CARDIOVASCULAR SYSTEM:

Heart:
Location: Mediastinum
Size: Fist; wt= 300 g (10.6 oz)
Characteristics: Four chambered muscular organ
Functions: Pumps blood to the tissues, supplying them
with oxygen and other nutrients
Composed of:
a. Endocardium Consists of the endothelial tissue and lines inside the heart and valves.
b. Myocardium Made up of muscle fibers and is responsible for the pumping action.
c.Epicardium Exterior layer of the heart.
Pericardium
Characteristics: Thin, fibrous sac
Functions: Surrounds the heart, protects it from
traumas and infections.
Composed of:
a. Visceral pericardium Adhering to the epicardium
b. Parietal pericardium A tough fibrous tissue that attaches to the great vessels, diaphragm, sternum,
and vertebral column and supports the heart in the mediastinum.
c. pericardial space - space between two layers.
- normally filled with 20 mL of fluid, lubricates the surface of the heart and
reduces friction during systole.
Four chambers of the -Separated by the septum
heart -pumping action of the heart accomplished
by rhythmic relaxation and contraction of
the heart.
a. Diastole -Relaxation phase
-all four chambers relax simultaneously.
-allows the ventricle to fill in preparation for contraction.
-period of ventricular filling.
b. Systole -events in the heart during contraction of the two top chambers and 2 bottom chanbers.
- Atrial systole occurs first just at the of diastole, followed by ventricular systole.
- this sync, allows the ventricles to completely fill prior to ejection of blood from their
chambers.
 Composed of:
a. Atria Upper collecting chambers
b.Ventricle Lower collecting chambers
Blood flow:

IVC

SVC

RA

TRICUSPID VALVE -prevents regurgitation.

RV

PULMONARY ARTERY

PULMONIC VALVE

BLOOD FROM THE LUNGS

LA

MITRAL VALVE- guarding atrium; prevents regurgitation.

LV

AORTIC VALVE

AORTA

SYSTEMIC CIRCULATION
FOUR VALVES OF THE HEART -keeps blood flowing in one direction
a. Atrioventricular valves (tricuspid/ mitral valve) Prevents backflow of blood into the atria at the
start of each contraction.
b. Pulmonic and aortic valve -Prevents blood from regurgitating into the
ventricles of each ventricular contraction.
-“semilunar valves”
- Ventricular wall must expand in order to
accommodate rapid ventricular filling.
Name Description Characteristics Etiology Clinical manifestations Nsg. Mangement
Sinus tachycardia rate is greater than RATE: 100 to 180 bpm Causes: Occasional palpitations Prescribed treatment
100 P WAVES: precede each (asymptomatic) Hypotension Carotid massage
QRS. Exercise Angina with CVD Neta-adrenergic
PR INTERVAL: normal Anxiety blockers
QRS COMPLEX: normal Fever
CONDUCTION: normal Drugs
RHYTHM: normal Anemia
Heart failure
Hypovolemia
Shock
Sinus Bradycardia Heart rate is less than RATE: less than 60 -Drugs Fatigue Maintain adequate CO
60 bpm P WAVES: precede each Vagal stimulation Lightheadedness Anticholinergic drug
QRS Hypoendocrine Syncope (atropine
PR INTERVAL: normal states
QRS COMPLEX: normal anorexia
RHYTHM: normal hypothermia
CONDUCTION: normal sinus node
involvement in MI

