The document outlines the control and function of the cardiovascular system, including heart structure, blood flow, and electrical conduction. It highlights disorders related to blood flow, blood pressure, and cardiac function, emphasizing hypertension prevalence and its classifications. Additionally, it discusses the impact of hypertension on various organs and details about congenital heart defects in infants and children.

1. Circulatory Function
Brenda Nabawanuka

2. Outline
1. Control of cardiovascular function
2. Disorders of blood flow and blood
pressure
3. Disorders of cardiac function
4. Heart failure and circulatory shock

3. Control of cardiovascular function

4. The Heart
 Gross structures
 Musculature-pericardium, fibrous & serous
epicardium, visceral serous pericardium,
myocardium (heart muscle)
 Muscle cell (microscopic structures), central nucleus,
sarcoplasm, sarcolemma, sarcomere-the contractile
unit, intercalated discs
 Pattern of blood flow through the structures of the
heart; atria, ventricles, valves

5. Transition from fetal to pulmonary circulation
• the umbilical cord is cut
• systemic vascular resistance is increased
• pressure in the L side of the heart increases
• foramen ovale closes
• breathing is initiated
• pulmonary vascular resistance falls
• blood that was shunted through the PDA now goes
to the lungs.

7. Fetal (prenatal) circulation. Pulmonary (postnatal) circulation

8. Chambers
Right side of Heart
•Right atrium – the thin-walled atrium, low relative pressure
receives blood from superior and inferior vena cava, the
coronary sinus and thebesian veins. The outflow of blood
through tricuspid valve.
•Right ventricle – relatively thin muscle wall, crescent-shaped,
papillary muscles, chordae tendineae, low pressure. Outflow
through the pulmonic valve to the pulmonary artery.

9. Chambers
Left side of the heart
•Left atrium, - thicker muscle, medium pressure of blood, inflow
of blood through the four pulmonary veins.
Outflow is through the mitral valve.
•Left ventricle – largest muscle mass, high pressure blood flow,
papillary muscles, spring-like pump action.
Outflow of blood through the aortic valve and the aorta.

11. Valves
 Atrioventricular Valves:
 Tricuspid – has three leaflets, controlled by papillary
muscles; chordate tendineae
 Mitral valve – two cusps, controlled by papillary muscles
and the chordae tendineae
 Semilunar Valves:
 Pulmonic valve – three-leaflet valve, formed by fibrous
ring, tendinous tubercle midpoint free edges
 Aortic valve – three leaflets, also formed by fibrous ring,
tendinous tubercle midpoint free edges.

13. Vasculature of the Heart
 Right coronary artery – most branches of this artery
anastomose distally with left anterior descending.
 Left coronary artery – divides into two main branches,
left ant. descending and left circumflex artery.
 Great cardiac vein – largest system, forms coronary
sinus, drains left ventricle primarily.
 Anterior cardiac veins – empty directly into right
atrium.
 Thebesian veins – smallest system, empty into right
atrium

14. Conduction System of the Heart
 SA (Sino-atrial node)
 Atrial preferential pathways – anterior
internodal, middle, posterior
internodal
 AV (Atrio-ventricular node)
 Bundle of HIS
 Left Bundle Branch
 Right Bundle Branch
 Purkinje fibres

16. Contractility of Heart Muscle
 Heart muscle possesses the following properties:
Automaticity - pacemaker ability
Conductivity - each cell has the ability to conduct
impulses
Contractility - ability to contract (make
each cell shorter or longer)
Irritability - each cell has ability to contract on
its own, to send impulses to cells without it first
being stimulated from another source

17.  These properties make the myocardium
different from other muscle cells in the body
 Various factors affect the activity of cardiac muscle
The availability of oxygen,
afterload,
nervous control,
muscle condition
Drugs

18. Blood Flow through the heart
Physical characteristics important to blood flow:
 Diameter of the
blood vessels
 Cross-section areas
of the chambers and
vessels
 Length of the vessels
 Quantities of blood:
 Heart 18%
 Pulmonary vessels 12%
 Large arteries 8%
 Small arteries 5%
 Arterioles 2%
 Capillaries 5%
 Small veins 25%
 Large veins 25%

19. Velocities of blood flow
 Directly related to the amount of circulating
blood volume and the area of the vessels.
 Blood returns to the heart from the general
circulation.
 Almost 50% of all blood in the body is in the
systemic veins of the body.
 The small veins usually offer little resistance
to blood flow.

