Download the basics - Cardiovascular Nursing Education Associates

5/29/2012
BACK TO THE BASICS: ASSESSING YOUR
PATIENT’S CARDIOVASCULAR STATUS
WITHOUT ALL THE BELLS AND WHISTLES.
NTI 2012
Session Number: 381
Presented By: Cynthia L. Webner, DNP, RN, CCNS, CCRN-CMC
www.cardionursing.com
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5/29/2012
CARDIAC DIASTOLE (ATRIAL & VENTRICULAR):
EARLY PASSIVE VENTRICULAR FILLING
3
ATRIAL SYSTOLE & VENTRICULAR DIASTOLE:
LATE ACTIVE VENTRICULAR FILLING
Atrial Kick
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BEGINNING VENTRICULAR SYSTOLE:
ISOVOLUMIC CONTRACTION
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VENTRICULAR SYSTOLE: EJECTION
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HEART SOUNDS – THE BASIS FOR THE SOUNDS
•
Diastole
•
• Passive Ventricular Filling
• S3
• Active Ventricular Filling
• Atrial Kick – S4
• Valves Open
• Mitral
• Tricuspid
• Don’t open well
• Stenosis
• Valves Closed
• Aortic
• Pulmonic
• Don’t close well
• Regurgitation
Systole
• Isovolumic contraction
• Ejection of LV Contents
• Valves Open:
• Aortic
• Pulmonic
• Don’t open well
• Stenosis
• Valves Closed
• Mitral
• Tricuspid
• Don’t close well
• Regurgitation
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BASIC HEART SOUNDS
S1
• Closure of the M itral (M 1)
valve and the Tricuspid (T1)
valve
• Beginning of Ventricular
Systole and Atrial Diastole
• Location: M itral area
• Intensity: Directly related to
force of contraction
• Duration: Short
• Quality: Dull
• Pitch: High
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BASIC HEART SOUNDS
S2
• Closure of Aortic (A2) and
Pulmonic (P2) Valve
• End of Ventricular Systole
• Location: Pulmonic area
• Intensity: Directly related to
closing pressure in the aorta
and pulmonary artery
• Duration: Shorter than S1
• Quality: Booming
• Pitch: High
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DIASTOLIC FILLING SOUNDS
S3 - VENTRICULAR GALLOP
• Early diastolic filling sound
• Caused by increased pressure and resistance
to filling.
• Most frequently associated w ith sy stolic
dy sfunction
• Associated w ith:
• Fluid ov erload state
• Right or left v entricular failure
• Ischemia
• Aortic regurgitation
• Mitral regurgitation
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DIASTOLIC FILLING SOUNDS
S3 - VENTRICULAR GALLOP
• Patient position: left lateral decubitus
position
• Location:
• Left-sided S3 – mitral area.
• Right-sided S3 – tricuspid area.
• Intensity
• Left-sided heard best during expiration.
• Right-sided heard best during
inspiration.
•
•
•
•
Duration: short.
Quality : dull, thud like.
Pitch: low .
May be normal in children, y oung
adults (up to 35-40) and in the 3rd
trimester of pregnancy.
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DIASTOLIC FILLING SOUNDS
S4 - ATRIAL GALLOP
• Late diastolic filling sound
• Caused by atrial contraction and the
propulsion of blood into a noncompliant
(stiff) ventricle.
• Most frequently associated with diastolic
dysfunction
• Associated with:
•
•
•
•
•
•
Fluid overload state
Systemic hypertension
Restrictive cardiomyopathy
Ischemia
Aortic stenosis
Hypertrophic cardiomyopathy
• May be normal in athletes
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DIASTOLIC FILLING SOUNDS
S4 - ATRIAL GALLOP
• Patient position: left lateral decubitus
position.
•
Location
• Left-sided S4 – mitral area.
• Right-sided S4 – tricuspid area.
•
Intensity
• Left-sided louder on ex piration.
• Right-sided louder on inspiration.
• Duration: Short
• Quality: Thud like
• Pitch: Low
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MURMURS
• High blood flow through a normal or abnormal valve
• Forward flow through a narrowed or irregular orifice into a
dilated chamber or vessel
• Backward or regurgitant flow through an incompetent valve
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HEART SOUNDS:
THE BASIS FOR THE SOUNDS
•
Diastole
• Passive Ventricular Filling
• S3
• Active Ventricular Filling
• Atrial Kick – S4
• Valves Open
• Mitral
• Tricuspid
• Don’t open well
• Stenosis
• Valves Closed
• Aortic
• Pulmonic
• Don’t close well
• Regurgitation
•
Systole
• Isovolumic contraction
• Ejection of LV Contents
• Valves Open:
• Aortic
• Pulmonic
• Don’t open well
• Stenosis
• Valves Closed
• Mitral
• Tricuspid
• Don’t close well
• Regurgitation
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PARADIGM SHIFT
• Hemodynamics does not equal invasive monitoring
• One must be comfortable with shades of grey!!
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The Heart as a Pump
Goal: Forward
propulsion of blood
to perfuse the body.
