AP test #1 outline #3 (PDF)

Required Reading:
Capriotti, Theresa, Parker Fizzell, Joan (2016). Pathophysiology: Introductory
Concepts and Clinical Perspectives. F.A. Davis: Philadelphia, PA.
Pages: 346-348, 356, 371-374, 376-378, & 382-395.
Electronic Pages: Page number on electronic page of the E-book correlates to
print version.

It

Describes the process of

a

contraction

heart

Davis Advantage (Online) Pathophysiology I Class
Cardiac Function and Assessment
Left and Right Heart Failure

Nursing: A Concept-Based Approach to Learning. Volume 1. (2019), (3rd ed.).
Pearson: Boston, MA. Pages: 1115-1116, 1140-1142, 1193, 1229-1230,
1232-1235, 1270-1273, 1275-1276.
Exemplar 16 F Heart Failure
Exemplar 16 I Dysrhythmias
Required Web Sites (current as of 12/26/19):
3D Medical Animation Congestive Heart Failure Animation 3:40
http://www.youtube.com/watch?v=3YddwXPWVSc
Cardiac depolarization & repolarization 7:47
https://www.youtube.com/watch?v=zBj6btjdYHU
Optional Web Sites (current as of 12/26/19):
American Heart Association
http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Types-of-HeartFailure_UCM_306323_Article.jsp#mainContent
ECG Interpretation 11:10 Much Deeper & detailed
https://www.youtube.com/watch?v=JerLlI0f9IU
Overview Health Education Video: Heart Failure 5:50
http://www.youtube.com/watch?v=mhYeO2fwSps
Rhythm (EKG) Simulator
https://www.skillstat.com/tools/ecg-simulator
The ECG Course- Rate & Rhythm 18:31
https://www.youtube.com/watch?v=F9yf08-jRtY
Learning Objectives:
The student will:
1) Utilize theories and concepts to build an understanding of the manifestations of chronic pathophysiological conditions
involving perfusion related to the cardiovascular system.
2) Incorporate theory and research utilizing data from multiple evidence based sources to build an understanding of chronic
pathophysiological conditions involving perfusion related to the cardiovascular system.
3) Explain the common mechanisms of chronic disease progression of conditions involving perfusion related to the
cardiovascular system.
4) Determine protective and predictive factors which influence the health of patients with chronic conditions involving perfusion
of the cardiovascular system.

Outline
NOTE: C is for Capriotti and P is for Pearson
1. Describe the following: Page: C 371-374, P 1115-1116
volume

Preload:

to

The

blood

of 0

venous return

in the

to preload

after diastole

In

the Re atrium
blood

must overcome to pump
The amount of resistance the ventricles
most commonly referstothe L

Afterload:

0

Inotropic State:

of contraction of the

The force

muscles

each minute
of 0 Pumped out of the
FailureEEE
out per minute
Cardiac Output:The amount of blood the D pumps
to cardiac output
with each contraction
l I i r il I i ri
leaves the L ventricle
Ejection Fraction:
0
measurement
much
how
of
A
blood

volume

Stroke Volume:

The

Expressed as

Cardiac Reserve:

a

The work

Frank-Starling’s Law:

is required
is able to Proform beyond what

the

relationship

Afterloadto inverse

9

of strd

rradi

g

relationship

How we evaluate
afar

So
g to

effectiveness

Pre1

cardiacoutput

co

ta

9

ta
2. Contrast the normal heart from a heart in failure. Page: C 371, P 1228

fi
i

ii

if

Healthy

i
C

HF

µ f

unable
eineimen

3. Contrast the term Heart Failure (HF) with Chronic or Congestive Heart Failure (CHF) Page: C 382-383

less

more common

common

4. Describe the risk factors for HF. Page: C 382, P 1232

Hypertension greatest
myocardial infarction estrogen
young age
f
tax
equalizes after menopause
CAD
americans
African

