❑ Smoking cessation

❑ Medication
❑ Low dose CCB or Alpha-blocker – to reduce the
frequency and severity of attacks
Venous disorders:
Deep Venous Thrombosis
❑ A blood clot (thrombus) forms on the wall of a vein,
accompanied by inflammation of the vein wall and
some degree of obstructed venous blood.
❑ Mostly forms in thigh or lower leg.
❑ Thrombus may break loose and travel through the
circulation (as emboli) to cause life-threatening
complications such as pulmonary embolism.

❑ Pathophysiology
❑ Stasis of blood
❑ Vessel damage
❑ Increased blood coagulability
Deep Venous Thrombosis –
Manifestations
❑ Usually asymptomatic
❑ Dull, aching pain in affected extremity, especially
when walking
❑ Possible tenderness, warmth, erythema along
affected vein
❑ Cyanosis of affected extremity
❑ Swelling (edema) of affected extremity
Deep Venous Thrombosis –
Diagnostic Tests
❑ Duplex venous ultrasonography
❑ Noninvasive, can visualize the vein and measure the
velocity of blood flow in the veins.
❑ Plethysmography
❑ Noninvasive, can measure changes in blood flow
through the veins.
❑ Ascending contrast venography
❑ Invasive,uses an injected contrast medium to assess the
location and extent of venous thrombosis.
Deep Venous Thrombosis – Treatments

❑ Medication
❑ Anticoagulants

➢ Heparin/Low-molecular-weight heparin
➢ inhibitthe effects of thrombin and prevent the conversion of
fibrinogen to fibrin.
➢ Monitor APTT

➢ Warfarin
➢ interfereswith synthesis of vitamin K-dependent clotting
factors by the liver, leading to depletion of these factors.
➢ Monitor PT/INR
Deep Venous Thrombosis – Treatments

❑ Supportive treatment
❑ Bedrest in acute phase
❑ Elevation of legs

❑ Use of elastic compression stockings or pneumatic

compression device
❑ Surgery
❑ Venous thrombectomy – when thrombi lodge in the
femoral vein and their removal is necessary to prevent
pulmonary embolism or gangrene.
❑ IVC filter – to capture emboli from the pelvis and lower
extremities, preventing pulmonary embolism
Deep Venous Thrombosis –
Nursing Interventions
❑ Follow supportive treatment
❑ Monitor blood tests for clotting time to evaluate the
medication effects (follow up blood test is needed)
❑ Monitor respiratory status for complication of
pulmonary embolism
❑ Monitor calf and thigh diameter of the affected
extremity
❑ Pain management
❑ Promote mobility – encourage ROM exercise, frequent
position changes, etc.
❑ Foot care
❑ Avoid cross leg, use a recliner chair when sitting
Venous disorders:
Varicose Veins
❑ Problems with valves: fragile, weakened,
damaged, deteriorate over time → pooling of
blood in veins

❑ Manifestations
❑ veins near the skin’s surface
➢ bulging and twisted
➢ discoloration: dark purple or blue
➢ dilatation & elongation of
saphenous valves
➢ achy or heavy feeling of legs
➢ pain worsen after sitting or standing for a long time
Varicose Veins
Risk Factors
❑ family history

❑ age

❑ pregnancy

❑ overweight or obesity

❑ lack of movement

❑ standing or sitting for long periods of

time
❑ female, hormonal changes

Diagnostic tests
❑ Duplex venous ultrasonography

❑ visualize the vessels & measure the velocity of blood flow

Varicose Veins – Treatments
❑ Self-care
❑ exercising, losing weight, not wearing tight clothes,
elevating the legs, and avoiding long periods of
standing or sitting
❑ Compression stockings
❑ Sclerotherapy
❑A sclerosing solution is injected into the vein that scars
and closes those veins. In a few weeks, treated varicose
veins should fade.
Varicose Veins – Treatments
❑ High ligation and vein stripping
❑ tying off a vein before it joins a deep vein and
removing the vein through small incisions
❑ Ambulatory phlebectomy
❑ removes smaller varicose veins through a series of tiny
skin punctures
❑ Endoscopic vein surgery
❑ for client involving leg ulcers with other techniques fail
❑ uses a thin video camera inserted in leg to visualize
and close varicose veins and then removes the veins
through small incisions
Varicose Veins – Nursing Interventions

❑ Pain management
❑ Use of elastic compression stockings
❑ Promote regular exercise
❑ Advise to elevate the legs for 15-20 minutes
several times a day and during sleep
❑ Promote foot and skin care to avoid injury
Lymphatic disorders:
Lymphedema
❑ Caused by inflammation, obstruction or removal of
lymphatic vessels.
❑ Characterized by extremity edema due to
accumulation of lymph
❑ Female > Male
Lymphedema - Manifestations
❑ Swelling of part or all of your arm or leg, including
fingers or toes
❑ A feeling of heaviness or tightness
❑ Restricted range of motion
❑ Aching or discomfort
❑ Recurring infections
❑ Hardening and thickening of the skin (fibrosis)
Lymphedema - Treatments
❑ Supportive treatment
❑ Meticulous skin and foot care – to prevent infection.
❑ Exercise and leg elevation – to promote lymph flow.