20.  The large veins do offer much resistance
to the flow of blood to the heart.
 The patient who is more active will have
better flow of blood back to the heart.
 With reduced activity, the blood tends to
pool in the large vessels and can lead to
severe venous stasis.

21.  From the right atrium
blood flows to the right ventricle and is
then propelled into pulmonary circulation.
After blood is aerated with fresh oxygen,
it is returned to the left side of the heart
into the left atrium

22.  From the left atrium
The blood is ejected into the left
ventricle.
The left ventricle then pumps the blood
out of the heart into the general
circulation.
The aorta is the first vessel to carry
blood,
At the same time, the coronary arteries
are being fed oxygenated blood to
circulate through the heart.

23. Cardiac Output
Preload
Afterload Contractility
Heart Rate Stroke Volume
= X
Factors that affect Cardiac Output

24. PreLoad
 The volume of blood/amount of fiber stretch in the ventricles at the
end of diastole (i.e., before the next contraction)
 Fluid volume increases
 Vasoconstriction (“squeezes” blood from vascular system into
heart)
 Preload decreases with
 Fluid volume losses
 Vasodilation (able to “hold” more blood, therefore less returning to
heart)
 The greater the heart muscle fibers are stretched (b/c of increases in
volume), the greater their subsequent force of contraction – but only up
to a point. Beyond that point, fibers get over-stretched and the force of
contraction is reduced
 Excessive preload = excessive stretch reduced contraction reduced
→ →
SV/CO

25. Cardiac
Output

26. Afterload
 Afterload
 The resistance against which the
ventricle must pump. Excessive
afterload = difficult to pump blood →
reduced CO/SV
 Afterload increased with:
Hypertension
Vasoconstriction
 Afterload decreased with:
Vasodilation

27. contractility
Contractility
 Ability of the heart muscle to contract; relates to the strength of
contraction.
 Contractility decreased with:
 infarcted tissue – no contractile strength
 ischemic tissue – reduced contractile strength.
 Electrolyte/acid-base imbalance
 Negative inotropes (medications that decrease contractility, such as
beta blockers).
 Contractility increased with:
 Sympathetic stimulation (effects of epinephrine)
 Positive inotropes (medications that increase contractility, such as
digoxin, sympathomimmetics

28. Neural control of circulatory function

29. Autonomic nerve impulses alter the
activities of the S-A and A-V nodes
Regulation of the cardiac cycle

30. Summary of long term BP control
 Cardiac output and BP depend on renal control of
extra-cellular fluid volume via:
 Pressure natriuresis, (increased renal filtration)
 Changes in:
Vasopressin
Aldosterone
Atrial natiuretic peptide
All under the control of altered cardiovascular
receptor signaling

31. Arginine Vasopressin (AVP)
• Enhances water retention
• Causes vasoconstriction
• Secretion increased by aortic baroreceptors and
atrial sensors

32. Baroreceptor reflex
Blood pressure falls
Aortic arch Carotid sinus
Constriction of veins
& arterioles
Increased stroke
volume
Increased heart
rate
Vasoconstriction Cardiac stimulation Cardiac inhibition
Nucleus tractus solitarius
Increased peripheral
resistance
Increased cardiac
output
Increased blood
pressure
Neural integration
Sensors
Effectors

33. Disorders of blood flow and
blood pressure

34. Blood Pressure
 Blood pressure is probably one of the most important
measures of the overall cardiovascular system
 Normal blood pressure is determined by the cardiac
output, the velocity, the resistance of the blood
vessels
 Systolic pressure refers to the initial force of
contraction of the heart.
 Diastolic pressure refers to the pressure of the blood
vessels after the initial force of contraction of the heart.

35. HYPERTENSION
 Factors Influencing Blood Pressure
Blood Pressure = Cardiac Output x Systemic Vascular
Resistance

36. Problem Magnitude
 In Uganda the overall prevalence of 26.4%.
 Prevalence was highest in the central region at 28.5%
 Followed by the eastern region at 26.4%
 Western region at 26.3%
 Northern region at 23.3%.
 Prevalence in urban areas was 28.9%, and 25.8%
in rural areas.
 Worldwide prevalence estimates for HTN may be as much as 1
billion.
 7.1 million deaths per year may be attributable to hypertension.