Family history

f

protective
good
Lifestyle
Obesity

cardio

diabetes t

meds

Sleep

gg

apnea

in
booze

conditions

2

5. Summarize the following compensatory mechanisms involved with HF: Page: C 376-378, 384-388, P 1229-1230.
RAAS
Friend
canine

atriaimxocxtef.ie

Natriuretic Peptides

0 about to enter

To

TB DetectedhighoiiiandreleasedAwptoinducenatriuresisexcretionofNattOw

thatand9H2O

GFR 9 Blocks RAAS Released
during HF

Endothelin

arterial

t

Blood

ftp.Nwpptqk

venous

B type

S endothelium vasculature inHF Normally 9Post MI

secretedby

p resistance asaist L ventricle

Vasoconstrictor

Tumor Necrosis Factor-Alpha (TNF-alpha)

eat in patients

with HF

ft

Inotrophic State

Zoo

Hyperatrophy
Fibrotic changes

Inflammatory

It

that

Nitric Oxide (NO)

Potent vasodialator

simulates

Released by the posterior

cells

endothelial Qi

vascular
produced by

Antidiuretic Hormone (ADH)

cell death

i

cytokine

water

90 t Vasoconstrictor

8 pituitary stand

Autonomic Nervous System (ANS) Regulation

Parasympathetic
csthimoY.IT

rgie

contjfIIe
b

receptors

I U 41

I

sympathetic

q

b
stimulates

i

I
fp

Force

contraction

Heart1kidney

Beta 7

Rate

adrenergic

Bad

receptors

Regulation

6. Differentiate between Systolic and Diastolic heart failure. Page: C 383, P 1230

Normal

systolic

I

chit

if

I

ventricles Fill normally
with

Diastolic dysfunction

disfunction
l Ll Ll

Ll Ll l

I

it

mint

I

N

i

weak distendedventricle

Struggles to

pumpforward

stfu
N
Stiff nonelastic ventricle
cannot fullyexpand thus fill
with less 0

7. Correlate the pathophysiology to the clinical manifestations of left sided HF (LVF). Page: C 384-389, 391-392, P 1230-12

Hydrostaticpressurebacksup into
andpulmonaryvasculature

Dyspnea:
Cough:

ii

n
Be

Crackles:

a

f Ll Ll 1

atrium

qf

pulmonaryedema

is n iioiri

i

nii

Can be heard in a stethoscope
via
the openingandClosingof the
alveoliagainstthefluid

Orthopnea:

Paroxysmal nocturnal dyspnea:

Nocturia :

S3:

Results

poop ask about

Other manifestations:

anorexia

s

I

i

Pulmonary edema:

thin

yy

Weak E ventricle

Confusion/Anxiety:
Fatigue:

y

t

cannot

i

daiz.minarni.in

ft

aorota

starting point for

in 4,7 Confusionanxiety

1
Fatigue

pathological Sympoms

this
loss

nausia headache memory

and insomnia 2

8. Correlate the pathophysiology to the clinical manifestations of right-sided (RVF) heart failure. Page: C 389-392, P 1232-1233

gravity pulls the excess fluid
from RUF HF to the lower extremities

Dependent edema: when
Weight gain:

fluid
Ascites:

Edem

occurs

as

result of the buildup

a

to poor drainage

due

Jugular venous distention: As pressurebuilds in the venous sign
system bulging of a blue vein on theneckbecomes a Clinical
Abdominal pain:

Abdominal

associated

occurs in RVE

Fatigue:

yv

This

im aired

can

can

of backwards
sign

hurt

These

Anorexia, nausea and bloating:

are

distension

are
conditions that
with poor G I drainage which

occur

as

a

result of

intestinal absorbtionl metabolism
due to venous congestion

K

of

leads to
nTIaticeIinessnureaihctahfysasterointesina'veins

IE

t.HL.li

resulting

i

g

yfy

n

Fg

j
V

weak musclestruggles topush
Thin
Forwardcauses a backup of

Of

0

hydrostaticpressureThisbackupcontinues
intothePeatriumthevenacanvas andtherestof

venoussystem

BE
systemic venous systempressure 9

9. Describe the complications and progression of HF. Page: C 386, 388, 395, P 1232

class 1

Causes no side effects

no limitation to activity

AmericaHeart

Association stage

µ

sightlimitationto activity comfortable at rest but activitycausesfatigue
palpitations or dyspnea
Ias 3 marked limitationwithactivity Comfortable at rest but even a little
Class 2

