Download Heart Failure

Cardiovascular Anatomy &
Physiology
Objectives
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Function
Anatomy
Cells
Cardiac Output
Oxygen Transport
Pathologies
Cardiovascular Function


Deliver oxygenated blood
to tissues- where diffusion
and filtration occur
Transport blood back to
lungs- where oxygen and
carbon dioxide exchange
occur
Cardiovascular System
Cardiovascular Structures
Human Heart
Surface anatomy of the human heart.
The heart is demarcated by:
-1. A point 9 cm to the left of the
midsternal line (lower left or apex of
the heart)
-2. The seventh right sternocostal
articulation (lower right side of heart)
3.
2.
4.
1.
-3. The upper border of the third right
costal cartilage 1 cm from the right
sternal line (upper right side of heart)
-4. The lower border of the second left
costal cartilage 2.5 cm from the left
lateral sternal line (upper left side of
heart)
Cells of the
Cardiovascular System
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Cardiac cells
– pacemaker cells
– cardiac myocytes
Vascular cells
– endothelial cells
– smooth muscle cells
Cardiac Myocytes
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Conduct AP cell-to-cell via gap
junctions
Are packed with contractile elements
Have well developed sarcoplasmic
reticulum which sequesters calcium
Are dependent on extracellular calcium
for contraction
How does membrane depolarization
lead to mechanical contraction?
Action Potential
Calcium influx from ECF
Calcium release from SR
Increased intracellular free calcium
actin-myosin crossbridging
myocardial cell shortening
Cardiac Muscle Cell
Ca
Ach
receptor
Ca++
channel
ATP
Ca
beta
receptors
cAMP
Ca
Na
Ca
Na
ATP
Na channel
K
SR
Na
K
K channel
digoxin
ANS effects on heart and vessels
Heart
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inotropy
chronotropy
dromotropy
lusitropy
SNS
PSNS
+
+
+
+
-
constrict
constrict
dilate
no effect
Vessels
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pulmonary/coronary
most others
Cardiac Output
THE most important variable in cardiac
function!
CO = HR x SV
Oxygen Transport
pO2 lungs = 80-100 mm Hg
pO2 tissues = 30-40 mm Hg
SaO2 lungs = 95-100%
SaO2 tissues = 60-80%
PaO2
Saturation
100
90
80
70
60
50
40
98%
96%
94%
92%
89%
83%
75%
Shifts in Hb-O2 Affinity

Shift to right: affinity
– acidemia
– hyperthermia
– hypercarbia
– increased 2,3DPG

Shift to left: affinity
– alkalemia
– hypothermia
– hypocarbia
– decreased 2,3DPG
Figure: 13-15
The oxyhemoglobin dissociation
curve
Carbon Dioxide Transport
Physical Solution: (5%)
PaCO2 X .06
Carbaminohemoglobin: (15%)
HB
N
H
COOBicarbonate ion (80%)
CO2 + H2O
H2CO3
H+ + HCO3-
Red Cell Production
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iron
folate
vitamin B12
erythropoietin
functional stem cells
Figure: 13-17
The erythropoietin response to anemia,
hypoxia, polycythemia
Cardiovascular Pathology
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Anemia
Heart Failure
Valvular Defects
Cardiomyopathies
Congenital Defects
Vascular Insufficiency
General Signs and
Symptoms of Anemia
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Increased respiration
Increased heart rate
Fatigue
Decreased activity tolerance
Pallor
Murmur
Heart Failure
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Def: Inability to effectively PUMP the amount of
blood delivered to the heart
Left ventricular ejection fraction (EF)
– Normal values: 60-80%
– Important measure of heart failure