-normal in athletes
Premature Ventricular -Increased RATE: 60 TO 100 BPM Irritability of (asymptomatic) Assessment
Tachycardia automaticity of P WAVES: no P waves ventricular Palpitations Severe, may lead to
ventricular muscle PR INTERVAL: no PR muscles Weakness Fibrillation or V tach.
cells. interval Exercise Lightheadedness Admin lidocaine- short
- harmful if more than QRS COMPLEX: Increasd term
6. -wide and bizarre (0.1 catecholamines Procainamide- long
second) Electrolyte term
-multifocal Imbalance
-results in many different Digoxin Toxicity
configurations Hypoxia
RHYTHM: Bigeminy Myocardial Damage
CONDUCTION: retrograde
through the conduction
system
Name Description Characteristics Etiology Clinical manifestations Nsg. Mangement
Ventricular Three or more RATE: 100-250 Irritability of Light-headedness Antiarrhythmic drud
Tachycardia consecutive PVC’s P wave: blurred ; QRS has ventricular muscle Weakness Lidocaine
no association with the P Dyspnea Procainamide/
Decreased in diastolic wave Unconscious Amiodarone
filling PR interval: not present Cardioversion –if meds
QRS complex: wide and unsuccessful.
bizarre, T wave is in the Severe- defibrillation
opposite direction
Conduction: abnormal in
ventricular tissue
Rhythm: usually regular
Ventricular fibrillation Rapid, ineffective RATE: rapid and Untreated VT LOC Assist with
quivering of ventricles uncoordinated Digoxin and Pulselessness defibrillation
that may be rapidly P wave: not seen quinidine toxicity Loss of BP Antiarrythmic med
fatal. PR interval: not seen Hypothermia Cessation of Avoid automated
QRS complex: undulation respirations external devices
with no specific pattern Possible seizures
Conduction: unorganized; Sudden death
foci firing at once
Rhythm: Irregular with
rhythm
Disease Definition Diagnostic exams Etiology Clinical manifestations Nsg. Management
Coronary artery Narrowing of large ECG 1. Advanced age  Angina  Nitrates
disease and medium sized 1. ST depression 2. Chronic stress  N and V  Antiplatelets
coronary arteries 2. T wave inversion 3. DM  Dizziness  Antilipidemics
due to intimal 4. Family history  Syncope  Beta-adrenergic
plaque formation 5. Contraceptives  Diaphoresis, cool blockers
6. Hyperlipidemia clammy skin  Ca channel
7. Hypertension  Apprehension or blockers
8. Male/ post a sense of
menopausal female impending doom  *Anginal attack
9. Obesity 1. Stop all activity, Place
10. Sedentary lifestyle one NTG tablet under
11. Smoking the tongue adnw ait
for 5 min,

2. Stay with him at all

times

3. STAT 12- lead ECG

4. Family teaching

 *Treatment:
1. PTCA- percutaneous
transluminal Coronary
angioplasty

2. CABG- coronary
Artery bypass graft

 *family Teaching
1. Participate in
cardiac rehab.
2. Advise family to
take CPR course
Disease Definition Diagnostic exams Etiology Clinical manifestations Nsg. Management
Myocardial 1. Destruction of ECG 1. Atherosclerosis Chest pain Drug therapy
Infarction myocardial T wave to be larger 2. Coronary Artery Diaphoresis Morphine
tissue in and inverted Spasm N and V Nitrates
regions of the (epicardial MI) 3. Complete arterial Dyspnea Antilipidemics
heart . St segment elevated occlusion by Palpitations or syncope Thrombolytics
(endocardial MI) embolism or Anxiety Anticoagulants
2. Deprivation of thrombus Tachycardia/ bradycardia Assess Px
adequate blood Serum enzyme tests: 4. Decreased coronary Dec. BP Monitor cardiac enzymes
supply. Creatinine blood flow due to Altered S3 (L ventricular Hemodynamic
phosphokinase hemorrhage or failure) parameters
Lactate shock Anxiety
dehydrogenase Diet: liquid diet
Troponin Low sodium diet
Low fat
WBC elevated
Treatment
PTCA
CABG
Family teaching
CARDIAC Goal: Objective: Causes: NSG. Management CATEGORIES:
REHABILITATIO help px live a life CVD:  CBR 1. Right
N that is full, vital, Limit the effects ASHD Semifowlers position- -L sided HF
and productive but and progression of MI promote oxygenation -Cor pulmonale
within the hearts atherosclerosis HYPERTENSION  Nitroglycerin -R ventricular
ability RHD 1. Inorder to preserve med: infarction
Return px to work Ischemic Heart Disease do not place on light.
and pre-illness Arrythmias 2. Lifetime: 6 mths 2.Left
lifestyle Valvular disease 3. Vasodilatory function -Disease of coronary
(check BP) arteries
Enhance the Non- CVD 4. If not relieved give every Hypertension
pfychosocial and Pregnancy and childbirth 5 min. Cardiomyopathy
vocational status of Severe Physical and mental  O2- tissue hypoxia RHD
the Px stress  ECG- Hemodynamic
Throtoxicosis procedure
Prevent another Acute Blood Loss  Stool softeners-dec.
cardiac event Severe infection constipation
COPD -risk of bradycardia

 Thrombolytic
Therapy- effective
during 3 to 5 hrs.
After therapy—take heparin:
to prevent recurence
 Admin
antiarryhythmias

 Maintain a quite envi.

