NURS 301 Test 2 Study Guide
Ch. 32-38: Cardiovascular Unit Part 1
Anatomy and Physiology Review
● The Heart
o Endocardium- thin inner lining of the heart
o Myocardium- Middle muscular layer
o Epicardium- Outer fibrous membrane
o Pericardium- 2 layered “sac” that surrounds the heart; consists of
Visceral layer (inner) and Parietal layer (outer)
- Pericardial sac contains 10-30 mL of pericardial fluid that prevents
a friction rub
➔Increased pericardial fluid= cardiac tamponade
➔Decreased pericardial fluid= Friction rub
Systemic Circulation: Blood Flow through the Heart
1. Right atrium receives blood from the superior and inferior vena cava and
coronary sinus
2. Blood passes from right atrium through the tricuspid valve to the right ventricle
3. Blood passes from the right ventricle through the pulmonic valve into the
pulmonary artery and to the lungs for oxygenation
4. Pulmonary vein returns freshly oxygenated blood back to the left atrium
5. Blood passes from left atrium to the left ventricle through the mitral valve
6. Blood exits the left ventricle through the aortic valve out into the aorta and to the
body
o A/V valves: Tricuspid and Bicuspid (mitral)
o Semilunar valves: Pulmonic and aortic
o Exception: Arteries normally always carry oxygenated blood, but the
pulmonary artery is the exception! It carries deoxygenated blood to the
lungs, and the pulmonary vein carries oxygenated blood back to the heart
from the lungs
o Remember: Tissue Paper My Assets! (Valves right to left in order of
blood flow)
Coronary Circulation: Myocardial Blood Supply
o The heart has its own circulatory system
o Right above the cusps of the aortic valve are the Sinuses of Valsalva
which open into the right and left coronary artery
o Blood flows to the heart muscle during diastole
- Myocardium receives blood during diastole!
o Right coronary artery supplies the right atrium and the right ventricle
(part of the posterior left ventricle)
o Left coronary artery branches into the left anterior descending and the
left circumflex artery that supply the left atrium and left ventricle
o Definitions:
A. Ischemia= Tissue Hypoxia; Inadequate blood flow to meet the
myocardial oxygen needs
- Reversible lack of oxygen to tissues causing hypoxia
- The pain that goes along with myocardial ischemia is called
angina pectoris
B. Infarction= Result of permanent loss of blood supply and cellular
death; Irreversible tissue death
C. Perfusion= Measure of blood flow and oxygen delivery to tissues.
No perfusion can lead to MI, stroke, or acute renal failure! Check
bowel sounds, pedal pulses 2 Check kidney perfusion by
measuring urinary output. A patient should produce at least 30
mL/hr Conduction System a) SA Node- specialized nerve tissue
(the heart’s pacemaker). The SA node is located at the top of the
right atrium If a patient has a “sinus rhythm,” it means the bat
originated from the SA node. However, “sinus” can include brady,
normal, or tachy rates b) Action Potential- Electrical impulse travels
through the heart and leads to contraction c) Contraction- Occurs
when calcium flows into cardiac cells after depolarization d) AV
Node- allows time for atria to fill by providing a break in the
contraction Mid way point; a pause to allow the atria to fill e)
Bundle of His- Picks up the impulse and spreads it over the
ventricles by way of the Purkinje Fibers f) Repolarization- cells
return to former state g) Systole- absolute refractory period during
which the cardiac muscle gradually recovers and is excitable again.