Etiologies: Many, but 2 main causes are
hypertension and ischemia
–
–
–
–
–
MI
CIHD
Valve Disease
Congenital Defects
Cardiomyopathy
Figure: 19-5
Interdependence of left and right heart
function
Clinical presentation of CHF
Differs for left, right, or both ventricle failure
Left Ventricular Failure (LVF)
Right Ventricular Failure (RVF)
Forward Failure
Poor cardiac pumping = reduced CO
Backward Failure
Congestion of blood behind the heart
Figure: 19-7
Manifestations of left heart failure
Clinical presentation of LVF
most common presentation for CHF
Often leads to RVF (biventricular failure)
Common causes
Left ventricular infarction
Cardiomyopathy
Aortic and mitral valvular disease
Systemic hypertension
Forward effects – reduced CO leads to hypoxia
Brain hypoxia – restlessness, mental fatigue,
confusion, anxiety, impaired memory
Cardinal symptom – dyspnea (early sign)
Hypoxemia results from impaired gas exchange
Cyanosis results from deOxyHgb (late sign)
Arterial Blood Gas analysis
Cyanotic
Elevated Left arterial pressure
Acute cardiogenic pulmonary edema – life threatening
Bolt-upright posture
Dyspnea and anxiety
Lungs are congested but systemic venous system is not
Summary
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Anemia
Heart Failure
Valvular Defects
Cardiomyopathy
Congenital Defects
Vascular Insufficiency
Valvular Disorders
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Abnormalities of Valve function:
– Stenosis & Regurgitation
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Etiology
– congenital
– rheumatic
– degenerative calcification
– infective
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Diagnostic Evaluation: Echo-doppler
Common Valve Disorders
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Mitral Stenosis
Mitral Regurgitation
Aortic Stenosis
Aortic Regurgitation
Mitral valve lies between the left atrium and left ventricle.
Stenosis – obstruction to blood flow thru cardiac valves that are
not opening completely
Regurgitation – retrograde blood flow through a cardiac valve
when the valve is closed
Differential Diagnosis of
Murmur

Mitral Stenosis
– Increased Left Arterial Pressure
– Loud S1 opening snap at apex
– Murmur rare, if present, short diastolic
– atrial fibrillation is common
Mitral Stenosis
120
90
60
30
0
LA/LV
gradient
Differential Diagnosis of
Murmur
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Mitral Regurgitation
– Systolic Murmur
– Radiates to left axilla
– Pansystolic, blowing
– Prominent S3
Mitral Regurgitation
120
90
60
large regurgitant V-wave
30
0
Differential Diagnosis of
Murmur
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Aortic Stenosis
– Mid systolic
– Crescendo-decrescendo
– Radiates to neck
– S4 prominent
– Angina, syncope common
Aortic Stenosis
180
120
90
40
0
LV/Aortic
pressure gradient
Differential Diagnosis of
Murmur