 MIO
HEART Syndrome of CHEST RADIOGRAPH LEFT SIDED: Medications:
FAILURE pulmonary or Dyspnea  Cardiac glycosides
systemic Cardiomegaly Crackles  Diuretics
circulatory Vascular congestion Frothy blood tinged  Angiotensin
congestion caused sputum converting enzyme
by decreased ELECTROCARDIOGRAM: Tachycardia with inhibitors
myocardial Hypertrophy s3sound  Vasodilator therapy
contractility. Myocardial damage Pale cool extremities  Antilipemics
Peripheral and central
ABG cyanosis Provide ongoing assessment:
Decreased partial Dec. peripheral pulses  Multilumen pulmonary
pressure of arterial Dec. urinary output artery catheter:
oxygen Easy fatigability -Hemodynamic parameters
Increased partial Insomnia  Heart rate and rhythm
pressure of arterial
carbon dioxide RIGHT SIDED  Weigh client
Edema
PULSE OXIMETER Wt. gain  Monitor serum
Less than 95 % Nausea electrolyte
Anorexia
MULTILUMEN JVD
PULMONARY ARTERY Liver congestion  Prevent complication of
L SIDE: immobility: Apply
Elevated pulmonary antiembolism stockings
artery and capillary
wedge pressures  Provide a low low sodium
diet- dec. fluid retention
R side: and subsequently the
Elevated CVP workload of the heart.

 Provide a client and

family teaching

 Internal ballon- mech.

Device that diverts
blood to an ext pump.
 Chest pain upon : DRUG THERAPY:
ANGINA LABS and Dx’s test: Physical exertion  Nitrates
 ECG Exposure to cold  Beta blockers
Types:  Exercise stress Eating a heavy meal  Ca channel
 Stable angina- test stress blockers
paroxysmal chest  Echocardiogram  Antiplatelet
pain. Predictable.  C-reactive protein  anti coagulant
 Unstable angina- pre  Coronary medications
infarction. Angiography 1. aspirin
Unpredictable  Cardiac 2. eplidogrel
degree catheterization 3. heparin
4. LMWH
 Variant angina-
similar to classic
angina. Appears at
early HRS of the
day.
 Nocturnal Angina-
during night
 Angina Decubitus-
recline and lessens
when the clients
stands up
 Intractable- not
responsive to
intervention
 Post infarction-
occurs after heart
attack
 Assessment Treatment Dx’s test:
 Chest radiograph
Acute Pulmonary edema Heart failure Restlessness and CBR vascular congestion of
-L side HF vague uneasiness Semifowlers position lung fields (butterfly
CO reduced increased left Oxygen (40 to 70) appearance)
atrial pressure Profound dyspnea Drug therapy
Digitalis  Multilumen
Increased pulmonary vein Pallor Diuretics Pulmonary artery
and capillary pressure Vasodilators catheter-
exceeding intravascular Cough Morphine IV Elevated central venous
osmotic pressure Aminophylline Pulmonary artery
Productive frothy Rotating Tourniquet Capillary wedge
Serous fluid is forced blood tinged – or phlebotomy pressures
rapidly into the alveoli classic symptom Hemodynamic
Monitoring –CVP  ABG
Reaches the bronchioles and sputum Endotracheal/ Decreased partial
bronchi nasotracheal pressure of arterial
Audible wheezing intubation oxygen Co2