FLOW IS DETERMINED
BY:
√PRESSURE
√ RESISTANCE
√ VOLUME
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RIGHT SIDED VERSUS LEFT SIDED SYSTEM
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BASIC HEMODYNAMIC FORMULA
Cardiac Output
Heart Rate X Stroke Volume
Preload
Afterload Contractility
Same four components also determine myocardial oxygen demand20
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PRELOAD
The ventricle is preloaded for ejection.
It’s about stretch!
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PRELOAD
• End-diastolic stretch on myocardial
muscles fibers
• Determined by:
• Volume of blood filling the
ventricle at end of diastole
• Greater the volume the greater
the stretch (muscle fiber length)
Ð
• Greater the stretch the greater
the contraction
Ð
• Greater the contraction the
greater cardiac output
TO A POINT
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NON INVASIVE ASSESSMENT OF PRELOAD
Right Ventricular Preload
Left Ventricular Preload
•
JVD
•
Orthopnea / PND/ Dyspnea
•
Hepatojugular reflux
•
CXR report of vascular / interstitial edema
•
Peripheral edema *
•
Rales/crackles
•
Weight*
• Consider role of lymph drainage
•
S3 Gallop
•
Frothy sputum
•
Hypoxemia from decreased diffusion of
oxygen
•
Pre-renal AKI (BUN/creatinine ratio 20:1)
•
Weight*
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MEASURING JVD
• Raise HOB 30 – 45
degrees
• Normal JVP level is < 3 cm
above the sternal angle
• Internal preferred
• Sternal angle is 5cm above
right atrium
• M ay use external
• Use tangential light
• Use centimeter ruler
• JVP of 3 cm + 5cm =
estimated CVP of 8cm H2O
• Difficult to assess if
HR>100
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Estimated CVP> 8 cmH2O
ŒIncreased blood volume
ΠUsually RV failure
ΠTricuspid valve regurgitation
ΠPulmonary hypertension
JVD (JUGULAR VENOUS DISTENSION)
Additional assessment tip:
Sitting or standing patient up to see top of column.
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JVD (Jugular Venous Distension)
Jugular Vein
No pulsations palpable.
Carotid Artery
Palpable pulsations.
Pulsations obliterated by pressure above the clavicle. Pulsations not obliterated by pressure above the
clavicle.
Level of pulse wave decreased on inspiration;
increased on ex piration.
No effects of respiration on pulse.
Usually two pulsations per systole (x and y
descents).
One pulsation per systole.
Prominent descents.
Descents not prominent.
Pulsations sometimes more prominent with
abdominal pressure.
No effect of abdominal pressure on pulsations.
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FACTORS INFLUENCING PRELOAD
• Body Position
• Circulating blood volume
• Venous Tone
• Hypervolemia
• Intrathoracic pressure
• Third spacing
• Intrapericardial pressure
• Dysrhythmias
• Atrial Kick
• LV Function
• Hypovolemia
• Distribution of blood
volume
• Sepsis
• Anaphylaxis
• Venous vasodilators
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AFTERLOAD
After the ventricle is loaded,
it must work to eject the contents!
It’s about pressure!
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AFTERLOAD
• Pressure ventricle needs to
overcome to eject blood volume
• Left ventricle:
• Systemic vascular resistance (SVR)
• Other components
• Valve compliance
• Viscosity of blood
• Arterial wall compliance
• Aortic compliance
• Right ventricle:
• Pulmonary vascular resistance
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BP AND AFTERLOAD
• Blood pressure does not equal afterload
Blood Pressure (MAP) =
Cardiac Output x Systemic Vascular
Resistance (Afterload)
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BP = CO X SVR
• Low BP could be due to:
• Low CO
• HR too slow or too fast
• Preload too low or too high
• Contractility low
• Low SVR
• Vasodilation due to sepsis, anaphylaxis, altered
neurological function, drugs
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MORE ON VASCULAR TONE
• Increased vascular tone is usually associated with
compensation for low Stroke Volume
• Acute Cardiogenic shock
• Hypovolemic shock
• Decreased vascular tone is usually due to abnormally
pathology
• Sepsis
• Anaphylaxis
• Altered neurological control
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NON INVASIVE ASSESSMENT OF AFTERLOAD
Right Ventricular Afterload
Left Ventricular Afterload
• NOTE: Any hypoxemia,
positive pressure
ventilation, and PEEP
increase the workload of
the right ventricle.
• Diastolic BP is closest
noninvasive
measurement
• Evaluate the pulse
pressure
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USE OF PULSE PRESSURE & HEART RATE
• PP < 35 with tachycardia • PP > 35 with tachycardia
(in absence of beta
blocker)
• Early sign of oxygenation
failure
• Early sign of inadequate
blood volume
• Delivery cannot meet
demand
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CAUSES OF
INCREASED
LV AFTERLOAD
CAUSES OF
DECREASED
LV AFTERLOAD
• Arterial vasoconstrictors
• Arterial vasodilators
• Hypertension
• Hyperthermia
• Aortic valve stenosis
• Vasogenic shock states (sepsis
and anaphylactic) where the
body cannot compensate with
vasoconstriction
• Increased blood viscosity
• Hypothermia
• Compensatory
vasoconstriction from
hypotension in shock
• Chronic Aortic Regurgitation –
hyperdynamic cardiac output
therefore lowering systemic
vascular resistance
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INCREASED RIGHT SIDED AFTERLOAD
• Pulmonary hypertension
• mPAP > 25 mmHg or > 30 mmHg w ith ex ercise
• PVR > 250 dy nes/sec/cm -5
• Causes
•
•
•
•
•
•
Hy pox emia
Acidosis
Inflammation
Hy pothermia
Ex cess sy mpathetic stimulation
Pulmonary endothelial dy sfunction
• Impaired nitric oxide and prostacyclin (PGI2) release
• Primary pulmonary hy pertension
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CONTRACTILITY
• Ability of myocardium to
contract independent of
preload or afterload
• Velocity and extent of
myocardial fiber shortening
• Inotropic state
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CONTRACTILITY
• Related to degree of myocardial fiber stretch (preload) and wall
tension (afterload).