Aortic Regurgitation
– Diastolic murmur
– Bounding Pulse “waterhammer”
– Wide pulse pressure
Aortic Regurgitation
180
120
aortic pressure
with Aortic
Regurgitation
90
40
0
normal
aortic
pressure
Cardiomyopathy
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Dilated
– enlarged heart chambers
– poor contractility
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Hypertrophic
– outflow obstruction
– ischemia
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Restrictive
– impaired diastolic filling
Congenital Heart Defects
Acyanotic
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L to R shunt
– Atrial Septal Defect
– Ventricular Septal
Defect
– Patent Ductus
Arteriosus
Cyanotic
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R to L shunt
– Transposition
– Tetralogy of Fallot
Shock
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Defining Characteristic: Oxygen Delivery to one or
more tissues is below basal requirements leading to
hypoxic and immunologic injury.
Types of Shock:
– Hypovolemic
– Cardiogenic
– Distributive (e.g. anaphylactic, septic, neurogenic)
Manifestations: Signs and symptoms of tissue ischemia
and death.
Diagnosis of Shock
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Tachycardia
Hypotension (orthostatic)
Peripheral hypoperfusion
(slow capillary refill, cool, mottled)
Oliguria or anuria
Metabolic acidosis
In septic shock: fever, chills
General Treatment Measures
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Supine position
Oxygen
Analgesics
Labs: CBC, ABG, Renal panel, Type & X, UA
Cardiac Monitoring
CVP Monitoring (at least)
Volume replacement
(colloid vs crystalloid vs blood)
Vasoactive Drugs
Septic Shock
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Usually caused by gram negative bacteria.
Monoclonal antibody to endotoxin may be
used.
Don’t be fooled by high cardiac output, still
have insufficient blood volume to fill the
tank.
Oxygen consumption is often low due to
abnormal distribution and shunt. Look for
increased consumption with treatment.
Mortality is high: 40-80%
Vascular System
Arterial Insufficiency
Venous Insufficiency
Risks for Vascular
Insufficiency
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Arterial
– smoking
– atherosclerosis
– inflammatory:Buerger
s
– trauma
– DIC
– emboli from LV
– vasospasm
– diabetes mellitus
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Venous
– stasis of bloodflow
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immobility
R heart failure
prolonged standing
obesity
pregnancy
– trauma
– hypercoagulable
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high platelets
high hematocrit
Pathophysiology of
Insufficiency
Heart Pump
venous
arterial
ischemia
edema
capillary
Arterial Insufficiency
Flow Downstream
ischemia
acute
Pain
Pallor
Pulselessness
Paresis
Paralysis
Poikilothermy
chronic
Intermittent claudication
Atrophy (skin, hair)
Thickening of nails
Venous Insufficiency
Obstruction of Venous Drainage
capillary hydrostatic pressure
edema, stasis
pain
risk of pulmonary
embolus
stasis ulcers
and skin changes
Thrombophlebitis
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Deep Vein (DVT)
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– Extremity Edema
– General leg pain
– Fever
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– local Inflammation
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High Risk of PE
Treatment
– immobilize
– anticoagulate
– treat risk factors
Superficial
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warm
tender
red
swollen
– Collateral veins
minimize edema
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Low Risk of PE
Assessment of Cardiac
Function
Electrical Function
Contractile Function
Is Electrical Conduction
Normal?
R
P
T
Q
S
ECG Assessment
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Rate?
Conduction Abnormality?
– Dysrhythmias
– Conduction blocks