Cyanosis Px’s with cardiac

failure- careful in
Tachycardia positioning
- Semi-
fowlers-
- Inc. in fluid in
change of
positions
- Lungs is
affected
STRUCTURAL HEART Clinical manifestations Dx Surgical management
FAILURE
Chest Xray Pallative surgery
Congenital Heart Failure Echocardiogram CABG -closure or
a. Volume overload  CHF patch graft
-occurs when greater than  Murmur performed
normal amount of blood  Risk for bacterial
enters either the ventricular endocarditis and Atrial septal defect:
chambers. pulmonary vascular Surgical Dacron patch
obstructive CP bypass
b.Ventricular Septal Defect  Tachypneic
-abnormal opening between R  Diaphoretic
and L ventricles.  Fatigue
 Emboli formation
OBSTRUCTION OF THE MANIFESTATIONS: High risk for: Surgical management
FORWARD FLOW HPN
s/sx of CHF in infant Ruptured aorta Resection of the
Coarctation of the aorta high BP and bounding pulse Aortic aneurysm coarcted portion with
in the arms Stroke an end to end
-caused by narrowing of Weak or absent femoral anastomosis of the
aorta that impedes blood pulse aorta
flow, can occur anywhere Coll lower extremities
between the origin of the Children exp: Enlargement of the
aortic arch and bifurcation Headache constricted section
of the aorta in the lower Dizziness
abd. Fainting Percutaneous balloon
Epistaxis resulting from angioplasty
hypertension

Aortic Stenosis Murmur

-fusion of the three cusps of Dec cardiac output with Aortic Valvulotomy
the aortic valve faint pulses Balloon angioplasty
-causing resistance to the Hypotension
blood flow in the L ventricles Tachycardia
-L ventricular Hypertrophy Poor feeding
-Pulmonary Vascular
congestion Children show signs of:
-Hypertrophy of the L Exercise intolerance
ventricular wall lead to Chest pain
decrease end diastolic dizziness
pressure; results to
pulmonary venous and
pulmonary arterial HPN

Disease Pathophysiology Assessment Treatment Dx’s exams Etiology

CONGENITAL PULMONIC Manifestations: Treatment;
STENOSIS Surgery
Murmur
-narrowing of pulmonary Mild cyanosis of CHF Transventricular valvutomy
valve Cyanosis
-resistance to blood flow Severe: CHF Pulmonary valvutomy
causes R ventricular
hypertrophy and decreased
pulmonary BF

PULMONARY ATRESIA-
extreme form of pulmonary
stenosis in that there is
total fusion of the
commisures and no blood
flow to the lungs