During contraction, the heart briefly loses its self excitability o
Auscultation: S1= Closing of AV valves (lub) S2= Closing of SL
valves (dub) S3= Ventricular gallop (“KenTUCKy”)- d/t fluid
overload, CHF, or murmur; common in peds S4= Atrial Kick
(TENessee) EKG 1) P-Wave= Depolarization (contraction) of the
atrium 2) PR Interval= Measure of the time required for the impulse
to spread from the SA node to the ventricle (from top to bottom of
heart) 3) QRS Interval= Depolarization (contraction) of ventricles 4)
T-Wave= Repolarization of ventricles 5) U-Wave= If present, may
mean hypokalemia or repolarization abnormalities Three
Electrolyes that Influence the Heart: o Potassium o Calcium o
Magnesium ST elevation of 1 mm off baseline indicates ischemia
and/or infarction! “STEMI”= tombstone on EKG! EKG Strip: (Know
the times! Assume each strip is 6 seconds, so multiply “R’s” by 10
to get HR) o Each small box is 0.04 seconds, each large box is
0.20 seconds o P wave= 0.06-0.12 seconds o PR Interval=
0.12-0.20 seconds o QRS Complex= 0.04-0.12 seconds Cardiac
Output CO= amount of blood pumped per minute. CO= HR (heart
rate) x SV (blood ejected per beat in mL) o Cardiac Output: WNL=
4-8 L/min (LITERS) o Stroke Volume: WNL 60-70 mL/beat
(MILILITERS) Ex. CO= HR x SV = 70 bmp x 70 mL = 490 mL/min
4.9 L/min Normal Blood Volume: (since CO=4-8 L/min, you pump
entire blood volume within 1 minute!) o Female: 4-6 L o Male: 4-8 L
Generally, if heart rate goes up, cardiac output will go up. But this is
only true to a certain point. If HR is greater than 120 bpm
sustained, CO would decrease b/c chambers don’t have time to fill
causing the stroke volume to decrease! o It is ok to have a HR
>120 bmp acutely, but just don’t discharge the patient until it is
managed Three Components of SV: (Cardiac meds will affect one
of these) 1) Preload= Volume! The volume of blood in the
ventricles at the end of diastole, before the next contraction End
diastolic volume (EDV) determines the amount of “stretch” placed
on the myocardial fibers Ex. An ejection fraction of 70% means
30% of blood remains in ventricle after contraction Causes of
increased preload: (too much blood left in the heart)
Hypervolemia/fluid overload Cardiac valve regurgitation (murmurs
allow for back up) Pump failure/CHF Multiple blood transfusions
Salt tablet Causes of decreased preload: (not enough blood return
to the heart) Hypovolemia/Low circulatory blood volume
Hemorrhagic shock/Bleeding Lasix Dehydration Diabetes
insipidus (no ADH) Anaphylaxis (vasodilation) 2) Afterload=
Resistance! Reflects the vascular resistance against which the left
ventricle pumps Affected by size of ventricle, vascular wall tension,
and arterial blood pressure Causes of increased afterload:
Vasoconstriction or meds that vasoconstrict Hypertension Fight or
flight Smoking Stress Causes of decreased afterload: Calcium
channel blockers or other vasodilators Hypotension Distributive
shock 3) Contractility= Squeeze! Speaks to how “in shape” the
muscle is When contractility rises, the SV rises by increasing the
emptying of the ventricles Causes of increased contractility:
Epinephrine/norepinephrine SNS Stress Positive inotropes such
as Digoxin Causes of decreased contractility: Increased aging o *
Increasing preload, afterload, or contractility increases the workload
of the heart and increases the need for oxygen. We need to
manage our stress and hypertension! 4 o Starling’s Law: To a point,
the more the fibers are stretched, the greater their force of
contraction. The more fluid/stretch, the greater the contraction. But
if the fibers are overstretched, they will break! Regulation of
Cardiovascular System Autonomic Nervous System regulates the
SNS (excitatory) and the PNS (inhibitory) o Sympathetic (beta 1
receptors) increase heart rate and contractility o Parasympathetic
(vagus nerve) decreases heart rate o Exercise, temperature, and
medications exert their effects on the heart through the ANS! o
Example of Negative Feedback System! Baroreceptors (“Baro”=
pressure) o Location: Aortic arch, carotid sinus, vena cava, atria,
and pulmonary arteries o Sense pressure changes within the
arterial system o Send messages to the vasomotor center (brain
stem) o Increased blood pressure inhibits the sympathetic beta 1
receptors and enhances the parasympathetic system to decrease
HR and cause peripheral vasodilation o Make sure you check HR
and BP before giving vasodilators such as ACE inhibitors or CCB’s!
Blood Pressure The pressure exerted by blood against the walls of
the arterial system Systolic is the peak pressure against the
arteries when the heart contracts Diastolic is the residual pressure
during ventricular relaxation BP= CO x SVR (systemic vascular
resistance) Can be measured invasively through arterial pressures.
A catheter is inserted into an artery (an “art line”) for continuous
monitoring Can be measured non-invasively through a manual cuff
Korotkoff Sounds o Auscultate first tapping- spurt of blood into
constricted artery (systolic BP) o Disappearance of the tap is the
diastolic pressure Pulse Pressure= Difference between SBP and
DBP o Ex. If a patient has a BP of 120/80, their pulse pressure is
40 o Monitor the pulse pressure of a fresh post op patient! A
narrowing pulse pressure means bleeding or hypovolemia!
(120/60…120/70…110/70) o Widening PP means neuro problem!
(120/80…130/70…140/60) o A stable PP but decreasing BP means
dehydration (120/80…110/70…100/60) o Isolated systolic
hypertension can cause a widened PP at baseline, this is a normal
effect of aging (120/80…150/80…180/80) **Mean Arterial Pressure
(MAP)= Average pressure within the arterial system that is felt by
organs in the body; a “perfusion measure” o MAP= DBP + 1/3 PP
Ex. Patient has a BP of 120/60 MAP= 60 + 1/3 (120-60) = 60 + 20 =
80 o Normal value for MAP= 70-100 o You need a MAP ≥60-70 to
perfuse the vital organs! Effects of Aging on CV System Increased
