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52 Cards in this Set

  • Front
  • Back
Divided into 2 sides- which receive and send blood to different parts of the body

– Left- receives blood from the lungs and sends blood to the body

– Right- receives blood from the body and sends it to the lungs
A thick wall separates the right side of the heart from the left side
Heart Chambers

The heart has 4 chambers
Upper chambers
– Right and left ATRIA
Receiving chambers for blood
Lower chambers
– Right and left ventricle Pumping chambers for blood
The right atrium receives
deoxygenated blood from the venous system and sends it to the right ventricle
The right ventricle
pumps that blood to the lungs to be oxygenated
The left atrium receives
oxygenated blood from the lungs and sends it to the left ventricle
The left ventricle
pumps all the blood to all the cells and tissues in the body
lines the inside of cardiac chamber, made of thin endothelial cells
middle layer, made of muscle fibers and responsible for pumping
made of fibrous and loose connective tissue, also known as visceral pericardium (sac that surrounds and protects the heart)
tricuspid valve

mitral valve, also called bicuspid
- separates the RA and RV

-separates the LA and LV
pulmonary valve

aortic valve
-separates the right ventricle and the pulmonary artery

-separates the left ventricle from the aorta
branches off to supply the nerve tissue of the conduction system
branches off into the LAD and circumflex artery

supplies blood to LA, LV, and septum
The term cardiac cycle refers to what?
cardiac cycle refers to the contraction (systole) and relaxation (diastole) of both the atria and ventricles

The chambers fill with blood, contract and relax
-negative state inside myocardial cell
-positive state inside myocardial cell
-Once contraction occurs the charges inside the cells returns to normal until the next stimulus is sent. This process

Amount of blood pumped out of the left ventricle in one minute 4-8L/min

Cardiac output can be increased by:
increasing heart rate
– increasing stroke volume
Volume of blood ejected with each ventricular contraction
– normal 65-70 ml
Cardiac Output = HR X stroke volume
Factors That Affect Stroke Volume Preload

– amount of blood that is in the ventricles during the filling stage

u increase preload=increase SV= increase CO
Factors That Affect Stroke Volume Contractility
ability of muscle fibers to produce contraction

u factors that have (+) inotropic effects increase and those with (-) inotropic effects decrease
Factors That Affect Stroke Volume Afterload
amount of pressure ventricles must overcome to eject the blood volume it holds
- increases with vasoconstriction
- decreases with vasodilation
Begin with chief complaint and history of present illness
Medical history
Family history
Review of Systems
– head to toe assessment
Lung Sounds
should not hear any “noises”

if lungs are “wet” sign of Lt. sided heart failure or fluid overload
may have productive or none productive coughs

– frothy sputum can indicate CHF
Blood Pressure
– check in both arms

– Orthostatic BP

– as BP decreases the HR should increase
– inspect for intactness, cap. refill, temperature, turgor, and color
Heart Sounds
– the valves closing produces the “lub dub” sound
- “lub” is S1(atrioventricular valves closing)
- “dub” S2 (semilunar valves closing)
Abnormal Heart Sounds
– Murmurs
– Rubs
-sound produced by turbulent blood flow across valves
-heard when pericardium is inflamed can be pericardial or pleural
Peripheral Edema
– sign of fluid overload and the inability of the heart to compensate for imbalance
Areas for Edema
the fluid is “backing up” into the tissues

sign of Rt sided heart failure
Areas for Edema
– the fluid is “backing up” into the lungs

sign of Lt. sided failure
Mental Status
may be decreased R/T:

decrease level of O2 to brain

electrolyte imbalance

SOB or Chest Pain can cause anxiety
Jugular Vein
– if Rt side of heart backs up, the blood can’t drain from jugulars, causing distention

– sit patient up 45 degrees and assess for distention
weight upon admission and then daily

– increase > 2 lbs in 24-48 hrs is a weight gain of 1 liter of fluid

– ***best indicator of fluid balance***
Different Enzymes to diagnose cardiac disease
protein involved in contractility of muscles

– Troponin I is specific to the heart

u released after myocardial infarction and increases in 4-6 hrs from onset of s/s

u peaks in 14 to 18 hrs will return to normal in 7 days
Different Enzymes to diagnose cardiac disease
Creatinine Kinase (CK)
indicative of muscle damage
Found in 3 tissues:
– Brain
– Skeletal muscle
– **Heart (CKMB)**
elevates in 4-12 hrs after damage, peaks in 24 hrs, and returns to normal in 3-4 days
Different Enzymes to diagnose cardiac disease
Lipid Profile
cholesterol, triglycerides, phospholipids
– major contributor to CAD
– produced in the liver
– usually elevated with the LDL
– normal 40-150
Lipid Profile
– produced by the liver, used to form bile salts for digestion of fats and for production of adrenal, ovarian and testicular hormones

– if > 200 mg/dl at risk for CAD, HTN, MI
Forms of cholesterol
– a. high density (HDL
promote excretion of LDL’s and VLDL’s
risk for CAD is decreased if HDL’s are elevated
normal 30-70
Forms of cholesterol
b. low density (LDL)
if elevated, risk for CAD
normal60 -160
– c. very low density (VLDL)
A diagnostic test performed in an operative setting

– Done for a variety of purposes

A catheter is advanced into the vascular system and dye is injected into the heart’s veins, arteries, and vessels to check for damage or blockages

A catheter is advanced into the vascular system and dye is injected into the heart’s veins, arteries, and vessels to check for damage or blockages
NPO after MN

Assess for allergies to iodine, radiographic dye, and latex


Consent for procedure


Post care instructions
keep sand bag in place for bleeding
check pedal pulses
keep leg straight @ least 6 hrs.
Systolic Blood Pressure

Determined by:
– the force and volume of blood that the left ventricle ejects during systole

– The ability of the arterial system to distend at the time of ventricular contraction

Narrowing of the arterioles increases peripheral resistance

– Which increases BP
Diastolic Blood Pressure
Reflects arterial pressure during ventricular relaxation

If arterioles are resistant, blood is under greater pressure
Stage 1 hypertension
Stage 2 hypertension
– 120/80 to 139/89
– 140/90 to 159/99
– >160/100
Causes the heart to work harder to pump against the increases resistance

Size of heart muscle increases
When the heart can no longer pump adequately to meet the body’s metabolic needs, heart failure occurs
The extra work and greater mass increase the heart’s need for oxygen
If the myocardium does not receive sufficient oxygenated blood, myocardial ischemia occurs
Can result in a myocardial infarction
ACE Inhibitors
Prevents Angiotensin I from converting to Angiotensin II

Promote fluid and sodium loss and decrease peripheral vascular resistance
Angiotensin Receptor Blockers
Angiotensin II receptor antagonist

Blocks effects of angiotensin II

Relax vascular smooth muscle

Increase salt and water excretion
Calcium Channel Blockers
Block calcium ions through specific channels of the cell membrane in the blood vessels

Dilate coronary and peripheral arteries


Inhibit reabsorption of sodium in distal convoluted tubules

Promote sodium and water excretion, thus reducing circulating blood volume
Accelerated and Malignant Hypertension
-Markedly elevated BP, accompanied by hemorrhages and exudates in the eyes
– Dangerously elevated BP accompanied by papilledema
Accelerated and Malignant Hypertension S/S
Onset of sudden severe back pain with hypotension **
Nursing Management of
Accelerated and Malignant Hypertension
Lower BP within 1-2 hours

Report a systolic BP of 160 or diastolic of 115 or higher