• Influences myocardial oxygen consumption
• Ï contractility
Ö Ï myocardial workload
Ö Ï myocardial oxygen consumption
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IMPORTANT POINTS ABOUT CONTRACTILITY
• No accurate w ay to measure contractility
Noninvasive Assessment: Ejection Fraction
• Low cardiac output does not necessarily mean diminished contractility
(i.e. hy pov olemia)
• Correct preload and afterload problems first in a patient w ith a low
ejection fraction.
• Increasing contractility w ith medications w ill also increase my ocardial
ox y gen demand.
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FACTORS ALTERING CONTRACTILITY
•
Decreased contractility
•
• Excessive preload or afterload
• Drugs – negative inotropes
Increased contractility
• Drugs
• Positive inotropes
• Myocardial damage
• Hyperthyroidism
• Ischemia
• Adrenal Medulla Tumor
• Cardiomyopathy
• Hypothyroidism
• Changes in ionic environment:
hypoxia, acidosis or electrolyte
imbalance
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HEART RATE
• M athematically heart rate increases cardiac output
• Physiological limit where increased heart rate will
decrease cardiac output due to decreased filling
time (decreased preload)
• Consider as first line strategy to increase cardiac
output when temporary pacemaker in place
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ADJUSTING TO MAINTAIN CARDIAC OUTPUT
THE BODY KNOWS THE ALGORHYTHM
• When perfusion to the tissues decrease for whatever
reason the body launches a response
• The body begins to adjust to improve cardiac output
• Two primary responses
• Sympathetic nervous system
• Renin angiotensin aldosterone system
ACTIVATION OF SNS
• First Responder
• Decreased CO → ↓ BP → activates baroreceptors and vasomotor
regulatory centers in medulla
• Increase circulating catecholamines
• Stimulates alpha and beta receptors
• Increase HR
• Peripheral vasoconstriction
• Contractility
Positive effect: ↑ CO and BP
Negative effect: ↑ O2 demand → ischemia, arrhythmias, sudden death
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ACTIVATION OF RAAS
• Kidney’s response to decreased perfusion
due to decreasing CO
• Concentrations of angiotensin II, and
aldosterone rise as end result
• Potent vasoconstriction
• Venous – enhanced preload
• Arterial – enhanced afterload
• Enhanced Aldactone
• Sodium/water absorption increases
• Enhanced preload
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DELIVERY OF OXYGEN TO THE TISSUES
Oxygen
Hemoglobin
Cardiac Output
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OXYGEN DELIVERY TO TISSUES
• Oxygen delivery measured as DO2
• Volume of oxygen delivered to tissues each minute
• DO2 = cardiac output x arterial oxygen content
• Arterial oxygen content = hemoglobin x arterial
oxygen saturation
• DO2 formula = CO x HGB x SaO2 x 13.4 (constant)
• Normal DO2 = 900- 1100 ml/min (1000 ml/min)
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OXYGEN CONSUMPTION / RESERVE
• Oxygen consumption is
measured as VO2
• Volume of oxygen
consumed by the
tissues each minute
• Normal VO2: 200–300
ml / min (250 ml / min)
• Measured by mixed
venous oxygen
saturation (SVO2)
• Normal 60-80% (75%)
• May also be measured
by SCV02
• Normal 80-85%
• Trends the same as SV02
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KEY POINTS
• Tissues were delivered 1000 ml / min (DO2)
• Tissues uses 250 ml / min (VO2)
• This leaves a 75% reserve in venous blood
• Oxygen delivery and oxygen consumption are
independent until a critical point of oxygen delivery is
reached
• Tissues will extract the amount of oxygen needed
independent of delivery because delivery exceeds need
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CAUSES OF INCREASED VO2
• Fev er per 1 degree C
• 10%
• Shiv ering
• 50-100%
• Suctioning
• 7-70%
• Sepsis
• 5-10%
• Non Family Visitor
• 22%
• Position Change
• 31%
• Sling Scale Weight
• 36%
• Bath
• 23%
• CXR
• 25%
• Multi Organ Failure
• 20-80%
CNEA / KEY CHOICE
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RELATIONSHIP OF DELIVERY TO CONSUMPTION
DO2
VO2 (extraction is
SVO2 (SV0 2 will
independent of delivery) improve when you
increase delivery)
1000 cc
250 cc (25%)
75%
750 cc
250 cc (33%)
67%
500 cc
250 cc (50%)
50%
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WHEN YOU HAVE ALTERATIONS IN OXYGEN
SATURATION, HEMOGLOBIN OR CARDIAC
OUTPUT YOU MAY HAVE ALTERATIONS IN
OXYGENATION.
