Cardio Function 2015

ASSESSMENT OF
CARDIOVASCULAR
FUNCTION
Nelia B Perez RN, MS
PCU - MJCN
nhelzki-2014
ncm-103

LECTURE OBJECTIVES
1. Review anatomy & physiology
of the cardiovascular system.
2. Discuss relevant aspects of the
patient history.
3. Describe physical assessment
of cardiovascular status.
4. Review diagnostic procedures,
tests and medications relative to
the cardiovascular system.
nhelzki-2014 ncm-103

Anatomy & Physiology
Functions of the heart &
CV system
• Pumps blood to tissues
to supply O2 & nutrients
• Remove CO2 &
metabolic wastes
(What makes it “tick”!)

CARDIAC CELLS HAVE UNIQUE
PROPERTIES
• AUTOMATICITY  CELLS
CONTRACT INDEPENDENTLY
(THEY INITIATE THEIR OWN IMPULSE)
• EXCITABILITY  ION SHIFT
• CONDUCTIVITY 
TRANSMIT IMPULSE TO
ANOTHER CARDIAC CELL
• CONTRACTILITY  HOW
WELL THE CELL CONTRACTS

PERICARDIUM / PERICARDIAL SAC
• Protects heart from trauma
• Serous fluid lubricates
and prevents friction
• Prevents heart from over
filling

CORONARY ARTERIES
Right & Left arteries encircle the heart
and supply blood to the myocardium
during ventricular relaxation( diastole)
LEFT MAIN CORONARY ARTERY
L ANTERIOR DESCENDING
(LAD)
L CIRCUMFLEX (LCX)
RIGHT CORONARY ARTERY
POSTERIOR
MARGINAL

CORONARY ARTERIES
(R) ARTERY
(L) ARTERY
LAD
CIRCUMFLEX

CONTRACTION OF CARDIAC
MUSCLE
The heart can’t pump unless an
electrical stimulus occurs
Action Potential (AP) – electrical
change
(depolarization = contraction)
Brought about by release of
calcium
(+ charge) into cells- mechanical
change
Intrinsic Pacemakers – depolarize
and generate the AP

CONTRACTION OF CARDIAC
MUSCLE
The pacemaker with the fastest rate of
depolarization stimulates the AP
• SA node (60-100 bpm)- Upper R atrium-
capable of initiating electrical impulse
• AV node (40-60 bpm)- Lower R atrium
• Other pacemakers ( 40 bpm)
-what can affect SA/AV node function ?

1. Cardiac Innervation:
■ Sympathetic NS → ↑ excitability.
■ Parasympathetic NS (vagus) → ↓ excitability.
2. Effect of ions concentration in ECF:
■ ↑ Ca2+
→ ↑ excitability.
■ ↑ K+
→ ↓ excitability.
3. Physical factors:
■ ↑ temperature → ↑ excitability.
■ ↓ temperature → ↓ excitability.
Factors affecting myocardial excitability

4. Blood flow:
■ Insufficient bl flow to cardiac ms ↓ excitability &
myocardial metabolism for 3 reasons:
(1) lack of O2,
(2) excess accumulation of CO2, &
(3) lack of sufficient food nutrients.
5. Chemical factors (drugs):
■ Digitalis → ↑ excitability.
Factors affecting myocardial excitability (continued)

1. Cardiac innervation.
2. Effect of ions concentration in
ECF.
3. Physical factors.
4. Blood flow.
5. Chemical factors (drugs).
Factors affecting myocardial
conductivity:

■ Sympathetic NS → ↑ conductivity.
■ Parasympathetic NS (vagus) → ↓ conductivity.
2. Effect of ions concentration in ECF:
■ ↑ Ca2+
→ ↑ conductivity.
■ ↑ K+
→ ↓ conductivity.
■ ↑ temperature → ↑ conductivity.
■ ↓ temperature → ↓ conductivity.
Factors affecting myocardial conductivity
(continued)

4. Blood flow:
■ Insufficient bl flow to cardiac ms ↓ conductivity &
myocardial metabolism for 3 reasons:
(1) lack of O2,
(2) excess accumulation of CO2, &
(3) lack of sufficient food nutrients.
■ Digitalis → ↑ conductivity.
Factors affecting myocardial conductivity
(continued)