CONDITIONS OF
DESATURATION
Tetralogy of fallot
a. structural defect –
complex of shunting of the
blood due to multiple
structural alterations
b. Ventricular Septal defect
c. Pulmonic Stenosis
d. Overriding of the aorta
e.R ventricular hypertrophy
Assessment: MANAGEMENT:
Infant:
-acutely cyanotic progresses Knee chest and squatting
as pulmonic stenosis worsens position
-murmur - Cuts offcirculation
-episode of cyanosis, Volume resuscitation
hypoxia, blue spells or tet Oxygen- ineffective in
spells treating hypoxic spells
Characterized by:
Sudden, marked inc. of Pharmacologic
cyanosis followed by
syncope, hypoxic brain and Betablocker
injury Morphine
Phenylephrine HCL
Children:
Inc. cyanosis, squatting, Surgery
clubbing of fingers, poor Pallative shunt
growth may occur
Closure of Vsd- complete
Dec. exercise tolerance repair
Inc. DOB
Eating difficulties
Squatting SOB
Clubbing of fingers and toes
PATENT DUCTUS Manifestations: Med mgmt:
ARTERIOSUS Asymptomatic Indomethacin- helps close
Sx CHF the PDA in premature
-failure of the fetal ductus MURMUR- machinery like infants. Stimulate PDA to
ateriosus to close w/in the Widened PP constrict tighten closing
1st wk of life Bounding Pulse the connection.
Risk for bacterial endocarditis
-continued patency of this Pulmonary vascular Obstructive
vessel allows blood to flow
from the higher pressure ADULTS:
aorta to the lower pressure Dyspnea
aorta to the lower Fatigability
pulmonary artery causing a
L to R shunt
TRANSPOSITION OF Assessment: MAngement: Interventions:
GREAT ARTERIES Infants- cyanosis V/s
Mechanical ventilation Respi stat.
Pulmonary artery leaves L Children Pharmacologic support for Auscultate breath sounds
ventricle, and the aorta - Cyanosis poor cardiac output for crackles, rhonchi, or
exits from the R ventricle - Respi infections Prostaglandin rales
with no communication - diminished exercise Correction of metabolic Admin. O2
between the systemic and tolerance acidosis Provide endotracheal tube
pulmonary circulation - fatigabilityclubbing of and ventilator care
fingers Monitor for hypercyanotic
spells
Asses for S/sx of CHF
Peripheral pulses
IO
Wt. daily
Fluid restriction
Admin. Meds
Stress free
Prepare family for
possibility of surgery
CARDIOMYOPATHY
-heart muscle disorder of
unknown etiology
-heart muscle disorder
associated with cardiac
dysfunction
-dominant feature:
involvement of heart muscle
itself
-Four conditions that
increases threshold:
Chronic alcohol ingestion
Pregnancy
Systemic HPN
Various infections
Categories:
DILATED cardiomyopathy
-known as congestive
cardiomyopathy
-the heart chambers are
dilated and ventricular
contraction is impaired
-common type
- heart ejects less than 40 % of
the blood in the L ventricle-
red. CO may lead to HF
Hypertrophic Cardiomyopathy
-characterized by decreased
compliance of the L ventricle
and hypertrophy of the
ventricle muscle mass
a. impaired ventricular filling
b. Small end diastolic pressure
c.Low cardiac output
Characterized by Massive
Ventricular Hypertrophy
Heart Muscle asymmetrically
increase in size and mass esp.
along the septum
Restrictive cardiomyopathy
-least common
CAUSES:
Idiopathic
Result of damage to the
myocardium, produced by a
variety of toxic, metabolic
or infectious agents. It may
be due to fibrous change of
the myocardium from a
prev. MI
1. Obstructive – septum
thickens and bulges into
the L ventricle. This will
block the blood out out of
the ventricle
2.Non obstructive –
thickened heart muscle
does not block the flow of
blood out of the ventricle
amy become thicker or may
happen only at the bottom
Assessment: Treatment
S/ sx of L ventricular Diuretics
failure Cardiac Glycosides
Weakness, fatigue Vasodilators
Activity intolerance Anti dysrhythmias
Chest pain Instruct the client to
Dysrhythmias avoid ingestion of alcohol
Eventually signs of R Heart Transplant
ventricular failure
s/sx chest pain Instruct the px to report
dizziness s/sx of dizziness or
SOB fainting
Fainting Intruct the Px to avoid
ingestion of alcohol
Exertional Dyspnea
Syncope
Chest pain @rest, not
relieved by nitrates
Dysrhythmias
DIGITALIS TOXICITY Guidelines for digitalis prep:
GI: 1. Take pulse for 1 minute
Anorexia 2. Heartbeat is below 60, dc drug
N and V 3.S/sx for digitalis toxicity
Diarrhea 4.hypokalemic – withhold drug and
Abd. Cramps notify doctor

CNS:
Fatigue
Lethargy
Depression restlessness irritability
Drowsiness
Convulsions
Neuralgia
Delusions
Hallucination
Aphasia
Memory loss

CVS
Bradycardia
Ventricular bigeminy
Trigeminy
VT
AV block
Atrial tachycardia

Eyes:
Flickering flashes of light
Halo around lights
Photophobia
Blurring
Diplopia

Dopamine and Dobutamine
-facilitate myocardial contractility
And enhanced stroke volume
Scomata (blind spots on visual field
Dopamine Dobutamine
renal dose- less than 4 ug/ kg/ min -inc. HR and produces more
-stimulates dopaminergic receptors myocardial contractility than
in the renal, mesenteric, cerebral dopamine
and coronary vascular bed which
causes vasodilation:
Inc. renal flow
Increase GFR and Na excretion
Moderate dose- 4-8 ug / kg/ min
- inc. HR. SV and Co
Large dose8
-vasoconstriction
PHARMACOLOGIC THERAPIES FOR HEART
PROBLEMS:

Sinus Tachycardia: Sinus Bradycardia PVC

Beta blockers Atropine- 0.5 as an IV bolus every 3-5 m until Short term- lidocaine
Ca channel blocker 3 mg Long- procainamide