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HOW CARDIAC CONDITIONS ALTER
MYOCARDIAL PERFORMANCE
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SYSTOLIC VS DIASTOLIC DYSFUNCTION
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SYSTOLIC DYSFUNCTION
• Impaired wall motion and ejection
• Dilated chamber
• 2/3 of Heart Failure Population
• Hallmark: Decreased LV Ejection Fraction < 40%
• Ischemia is cause in 2/3 of patients
• Multiple other causes including
• Mitral Regurgitation
• Dilated Cardiomyopathy
• Untreated diastolic dysfunction
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DIASTOLIC DYSFUNCTION
•
•
•
•
•
Filling impairment
Normal chamber size
20 to 40% of patients with HF have preserved LV function
Normal EF or elevated
Caused by
•
•
•
•
•
•
Hypertension
Restrictive myopathy
Ischemic heart disease
Ventricular hypertrophy
Valve disease
Idiopathic
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DIASTOLIC DYSFUNCTION
• Diagnosis is made when rate of ventricular filling
is slow
• Elevated left ventricular filling pressures when
volume and contractility are normal
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HEART FAILURE
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HEART FAILURE DEFINED
• Heart Failure is a
complex clinical
syndrome resulting
from any structural or
functional cardiac
disorder impairing the
ability of the ventricle
to either fill or eject
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HEART FAILURE PATHOPHYSIOLOGY
• Complex process involving continually
emerging symptoms and deterioration
• M yocardial dysfunction initially results
from any number of triggers
• Compensatory mechanisms designed
to improve cardiac output eventually
cause harm
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PATHOPHYSIOLOGY
THE REAL CULPRIT: NEUROHORMONAL RESPONSE
Two significant events occur
• Sy mpathetic Nerv ous Sy stem (SNS) stimulation
•
Increase Heart Rate
•
Increase Contractility
• Activ ation of the Renin-Angiotensin-Aldosterone Sy stem (RAAS)
• Vasoconstriction
• Venous – Increased Preload
• Arterial – Increased Afterload
• Enhanced Aldactone: Sodium and Water Retentions
• Increased preload
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STAGES OF HEART FAILURE
AMERICAN COLLEGE OF CARDIOLOGY / AMERICAN HEART ASSOCIATION GUIDELINES
Stage A
Stage B
Stage C
Stage D
At high risk f or HF but
without structural heart
disease or sy mptoms
of HF.
Structural heart
disease but without
signs or sy mptoms
of Heart Failure
Structural heart
disease with prior or
current sy mptoms of
HF.
Ref ractory HF
requiring
specialized
interv entions.
HPTN
CAD
DM
Obesity
Metabolic syndrome
Family HX CM
Prev ious MI
LV Remodeling
including LVH and
low EF
Asy mptomatic
v alv ular disease
Know structural
disease and SOB,
f atigue, reduced
exercise tolerance.
Marked
sy mptoms of HF
at rest despite
maximal medical
therapy.
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STAGES TO GUIDE THERAPY
Stage A
Stage B
Class IA-C)
•Treat HTN
•Treat DM
• Smoking
Cessation
• Treat Lipids
• Regular
Exercise
• DC Alcohol /
Drug Use
•Treat thy roid
disorders
• ACE-I in select
patients
• All measures
as stage A
Stage C
•All measures under stage A
• Dietary salt restriction
• Daily Weight
• Medications for routine use:
•ACE-I in
Diuretics
select patients
ACE – I
• Beta Blockers
Beta-Blockers
in select
Digitalis
patients
Aldosterone Antagonists
Hydralizine/Isordil
African Americans
• Implantable
def ibrillators
• Exercise training
• Devices in select patients
Resynchronization Therapy
Implantable defibrillators
Stage D
• All measures
under A, B and C
• Mechanical assist
• Transplantation
• Palliativ e Care
• Hospice
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CARDIAC RESYNCHRONIZATION
THERAPY
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NORMAL VENTRICULAR DEPOLARIZATION
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VENTRICULAR DEPOLARIZATION
WITH LBBB
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VALVULAR HEART DISEASE
Aortic Stenosis
Mitral Regurgitation
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VALVE DYSFUNCTION
Decreased Cardiac
Output
Compensatory
Changes
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PATHOPHYSIOLOGY
Remember:
Stenosis = Pressure
Regurgitation = Volume
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AORTIC STENOSIS
PATHOPHYSIOLOGY
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COMPENSATORY MECHANISMS
Aortic Valve Orifice Narrows
Î ____Afterload
Î ____LV Workload
Î ____LV Wall M ass
Î ____LV Hypertrophy
Î ___________ Dysfunction
Works well for years – even decades.