2. Oxygen supply.
3. Calcium & potassium ions
concentration in ECF.
5. Hormonal & chemical factors
(drugs).
6. Mechanical factors.
contractility: (Inotropic effectors)

■ Sympathetic NS → ↑ force of contraction.
■ Parasympathetic NS (vagus) → ↓ atrial force of
contraction w no significant effect on ventricular ms.
Factors affecting myocardial contractility (continued)

2. Oxygen supply:
■ Hypoxia → ↓ contractility.
3. Calcium & potassium ions
concentration in ECF:
■ ↑ Ca2+
→ ↑ contractility.
■ ↑ K+
→ ↓ contractility.
■ Warming → ↑ contractility.
■ Cooling → ↓ contractility.
Factors affecting myocardial contractility
(continued)

5. Hormonal & chemical factors
(drugs):
■ +ve inotropics:
(Adrenaline, noradrenaline,
alkalosis, digitalis, Ca2+
, caffeine,…)
■ -ve inotropics:
(Acetylcholine, acidosis, ether,
chloroform, some bacterial toxins (e.g.
diphtheria toxins), K+
, …)
(continued)

6. Mechanical factors:
a. Cardiac ms. obeys ‘all or none law’:
i.e. minimal or threshold stimuli lead to
maximal cardiac contraction, because
cardiac ms. behaves as a syncytium.
(continued)

b. Cardiac ms. can’t be stimulated
while it is contracted, because its
excitability during contraction is zero
due to long ARP, so it can’t be
tetanized.
c. Cardiac ms. can perform both
isometric & isotonic types of
contractions.
(continued)

d. Starling’s law of the heart:
■ “Length-tension relationship”
‘Within limits, the greater the initial length of the
fiber, the stronger will be the force of its contraction;
However, overstretching the fiber as in heart
failure its power of contractility decreases’ i.e. within
limits, the power of contraction is directly proportional
to the initial length of the ms.
■ Cardiac ms accommodates itself (up to certain limit)
to the changes in venous return.
(continued)

e. Cardiac ms shows staircase
phenomenon (gradation), if providing
all other conditions kept constant.
i.e. if an isolated heart is stimulated
by successive equal & effective
stimuli, the 1st
few contractions show
a gradual ↑ in the magnitude of
contraction.
(continued)

2. Effect of ions concentration in ECF.
4. Chemical factors (drugs).
rhythmicity
(chronotropic effectors):

a. Sympathetic stimuli:
→ Tachycardia, by ↑ spontaneous depolarization
of SA- node.
How?
■ ↓ SA- node membrane permeability to K+
→ less K+
efflux.
■ ↑ membrane permeability to Ca2+
→ more Ca2+
influx.
■ As a result, the slope of depolarization ↑, causing ↑
rate of SA- node firing & ↑ HR.
Factors affecting myocardial rhythmicity:

b. Parasympathetic stimuli (vagus):
→ Bradycardia, by ↓ spontaneous depolarization
of SA- node.
How?
■ ↑ SA- node membrane permeability to K+
→ more K+
efflux.
■ ↓ membrane permeability to Ca2+
→ less Ca2+
influx.
■ As a result, the prepotential slope ↓, causing ↓ rate of
SA- node firing & ↓ HR.
1. Cardiac Innervation (continued)

a. Warming: → ↑ rhythmicity.
b. Cooling: → ↓ rhythmicity.
c. Exercise: → ↑ HR as a result of ↑ sympathetic
n. stimulation & ↓ vagal inhibition to SA- node.
d. Endurance-trained athletes: Resting
bradycardia due to high vagal activity.

a. Thyroid hormones & catecholamines:
→ ↑ rhythmicity.
b. Ach:
→ ↓ rhythmicity.
c. Hypoxia:
→ ↓ rhythmicity.

DISRUPTION IN SERUM
ELECTROLYES CAN RESULT IN
ALTERATION IN CARDIAC CYCLE
• Potassium
• Calcium
• Sodium
• Magnesium

MONITORING MOVEMENT OF THE
CARDIAC ACTION POTENTIAL
(AP)
• EKG – monitors the movement of the
AP, in other words, the electrical
changes.
• How are the mechanical changes
( cardiac output ) monitored ?

CARDIAC CYCLE
CARDIAC CYCLE – all the
activities occurring in the
heart during one
contraction, and
subsequent period of
relaxation. Graphically
represented on an EKG
(ECG).