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Ischemia/Infarction?
LVH?
Cardiovascular
Pathophysiology
Afterload – The resistance that must be overcome to eject blood
from a cardiac chamber. Left ventricular afterload is correlative with
the resistance in the systemic vasculature.
Preload – The volume of blood that remains in the cardiac chamber
prior to systole.
Classification of
Hypertension
Category
SBP
DBP
Recommended
Followup
Normal
<130
<85
Recheck in 2 years
130-139
85-89
Recheck in 1 year
Stage 1 (mild)
140-159
90-99
Confirm within 2 mo
Stage 2 (mod)
160-179 100-109
Eval or refer 1 mo
Stage 3 (severe)
180-209 110-119
Eval or refer 1 week
High Normal
Hypertension
Stage 4 (very sev)
>210
>120
Eval or refer
immediately
Differential Diagnosis of
Hypertension
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Primary Hypertension (95%)
Secondary Hypertension
– Contraceptive use
– Renal disease
– Renal artery stenosis
– Cushing’s syndrome
– Pheochromocytoma
– Pregnancy induced hypertension
Treatment?
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Diuretics, beta blockers, ACE
inhibitors, calcium channel blockers,
alpha blockers
Consider age, ethnicity, coexisting
disorders, cost, lipid profile
Figure: 18-2
Lipoprotein transport
Chylomicron
85% triglyceride
5% cholesterol
VLDL
55% triglyceride
20% cholesterol
LDL
5% triglyceride
55% cholesterol
20% protein
HDL
5% triglyceride
20% cholesterol
50% protein
Figure: 18-3
Type I - IV atherosclerotic plaques
Types I-III
Asymptomatic
Arterial wall narrowing
Types IV-VI
Predispose to ischemic
episodes
Ischemic Heart Disease
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Etiology:
– Coronary Atherosclerosis
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Risks:
Clinical Syndromes:
– angina pectoris
– myocardial infarction
– chronic ischemic heart disease
– sudden cardiac death
Pathogenesis of
Atherosclerosis
Lipid accumulates in vascular wall
Macrophages infiltrate the wall and
oxidize the lipids
Cell injury and release of local growth factors
(Angiotensin II)
Plaque formation on intimal wall
Demand > Supply: Angina
Perfusion pressure
fixed stenosis
oxygen content
SUPPLY
afterload
contractility
preload
heart rate
DEMAND
How to increase supply?
How to decrease demand?
Pathogenesis of Ischemia
Plaque Disruption or Breakdown
Tissue Thromboplastin Exposed
Platelet Aggregation and Clotting Cascade Activated
Thrombus Formation
Acute Ischemia
Ischemic Syndromes
Stable
Angina
Unstable
Angina
MI
Patho:
Fixed stenosis Thrombus
>75%
+ lysis
Thrombus
with occlusion
Pain:
predictable
relieved by
rest (3-5 min)
unpredictable
not relieved
rest
unpredictable
not relieved
rest (>15-30)
not elevated
elevated
Serum Enz: not elevated
ECG Changes with
Ischemia
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Indicative Leads show:
Ischemia: ST elevation or depression
T-wave peaking, flattening,
inversion
Bigger than normal Q-waves
ST elevation
Q
Sequela of Myocardial
Infarction
Decreased Myocardial Perfusion
Partially ischemic cells
Totally ischemic cells
Anaerobic metabolism
and lack of ATP
No ATP
Cell rupture and death
Ion leak across
cell membrane
ST changes
Dysrhythmias
Q-waves
Elevated
Enzymes
Figure: 18-9
Summary of events following MI
Figure: 18-8
Time course of serum marker elevations
after MI
Serum markers
released from damaged
cardiac cells
Cardiac isozymes – MI indicators
creatine kinase (CK-MB)
only present up to 72 hrs
troponin I (present longer)
troponin T (present longer)
Compensatory Response to
Decreased Stroke Volume
Decreased Stroke Volume
IMMEDIATE
baroreceptor
activation
HOURS
RAS activity
WEEKS
Increased LV
wall tension
fluid retained
SNS
SV,
CO
preload
SV,
CO
ventricular
hypertrophy
SV,
CO
Differential Diagnosis of
Chest Pain
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Cardiac ischemia
Chest wall trauma, costochondritis
Pleural pain - pneumonias
Pneumothorax
Gastrointestinal (GERD)
Treatment of Cardiac
Ischemia