Compensatory system ultimately fails Î Symptoms
http://www.marvistavet.com/assets/images/aortic_stenosis.gif
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ALTERATION IN MYOCARDIAL PERFORMANCE
AORTIC STENOSIS
• Diastolic Dysfunction
• Poor Ventricular Filling
• To improve filling
• Preload
• Volume management
may be precarious
• Longer diastole
(slower heart rates)
• Gently adjust volume
either way
• Relaxed left
ventricle
• Cautious use of venous
vasodilators
• Elevated heart rate
impacts filling time
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ALTERATION IN MYOCARDIAL PERFORMANCE
AORTIC STENOSIS
• Afterload
• Elevated due to stenotic aortic
valve
• SVR remains normal if cardiac
output maintains perfusion
• Arterial vasodilatation with
exercise needs an effective
increase in cardiac output to
prevent hypotension
• Contractility
• Increased left ventricular
ejection fraction
• Strong pump
• Heart Rate
• Increased heart rate will
decrease filling time
• Severity of AS may
prevent effective increase
in CO
• May develop dizziness
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SYSTOLIC EJECTION MURMUR
• May be present before any significant hemodynamic changes occur
• More severe AS Î longer murmur
• Timing: Midsystolic
• Location: Best heard over aortic area
• Radiation: Toward neck and shoulders
• May radiate to apex
• Configuration: Crescendo-decrescendo
• Pitch: Medium to high
• Quality: Harsh
75
S4 - ATRIAL GALLOP
• Late diastolic filling sound
• Caused by atrial contraction and the
propulsion of blood into a noncompliant
(stiff) ventricle.
• Most frequently associated with diastolic
dysfunction
• Associated with:
•
•
•
•
•
•
Fluid overload state
Systemic hypertension
Restrictive cardiomyopathy
Ischemia
Aortic stenosis
Hypertrophic cardiomyopathy
• May be normal in athletes
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5/29/2012
LEFT OR RIGHT SIDED S4
• Patient position: left lateral decubitus position.
•
Location
•
•
•
Left-sided S4 – mitral area.
Right-sided S4 – tricuspid area.
Intensity
•
Left-sided louder on expiration.
•
Right-sided louder on inspiration.
• Duration: Short
• Quality : Thud like
• Pitch: Low
• D:\Track07.cda
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MITRAL REGURGITATION
PATHOPHYSIOLOGY
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MITRAL REGURGITATION
PATHOPHYSIOLOGY
During systole as the LV contracts blood is ejected from left ventricle
through the open aortic valve AND some is diverted retrograde
through dysfunctional mitral valve
Ä ______left atrial volume and pressure AND
Ä left atrium responds by _________
Ä atrium sends _________volum e to ventricle
Ä LV adjusts by ________________ AND
Ä LV increases _____________to assure forward flow
Works well for years – even decades.
Compensatory system ultimately fails Î __________ Dysfunction
Î Symptoms
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ALTERATION IN MYOCARDIAL PERFORMANCE
MITRAL REGURGITATION
• Systolic Dysfunction
• Reduced ejection
• Afterload
• SVR increased
• Preload
• Elevated
• Reduced ejection activates
normal compensatory
mechanisms
• Sympathetic nervous
system
• Renin angiotensin system
• Contractility
• Reduced
• Heart Rate
• Elevated with compensatory
changes
• Too much or too little volume
problematic
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MITRAL REGURGITATION
SYSTOLIC MURMUR
• Timing: Holosystolic
• Location: Mitral area
• May be louder in aortic area depending on leaflet involved
• Radiation: To the left axilla or posteriorly over lung bases
• Quality: Blowing, harsh or musical
• Configuration: Plateau
• Pitch: High
81
CARDIOMYOPATHY
Dilated
Restrictive
Hypertrophic
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CARDIOMYOPATHY
• Heterogeneous group of diseases of the myocardium
• Associated with mechanical and / or electrical
dysfunction
• Usually (but not invariable) exhibit inappropriate
ventricular hypertrophy or dilation
• Due to a variety of causes
•
Maron, B.J. et al Contemporary Definitions and Classification of the Cardiomyopathies: An American Heart
Association Scientific Statement From the Council on Clinical Cardiology, Heart Failure and Transplantation
Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology
Interdisciplinary Working Groups; and Council on Epidemiology and Prevention Circulation, Apr 2006; 113:
1807 - 1816.