CARDIAC CYCLE
EKG – A 12 lead
EKG is a
graphic record
of the electrical
forces
produced by
the heart

CARDIAC CYCLE
Polarized (resting) cell – represented on
EKG as baseline or isoelectric line
Depolarization – impulse over specialized
cardiac cells (not neuromuscular
impulse)
Repolarized cell – returns to normal. Na
moves out of cell, K moves in – requires
ATP
How will ischemic tissue change the
cardiac cycle ?

ELECTRODE POSITIONS
“LEADS”
• Leads measure electrical activity
between 2 points
• Movement toward ⊕ electrode causes
positive deflection
• Movement away from ⊕ electrode
causes negative deflection

ELECTRODE POSITIONS
A 12 Lead EKG shows electrical activity
from 12 different positions in the heart,
concentrating on (L) ventricle
A 14 Lead EKG includes (R) ventricle
activity

Cardiac output
• SV-
• CO-
• Preload-
• Afterload-
• Ejection fraction
• GOAL is to maintain adequate MAP so
perfusion of oxygenated blood to vital
organs occurs

Regulation of cardiac function & BP
• Autonomic nervous system
• Sympathetic norepinephrine
• Parasympathetic – acetylcholine
• Stimulation of adrenals by SNS –
norepinephrine
• Peripheral baro receptors
• Stretch receptors
• chemorecptors
• hormones

STROKE VOLUME (SV) & CARDIAC
OUTPUT (CO)
• SV – amount of blood ejected by 1
ventricle in 1 beat
• CO – volume ejected in 1 min
Control of SV and HR = SV&HR are
continually adjusted by the body, and
are affected by the return of blood from
the tissues (think of exercise)
CO = SVxHR

STROKE VOLUME (SV) &
CARDIAC OUTPUT (CO)
Extrinsic control of HR is a more
powerful way of controlling CO
than changing SV
11  CVP causes stretching of (R)
atrial muscle which stimulates
SNS &  HR (to help pump all
the blood returned to it)
Remember “Starling’s Law”

STROKE VOLUME (SV) &
CARDIAC OUTPUT (CO)
2. Stretch baroreceptors (aorta &
carotid) detect in pressure which
stimulates SNS & HR  (to ensure
adequate blood supply to heart/
brain)
3. If  pressure detected, then PSNS is
stimulated & HR is slowed (vagus
nerve) (prevents excess arterial
pressure which can damage organs)

CARDIAC LOAD
Preload = degree of myocardial fiber
stretch at the end of diastole and just
before contraction
Afterload = pressure against which
ventricles must eject blood. This
pressure is affected by systemic
vascular resistance (SVR)

Blood Pressure
•Reflects the driving pressures produced by the ventricles
•Because arterial pressure is pulsatile, a single value is used to represent the overall driving
pressure. This is called the mean arterial pressure.
MAP = diastolic P + 1/3(systolic P-diastolic P)
Why does diastolic pressure account for a greater proportion of the overall
value?
SVR = systemic
vascular resistance
CO = cardiac output
SV = stroke volume
MAP = Q x Rarterioles
Explain how these two equations are equivalent

What factors influence blood
pressure?
•Blood volume
•Vascular resistance
•Autoregulation
•Autonomic influences

Regulation of Blood Pressure
• Main coordinating center is in
the medulla oblongata of the
brain; medullary cardiovascular
control center
• Reflex control of blood pressure
•Baroreceptor reflex

Age related changes
• Decreased myocardial contractility
• Thickening of endocardium & valves
• Coronary arteries rigid & thickened
• Decreased elasticity of vessel walls
• Decreased internal diameter of vessels

CARDIAC ASSESSMENT
Cardiac status of all patients should be
routinely assessed. Everyone has a
1. Objective
2. Subjective
CP
Dyspnea
Fatigue
What else ?

IMMEDIATE NURSING INTERVENTIONS FOR
ACUTE CARDIAC EVENT
MOVIE Acronym
M- Monitor for pain
O- O2 and pulse ox
V- Vital signs
I- Intravenous fluids
E- EKG monitoring
Anything else??

