CIRCULATORY SYSTEM connective tissue and serves to prevent

over distension of the heart.

 It is a fluid-filled network of tubes
 In between the parietal and visceral
through which materials move
pericardium is a serous fluid (5-10ml)
between the environment and the cells
in the pericardial sac, that prevents
of a multicellular animal.
friction between the two pericardial
Major Components OF CIRCULATORY SYSTEM membranes as the heart beats.

 Heart Layers of the heart are as follows:

 Blood a. Epicardium- outermost layer, a smooth
 Blood vessels- veins, arteries, outer surface of the heart
capillaries b. Myocardium- thick middle layer
composed primarily of cardiac muscle
Anatomy and Physiology of the Heart cells heart where the four chambers are
Heart made. Responsible for the heart’s
 Primary function is to pump blood ability to contract
through the arteries, capillaries and c. Endocardium
veins  Innermost layer of the heart
 Pumps blood which creates blood composed of thin connective tissue
pressure, circulates oxygen nutrients  It lines the chambers and covers the
and other substances heart valves of the heart
LOCATION SIZE and the Shape of the Heart  important characteristic is its
 It weighs 300g and approximately the smoothness that prevents
size of the fist, 5 inches in length and 3 abnormal blood clotting
inches wide.
 The shape of the heart is somewhat CHAMBERS OF THE HEART
cone like in appearance.  the four chambers of the hear are as
 Mediastinum- the central section of the follows:
thorax (chest cavity). It is in this area  right atrium and right ventricle which
that the heart is house, lying in front of are thin and separated by the
the spinal column, behind the sternum interatrial septum
and between the lungs  left atrium and left ventricle have
 Two thirds of the heart lies to the left of thicker walls and separated by
the midline, the apex of the heart just interventricular septum
above the diaphragm and the base of
the heart lies at approximately the level RIGHT ATRIUM
of the third rib  receives deoxygenated blood from the
 The heart is enclosed by body by way of the Superior vena cava
pericardium/pericardial sac which (SVC) and inferior vena cava (IVC).
consist of two layers  From the RA, blood will flow to the
1. Visceral pericardium- thin serous inner right atrioventricular valve or tricuspid
layer which surrounds the heart. valve into the right Ventricle (RV)
2. Parietal pericardium- outer layer,
consist of tough, nonelastic, fibrous
  Tricuspid valve- prevents back flow of VALVES of the Heart
blood from the RA to RV, when the RV  There are two set of valves: The
contracts. atrioventricular and semi lunar valves
 Located between RA and RV
ATRIOVENTRICULAR valves
RIGHT VENTRICLE - are tricuspid valve and bicuspid (mitral)
 Receives blood from the RA and ejects valve, located in between atria and
this blood into the lungs via Pulmonary ventricles
artery. - allow blood to flow from the atria into
 At the junction of this large artery and the ventricles
the RV is the Pulmonary Semilunar - Effective in preventing backflow of
valve blood into the ATRIA.
Pulmonary valve- prevents back flow of blood  Tricuspid- name for its three cups,
from the pulmonary artery to the RV when RV located between RA and RV. Free edge
relax. of each of these three cups extend into
the ventricles where they attach to the
LEFT ATRIUM chordae tendineae.
 Receives oxygenated blood from the  Chordae tendeneae are fine chords of
lungs by way of four pulmonary veins. dense connective tissue that attached
 This blood will flow into the left to the papillary muscles in the wall of
ventricle through Mitral or Bicuspid the ventricles. The chordae tendeneae
valve. supports the AV valves during
Mitral/Bicuspid- it prevents back flow of ventricular systole to prevent valvular
blood from LV to LA when LV contracts prolapse in the Atrium.
 Other function:
- Produce hormone involve in BP Papilliary muscles and chordae tendeneae- it
maintenance. When the walls of the prevents inversion of the AV valves when the
atria are stretched by increase blood ventricles contract.
volume or blood pressure, the cells  MITRAL/Bicuspid- located between LA
produced Atrial natriuretic peptide. and LV

LEFT VENTRICLE SEMILUNAR VALVES

 Receives blood from the left atrium and - are the aortic valve and pulmonic valve.
ejects blood into systemic arterial - Prevent backflow of blood into the
circulation. ventricles
 Pumps blood to the body through the  Aortic valve- lies between the LV and
AORTA. the aorta.
 At the junction of aorta and LV is the  Pulmonic valve- lies between RV and
Aortic Semilunar valve/Aortic Valve. pulmonary artery.
- This valve is closed when the LV relaxes, During ventricular systole- the AV valves are
to prevent back flow of blood from the close and the semilunar valves are open.
Aorta to the Left Ventricle. During ventricular diastole- the semilunar
valves are close, and the AV are open.
CORONARY ARTERIES waste products between the blood and
 The coronary arteries originated from body tissues
the aorta just behind the aortic valve  Connectors between arteries and veins
 The two main coronary arteries are
Left Coronary Artery (LCA) and the Blood Flow in the Body
Right Coronary Artery (RCA) – supply 1. Deoxygenated blood returns from the
blood to the myocardium rest of the body through the superior
 The LCA divides into two branches and inferior vena cava.
namely: the Circumflex Coronary 2. The right atrium receives the
Artery (CCA) and Left Anterior deoxygenated blood.
Descending Artery (LADA) 3. Blood then enters the right ventricle
 CCA- supplies the LA, posterior lateral through the tricuspid valve.
surface of the LV. 4. Contraction of the right ventricle
 LADA- supplies the anterior wall of the pushes blood through the pulmonary
LV, the anterior interventricular semilunar valve into the pulmonary
septum, the anterior papillary muscles arteries in which it travels to the lungs.
and the apex of the heart. 5. After passing through the capillaries of
 RCA- supplies the RA, RV, a portion of the lungs, the blood which is now
the septum, SA node, AV node, and the oxygenated returns to the heart in the
inferior portion of the ventricle. pulmonary veins.
6. The Left atrium receives blood from
CORONARY SINUS the pulmonary vein.
 Receives deoxygenated blood from the 7. Blood passes through the mitral valve
veins of the myocardium into the left ventricle.
8. Contraction of the left ventricle pushes
VEINS blood through the aortic semilunar
 Are blood vessels that carries blood valve into the aorta. Blood travels to
towards the heart. all regions of the body where it feeds
 Branch off into smaller vessels is called cells with oxygen.
venules
 Operates under low pressure, thin Cardiac Cycle and Heart Sounds
 Carry deoxygenated blood - Simultaneous contraction of the two
atria, followed by simultaneous
SUPERIOR VENACAVA contraction of the ventricles
 Drains blood from the head to the neck Systole
 Contraction and emptying of the atria
INFERIOR venacava and ventricles
 Collects blood from the lower portion of  Aortic and pulmonic valve are open,
the body. mitral and tricuspid valve close
Diastole
CAPILLARIES  relaxation and filling of atria and
 Are tiny blood vessels that allow for the ventricles
exchange of oxygen, nutrients and  aortic and pulmonic are close, mitral
and tricuspid valve are open.
Creates the two heart sounds  Strength of the cardiac cells to contract or
- Lub- the first sound that is the loudest shorten
and longest sound caused by ventricular AFTERLOAD
systole closing the AV valves.  The amount of tension in the ventricle
- Dub- the second sound caused by the during contraction to eject blood from the
closure of aortic and pulmonary left ventricle into the aorta.
semilunar valves.
- If any of these valves does not close
ANS influences on Cardiac Activity
properly, an extra sound called heart
murmur may be heard SNS
- Heart murmur- is abnormal extra heart  responsible for preparation of the body for
physical activity (Fight or Flight).
sound by malfunctioning of the heart
 releases norepinephrine
valves.
PNS
regulates the calmer (Rest and Digest)