83
DILATED CARDIOMYOPATHY
• Most common form of cardiomyopathy
• Dilated LV with LVEF < 40%
• Systolic Dysfunction
• Causes
•
•
•
•
•
•
•
•
•
•
Idiopathic
Ischemic
Genetic disorders
Hypertension
Viral / Bacterial Infection
Hyperthyroidism
Valvular Heart Disease
Chemotherapy
Peripartum Syndrome Related to Toxicity
Cardiotoxic Effects of Drugs or alcohol
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STAGES TO GUIDE THERAPY
Stage A
Stage B
Class IA-C)
•Treat HTN
•Treat DM
• Smoking
Cessation
• Treat Lipids
• Regular
Exercise
• DC Alcohol /
Drug Use
•Treat thy roid
disorders
• ACE-I in select
patients
• All measures
as stage A
Stage C
Stage D
•All measures under stage A
• Dietary salt restriction
• Daily Weight
• Medications for routine use:
•ACE-I in
Diuretics
select patients
ACE – I
• Beta Blockers
Beta-Blockers
in select
Digitalis
patients
Aldosterone Antagonists
Hydralizine/Isordil
African Americans
• Implantable
def ibrillators
• Exercise training
• Devices in select patients
Resynchronization Therapy
Implantable defibrillators
• All measures
under A, B and C
• Mechanical assist
• Transplantation
• Palliativ e Care
• Hospice
85
RESTRICTIVE CARDIOMYOPATHY
• Rigidity of myocardial wall
• Results in decreased ability of chamber walls to expand during
ventricular diastole
• Diastolic Dysfunction
• Least common form of Cardiomyopathy
• 5% of all primary heart muscle diseases
(Goswami & Reddy, 2003)
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RESTRICTIVE CARDIOMYOPATHY
Primary Causes
•
Endomyocardial Diseases
Secondary Causes
•
• Eosinophilic Endomyocardial Fibrosis
Infiltrative disorders
• Amyloidosis
• Endocardial Fibrosis
• 90% of RCM in North
America
• Cardiac Transplant
• Sarcoidosis
• Anthracycline Toxicity
• Radiation carditis
•
Idiopathic
•
Loffler’s Endocarditis
•
Storage Diseases
• Hemochromatosis
• Glycogen storage disease
• Fabry’s Disease
87
ALTERATION IN MYOCARDIAL PERFORMANCE
RESTRICTIVE CARDIOMYOPATHY
• Diastolic Dysfunction
• Poor Ventricular Filling
• Work to improve filling
• Preload
• Volume management
may be precarious
• Longer diastole
(slower heart rates)
• Gently adjust volume
either way
• Relaxed left
ventricle
• Use caution with
venous vasodilators
• Elevated heart rate
impacts filling time
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ALTERATION IN MYOCARDIAL PERFORMANCE
RESTRICTIVE CARDIOMYOPATHY
• Afterload
• No change in afterload
• Contractility
• Not initially impacted.
• Heart Rate
• Increased heart rate will
decrease filling time
• Can develop arrhythmias
due to infiltrates
89
HYPERTROPHIC
CARDIOMYOPATHY
1 of every 500 (Maron et al, 2003)
Primary genetic cardiomyopathy
Effects men and women equally
Hypertrophy of myocardial muscle mass in the absence
of increased ventricular afterload
• Associated with decreased ventricular filling and
decreased cardiac output
• Diastolic dysfunction
• M ost common cause of sudden death in young adults
• Cause unknown
•
•
•
•
• 50% transmitted genetically
90
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5/29/2012
HYPERTROPHIC CARDIOMYOPATHY
• Disarray of cardiac myofibrils with hypertrophy of myocytes
• Cells take on a variety of shapes
• Myocardial scarring and fibrosis occurs
91
HYPERTROPHIC
CARDIOMYOPATHY
• Usually only effects Left
Ventricle
• Changes may be symmetrical
• Asymmetrical septal
hypertrophy is more common
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ALTERATION IN MYOCARDIAL PERFORMANCE
RESTRICTIVE CARDIOMYOPATHY
• Diastolic Dysfunction
• Poor Ventricular Filling
• Work to improve filling
• Preload
• Volume management
may be precarious
• Longer diastole
(slower heart rates)
• Gently adjust volume
either way
• Relaxed left
ventricle
• Use caution with
venous vasodilators
• Elevated heart rate
impacts filling time
93
ALTERATION IN MYOCARDIAL PERFORMANCE
RESTRICTIVE CARDIOMYOPATHY
• Afterload
• No change in afterload
• Contractility
• Usually increased.
• Increased with obstruction
• Heart Rate
• Increased heart rate will
decrease filling time
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5/29/2012
ASSESSMENT IN ACUTE DECOMPENSATION
95
ASSESSING FOR ADEQUATE CARDIAC OUTPUT
Forwards Flow:
CI, Skin temp (warm or cold)
5
4
3
Normal Hemodynamics (I)
No pulmonary congestion:
• PWP < 18; Dry lungs
No hypoperfusion:
• CI > 2.2; Warm skin
2
Forwards Failure (III)
1
No pulmonary congestion
• PWP < 18; Dry lungs
Hypoperfusion
• CI < 2.2; Cold skin
Backwards Failure (II)
Pulmonary congestion
• PWP > 18; Wet lungs
No hypoperfusion
• CI > 2.2; Warm skin
The Shock Box (IV)
Pulmonary congestion
• PWP > 18; Wet lungs
Hypoperfusion
• CI < 2.2; Cold skin
0
2
4
6
8
10 12 14 16 18 20 22 24 26 28 30 32 34 36
Preload: PWP, lung sounds (dry or wet)
96
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5/29/2012
FLUID OVERLOAD VS. HYPOPERFUSION
• Fluid Overload
• Hypoperfusion
• Weight gain
• Narrow pulse pressure
• Peripheral edema
• Resting tachycardia
• Jugular venous distention
• Cool Skin
• SOB
• Altered mentation
• Crackles in lungs