Pain Assessment
SLIDA or
Precipitating/alleviating factors
Quality
Radiation
Severity
Timing

OTHER ELEMENTS OF
CARDIAC ASSESSMENT
• Previous cardiac hx
• Other medical conditions that may
affect heart function
• Chest injury
• Previous heart surgery
• Past medical hx
• Medications: prescribed, OTC, herbals
• Activity tolerance
• Health habits
• Family hx

EXAMINATION
• Inspection
• Palpation
• Percussion-?
• Auscultation = S1, S2 at PMI
Aortic
Pulmonic
Tricuspid
Mitral

Heart Rhythm
Regular, Irregular, Regular Irregular
Abnormal Sounds: Gallops
Murmurs
Bruits
S3 ventricular gallop – heard in early
diastole
S4 atrial gallop – generally abnormal

Assessment of Murmurs
Turbulent blood flow in valvular disorders
and septal defects
Timing of murmurs is a must!
Systolic murmurs occur between S1 & S2
Diastolic murmurs occur between
S2 & S1
Grade 1 – 6 identifies intensity of murmur

Other assessments
• Jugular vein pressure – assess JVD
which reflects increased filling
volume and pressure on (R) side of
heart
 JVD associated with (R) HF,
SVC obstruction (Normal is 3-
10cm H20)
• Pulse deficit – the difference
between apical HR and peripheral
pulse-associated with Afib, and
heart blocks
• Pulse pressure – the difference
between systolic & diastolic
pressurenhelzki-2014 ncm-103

Other assessments
• Respiratory: Lung sounds = rate,
rhythm, quality, sputum
• GI-Abdomen
• Peripheral Vascular:Lower extremities

Diagnostic Procedures
1. EKG 12 Lead
continuous cardiac monitoring
holter monitor
2. Chest x-ray – detects enlargement
of heart & pulmonary congestion

Diagnostic procedures
3. Echocardiography – ultrasound that
reveals size, shape and motion of
cardiac structures
Evaluates heart wall thickness, valve
structure, differentiates murmurs
4. TEE – transesophageal
echocardiography provides a clearer
image because less tissue for sound
waves to pass through

Diagnostic procedures
5. Angiography / cardiac catherization
determines coronary lesion size,
location, evaluate (L) ventricular
function, measures heart pressures
6. Exercise tolerance test
7. Radionuclide Imaging

1. Cardiac enzymes = enzymes are released
when cells are damaged (MI). Enzymes
are found in many tissues/muscles, and
some are specific to cardiac tissue.
Serial measurement can aid in dx, and
monitor course of MI
Cardiac enzymes =
CPK – MB (CK-MB),myoglobin, Troponin
In general, the greater the rise in the
serum level of an enzyme, the greater the
degree or extent of damage to the
muscle.
LDH
Lab Studies

LAB studies CONT
2. Electrolytes
3. Lipid panel
4. CBC
5. C – Reactive Protein
6. BNP- Human B-
Natriuretic Peptide
7. Blood coags-PT/PTT/INR

REVALIDATION TIME
Mary is attending a sophomore level nursing class
on anatomy and physiology. Which statement, if
made by Mary, demonstrates a good
understanding of the anatomy and physiology of
the heart?
A."The heart is encapsulated by a protective
coating called the endocardium.“
B."The SA node is considered the main regulator
of heart rate.“
C."The left atrium receives deoxygenated venous
blood from all peripheral tissues.“
D."Stroke volume is the amount of blood ejected by
the right ventricle during each diastole

Kirsten is completing her graduate clinical rotation in
a large urban teaching hospital in a medical
coronary care unit (CCU). Which observation
demonstrates a good understanding of completing
a thorough cardiac examination?
• A. In an obese client, an adult cuff size of 12 to 14
cm is preferable.
• B.The carotid artery on the neck is auscultated to
assess for the presence of a bruit.
• C.The apical impulse is auscultated over the fifth
intercostal space in the midclavicular line.
• D.Palpation is used to determine cardiac size.

Edward is a 40-year-old white male. He is an accountant who
works on average 11 hours per day. He reports feeling
stressed each day, even with mundane things such as a
traffic jam. His father had a massive myocardial infarction
at the age of 48. His mother has a history of congestive
heart failure. He seldom has time to exercise, but does eat
balanced meals when possible, although he does not get
to eat three meals a day. Select all factors that place
Edward at risk for heart disease.
• A.Family history
• B.Age
• C.Coping-stress tolerance
• D.Race
• E.Occupation

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