CARDIAC OUTPUT functions
 The volume of blood ejected from the left  Releases Acetylcholine
ventricle into the Aorta per minute CHEMORECEPTORS
 CO=SV x HR  Medulla Oblongata and special receptors
 Normal-5-6 L/minute are found in the carotid and aortic bodies
 Determine by three factors namely: which can regulate respiratory ACTIVITY.
preload, contractility and afterload  are sensitive to changes in arterial carbon
PRELOAD dioxide, oxygen, and pH.
 The amount of the ventricles stretch at the  A decrease pH or increase in paCO2 level
end of the diastole causes a reflex SNS response that result in
 Related to the volume of blood distending tachycardia, vasoconstriction and increased
the ventricles at the end of the diastole myocardial contractility
 the pressure in the ventricles at the end of  Decreased paCO2 and increased pH leads to
diastole. vasodilation
 It is determined by the amount of venous  A decrease pH or increase in paCO2 level
return leads to passive vasodialtion
 Increased Preload- fluids, SNS
(vasoconstriction), Decreased Preload Two Basic Myocardial Cell Groups
(Diuretics-Furosemide, Nitroglycerine 1. MYOCARDIAL WORKING CELLS
(vasodilator)  Are responsible for generating the physical
contraction of the heart
FRANK STARLING LAW  The primary function of MWC include both
 Starling Law conceptualizes that the greater CONTRACTION and RELAXATION
the myocardial stretch within physiologic 2. SPECIALIZED PEACEMAKER CELLS
limit, the more forceful the ventricular  Responsible for controlling the heart rate
contraction resulting to increase Stroke and the rhythm of the heart by
volume. coordinating regular depolarization
CONTRACTILITY  The primary function is for GENERATION
 a change in inotropic state of the muscle and CONDUCTION of electrical impulses
without a change in myocardial fiber length
or preload.
Primary Cardiac Cell Characteristics the muscle fibers of both atria
Automaticity resulting in DEPOLARIZATION
 is the ability of the heart to initiate  the natural peacemaker of the heart is -
impulses repetitively and has the most rapid rate of contraction,
spontaneously. Meaning the cardiac it depolarizes more rapidly than any
muscle cells can generate their own other part of the myocardium. The SA
electrical impulses spontaneously node triggers electrical impulses at a
without external (nervous) stimulation. firing rate of 60-100 beats per minute.
This intrinsic spontaneous  Furthermore, the SA node represents
depolarization frequency produces the P-wave (atrial contraction) on the
EKG tracing.
contraction of the myocardial cells.

INTERNODAL PATHWAYS
Excitability-
 distribute the electrical impulse from
 the ability of the cardiac cells to
the SA node throughout the ATRIA to
respond to a stimulus by initiating a
the AV node
cardiac impulse. It is called irritability
 The atria then depolarized and the
Conductivity
impulse for contraction is transmitted
 the ability of the cardiac cells to receive
to the atrioventricular (AV) node
to an impulse by transmitting the
 The transmission of impulses from the
impulse along cell membranes.
SA node to the AV node and to the rest
Contractility
of atrial myocardium brings ATRIAL
 the ability of the cardiac cells to shorten
SYSTOLE
and cause cardiac muscle contraction in
response to electrical stimulus.
AV (Atrioventricular) node
 Known as rhythmicity.
 Located on the floor of the right atrium
 Administration of epinephrine and
just above the tricuspid valve
dopamine can enhance contractility
 At the level of the AV node, the
electrical activity is delayed
ELECTRICAL HEART CONDUCTION SYSTEM
approximately 0.05sec.
 The cardiac cycle is a sequence of
 This delay allows for atrial contraction
mechanical events that is regulated by
and a complete filling of the ventricles.
the electrical activity of the
If there wasn’t a delay the atriums would
myocardium. The heart generates its not fully empty into the ventricles which
own beat, and the electrical impulses would cause problems.
follow a very specific route throughout  3 regions: AV junctional tissue between
the myocardium. the atria and node, the nodal area, and
AV junctional tissue between the node
Sinoatrial (SA) Node and Bundle of His
 Located in the upper portion of the  The only pathway for conduction of
Right Atrial wall of the heart near the atrial impulses to the VENTRICLES is
opening of SVC. SA node receives its the AV Bundle/ Bundle of His
blood supply from SA artery.  Slows impulse, intrinsic firing rate of
 Made up of cluster of cells capable of 40-60BPM
generating impulses travel throughout
  The electrical impulses is transmitted
into the Bundle of His and travel into
CARDIAC DEPOLARIZATION
the Purkinje fibers to the rest of the
ventricular myocardium to bring about POLARIZED STATE/Resting Potential
VENTRICULAR systole.  The RESTING state of the cardiac cells
wherein the inside of the cell is electrically
NEGATIVE relative to the outside of the cell.
AV JUNCTION
 Region where the AV node joins the DEPOLARIZATION
Bundle of His  Involves the movement of ions across the
 Similar to SA node, AV Junctional tissue cardiac cell membrane resulting in POSITIVE
polarity inside the cell membrane
contain fibers that can depolarize
REPOLARIZATION
spontaneously forming an electrical  The depolarized cell is polarized and
impulse that can spread to the heart positive charges are again on the outside,
chambers and negative charges on the inside of the
 Therefore if the SA node fails or slows cell.
KEY POINTS TO REMEMBER
below its normal range, the AV
1. MYOCARDIAL WORKING CELLS
junctional tissues can initiate electrical  Are responsible for generating the physical
activity to assume the role of Secondary contraction of the heart muscles
pacemaker  Contraction and relaxation
BUNDLE OF HIS 2. SPECIALIZED WORKING CELLS
 The conduction pathway that leads out  Responsible for controlling the heart rate
and the rhythm of the heart by coordinating
of the AV node regular depolarization
 Approximately 15mm long and lies at  The primary function is for GENERATION
the top of the interventricular septum and CONDUCTION of electrical impulses
 Called as Common Bundle- Two main 3. AUTOMATICITY
branches (left and right) that conduct  Is the ability of the cardiac peacemaker cells
to spontaneously generate their own
electrical activity from the Bundle of His
impulses without external stimulation
down to Purkinje Network 4. EXCITABILITY
 Contains pacemaker cells that have the  The ability of the cardiac cells to respond to
ability to self initiate electrical activity a stimulus by initiating a cardiac impulse. It
at an intrinsic firing rate of 40-60BPM is called IRRITABILITY.
5. CONDUCTIVITY- ability of cardiac cells to
receive and electrical impulse and then
PURKINJE’S NETWORK transmit to other cardiac cells.
 Spread impulse throughout the 6. CONTRACTILITY
ventricles resulting to ventricular  the ability of the cardiac cells to shorten
contraction and cause cardiac muscle contraction in
 Ventricular contraction is facilitated by response to electrical stimulus.
 Known as Rhythmicity.
the rapid spread of electrical impulse 7. K performs a major function in myocardial
through the Left and Right Bundle depolarization and repolarization
branches and Purkinje Fibers into the 8. Na plays a vital part in depolarization of the
ventricular muscle myocardium
 Possessed the intrinsic ability to serve 9. Ca renders an important function in
myocardial depolarization and myocardial
as peace maker
contraction
 Intrinsic firing rate of PF is 20-40BPM
 10. When cardiac cell is at rest, the K ion  Connectors between arteries and veins
concentration is GREATER INSIDE the cell,
and the NA ion concentration is GREATER BLOOD FUNCTIONS
OUTSIDE the cell. • Transportation-hormones, gasses,
11. By means of active mechanism transport nutrients, ions, heat
called NA-K EXCHANGE PUMP, K and Na • Regulation- pH, temperature, water
are move in and out the cell through cell balance in cells
membrane. • Protection- clotting, white cells
12. DEPOLARIZATION- is an electrical interferons, complement
occurrence resulting in myocardial
contraction involving the movement of ions Characteristics of BLOOD
across cardiac cell membranes Volume
13. REPOLARIZATION- the depolarized cell is  Female: 4-5 L
polarized and the POSITIVE charges are  Male: 5-6 L
again on the outside, and NEGATIVE Temperature
charges on the inside the cell. It is return to  38 C (100.4 F)
the RESTING STATE pH:
14. During the process of repolarization, the  7.35 - 7.45
cardiac cells is unable to respond to a new Viscosity
electrical stimulus; the cardiac cell cannot  relative to water
spontaneously depolarized and is referred
to as ABSOLUTE REFRACTORY METHOD Formation of Blood Cells
15. The relative refractory method is the period  Called hemopoiesis
when repolarization is almost complete and  Just before birth and throughout life
the cardiac cell can be stimulated to occurs in red bone marrow
contract prematurely if the stimulus is much  Contains pluripotent stem cells
stronger than normal.  In response to specific hormones these
develop through a series of changes to
Blood vessels form all of the blood cells
ARTERIES- It carries oxygenated blood AWAY from
the heart Composition/Component of the BLOOD
1. PLASMA
LAYERS of ARTERIES  Watery straw colored part of the blood
Tunica intima  Made up of water, proteins, glucose, fats
 Innermost layer and consist of and gases
endothelium and elastic membrane  Transport nutrients
Tunica Media  Maintain acid base balance
 Middle layer and consist of smooth muscle  Transport waste from the tissues
cells  ~91% water, 7% proteins, 1.5 % other
Tunica Adventitia solutes
 Outermost layer and made up of  Proteins: Albumin (54%)- osmosis and
connective tissue carriers;
 Globulins (38%)- antibodies
VEINS  Fibrinogen (7%)- clotting
 Carries blood BACK to the heart  Other: Electrolytes , nutrients, gases,
 Two largest veins: hormones, vitamins & waste products
 Superior Vena cava and Inferior venacava
2. The Formed Elements- (blood cells/cell
CAPILLARIES fragments)
 Tiny blood vessels that allow for the
exchange of O2, nutrients, and waste 1. RBC/Erythrocytes
products between the blood and body  Transport O2 and CO2 to and from tissues.
tissues  Contain Hemoglobin
  Has a lifespan of 90-120days ECG
2. White Blood Cells (WBC)  It is a graphical recording of the electrical
 Defenses: phagocytes, antibody activities of the heart.
production and antibacterial action  It is the first diagnostic test done when
 Phagocytes: cardiovascular disorder is suspected.
 Neutrophil- first responders  The procedure is PAINLESS.
 Monocytes macrophages (big eaters) INDICATIONS OF ECG
 Eosinophil- phagocitize antibody-antigen  MI and other CAD
complexes Involved in suppressing allergic  Cardiac Dysrhythmias
responses  Heart enlargement
 Basophil- intensify allergic reactions  Electrolytes imbalances- especially CA, NA
 Immune response- T-cells, B-cells& natural and K levels
killer (NK) cells  Inflammatory diseases of the heart
 Granulocytes- Neutrophils, Eosinophils,  Effects of drugs on the heart
Basophils
 Agranulocytes-Lymphocytes, Monocytes- ELECTRODE
that reside in your blood and tissues to  An adhesive pad that contains conductive
find and destroy germs (viruses, bacteria, gel and designed to be attached to the
fungi and protozoa) and eliminate infected patients skin
cells. Monocytes call on other white blood LEADS
cells to help treat injury and prevent - Electrodes connected to the monitor or EKG
infection. machine by wires
 4,000-11,000/l  Wires are color coded.
RHYTHM STRIP
WBC Life Span  The printed record of the electrical activity
• 5000-10,00 WBC /µl blood of the heart
• Limited number of bacteria can be eaten
• Life span is a few days
• During active infection may be hours The standard ECG consist of 12 leads
• Leukocytosis= increased WBC numbers  (I, II, III, AVR, AVL, AVF, V1, V2, V3, V4, V5,
response to stresses V6)
• Leukopenia = decreased WBC numbers  Used in prehospital and clinics settings
regularly to aid in screening patients who
3. PLATELETS potential candidates for fibrinolytic therapy
 Smallest cells in the blood  3 lead ECG- is use to detect life-threatening
 Essential for coagulation of blood dysrhythmias
 Plug damaged blood vessels Bipolar lead/Standard Limb Leads
 Promote blood clotting  Lead I II III - each have one positive
 Life span 5-9 days electrode and one negative electrode
 130,000-360,000/l  Current flows from the limbs through the
heart
General Properties of Whole Blood  Lead II and modified chest lead are the
Hematocrit most common leads used for cardiac
 RBCs as percent of total blood volume monitoring because of their ability to
 Female: 37%-48% visualized P waves.
 Male: 45%-52%  LA Lead (Black lead) - Should be placed
between the left shoulders and wrist away
Hemoglobin from the bony prominences as bone is a
 Female: 12-16 g/100 ml poor conductor of electricity
 Male: 13-18 g/100 ml  RA lead (white lead) should be placed at
the Right shoulder and wrist