37. Definition
• A systolic blood pressure ( SBP) >139 mmHg and/or
• A diastolic (DBP) >89 mmHg.
• Based on the average of two or more properly
measured, seated BP readings.
• On each of two or more office visits.

38. Follow-up based on initial BP
measurements for adults*
*Without acute end-organ damage
www.nhlbi.nih.gov

39. Classification
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40. Prehypertension
• SBP >120 mmHg and <139mmHg and/or
• DBP >80 mmHg and <89 mmHg.
• Prehypertension is not a disease category
rather a designation for individuals at high
risk of developing HTN.

41. Pre-HTN
• Individuals who are prehypertensive are
not candidates for drug therapy but
• Should be firmly and unambiguously
advised to practice lifestyle modification
• Those with pre-HTN, who also have
diabetes or kidney disease, drug therapy
is indicated if a trial of lifestyle
modification fails to reduce their BP to
130/80 mmHg or less.

42. Isolated Systolic Hypertension
• Not distinguished as a separate entity as
far as management is concerned.
• SBP should be primarily considered
during treatment and not just diastolic
BP.
• Systolic BP is more important
cardiovascular risk factor after age 50.
• Diastolic BP is more important before age
50.

43. Hypertensive Crises
• Hypertensive Urgencies: No progressive target-organ dysfunction.
(Accelerated Hypertension)
• Hypertensive Emergencies: Progressive end-organ dysfunction.
(Malignant Hypertension)
• Severe elevated BP in the upper range of stage II hypertension.
• Without progressive end-organ dysfunction.
• Examples: Highly elevated BP without severe headache,
shortness of breath or chest pain.
• Usually due to under-controlled HTN.

44. Hypertensive Urgencies
• Severe elevated BP in the upper range of
stage II hypertension.
• Without progressive end-organ
dysfunction.
• Examples: Highly elevated BP without
severe headache, shortness of breath or
chest pain.
• Usually due to under-controlled HTN.

45. Hypertensive Emergencies
• Severely elevated BP (>180/120mmHg).
• With progressive target organ dysfunction.
• Require emergent lowering of BP.
• Examples: Severely elevated BP with:
 Hypertensive encephalopathy
 Acute left ventricular failure with pulmonary
edema
 Acute MI or unstable angina pectoris
 Dissecting aortic aneurysm

46. Types of Hypertension
 Primary HTN:
also known as essential HTN.
accounts for 95% cases of HTN.
no universally established cause known.
 Secondary HTN:
less common cause of HTN ( 5%).
secondary to other potentially rectifiable
causes.

47. Causes of Secondary HTN
 Common
 Intrinsic renal disease
 Renovascular disease
 Mineralocorticoid excess
 Sleep Breathing disorder
 Uncommon
 Pheochromocytoma
 Glucocorticoid excess
 Coarctation of Aorta
 Hyper/hypothyroidism

48. Complications of Prolonged
Uncontrolled HTN
• Changes in the vessel wall leading to vessel
trauma and arteriosclerosis throughout the
vasculature
• Complications arise due to the “target organ”
dysfunction and ultimately failure.
• CVS (heart and blood vessels
• Kidneys
• Nervous system
• Eyes
• Damage to the blood vessels can be seen on
fundoscopy.

49. Atherosclerosis

50. • Effects On CVS
• Ventricular hypertrophy, dysfunction and failure.
• Arrhythmias
• Coronary artery disease, Acute MI
• Arterial aneurysm, dissection, and rupture.
• Effects on the kidneys
• Glomerular sclerosis leading to impaired kidney function and
finally end stage kidney disease.
• Ischemic kidney disease especially when renal artery stenosis
is the cause of HTN

51. • Effect on the nervous system
• Stroke, intracerebral and subarachnoid hemorrhage.
• Cerebral atrophy and dementia
• Effect on the eyes
• Retinopathy, retinal hemorrhages and impaired
vision.
• Vitreous hemorrhage, retinal detachment
• Neuropathy of the nerves leading to extraoccular
muscle paralysis and dysfunction

52. Retina Normal and
Hypertensive Retinopathy
Normal Retina Hypertensive Retinopathy
A: Hemorrhages
B: Exudates (Fatty Deposits)
C: Cotton Wool Spots (Micro
Strokes)
A B
C

53. Patient Evaluation Objectives
 (1) To assess lifestyle and identify
other cardiovascular risk factors or
concomitant disorders that may affect
prognosis and guide treatment
 (2) To reveal identifiable causes of
high BP
 (3) To assess the presence or absence
of target organ damage and CVD