Stable angina
– SL nitroglycerin
– Platelet inhibitor (e.g. ASA 325mg qod)
– beta blocker
– add long acting nitrate (remove at night)
– add calcium channel blocker (not
verapamil)
Treatment of Cardiac
Ischemia

If ECG shows signs of current ischemia
– Continuous ECG monitoring, Labs
– Oxygen
– Give ASA
– Relieve pain with SL nitro, morphine
– Evaluate for thrombolytic therapy
– Decrease MVO2: bedrest, pain relief, etc
– Manage dysrhythmias, hemodynamics
Heart Failure
Pathophysiological state
Abnormality of cardiac function to supply blood to meet demand
Pumps only from abnormally elevated diastolic filling pressure
Etiology
Myocardial failure
High demand on heart with near normal cardiac function
Inadequate adaptation of cardiac myocytes to increased wall stress
Causes circulatory failure but converse is not always true
Adaptations
Frank-Starling mechanism – increased preload sustains cardiac performance
Myocardial hypertrophy – mass of contractile tissue increases
Neurohumoral Activation –
Adrenergic cardiac nerves causes release of NE
Positive inotropy
Activation of RAA system – salt and water retention (increased preload, increased energy expense)
Release vasoconstrictive agents which increase afterload
Increased cAMP causes increased calcium entry
Positive inotropy, negative lusitropy
Increased energy expenditure and reduced CO which further stimulates RAA system
Calcium overload may cause arrythmia and sudden death
Cardiac AngII may cause negative lusitropy, positive inotropy, positive afterload, increased myocardial energy
expense
Congestive Heart Failure
Can result from most cardiac disorders.
Most common causes of CHF is myocardial ischemia from coronary
artery disease, hypertension and dilated cardiomyopathy
Systolic dysfunction
Reduced myocardial contractility
Congestion is result of fluid backup in heart
Common cause is myocardial cell death – MI (neg inotropy)
EF less than 50%
Chronic overexcitation of b receptor SNS may be exacerbate condition
B receptor blockers – treatment
Heart failure –
Signs, symptoms CHF
Reduced stroke volume
Reduced cardiac output
Reduced EF (typically < 40%; severe if EF<20%)
Congestive Heart Failure
Diastolic dysfunction
Reduced myocardial relaxation
Ventricle is not compliant and does not fill effectively
Ventricle filling dependent on Ca2+ uptake (active phase of diastolic relaxation)
Passive phase (myocardial stretch) impaired
Common cause is myocardial cell death – MI (neg inotropy)
Heart failure –
Signs, symptoms CHF (congestion; edema)
Reduced stroke volume
Reduced cardiac output
Near normal EF > 50%
Factors Affecting Cardiac
Output
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Heart Rate (chronotropy)
Contractility (inotropy)
Preload
Afterload
How is Heart Rate
Regulated?
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Intrinsic pacemaker rate = 100 bpm
Autonomic Influences
– SNS------> B1 receptor-------> Increased
HR
– PSNS-> Muscarinic (Ach)--> Decreased
HR
Stretch Reflex (Bainbridge):
Increased filling------> Increased HR
Drugs: ANS drugs, digitalis
What Factors Affect
Contractility?
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
Anything that increases Ca++ availability in the
heart muscle cell will increase Contractility.
Anything that decreases Ca++ availability in the
heart muscle cell will decrease Contractility.
What would be the effect of:
– SNS
– PSNS
– Digoxin
– Ca++ channel blocker
– B1 blocker
Preload: Volume Work of
the Heart
S.V.
preload
The Frank-Starling Law of the Heart:
Increased preload increases force of contraction
Afterload: Pressure work
of the Heart

Increased Afterload occurs with
increased resistance to ejection of
blood from the ventricle
– Increased Systemic Vascular Resistance
– Increased Diastolic Blood Pressure
– Aortic Stenosis

Increased Afterload: Decreased stroke
volume
Constitution of normal blood
Parameter
Value
45 ± 7 (38–52%) for males
Hematocrit
42 ± 5 (37–47%) for
females
pH
7.35–7.45
base excess
−3 to +3
PO2
10–13 kPa (80–100 mm
Hg)
PCO2
4.8–5.8 kPa (35–45 mm
Hg)
HCO3−
21–27 mM
Oxygen saturation
Oxygenated: 98–99%
Deoxygenated: 75%
ANEMIAS
ANEMIAS
How can the different types of
anemia be differentiated?