DIAGNOSTIC TEST
  Left Leg Lead (red Lead)-between left leg 3. If the patient is diaphoretic, attempt to dry the
and ankle area or use antiperspirant
 Right Leg Lead (Green Lead)- between the 4. Use conductive gel to ensure proper conduction
right hip and ankle, sometimes used as an 4. Proper placement of the leads
additional ground lead.
Lead Positive Negative WAVES, COMPLEXES and INTERVAL
Electrode Electrode
I Left arm Right arm P-WAVE- impulse spread across atria triggers atrial
II Left leg Right arm contraction
III Left leg Left arm  SA node fires first during the a normal
cardiac cycle. This firing send s the electrical
impulse outward to stimulate both atria
and manifest as the P wave
 Depolarization of the Atria both Left and
Augmented Leads Right atria
 currents flows from the heart outward to  Smooth and upward deflection
the extremities  Duration: 0.04-0.11sec
 referred to as unipolar lead having one true  Normal P wave is 3mm or less
pole.
PR INTERVAL
Augmented leads Position of flow
 Measure the time interval from the onset of
aVR-Augmented Frm the heart to R arm
atrial contraction to the onset of ventricular
voltage R arm
aVL-Augmented Frm the heart to L arm contraction
voltage, Left arm  Represents the Time interval needed for the
aVF-Augmented From the heart to the L impulse to travel from the SA node through
Voltage-Left foot foot the intermodal pathways in the atria
downward to the ventricles’
 Measured form the onset of P wave to the
CHEST LEADS onset of the Q wave of the QRS complex.
 from V1-V6  Normal PR interval is measured as three to
 knows as Unipolar leads or Precordial 5 small squares in EKG paper
leads  Duration: 0.12-0.20 sec
 Ck=hest leads look at the heart via  Shortened PR interval (less than .12sec)
horizontal (transverse plane) indicates that the impulse was outside the
 proper placement of the V leads is normal route
important to the correct interpretation of  Prolonged PR interval- delay in the
the 12 lead ECG strip electrical conduction pathway or AV block
th
V1- 4 ICS, R sternum QRS
V2-4th ICS, L sternum  Depolarization of the ventricles
V3-5th ICS, halfway between V2 and V3  Represents the conduction of the electrical
V4- 5th ICS, Left Midclavicular line impulse from the Bundle of His, throughout
V5- 5th ICS, Left anterior axillary line the ventricular muscle or ventricular
V6-5th ICS, Left midaxillary line depolarization/contraction of ventricles
V4R- 5th ICS, right midclavicular line  Duration: 0.05-0.10 sec
V5R- 5th ICS, right anterior axillary line  Narrow QRS indicates that the impulse is
not form in the ventricles and is thus
It is important that the pts skin be prepared before supraventricular or above the ventricles
attaching the leads. Steps
 Wide QRS- the impulse is either ventricular
1. clean the area with an alcohol swab and allow the
or supraventricular origin with aberrant
area to dry
conduction
2. Shave excess hair as indicated
Q wave T wave-ventricles returns to resting state
 The first negative deflection or downward  Repolarization of the ventricles; should
after the P wave exceed 5mm amplitude
 The first down stroke after the P wave  Provides the resting state of the myocardial
 3mm in depth work/ Resting phase of cardiac cycle/
 Pathologic Q wave indicates MI  Represents the return of ions to the
R wave appropriate side of the cell membrane
 The first positive deflection after the P
wave COMMON ECG changes
 5-10mm in height Hypokalemia
 High R waves indicate Ventricular  U-wave
Hypertrophy- because ehypertrophied  Depressed ST segment-
muscles requires a stronger electrical  Short T-Wave
current to depolarize. HYPERKALEMIA
S Wave  Prolonged QRS complex
 The negative deflection after the R wave  Elevated ST segment- ACUTE MI
and terminates at the upstroke of the T  Peak T wave
wave MI
J POINT  Elevated ST segment- acute MI
 It is where the QRS complex meets the ST  Inverted T wave- myocardial ischemia
segment  Pathologic Q wave
 Elevation or depression of 1 mm or more is QRS
an indication of Myocardial injury or  Wide QRS- PVC
schemia  Prolonged QRS- Hyperkalemia