• Decreased urine output
• Increased BUN/Creatinine
• Cheyne Stokes Respirations
97
STAGES OF SHOCK: SIGNS AND SYMPTOMS
• Sub clinical Hypoperfusion
• CI 2.2-2.5
• No clinical indications
of hypoperfusion yet
something seems
different or not right
• Compensatory with SNS
Stimulation
•
CI 2.0 – 2.2
• Restlessness / confusion
• Tachycardia
• Narrowed pulse pressure
• Tachypnea
• Cool Skin
• Oliguria
• Decreased Bowel sounds
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5/29/2012
STAGES OF SHOCK: SIGNS AND SYMPTOMS
• Shock: Progressive with
hypoperfusion (CI < 2.0)
• Dysrhythmias
• Hypotension
• Tachypnea
• Cold, clammy skin
• Anuria
• Absent bowel sounds
• Lethargy to coma
• Shock: Refractory with
profound hypoperfusion (CI <
1.8)
•
•
•
•
•
•
•
•
•
Life threatening dysrhythmias
Hypotension despite vasopressors
ARDS
DIC
Hepatic failure
ATN
Mesenteric ischemia
Myocardial ischemia
Cerebral ischemia
99
WHEN TO ALTER PRELOAD
• Pulmonary Congestion
• Subset II patients (Backwards Failure)
• Goal: Decrease preload
• Therapy: Diuretics, venous dilators
• Hypotension Secondary to Hypovolemia
• Subset III patients (Forward Failure)
• Goal: Increase preload
• Therapy: Fluids
100
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WHEN TO ALTER AFTERLOAD
• Combined forward and backward failure
• Subset IV patients: Shock Box
• Goal: Decrease pulmonary congestion and increase forward flow
• Therapy
• Arterial dilator drugs
• ACEI, ARBs, Nitroprusside, Ca++ blockers, Milrinone, Nesiritide
• IABP
101
WHEN TO ALTER CONTRACTILITY
• Subset III patients with adequate preload
• Subset IV patients: Shock box
• Assume a contractility problem
• Patients with low CO but optimal preload, afterload, and HR
CO = HR, preload, afterload, contractility
• Therapy:
• Inotropes (dobutamine, dopamine, milrinone, epinephrine,
digoxin)
• Increase MVO2, use with caution in acute MI
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5/29/2012
TREATMENT FOR ACUTE DECOMPENSATED
HEART FAILURE
103
ACUTE DECOMPENSATED HEART FAILURE
• Reduce Preload
• Diuretics
• Venous vasodilators
• Low dose Nitroglycerin
• Neseritide
• Increase Contractility
• Positive Inotropes
• Dobutamine
• Milronone
• Ultrafiltration
• Reduce Afterload
• Arterial vasodilators
• High dose Nitroglycerin
• Nitroprusside
• Neseritide
• Intra aortic balloon pump
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5/29/2012
Antman et al, 2004. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report
of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to 105
Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction).
106
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5/29/2012
REMEMBER
• Low BP could be due to:
• Low CO
• HR too slow or too fast
• Preload too low or too high
• Contractility low
• Low SVR
• Vasodilation due to sepsis, drugs, anaphylaxis
107
COMPARISON OF 2 HYPOTENSIVE PATIENTS
88/70
Vasodilators
82/30
Cardiogenic Shock
Septic Shock
Cause:
Decreased C.O.
Cause:
Decreased SVR
Treatment may
involve afterload
reduction to
increase cardiac
output
Treatment is
focused on filling
tank and restoring
vascular tone.
Vasopressors
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5/29/2012
CASE STUDY
If you listen to the patient and they will tell you
what is wrong with them!
109
PATIENT PRESENTATION
• 85 year old female living independently at home with
help of family is admitted to the hospital with
shortness of breath.
• She has become increasingly short of breath the past
2 days. Her weight is up 6 pounds from 3 days ago.
• She has not taken her medications for 4 days
because her prescriptions ran out and she was
waiting on her oldest son to get back in town to get
them filled.
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5/29/2012
HOME MEDS AND HISTORY
• Furosemide (only 20 mg daily)
• Lisinopril
• Metoprolol
• Aldactone
• Baby ASA
• Warfarin
• Synthroid
• OTC NSAIDs for pain
HISTORY
•
•
•
•
•
•
•
History of ischemic cardiomyopathy
CABG @ age 70
History of atrial fibrillation
History TIA
Last known ejection fraction 30%
Osteoarthritis
Hypothyroidism
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5/29/2012
STAGES OF HEART FAILURE
ACC / AHA
Stage A
Stage B
Stage C
Stage D
At high risk f or HF but
without structural
heart disease or
sy mptoms of HF.
Structural heart
disease but
without signs or
sy mptoms of
Heart Failure
Structural heart
disease with prior or
current sy mptoms of
HF.
Ref ractory HF
requiring
specialized
interv entions.
Know structural
disease and SOB,
f atigue, reduced
exercise tolerance.
Marked
sy mptoms of HF
at rest despite
maximal medical
therapy.
HPTN
CAD
DM
Obesity
Metabolic syndrome
Family HX CM
Prev ious MI
LV Remodeling
including LVH and
low EF
Asy mptomatic
v alv ular disease
113
CLASSIFICATION OF HEART FAILURE
NEW YORK HEART ASSOCIATION
Class I
Class II
Class III
Cardiac disease
Cardiac disease no Cardiac disease
resulting limitation with slight limitation with marked
in phy sical activity. of phy sical activity. limitation on
phy sical activity.