Laboratory Diagnosis of Anemia
– Low Hematocrit
– Low Hemoglobin
– Low RBC count

Red Cell Indices
– MCV (size) microcytic, normocytic
macrocytic
– MCHC (color) hypochromic, normochromic
MCV
MCV
low
Microcytic
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iron deficiency
hemoglobinopathy
chronic disease
lead poisoning
high
normal
Normocytic
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acute bleeding
aplastic
hemolytic
low erythropoietin
malignancy
Macrocytic
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low Vit B12
low folate
Polycythemia
Polycythemia
red cell mass
normal
increased
check erythropoietin
Relative
polycythemia
- hydrate
high
Secondary
- assess lung and
kidney function
low
Vera
- assess
wbc, platelets
Cardiovascular System
Physiology
Figure: 19-2
Compensatory mechanisms
in heart failure
These mechanisms attempt to improve cardiac output
SNS activation – early response to reduced CO
Increased heart rate
Increased contractility
Increased arterial vasoconstriction
Increased renin release
Chronic SNS activation
Increased afterload
Increased workload = Reduced CO
Decreased CO reduces kidney perfusion
Activates RAA system ultimately leading to increased fluid retention
Decreased EF = Increased Preload = Reduced CO = Reduced GFR =
Increased Fluid Retention = Increased RAS activation =
Increased Blood volume= Increased Chamber volume =
Increased Contraction (myocardial stretching)
Higher Preload = Increased Contractility = Increased CO
Left Heart Failure
Forward Failure
Poor cardiac pumping = reduced CO
Backward Failure
Congestion of blood behind the heart
LVF
Forward
effects
Backward
effects
EF
Left Ventricular
preload
CO
Fluid
retention
RAS
activation
Tissue
perfusion
Left atrial
pressure
Pulmonary
Pressure
Pulmonary
Congestion & edema
(dysfunction)
Right ventricular
afterload
Right ventricular
hypertrophy
Forward Failure
Poor cardiac pumping = reduced CO
Right Heart Failure
Backward Failure
Congestion of blood behind the heart
RVF
Forward
effects
Backward
effects
EF
Output to LV
Right Ventricular
preload
Left ventricular
CO
Right atrial
pressure
Systemic Venous
Congestion
Fluid
retention
RAS
activation
Tissue
perfusion
Figure: 19-9
Manifestations of right heart failure
Clinical presentation of RVF
Often results from LVF
Common causes
LVF
Right MI
Pulmonary disorders that increase pulmonary resistance
increased right ventricular afterload
reduce lung vascularization
hypoxemia, emphysema, embolus
RV compensates by increasing preload and
hypertrophy
Cardiomyopathy
Aortic and mitral valvular disease
Systemic hypertension
Forward effects – reduces CO via action on LV
Backward effects – congestion of systemic venous system
Impaired function of liver, portal system, spleen,
kidneys, peripheral subcuatenous tissues, brain
Edema apparent in lower extremities
Systemic system is congested but pulmonary system is
not
In biventricular heart failure – both systemic venous and pulmonary systems are congested
Principles of Heart Failure
Treatment

GOAL: Optimize Cardiac Output and
Minimize Cardiac Workload
– Management of Preload
– Management of Afterload
– Management of Contractility
Drugs used in the management of Heart Failure (table 19-3)
Phases of the Ventricular
Action Potential
Hyperpolarized (+)
1
2
K+ out
Ca++ in
0
Na+ in
-70 mV
Depolarized (-)
4
3
K+ out
CO2 transport in Blood
Also see
Fig 13-16
1.
2.
3.
Dissolved CO2
Carbaminoglobin
Bicarbonate ion
Chloride
shift
Cardiovascular System
Cardiovascular Structures
Structure diagram of the human heart from an anterior view.
Blue components indicate de-oxygenated blood pathways and
red components indicate oxygenated pathways.
Pacemaker Cells
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SA node, AV node, Purkinje fibers
Spontaneously generate action
potentials
Vary rate in response to ANS
Action potentials are associated with
opening of slow calcium ion channels
Almost no contractile elements
What is the basis of
automaticity?
Spontaneous Phase 4 depolarization
threshold
Ca
K out
-40 mV
Na
RMP
pacemaker cells are leaky to sodium at rest
-60 mV
ANS Influences on Ion Flux


Sympathetic:
NE, E stimulates Beta
receptors leading to
opening of Na/Ca
channels. The cell
depolarizes faster.
Parasympathetic: acetylcholine stimulates
muscarinic receptors
leading to opening of K
channels. Potassium leak
out offsets sodium influx.
The cell depolarizes
slower.
Autonomic NERVES
SNS (T1-L2)
Ach
N1
NE
nicotinic
a1, a2
b1, b2, b3
receptor
PSNS (Cn IX, X)
Ach
N1
Ach
nicotinic
M1 to M5
muscarinic
receptor
alpha-MN
N2 (nicotinic)
Ach
muscle