ST Segment Prolonged Q-T interval

 the first negative deflection after the R  Digitalis toxicity
wave  Long term quinidine
 Represents the plateau phase of the action  Long term procainamide
potential  hypoglycemia
 The interval during which the ventricles HEMODYNAMIC MONITORING
are depolarized and ventricular
 is the assessment of the patients circulatory
repolarization begins
status; it includes measurement of heart
rate, PAP, PCWP, CVP, cardiac output and
ST SEGMENT DEPRESSION
blood volume
 Due to myocardial ischemia secondary to
myocardial tissue hypoxia CVP
 Hypoxia results in altered repolarization  Monitors the pressures within the right
contribute to ST segment depression atrium
 Characterized by dip below the isoelectric  Monitors the blood volume, adequacy of
line of 1-2mm or 1-2 small boxes in the ECG venous return to the heart, pump function
strip of the right side of the heart
 Immediate O2 administration  To serve as guide for fluid replacement
ST segment Elevation  To administer blood products, TPN
 Due to myocardial injury secondary to  To obtain venous access when peripheral
acute myocardial infarction vein sites are inadequate
 Other causes coronary artery  To insert a temporary peacemaker
spasm,pericarditis and ventricular  To obtain central venous sample
aneurysm
  Requires the threading of a catheter into a
large central vein (subclavian, internal Nursing Interventions (Before)
jugular vein, median basilica, femoral).  Provide psychosocial support
 The catheter tip is positioned in the RA, or  Assess for allergy to iodine/seafood
upper portion of SVC  VS
 The level of water manometer should be  Withheld meals before the procedure
placed at the right, mid axillary, 4th ICS. This  Have the client to void. To promote
is the approximate level of the RA when the comport
client is in supine position  Administer sedative as order
 Position the client in SUPINE during the  Do cardiac monitoring
initial reading. To get accurate readings.  Tell client that warm or flushing sensation
Position can affect CVP readings will be feel as the contrast medium is
 Strict asepsis. To prevent infection injected
 Normal reading:  Fluttering sensation is felt
 SVC= 0-12 cm H2O
 RA= 5-12 cm H2O After the procedure
 CVP near zero- hypovolemia/ DHN-  Bed rest
hypotension, oliguria and rapid, weak,  Monitor VS especially peripheral pulses
thread pulse  Monitor EKG
 High CVP (15-20cm H2O)- hypervolemia-  Apply pressure dressing/ice pack
hypertension. Polyuria, bounding pulse.  Immobilized affected extremity in extension
PAP PCWP  Monitor extremities for color, temp, pulse
 Monitor pressure in the RA, RV, PA, and and sensation
distal branches of pulmonary artery (PCWP)
 It reflects pressure in the LEFT Atrium COMPLICATIONS
 Swan Ganz catheter is inserted via ante  Dysrhythmia
cubital vein into the right side of the heart  Pericardial tamponade
and is floated into the pulmonary artery  MI, pulmonary edema
 Elevated PAP and PCWP-indicate LSHF  Perforation of great vessels of the heart
 Normal range: Angiography/Arteriography
 PAP= 4-12mmHg PCWP= 4-12mm Hg
 Involves introduction of contrast medium
 PCWP reading above 25mm Hg indicate
into the vascular system to outline the
PULMONARY EDEMA
heart and blood vessels
Nursing Interventions
 Inflate balloon only for PCWP readings,  It may be done during cardiac
deflate between reading catheterization
 Observe catheter insertion site; culture site
q 48 hrs as ordered  Observe hypotension after the procedure
 Assess extremity for color, temp, capillary
filling and sensation

COMPLICATIONS
Pneumothorax, hemothorax, air embolism,
hematoma, cardiac tamponade