V TACH ASHD ANGINA

Amiodarone –IV for stable Px Low dose aspirin NITRATES
Procainamide Niacin or nicotinic acid Beta blockers
Sotalol Bile acid binding resins- Cholestyramine Ca channel blockers
Lidocaine –short Antipaltelet and anticoagulant meds (aspirin,
Isoproterenol- correct electrolyte imbalance Lowers cholesterol level clopidogrel, heparin, LMWH)
Lovastin
Pravastatin
simvastatin
MI Heart failures Acute pulmonary edema

Thrombolytics ACE inhibitors Digitalis

Anticoagu;lants and antiplateletrs Digitalis Diuretics
Analgesics Dopamine Vasodilators
ACE inhibitors Dobutamine Morphine IV
Stool softeners Diuretics Aminophyline
Vasodilating agents
Betablockers
Ca channel blockers
Conditions of desaturation Patent Ductus Arteriosus Dilated Cardiomyopathy

Beta blocker Indomethacin Diuretics

Morphine Cardiac glycosides
 Phenylephrine Hcl
Medical therapies:
Defibrillation
-SA node to resume it’s role as the
pace maker of the heart
-pulseless and unconscious
Cardioversion
-elective procedure
-use of electricity to convert
cardiac dysrythmia to NSR.
-electrical discharged is
synchronized with or triggered by
the client’s QRS complex for
avoidance of accidental discharge
during the repolarization phase
when the ventricle is vulnerable to
the development of VF.
-indications include tachycardia
developing in atrial, junctional,
ventricular
-QRS complex- present for
Before:
 Check ECG results for the
presence of VF and VT
 Pulse
 Remove any Topical
Nitroglycerin Patches
Before:
 Check ECG results for the
presence of VF and VT
 Pulse
 Remove any Topical
Nitroglycerin Patches
Vasodilators
Antidysrhythimias
During:
 Lubricate the paddles to
enhance conduction and prevent
skin burn
 Turn defibrillator on and
confirms that synchronizer
switch off.
 25-30 lbs of poressure
(anterolateral; paddles are
placed @ 2nd ICS Right and
anterior axillary line 5th ICS
left
 Stay away from bed
During:
Set machine within range 50-200
joules
Turn on synchronizer, deliver during
QRS complex and not on the
downslope of T wave(may inc. in
ventricular irritability, causing VF)
Lubricate pads
When ensuring O2, move pads away
Move away from bed
After:
Assess the pulse and ECG
First countershock , if unsuccessful,
defilbrate again
Terminate of resuscitation after
15-20 min of CPR andACLs
1st: 200
2nd:300
3rd:360 (max energy; last)
After:
Asses V/s
Maintain patent airway
Administer O2
Assess v/s and LOC
Asmin antiarrythmic drugs
Monitor for dysrythmias
Assess for chest burns
Provide emotional support
Document
successful conversion of the
dysrythmia
Automatic Implantable Device itended to convert life
Cardioverter- Defibrillator (AICD) threatening rhythms of the heart
which may cause sudden cardiac
death/ arrest
PACEMAKER After care Homecare
a. Temporary After insertion
Transcutaneous- for life Take pulse before getting out of
threatening situations Provide cont. ECG monitoring bed
Transvenous-
Chart the type of insertion, lead Check implantation everyday
Epicardial system, pacemaker mode and pacing Special precautions to prevent
guidelines disruption
Avoid strong magnetic forces
b.Permanent VS every 30 min ‘til stable Avoid placing excessive pressure
fixed rate Follow normal routines
Demand or stand by mode Be on guard for perforated Take note of follow up orders
ventricles

Asses for insertion sites for

infection

First 24 hrs, ROM in affected arm

—active ROM in 2 wks

Vagal Maneuvers Carotid massage Valsalva maneuver Cough CPR

-used to terminate tachydysrthmia -last pulse to be checked. -bring out parasympathetic impulses -cough and deep breathing
S1 S2 Abnormal heart
sounds:
Onset of systole Diastole
Apex of the heart Base of the heart
Closure of AV valves Closure of semilunar
valves