B

activitycausesfatigue1palpitations or dyspnea
discomfortcardiacinsuffiency at rest
to
activity
without
out
Unable
4
class
carry

D

10. Describe the tests that are used to diagnose HF. Page: C 392-394, P 1234-1235

Electrocardiogram
Echocardiogram
X Ray
Cardiac catheterization and audiography

multiple gated Acquision

scan

11. Describe the following terms: Page: C 347, P 1193, 1270
Dysrhythmia or arrhythmia Disorders of
Cardiac
sffrnaf.eeutiggl

r Generated at the SA node

certain

rhythm

Av node

Generated at the bundle of His Purkinje

Electrocardiogram (ECG or EKG)

muscle

the fingergyandventicular
5
energy at

A recording of

point S of the body

12. Describe the electrical conduction of a normal heart beat. Page: C 346, P 1114-1115

1 it Lll

t

iori
gg

I

j

r

t.IM

current
Purkinjefibers

vehicularmuscle

v

en.gn7eaaInnsumi.n

the SA node

2 Impulsetravels to the Av node
z Av node has a r way transmission down
the bundle of his

Ii

psiraiiinafeed.iiidenaa.tn

f

ii

b

Contraction

j

13. Describe the systematic approach to ECG interpretation. Page: C 348, P 1140-1142
Rate calculation

I 1141

k

Rhythm

beattheratetcosistanalthe

Iii
if
Fµ
It
ret.paaricineseg
Jt

SANodett7svo.av
Node
node

P waves

Atrial depolarization

thi j

PR and QRS Intervals

tr

EIas.E.me xietiiiep
r

PRInterval a

e

tnar.tana

betweenstartof

atrial depolarizationand start
of ventricledepolarization

A

Heartatrest

I wave

gg

Q

3

ventric

III

Cotntract depolarize

yp g p
I

2

f

to

contains the

Q Rands waves

the complex

Endocrine disorders
Sleep Apnea

14. Identify the risk factors for dysrhythmias. Page: P

disease like CAD
History of
Prior surgery
to BP

meds
lifestyle oaf

attack

Kasama

iii

15. What symptoms might a patient have if they are experiencing a dysrhythmia? Page: P 1271

Rapid
Slow

block

Rate
Rate

Pathway
a block in the conduction

beats or interruptnormal conduction sequence
Ectopic
16. Describe the defining characteristics, cause, and significance of the following rhythms . Page: C 356, P 1272-1273,
1275-1276
Sinus Rhythm:

through
an impulsetravels
which
in
normal
The
process

60 100 BPM

normal
Simplyput it is the

the

rhythm

are managed Risk
lol I 50 bpm irregularwith PRI Symptoms
may be due to A SNS activity

Sinus Tachycardia:

Sinus Bradycardia: LessthanGo b

pm treatedsymptomatically

of MI

PossiblePharm intervention or pacemakertherapy

May be due to 9 PNS activityCmentionsmetope Mayuse anticoagulants to B risk
to reduce Pulse

Atrial Fibrillation: 300 Goobpm

or stroke
Atrial Flutter:

The

240

ventricular

meds

irregular

360 Bpm

such

Meds

as

response

Additional

atria Mostcommontypeof
with
beta blockers

coordinated contraction of the

note
sympathetic
adrenergic

God
BY
HR controlled Maa

receptors

parasympathetic

cholinergic
receptors

of clot

arrhythmia

slow