Cardiac CATHETERIZATION
 To assess oxygen levels, pulmonary blood
flow, CO, heart structures
 Visualization of coronary artery
  Obesity. Results to increased cardiac
Assessment of Clients with Cardiovascular workload. The heart has to pump blood
Disorders supply to a larger body surface area. Maybe
rise in serum lipid levels.
1. Nursing History
 Hyperlipidemia. Hypercholesterolemia.
RISK Factors
Increased LDL cholesterol damages
NON-MODIFIABLE/ Unavoidable risk factors
endothelium and causes accumulation of
 Age. Persons above 40 of age are at risk to
fats on the endothelial lining which
develop cardiovascular disease due to
enhances the risk of atherosclerosis.
degenerative changes in the heart and
 Personality Type/ Behavior Factors. Type A
blood vessels
characterized by competitiveness,
 Gender. Males are more prone to CVD
impatience, aggressiveness and time
before the age of 65 years. Females have
urgency has been correlated to CAD
higher chance to CVD after the age of 65
 Contraceptive pills. It may precipitate
due to decreased estrogen levels in
thromboembolism and Hypertension. The
menopause, LDL/bad cholesterol increases
estrogen content of pills increases blood
to cause atherosclerosis.
viscosity which increases the risk of
 Race. Cardiovascular disorders are among
thromboembolism. It also stimulates the
the 10 leading causes of death worldwide.
liver to synthesize angiotensinogen which
 Heredity. Positive family history for CVD is
convert into angiotensinogen 1, a
at risk to develop the disease.
vasoconstrictor, which further acted upon
by pulmonary converting enzyme and
MODIFIABLE RISK FACTORS/ Avoidable risk factors
converted to Angiotensin 2 a very potent
 Stress-SNS response stimulation causes
vasoconstrictor.
secretion of norepinephrine to cause
 DM. Glucose from CHO cannot be
vasoconstriction and tachycardia.
transported into the cells due to insulin
 Diet. Increase intake of foods in high in
deficiency or increase resistance to insulin.
sodium, fats and cholesterol predispose to
The body mobilizes fats (lipolysis) to
CVD. High sodium retains water and
become a source of glucose. However, not
increase blood volume. High fats and
all fats mobilized are converted into
cholesterol predispose to atherosclerosis
glucose. Most of it remains as lipids.
Hyperlipidemia results.
 Exercise. Sedentary lifestyle increases the
risk to cardiovascular disorders.
PHYSICAL EXAMINATION
 Cigarette smoking. Nicotine causes
INSPECTION
vasoconstriction and spasms of the arteries a. SKIN COLOR- note for cyanosis, pallor or
which increases myocardial oxygen jaundice.
demand. It decreased levels of HDL. In  Pallor/Cyanosis- due to inadequate
smoking, more carbon dioxide is inhaled oxygenation
than oxygen  Jaundice-hemolysis of RBC. The bilirubin
 Alcohol. Related to HTN due to component of RBC is release in systemic
vasoconstriction. 30ml of alcohol causes circulation causing Indicates Right Sided
vasodilation. Heart Failure
 Hypertension. Increase systemic vascular b. NECK VEIN DISTENTION- due to venous
resistance, increased platelet adherence congestion
result from elevated BP c. Inspect the chest
  look for pulsations, symmetry of Patient Positioning for Heart Auscultation
movement and retractions
d. RESPIRATION Supine or sitting-up:
 Note for signs of dyspnea. Indicates  Use the diaphragm and listen at all 5
inadequate oxygenation. auscultation sites (noting S1 and S2 and if
e. Peripheral Edema- due to venous insufficiency there are any splits presents).
 In addition, distinguish S1 from S2. Then
repeat with the bell of the stethoscope…
PALPATION
noting any other extra sounds.
a. Peripheral Pulses
 Weak or bounding pulse and irregular
Left side: turn the patient onto their left side and
pulses- CARDIOVASCULAR DISEASE auscultate with the bell of the stethoscope at the
 Examine the pulses bilaterally. Peripheral APEX area and listen for S3, S4, or mitral stenosis
pulses should be equal. murmurs.
 Note amplitude (fullness) that depends on
pulse pressure. This gives an estimate of Sit up, lean forward, and have patient exhale: Listen
STROKE VOLUME with the diaphragm at the aortic and pulmonic sites
 Small volume pulse maybe from low stoke for murmurs.
volume and peripheral vasoconstriction (MI,
Shock, constrictive pericarditis.
5 AREAS of AUSCULTATION
b. Apical Pulse
AORTIC Area
 it is assessed at the POINT OF MAXIMUM
- right 2nd ICS
IMPULSE at 5th ICS or medial to the Left
- REPRESENTS S2 “dub”
Midclavicular line.
PULMONIC AREA
 Sit upright or lie on his side
 Left 2nd ICS REPRESENTS S2 “dub
c. PALPATE CAROTID ARTERY- reveals
character of pulse in the proximal aorta and
ERB’S Point
provides an indication of disease in LEFT
 3rd ICF Left Lateral sternum
VENTRICLE.
TRICUSPID AREA
d. Follow a systemic palpation sequence
- Left lower border 4th ICS REPRESENTS S1
covering the sternoclavicular, aortic,
“lub”
pulmonic, tricuspid and epigastric areas.
MITRAL AREA
YOU WON’T feel pulsation in these areas
- Left 5th ICS Mid clavicular line REPRESENTS
S1 “lub” (also the site of point of maximal
PERCUSSION
impulse)
 Pulmonary Edema- DULLNESS on
percussion of the chest.
The Base of the heart includes the aortic and
pulmonic areas, and S2 will be loudest at the base.
AUSCULTATION
Aortic and pulmonic murmurs are heard best at the
 If heart sounds are faint/hear abnormal
base with the patient leaning forward and sitting up
sounds listen again with the patient lying on
with the diaphragm of the stethoscope.
his side/ left lateral recumbent or seated
and leaning forward.
The Apex of the heart includes the tricuspid and
 LEFT LATERAL RECUMBENT POSITION- best
mitral areas, and S1 will be loudest at the apex. S3
suited for hearing LOW PITCHED sounds,
and S4 along with mitral stenosis murmurs will be
using the BELL of the stethoscope.
heard best at this position with the patient lying on
 FORWARD LEANING- to hear HIGH pitch
their left side with the bell of the stethoscope
sounds, used DIAPGRAM of the
stethoscope.
Heart Sounds
S1  These are audible vibrations of the heart
 is produced by asynchronous closure of and great vessels that are produced by
MITRAL and TRICUSPID VALVE turbulent blood flow.
 Dull, low pitch sound, described as “LUB”  blowing/swooshing noise from blood
 It signals the onset of ventricular systole turbulence in the chambers of the heart
 S1 is louder at the apex. (wall defect) or valve problem (stenosis or
S2 regurgitation)
 Sound produced at the end of ventricular  Indicate Incompetent or Stenotic Valves
contraction by asynchronous closure of  Heart valves are affected
AORTIC and PULMONIC VALVES
 High pitch, described as “DUB”
Types of Murmurs
 Shorter higher pitched sound than S1
Systolic murmur
S3/ Ventricular Diastolic Gallop  A heart murmur that occurs during a
 Is a faint, low pitch sound produced by heart muscle contraction.
rapid ventricular filing in early diastole after Diastolic murmur
S2.  A heart murmur that occurs during heart
 Caused by vibrations of ventricle filling from muscle relaxation between beats.
a resistant ventricle due to fluid volume Continuous murmur
overload or heart failure.  A heart murmur that occurs throughout
 Best heard at the apex, pt lying oh his left the cardiac cycle.
side.
 Commonly compared to the “y” sound in Grading of murmurs:
“Ken-tuck-y” Grade 1: hard to hear
 Disappears when the client sit up Grade 2: faint but heard
 heard after S2 and sounds like “LUB-DUB- Grade 3: easily to hear
TA” Grade 4: Loud with a chest thrill
Grade 5: Very loud…can hear when corner of the
 Commonly heard with High Cardiac Output chest piece is lifted off the chest
 Normal in children and young adults Grade 6: Loudest…can hear when whole chest piece
 Indicates Cardinal sign of CHF lifted off the chest
(VENTRICULAR FAILURE) in older adults
Pericardial Friction Rub
S4/Atrial Diastolic gallop  An extra heart sound originating from the
 Heard over tricuspid or mitral area (Lying pericardial sac
on left side)  Ask the client to lean forward and exhale
 Commonly described as sounding like  Use diaphragm of the stethoscope over the
“Ten-nes-see or heard before S1 and third interscostal space on the left side of
sounds like “TA-LUB-DUB” the chest
 Low frequency sounds  Short, High pitch and scratch sound
 Occurs nearly end of the diastole just  Indicates Pericarditis
before S1 after atrial contraction
 It is abnormal in all ages
 Can be heard in elderly clients COMMON MANIFESTATION OF HEART DISEASE
 Can be a sign of HPN, LEFT VENTRICULAR CHEST PAIN
HYPERTROPY, PULMONARY or AORTIC  Most common manifestation among
STENOSIS,) patients with cardiac disease
 Sudden or gradual and initially be difficult to
ascertain a cause
MURMUR
 due to decrease coronary tissue perfusion
and oxygenation
  Aerobic metabolism causes production of Emotional distress or a panic
LACTIC ACID. Lactic acid causes irritation of attack.
nerve endings in the myocardium that Characteristic
result to chest pain. 1. What precipitates or relives
dyspnea?
CHARACTERIZATION 2. How many pillows does the patient
1. Nature and Intensity sleep with at night?
 Ask the patient to described in his own  Use several pillows is an indication
words what the pain is like of ADVANCE HEART FAILURE
 Dull, sharp, burning, heaviness? 3. How far can patient walk or how many
 Ask the patient to rate the pain using PRS 1- flights of stairs can patient climb before
10. becoming dysneic?
2. Onset and duration
 when did the pain start? Types of Dyspnea
 how long did the pain episode last? Exertional
3. Location and radiation  Breathlessness on moderate
a. Ask the patient to point where it hurt most? exertion that is relieve by REST
POSITIVE LEVINE’S SIGN- clenched fist brought to  indicates DECREASE CARDIAC
patient’s chest. Indication of diffuse visceral pain RESERVE
with unstable cardiac disease. Orthopnea
b. Ask the patient if the pain seem to travel.  Difficulty of breathing when lying
(commonly radiate to left arm, jaw, back, abdominal down
 relieve by upright position
region
 the client need several pillows to
4. Precipitating and Relieving Factors
be able to sleep during the night.
a. What activity was patient doing just before
 A sign of MORE ADVANCE HEART
pain? (rapid walking, exposure to cold, eating spicy FAILURE
meal, or sitting quietly) Paroxysmal Nocturnal Dyspnea
b. What relieves the pain? Rest, medications or  Sudden dyspnea occurs at night 2-
change of position. 5 hours after the onset of sleep.
 Awakens patient with feeling of
SIGNIFICANCE OF PAIN suffocation
1. Ischemia- caused by increase in demand for  Sitting up relieves breathlessness.
coronary blood flow and oxygen delivery  During waking hours the client
2. Excruciating pain radiating to back and assumes upright position. This
flanks- acute dissecting aneurysm of the causes venous pooling of the
aorta. blood.
3. Sharp precordial pain (over the heart area)  When the client lies during the
radiating to left shoulder and upper back night, the blood from the lower
aggravated by respiration- ACUTE extremities are distributed to the
PERICARDITIS upper parts of the body and LUNG
CONGESTION may occur resulting
DYSPNEA/Shortness of Breath to DYSPNEA.
 an uncomfortable condition that makes  it takes 2-5 hours for the blood
it difficult to fully get air into your lungs. from the lower extremities to be
Problems with your heart and lungs can distributed in the upper
harm your breathing. Some people may extremities.
experience shortness of breath suddenly
for short periods of time. PALPITATION
Causes Shortness of Breath?  unpleasant awareness of the heart
beat
 Heart attack/ L CHF, Carbon monoxide  feelings or sensations that your
poisoning, Low blood pressure, Asthma heart is pounding
flare-up, Pneumonia, Pulmonary SIGNIFICANCE
embolism (blood clot in the lungs,
  POUNDING/ jumping sensation-
tachydysrhythmias FATIGUE
 SKIPPED beats- Premature or  due to low cardiac output. The heart is
ventricular beats, anemia, heart unable to provide sufficient blood to meet
failure, thyrotoxicosis the increase metabolic need of cells
 weakness or lack of energy tiring of the legs
EDEMA is caused by peripheral arterial or venous
 Increased hydrostatic pressure in disease.
the venous system causes shifting CYANOSIS
of plasma
- Bluish discoloration of the skin and mucous
 is abnormal accumulation of serous
membrane.
fluid in soft tissues
- Indicate poor cardiac output and tissue
 location of edema is influence
by gravity- fluids collects perfusion
bilaterally in the lower parts of the Central cyanosis
body.  Low oxygen saturation of arterial blood
 weight gain occurs before clinical  Tongue, buccal mucosa, lips
evidence of edema  Indication of cardiorespiratory disease,
heart failure and pulmonary edema
SIGNIFICANCE- LATE SIGN OF HEART Peripheral cyanosis
FAILURE  Reduced blood flow in the extremities due
to VASOCONSTRICTION
Grade 0:  Distal aspect of the extremities, tip of the
 no pitting edema. nose and earlobes
Grade: 1:  Cold exposure and peripheral vascular
 2 mm in depression disease
 Rebound time: immediate
Grade 2: JAUNDICE
 The pressure leaves an indentation of 3–4  Yellowish discoloration of the sclera of the
mm eyes
 rebounds in fewer than 15 seconds.  Sign of Right Sided Heart Failure/ chronic
Grade 3: hemolysis from prosthetic hear valves
 The pressure leaves an indentation of 5–6
mm that takes up to 30 seconds to FATTY SKIN DEPOSITS
rebound.  Associated with hyperlipidemia and CAD
Grade 4:
 The pressure leaves an indentation of 8 CLUBBING of the NAIL BEDS
mm or deeper.  Swollen nail base and loss of normal angle
 Very deep indentation  Associated with Congenital Heart Disease
 Rebound time: more than 20 sec and Col Pulmonale
 Thin brown line in the nail beds with
Degree of edema ENDOCARDITIS
a. MILD- 1/4 inch deep
b. MODERATE- ½ inch deep
c. SEVERE- ¾ - 1 inch deep