Ordinary activ ity
f ree of f atigue,
palpitation,
dy spnea or anginal
pain.
Comf ortable at rest
but ordinary activity
results in f atigue,
palpitations,
dy spnea, or anginal
pain.
Class IV
Cardiac disease
resulting in inability
to carry out any
phy sical activity
without discomf ort.
May hav e
sy
mptoms of
Comf ortable at rest
cardiac
but less than
insuf ficiency at rest.
ordinary activ ity
results in f atigue,
palpitations,
dy spnea, or anginal
pain.
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5/29/2012
PHYSICAL ASSESSMENT
BP: 88/70
HR: 110’s to 130’s
Rhythm: Atrial Fib
Frequent ventricular ectopy
RR 28-32
SaO2 88% on 4L nasal
cannula
Pale and cool to touch
Somewhat lethargic
M ild right sided weakness
Faint pedal pulses
Heart Sounds
S3
Systolic murmur 3/6
Lungs with crackles ½ up
bilaterally
JVD
Right Upper quadrant
tenderness
2+ peripheral edema to mid
calf
Urine output is 10cc in first hour
DIAGNOSTICS
First troponin .04
BNP 1200
K+ 5.1
H & H 9.2 / 30.1
BUN 42 / Creatinine 2.0
PaCO2 43 mmHg, PaO2 59 mmHg
Chest x-ray consistent with congestion and bilateral
pleural effusions
• ECG/ Rhythm
•
•
•
•
•
•
•
58
5/29/2012
EVALUATION
• Are tissues receiving adequate oxygenation?
• What are the 3 parameters that determine
delivery of oxygen to the tissues?
• What is probable cause of myocardial
decompensation?
59
5/29/2012
EVALUATION
BP: 88/70
HR: 110’s to 130’s
RR 28-32
Pale and cool to touch
Somew hat lethargic
S3
Systolic murmur 3/6 5 th ICS LMCL
Lungs: Crackles ½ up
JVD
RUQ quadrant tenderness
2+ edema
Urine output is 10cc/hr
SaO2 88% on 4L / NC
PaCO2 43 mmHg
PaO2 59 mmHg)
Mild right sided w eakness
K+ 5.1
H & H 9.2 / 30.1
BUN 42 / Creatinine 2.0
EVALUATION OF DELIVERY OF
OXYGEN
• Is SaO2 adequate?
•
•
•
•
What should PaO2 be?
What type of pulmonary problem is present?
How does it need to be treated?
Are there any concerns about ventilatory status?
• Is hemoglobin adequate?
• Is transfusion indicated?
• What needs considered?
• Is cardiac output adequate?
• What assessment indicators give you indication?
What is the value of the BUN/creatinine ratio?
60
5/29/2012
EVALUATION OF CARDIAC
OUTPUT
Cardiac Output
• What is the formula for
Cardiac Output?
• What non invasive
parameter correlates with
SV?
What would invasive hemodynamic
monitoring add?
Diagnosis?
Guiding therapy?
SVO2 value?
• Preload?
• JVD
• Lung sounds
• S3
• Afterload?
• Pulse pressure
• Contractility?
• EF
• HR?
• Compensation
• Beta blockade
HEMODYNAMIC PROFILE FOR CARDIOGENIC
SHOCK
• CO
• SV
• Preload
• Afterload
• Contractility
• HR
What is the profile
for our patient?
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5/29/2012
CAUSE OF DECOMPENSATION
• Stopping medications?
• MI?
• Valve dysfunction?
• Anemia?
• Atrial fibrillation?
• Impact of BBB?
Profiles of Advanced Heart Failure
Congestion at Rest
No
Low
Perfusion
at Rest
No
Yes
Warm and Wet
Warm and Dry
Congestion
No congestion
No hypoperfusion No hypoperfusion
CI 2.2
Yes
Cold and Dry
No congestion
Hypoperfusion
Cold and Wet
Congestion
Hypoperfusion
PWP 18
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5/29/2012
CORRECTING DECOMPENSATED
HEART FAILURE
• What parameters are a priority for
correcting?
• What are the results of therapy on
myocardial oxygen demand?
What is a non pharmacological method of
decreasing afterload?
Therapies of Advanced Heart Failure
Congestion at Rest
No
No
Low
Perfusion
at Rest CI 2.2
Yes
Yes
Preload Reduction
Diuretics
Nitrates
Inotropes
Dobutamine
Milrinone
Afterload Reduction
Hydralazine
Nitroprusside
Milrinone
Inotropes
PWP 18
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5/29/2012
ADDITIONAL QUESTIONS
• Co-existing pneumonia?
• Potassium
• Why so high?
What about
non steroidals?
• Right sided weakness
• New or old?
• Atrial fib
• New or old?
• Other reasons for warfarin?
CLINICAL ASSESSMENT WITHOUT BELLS
AND WHISTLES IS MORE CHALLENGING.
PROVIDERS AT THE BEDSIDE MAKE THE
DIFFERENCE IN THE LIFE AND DEATH OF
THE PATIENT.
Make sure your skills are the
best they should be.
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5/29/2012
www.cardionursing.com
BE THE BEST THAT YOU CAN BE EVERY
DAY. YOUR PATIENTS ARE COUNTING
ON IT!
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