❑ Elastic graduated compression stocking/intermittent

pneumatic compression device – to reduce edema.
❑ Medication
❑ Antibiotic – to prevent infection
❑ Diuretic – promote fluid loss
Lymphedema – Nursing Interventions

❑ Elevate affected extremities while seated and

during sleep.
❑ Apply elastic compression stockings as ordered.
❑ Careful cleansing and keep skin clean and dry.
❑ Encourage exercise.
❑ Monitor I&O.
❑ Restrict sodium intake if needed.
Common Nursing Diagnoses for Clients
with Cardiovascular Disorders
❑ Activity Intolerance
❑ Acute Pain
❑ Decreased Cardiac Output
❑ Impaired Physical Mobility
❑ Ineffective Peripheral Tissue Perfusion

❑ Impaired Gas Exchange

❑ Ineffective Airway Clearance
❑ Ineffective Breathing Pattern

❑ Anxiety
❑ Fatigue
References
American Heart Association. (2016). Advanced cardiovascular life support: provider manual.

American Heart Association. (2017). Part 5: Adult basic life support and cardiopulmonary resuscitation
quality.

American Heart Association. (2018). Highlight of the 2018 focused updates to the American Heart
Association Guidelines for CPR and ECC: Advanced Cardiovascular life support and pediatric advanced life
support.

Black, J. M., & Hawks, J. H. (2009). Medical-surgical nursing: Clinical management for positive outcomes
(8th ed.). St Louis, Mo.: W.B. Saunders.

Carpenito-Moyet, L. J. (2017). Nursing diagnosis: Application to clinical practice (15th ed.). Philadelphia,
PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Ellenbogen, K. A., & Wood, M. A. (2005). Cardiac pacing and ICDs (4th ed.). Oxford: Blackwell Publishing
Ltd.
References
Hinkle, J. L., & Cheever, K. H. (2014). Brunner and Saddarth’s textbook of medical surgical nursing (13th ed.). London:
Wolters Kluwer Health/ Lippincott Williams and Wilkins.

Hoen, B., & Duval, X. (2013). Infective endocarditis. The New England Journal of Medicine. 268, 1425–1433.

Hogan-Quigley, B., Palm, L. M., & Bickley, L. (2012). Bate’s nursing guide to physical examination and history taking.
Philadelphia: Lippincott Williams & Wilkins.

James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J., & Ortiz, E. (2014). 2014
evidence-based guideline for the management of high blood pressure in adults: Report from the Panel Members
Appointed to the Eighth Joint National Committee. Journal of American Medical Association, 311(5), 507-520.

Jun, S., & Gaetano, S. (2018). Update on peripheral artery disease: Epidemiology and evidence-based facts. Journal of
Atherosclerosis, 275,379-381.

LeMone, P., Burke, K., & Gubrud, P. (2015). Medical-surgical nursing: Clinical reasoning in patient care (6th ed.). Boston:
Pearson.

Mann, D. L., Zipes, D. P., Libby, P., & Bonow, R. O. (2015). Braunwald's heart disease: a textbook of cardiovascular
medicine (10th ed.). Philadelphia, PA : Elsevier/Saunders.
References
Martin, C., & McGrath, B. P. (2013). Ambulatory and home blood pressure measurement in
management of hypertension: White-coat hypertension. Clinical and Experimental Pharmacology and
Physiology, 41(1), 22-29.

Norgard, N. B., & Dinicolantonio, J. J. (2013). Clopidogrel, prasugrel or ticagrelor: A practical guide
to use of antiplatelet agents in patients with acute coronary syndrome. Postgraduate Medicine, 125(4),
91-102.

Ponikowski, P. et al. (2016). 2016 ESC guidelines for the diagnosis and treatment of acute and
chronic heart failure. European Heart Journal. Advance online publication.
doi:10.1093/eurheartj/ehw128.

Porth, C. M. (2015). Essentials of pathophysiology: Concepts of altered health states

(4th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.