SYNCOPE/DIZZINESS
 the client will experience generalized
weakness with inability to stand upright
followed by transient loss of consciousness.
SIGNIFICANCE
 decrease tissue perfusion
 fall of cardiac output with cerebral ischemia
 DYSRHYTHMIA related to cardiac disease
  Increase-polycythemia
 Decrease- blood loss, hemolytic anemia,
bone marrow suppression
LABORATORY and DIAGNOSTIC TEST
Laboratory BLOOD COAGULATION TEST
CBC
 For evaluation of general status Prothrombin Time (PT, Pro TIME)
 Elevated RBC indicates inadequate tissue  A protein produced by the liver for clotting
perfusion of blood.
 HYPOXIA stimulate renal secretion of  It measure the time required for clotting to
erythropoietin. This stimulates the bone occur after throboplastin and calcium are
marrow to increase RBC production added to decalcified plasma.
(polycythemia).  Valuable in evaluating the effectiveness of
 Elevated WBC’s may indicate infectious COUMADINE
heart diseases and MI.  Normal range is 11-16 sec
RBC  INCREASE: liver disease, Vit. K deficiency,
 carry oxygen from our lungs to the rest deficiency of factors II, V, VII or X
of our bodies.  DECREASE: thrombophlebitis, malignant
 Normal range= Male4.5-5.5M/cu.mm; tumor
Female: 4.1-5.1M/mm
 INCREASE: Polycythemia vera, inadequate C-heck why the medication is given and know the
tissue perfusion classification of the drug. You should know why the
 Decrease: loss and destruction of drug is give
erythrocytes, bone marrow suppression, H-ow will you know if the drug is effective. What
Anemia are the assessment parameters in monitoring the
WBC effects of the drugs.
 Normal range=5000-10000/cu.mm; E- xackly what time should the medication is given
 INCREASE- leukocytosis, infection,heart C-lient teaching tips. What would you tell your
diseases and MI patient to expect. Give instructions related to the
 Decrease- leukemia, autoimmune disease therapeutic and side effects
K-eys to giving it safely. You should identify the
ESR interventions to counteract the adverse/side effects
 Is a measurement of the rate at which of the drug.
RBC’s “settle out” of anticoagulated blood
in an hour. COUMADINE
 elevated in infectious heart disorders or MI C- Anticougulant; prevent thrombus formation; it
Normal Range does not dissolve clots
 Male: 15-20 mm/hr H- (-) thrombus
 Female: 20-30mm/hr E- No specific
Platelet C- Avoid green leafy vegetables as the Vit K content
 thrombocytes, are small, colorless cell of these vegetables interfere with the absorption of
fragments in our blood that form clots the drug
and stop or prevent bleeding. K- Assess for any sign of bleeding
 150-450k/cu.mm Keep Vit K at the bedside
 INC: poly vera; DEC: viral infections, SLE, Do not give patient any IM injection
idiophatic, dengue
Hemoglobin Partial Thromboplastin Time (PTT)
 substance in red blood cells that makes it  It measures the time required for clotting to
possible for blood to transport (carry) occur after a partial thromboplastin reagent
oxygen throughout the body. is added to the blood plasma.
(Hemoglobin is what gives red blood cells  The best single screening test for disorders
their color. in coagulation
 Male: 13-18g/dl; Female=12-16g/dl
  It is used to evaluate the effectiveness of Initial elevation: 4-6hrs
HEPARIN Peaks: 24-36 hrs
 Normal Range: 60-70 sec Returns to normal: 4-7 days

Activated Partial Thromboplastin Time (APTT) CREATININE PHOSPHOKINASE (CK-MB)

 Same purpose of PTT  Is the most cardiac specific enzyme
 Most specific test to evaluate the  It is an accurate indicator of myocardial
effectiveness of Heparin damage.
 Normal range: 30-45sec.  Normal range is:
Male: 50-325 mu/ml
HEPARIN Female: 50-250mu/ml
C- Anticoagulant; used to prevent clot enlargement Range with MI
H- Prolonged PTT  Onset: 3-6 hrs
E- No specific  Peaks: 12-18 hrs
C- Report signs of bleeding  Returns to normal in 3-4 days
K- monitor the PTT
Keep protamine sulfate at the bedside CREATININE KINASE (CK)
 is an enzyme found in the heart, brain,
Blood Urea Nitrogen (BUN) skeletal muscle, and other tissues.
 An indicator of renal function  Increased amounts of CK are released into
 Decreased cardiac output leads to low renal the blood when there is muscle damage.
tissue perfusion and reduction in GFR. BUN This test measures the amount of creatine
becomes elevated kinase in the blood.
 rise in 12 hrs
 peak in 36-72 hrs
 Normal range: 35-232 IU
Blood lipids  normalize in 3-5 days
Serum cholesterol
 NPO for 10-12 hrs LACTIC DEHYDROGENASE (LDH)
 150-200mg/dl  It plays an important role in cellular
Serum triglycerides respiration, the process by which glucose
 NPO for 10-12 hrs (sugar) from food is converted into usable
 140-200 mg/dl energy for our cells.
 LDH 1 the most sensitive indicator of
myocardial damage
SERUM ENZYME STUDIES  In MI, LDH 1 is elevated and its level
 When myocardial tissue is damage (MI) exceeds to LDH2 within 12 to 24 hrs.
certain enzymes or isoenzymes are release  Normal range 140 units per liter (U/L) to
into the bloodstream resulting to elevated 280 U/L
blood enzymes  LDH1 and LDH2- LDH2 is greater than LDH1;
except when the heart muscle is damage a
ASPARTATE AMINO TRANSPERASE reversal occurs.
 Formerly SGOT Range with MI
 Elevated indicates tissue necrosis Onset: rise in 12 hrs
 Used to indicate liver injury Peak: 24-48 hrs
 Found in liver, heart and skeletal muscle Returns to normal: 10-14 days
 Range:
Men= 10-40U/L; HYDROXYBUTYRATE DEHYDROGENASE (HBD)
Women= 9-25U/L  Elevation of HBD is always accompanied by
 Increase: liver diseases(heap, alcoholism, elevation of LDH levels
drug toxicity), Acute MI, anemia,  Valuable in detecting “SILENT MI” because
 Decrease= vit B 6 deficiency, CKD it remains elevate for a long period of time
 Range with MI  HBD and LDH are increase in MI
  Normal Range: 140-350 u  Detected as early as 30-60 minutes after
 Range with MI injury but declines rapidly 7 hours
Onset: 10-12 hrs
Peak: 48-72 hrs NURSING ALERT: the greater the peak in enzymes
Normal: 10-14days activity and the length of time the enzyme remains
at its peak level the serious the heart muscles
CARDIAC TROPONINS damage and a poor prognosis for the patient
 Troponins are a group of proteins found
in skeletal and heart (cardiac) muscle URINALYSIS
fibers that regulate muscular contraction. - To assess the effects of cardiovascular
 Troponin tests measure the level of diseases on renal function and the
cardiac-specific troponin in the blood to existence of renal or systemic diseases
help detect heart injury. (AGN, DM and hypertension)
 These proteins are released when the - Albuminuria is detected in the clients with
heart muscle has been damaged, such as HPT and CHF
occurs with a heart attack. The more - Myoglobinuria supports the diagnosis of
damage there is to the heart, the greater MI
the amount of troponin T and I there will
be in the blood. BUA
 There are three types of troponin - Reflects the adequacy of the renal tissue
proteins: troponin C, troponin T, and perfusion
troponin I - Cardiovascular disorders results to
 Most specific test to detect MI decrease renal tissue perfusion. This will
 T and I begins to rise 3-5 hrs after cause impairment of the ability of the
myocardial injury occurs kidneys to clear the plasma of end
products of metabolism like uric acid
Troponin I
 Modulates the contractile state Serum Electrolytes
 better cardiac marker than CK-MB and - Electrolytes affects cardiac contractility
should become the preferred cardiac specifically Na, Ka nd ca
enzyme when evaluating patients with - Na-135 to 145 mEQ/L
suspected myocardial infarction. - K- 3.5-5 mEq/L
 Normal range: 0 and 0.04 ng/mL - Ca 4.5 to 5.5 mE/L
 Rise in 3-5 hrs
 Peak: 14-18 hrs
 Remain elevated for 5-7 days (above DIAGNOSTIC TEST
1.5ng/ml indicates MI)
Troponin C ECG
 Binds calcium  It is a graphical recording of the electrical
Troponin T activities of the heart.
 Sensitive as CK MB in detecting myocardial  It is the first diagnostic test done when
 Is sensitive as CK MB for the detection of cardiovascular disorder is suspected.
myocardial injury above 0.ng/ml indicate  The procedure is PAINLESS.
MI. binds in I and C
 Rise in 3-5 hrs INDICATIONS OF ECG
 Remains elevated in for 14-21 days  MI and other CAD
 Cardiac Dysrhythmias
 Heart enlargement
MYOGLOBIN  Electrolytes imbalances- especially CA, NA
 Is a low molecular weight heme protein and K levels
found in cardiac and skeletal muscle.  Inflammatory diseases of the heart
 A sensitive indicator of early MI.  Effects of drugs on the heart
 Augmented leads Position of flow
ELECTRODE aVR-Augmented Frm the heart to R arm
 An adhesive pad that contains conductive voltage R arm
gel and designed to be attached to the aVL-Augmented Frm the heart to L arm
patients skin voltage, Left arm
LEADS aVF-Augmented From the heart to the L
- Electrodes connected to the monitor or EKG Voltage-Left foot foot
machine by wires
 Wires are color coded. CHEST LEADS
RHYTHM STRIP  from V1-V6
 The printed record of the electrical activity
 knows as Unipolar leads or Precordial
of the heart
leads
The standard ECG consist of 12 leads
 (I, II, III, AVR, AVL, AVF, V1, V2, V3, V4, V5,  Chest leads look at the heart via horizontal
V6) (transverse plane)
 Used in prehospital and clinics settings  proper placement of the V leads is
regularly to aid in screening patients who important to the correct interpretation of
potential candidates for fibrinolytic therapy the 12 lead ECG strip
 3 lead ECG- is use to detect life-threatening
dysrhythmias
Bipolar lead/Standard Limb Leads V1- 4th ICS, R sternum
 Lead I II III - each have one positive V2-4th ICS, L sternum
electrode and one negative electrode V3-5th ICS, halfway between V2 and V3
 Current flows from the limbs through the V4- 5th ICS, Left Midclavicular line
heart
V5- 5th ICS, Left anterior axillary line
 Lead II and modified chest lead are the
V6-5th ICS, Left midaxillary line
most common leads used for cardiac
monitoring because of their ability to V4R- 5th ICS, right midclavicular line
visualized P waves. V5R- 5th ICS, right anterior axillary line
 LA Lead (Black lead) - Should be placed
between the left shoulders and wrist away It is important that the pts skin be prepared before
from the bony prominences as bone is a attaching the leads. Steps
poor conductor of electricity 1. clean the area with an alcohol swab and allow the
 RA lead (white lead) should be placed at area to dry
the Right shoulder and wrist 2. Shave excess hair as indicated
 Left Leg Lead (red Lead)-between left leg 3. If the patient is diaphoretic, attempt to dry the
and ankle area or use antiperspirant
 Right Leg Lead (Green Lead)- between the 4. Use conductive gel to ensure proper conduction
right hip and ankle, sometimes used as an 4. Proper placement of the leads
additional ground lead.
Lead Positive Negative Electrode
WAVES, COMPLEXES and INTERVAL
Electrode
I Left arm Right arm P-WAVE- impulse spread across atria triggers atrial
II Left leg Right arm contraction
III Left leg Left arm  first little “hump” or “bump” you see
is known as the P-wave
 SA node is responsible for this.
Augmented Leads
 Study tip: The P-wave represents ATRIAL
 currents flows from the heart outward to
DEPOLARIZATION (depolarization is a big,
the extremities
 referred to as unipolar lead having one true fancy word for CONTRACTION).
pole.  SA node fires first during the a normal
cardiac cycle. This firing send as the
 electrical impulse outward to stimulate  The first negative deflection or downward
both atria and manifest as the P wave after the P wave
 P-wave represents Depolarization of the  The first down stroke after the P wave
Atria both Left and Right atria  3mm in depth
 Smooth and upward deflection  Pathologic Q wave indicates MI
 Duration: 0.04-0.11sec R wave
 Normal P wave is 3mm or less  The first positive deflection after the P
PR INTERVAL wave
 Measure the time interval from the onset of  5-10mm in height
atrial contraction to the onset of ventricular  High R waves indicate Ventricular
contraction Hypertrophy- because ehypertrophied
 Represents the Time interval needed for the muscles requires a stronger electrical
impulse to travel from the SA node through current to depolarize.
the intermodal pathways in the atria S Wave
downward to the ventricles  The negative deflection after the R wave
 the PR-interval starts at atrial contraction and terminates at the upstroke of the T
(remember atrial contraction is represented wave
by the P-wave) and ends at the beginning of  the final depolarization of the ventricles,
ventricle depolarization. So in other words, at the base of the heart.
it starts at the P-wave and ends at J POINT
the beginning of the QRS complex  It is where the QRS complex meets the ST
 Normal PR interval is measured as three to segment
5 small squares in EKG paper  Elevation or depression of 1 mm or more is
 Duration: 0.12-0.20 sec an indication of Myocardial injury or
 Shortened PR interval (less than .12sec) schemia
indicates that the impulse was outside the ST Segment
normal route  This segment starts at the J-point. The J-
 Prolonged PR interval- delay in the point is where you start to see an upward
electrical conduction pathway or AV block stroke after the S wave. The segment ends
QRS at the beginning of the T-wave.
 Depolarization of the ventricles or  The ST-segment represents when the
contraction of the ventricles ventricles are relaxing, also called
 This spike is called the QRS complex. The repolarizing.
bundle of His, bundle branches, and  The interval during which the ventricles
Purkinje fibers are responsible for this. are depolarized and ventricular
 Represents the conduction of the electrical repolarization begins
impulse from the Bundle of His, throughout
the ventricular muscle or ventricular
depolarization/contraction of ventricles
 Duration: 0.05-0.10 sec
 Narrow QRS indicates that the impulse is
not form in the ventricles and is thus ST SEGMENT DEPRESSION
supraventricular or above the ventricles  Due to myocardial ischemia secondary to
 Wide QRS- the impulse is either ventricular myocardial tissue hypoxia
or supraventricular origin with aberrant  Hypoxia results in altered repolarization
conduction contribute to ST segment depression
 Characterized by dip below the isoelectric
Q wave
line of 1-2mm or 1-2 small boxes in the ECG
strip
  Immediate O2 administration QRS
 Wide QRS- PVC
ST segment Elevation  Prolonged QRS- Hyperkalemia
 Due to myocardial injury secondary to
acute myocardial infarction Prolonged Q-T interval
 Other causes coronary artery  Digitalis toxicity
spasm,pericarditis and ventricular  Long term quinidine
aneurysm  Long term procainamide
T wave  Hypoglycemia
 This “bump” is called the t-wave and is
caused by the ventricles relaxing.
 ventricles returns to resting state HOLTER MONITORING
 represents Repolarization of the ventricles;
 The ventricles are so large that when they - A continuous 24 hr ECG monitoring
contract (depolarize) the form a large - To assess the activities that precipitates
electrical impulse that presents the QRS dysrhythmias and the TIME when the
complex. Therefore, (because they are so client experiences dysrhythmias
large) when they relax (repolarize) they - Portable monitoring system is called
form a small electrical impulse that telemetry unit
presents as the t-wave - The nurse should record the activities of
 should exceed 5mm amplitude the client or any unusual sensations
 Provides the resting state of the myocardial experience
work/ Resting phase of cardiac cycle/ INVASIVE HEMODYNAMIC MONITORING
 Represents the return of ions to the
appropriate side of the cell membrane  is the assessment of the patients circulatory
status; it includes measurement of heart
U-wave rate, PAP, PCWP, CVP, cardiac output and
 This is not very common, but I wanted to blood volume
show it to you and mention it.
Central Venous Pressure/ CVP
 The u-wave sometimes is seen after the t-
 Monitors the pressures within the right
wave. This is thought to be caused by the
atrium
relaxation of the Purkinje fibers.
 Monitors the blood volume, adequacy of
 However, the exact source of the U wave
venous return to the heart, pump function
remains unclear.
of the right side of the heart
COMMON ECG changes  To serve as guide for fluid replacement
Hypokalemia  To administer blood products, TPN
 U-wave  To obtain venous access when peripheral
 Depressed ST segment- vein sites are inadequate
 Short T-Wave  To insert a temporary peacemaker
HYPERKALEMIA  To obtain central venous sample
 Prolonged QRS complex  Requires the threading of a catheter into a
 Elevated ST segment- ACUTE MI large central vein (subclavian, internal
 Peak T wave jugular vein, median basilica, femoral).
MI  The catheter tip is positioned in the RA, or
 Elevated ST segment- acute MI upper portion of SVC
 Inverted T wave- myocardial ischemia  The level of water manometer should be
 Pathologic Q wave- permanent in ECG post placed at the right, mid axillary, 4th ICS. This
MI.
 is the approximate level of the RA when the - Can measure the ejection fraction (EF) or
client is in supine position the percentage of end diastolic blood
 Position the client in SUPINE during the volume that is ejected during systole.
initial reading. To get accurate readings. - EF provides information about the function
Position can affect CVP readings of the left ventricle during systole
 Strict asepsis. To prevent infection - No special preparation is required.
 Normal reading: - It is painless and takes approximately 30 to
 SVC= 0-12 cm H2O 60 minutes to complete
 RA= 5-12 cm H2O - The client has to remain still, in supine
 CVP near zero- hypovolemia/ DHN- position slightly turned to the left side,
hypotension, oliguria and rapid, weak, with HOB elevated 15 to 20 degrees
thread pulse
 High CVP (15-20cm H2O)- hypervolemia- Stress Testing or Exercise Testing/ Treadmill Test
hypertension. Polyuria, bounding pulse. -ECG is monitored during exercise on a
PAP PCWP treadmill or a bicycle-like device
 Monitor pressure in the RA, RV, PA, and The purpose of stress test are as follows:
distal branches of pulmonary artery (PCWP) - Identify ischemic heart disease
 It reflects pressure in the LEFT Atrium - Evaluate patients with chest pain
 Swan Ganz catheter is inserted via ante - Evaluate effectiveness of therapy
cubital vein into the right side of the heart - Develop individual fitness program during
and is floated into the pulmonary artery cardiac rehabilitation
 Elevated PAP and PCWP-indicate LSHF
 Normal range: Nursing Interventions:
 PAP= 4-12mmHg PCWP= 4-12mm Hg Patient teaching includes the following:
 PCWP reading above 25mm Hg indicate  Get adequate sleep the night before the
PULMONARY EDEMA test
Nursing Interventions  Avoid tea, coffee and alcohol on the day of
 Inflate balloon only for PCWP readings, the test. These may affect the test results
deflate between reading  No smoking and taking nitroglycerine 2
 Observe catheter insertion site; culture site hours before the test. To prevent postural
q 48 hrs as ordered hypotension
 Assess extremity for color, temp, capillary  Wear comfortable loose clothes
filling and sensation. To observe for ss and  Eat light breakfast or lunch 2 hours before
sx of circulatory impairment in the the test
extremity involve  Wear low heeled rubber soled shoes for
comfort during the test
COMPLICATION  Inform the physician if any usual
Pneumothorax, hemothorax, air embolism, sensations develop during the test (SOB,
hematoma, cardiac tamponade dizziness and fainting)
 Rest after the test
SONIC STUDIES
ECHO CARDIOGRAPHY Radiologic test
- Uses ultrasound to assess cardiac structure Chest X ray
and mobility such as valvular structure, - To determine the size and configuration of
chambers size and contents, ventricular the heart and size of the chambers
muscle, thickness and septal motion, - Avoid wearing metals
pericardial sac and ascending aorta Cardiac Fluoroscopy
- Facilitates observation of the heart from
varying views while the hear is in motion
Cardiac CATHETERIZATION Angiography/Arteriography
 To assess oxygen levels, pulmonary blood
 Involves introduction of contrast medium
flow, CO, heart structures
into the vascular system to outline the
 Visualization of coronary artery
heart and blood vessels
 Right sided heart catherization is done by
 It may be done during cardiac
insertion of catheter via cutdown into a
catheterization
large vein (Median cubital or brachial)
 Nursing interventions are similar to cardiac
 Left sided heart catheterization is done by
catheterization
passing a catheter into the aorta via
 Observe hypotension after the procedure
brachial or radial artery
because contrast medium used may cause
diuretic effects
Nursing Interventions (Before)
 Provide psychosocial support. To reduce
anxiety
 Assess for allergy to iodine/seafood.
 VS
 Withheld meals before the procedure. To
prevent nausea and vomiting
 Have the client to void. To promote
comport
 Administer sedative as order
 Do cardiac monitoring. To assess
dysrhythmias
 Done under local anesthesia
 Tell client that warm or flushing sensation
will be feel as the contrast medium is
injected
 Fluttering sensation is felt as the catheter
enters the chambers of the heart

After the procedure

 Bed rest
 Monitor VS especially peripheral pulses
 Monitor EKG
 Apply pressure dressing/ice pack over the
puncture site to prevent bleeding
 Immobilized affected extremity in extension
to promote circulation
 Monitor extremities for color, temp, pulse
and sensation
 Do not elevate the HOB more than 30
degrees if femoral site was used. Acute hip
flexion causes circulatory impairment

COMPLICATIONS
 Dysrhythmia
 Pericardial tamponade
 MI, pulmonary edema
 Perforation of great vessels of the heart
 pain,4 you may need a cardiac
catheterization.5
 Cardiac catheterization produces
images that can identify the location
and severity of blockages in the
coronary arteries, show your overall
heart function and the condition of
individual cardiac chambers (cardiac
ventriculography), and determine
whether your heart valves are
narrow, stiff, or leaky.
Cardiac catheterization1
 This test is also done preoperatively
 (also referred to as cardiac cath or
for planning cardiac procedures that
heart cath) is an invasive procedure
involve treatment of narrow or
used to evaluate and treat heart
blocked coronary arteries, such
conditions. A thin, long, flexible tube
as coronary artery bypass
is inserted, usually in the arm or
surgery, angioplasty, and stenting.
groin, and is guided to the blood
 can also be used to take a sample of
vessels of your heart.
tissue if you have a possibility of an
 Angiography is almost always done
infection or inflammation of the
during the procedure, which involves
heart,
injecting dye into your vessels so
 to measure oxygen levels for
they can be visualized with imaging,
assessment of cardiac and
typically an X-ray or an intravascular
pulmonary disease, or
ultrasound.
 to determine the pressure in various
 Your healthcare provider may use
areas of the heart (right heart
this to help diagnose a concern,
catheterization)
deliver medication, or repair heart
 can be used as one of the diagnostic
defects and disease.
tests for heart valve disease,
congestive heart failure,
Purpose of Test cardiomyopathy, or heart failure.

Therapeutic Uses
 to access your coronary arteries for
blockages and to assess heart muscle  useful in the treatment of heart
function and the structure and problems.
function of your heart valves.
 The catheterization procedure can  used to relieve blockages in the
also be used to deliver therapy for coronary arteries with angioplasty
many cardiac conditions. (widening the arteries), to remove
obstructive material (thrombectomy),
Diagnostic Uses and for stent placement (a tube that
 If you have signs of atherosclerosis remains in place to keep the artery
or coronary artery disease (blockage open).
in your heart vessels) such as
fatigue, shortness of breath, or chest  treat heart valve conditions such as
mitral stenosis and aortic
 stenosis (valvuloplasty) and heart Serious and less common complications
rhythm irregularities (cardiac include:
ablation), or to repair patent foramen
ovale.  An allergic reaction to the dye: This
 Sometimes a cardiac catheterization can cause flushing, a rash, extreme
with an angioplasty is done urgently shortness of breath, hypertension or
for the diagnosis and treatment of a hypotension, or heart rhythm
heart attack to restore blood flow to a irregularities and is treated as an
coronary artery, with the aim of emergency, usually with
preventing permanent heart damage. epinephrine.
Limitations  Artery damage: This can occur in
 Certain heart problems, such as any artery between the location of
congenital heart defects, heart valve catheter insertion all the way to the
disease, and heart failure, may be arteries in the heart, causing a defect
detected by catheterization and called a pseudoaneurysm.10
angiography, but are better evaluated  Perforation of the heart wall: This
with cardiac echo, cardiac MRI, or can cause a life-threatening
cardiac CT; arrhythmias are best condition, cardiac tamponade.
evaluated with an electrocardiogram  Sudden blockage of a coronary
(ECG or EKG), ambulatory artery, which can lead to a heart
monitoring, or an electrophysiology attack.
study.  Extensive bleeding.
Stroke.
Risks and 

Contraindications
Cardiac catheterization and angiography are
relatively safe, but because they are invasive
procedures involving the heart, several
complications are possible. For this reason, a
cardiac catheterization is performed only
when the treatment is expected to be highly
beneficial or when there is a strong
likelihood that the information gained from
the procedure will be of significant benefit.

 Common complications of cardiac

catheterization include minor
bleeding at the site of catheter
insertion, usually in the arm or the
groin, temporary heart rhythm
disturbances caused by the catheter
irritating the heart muscle, and
temporary changes in the blood
pressure.