54. (1) Cardiovascular Risk factors
• Hypertension
• Cigarette smoking
• Obesity (body mass index ≥30 kg/m2)
• Physical inactivity
• Dyslipidemia
• Diabetes mellitus
• Microalbuminuria or estimated GFR <60 mL/min
• Age (older than 55 for men, 65 for women)
• Family history of premature cardiovascular disease
(men under age 55 or women under age 65)

55. (2) Identifiable Causes of HTN
• Sleep apnea
• Drug-induced or related causes
• Chronic kidney disease
• Primary aldosteronism
• Renovascular disease
• Chronic steroid therapy and Cushing’s
syndrome
• Pheochromocytoma
• Coarctation of the aorta
• Thyroid or parathyroid disease

56. (3) Target Organ Damage
• Heart
 Left ventricular hypertrophy
 Angina or prior myocardial infarction
 Prior coronary revascularization
 Heart failure
• Brain
 Stroke or transient ischemic attack
• Chronic kidney disease
• Peripheral arterial disease
• Retinopathy

57. Disorders of cardiac function

58. Ductus Arteriosus
• An opening in fetal circ. between the pulmonary
artery (PA) and aorta (Ao).
• In fetal circulation, most of the blood bypasses
the lungs and returns to systemic circulation by way
of the PDA (PA to Ao).
• In transition to pulmonary circulation, the PDA
constricts over 10-15hrs; permanent closure should
occur by 3wks of age,
UNLESS SATURATION REMAINS LOW

59. Image

60. Hypoxemia in the infant
• Below 95% pulse oximetry.
• Cyanosis results from hypoxemia
• Perioral cyanosis indicates central hypoxemia
• Acrocyanosis does not.

61. Response to Hypoxemia
• Acute: HR increases
• Chronic: bone marrow produces more RBC
to increase the amount of Hgb available
for oxygen transport.
• Hct>50 is called polycythemia.
• Increased blood viscosity increases risk of
thromboembolism.

62. Cardiac Functioning
• 02 requirements are high the first few
weeks of life
• Normally, HR increases to provide
adequate oxygen transport
• Infant has little cardiac output reserve
capacity
• Cardiac output depends almost
completely on HR until the heart is fully
developed (age 5 yr).

63. Compliance in the infant
• In infancy, muscle fibers are less
developed and organized
• Results in less functional capacity or less
compliance
• Less compliance means the infant is
unable or less able to distend or expand
the ventricles to achieve an increase
stroke volume in order to compensate for
increased demands.

64. Severe Hypoxemia
• children respond with bradycardia
• cardiac arrest generally results from
prolonged hypoxemia related to respiratory
failure or shock
• in adults, hypoxemia usually results from
direct insult to the heart.
• therefore, in children, bradycardia is a
significant warning sign of cardiac arrest.
• appropriate Rx for hypoxemia reverses
bradycardia.

65. Pulmonary Artery
Hypertension
• Irreversible condition that results from R sided
heart circulation being overloaded and therefore
shunting excessive blood to the lungs.
• Overloads the R side of the heart, overloads the
pulmonary system causing increased pulmonary
vascular resistance (life threatening).

66. Obstructive Congenital
Defects
• Due to abnormally small pulmonary vessels
• Which restrict flow of blood, so the heart
hypertrophies to work harder to provide
the blood flow to organs.
• However, CO increases initially but
eventually hypertrophied muscle becomes
ineffective.
• Initially R sided failure, progressing to L
sided and eventual bilateral failure

67. CHF in the infant
• Can be subtle
• Good assessment skills are a must
• Tires easily, especially during feeding
• Initial weight loss
• Diaphoresis, irritability, frequent
infection.

68. CHF in older children
• Exercise intolerance
• Dyspnea
• Abdominal pain or distention
• Peripheral edema.

69. Symptoms of progressive
disease
• Tachycardia, tachypnea, pallor or
cyanosis, F/G/R, cough, crackles.
• Fluid volume overload: periorbital and
facial edema, JVD, hepatomegaly, ascites.
• Increased weight gain, bounding pulses,
edema of dependent body parts.

70. Cardiomegaly
• Occurs at the heart attempts to maintain
CO
• If CHF is not adequately treated,
precursors of Cardiogenic Shock arise:
cyanosis, weak peripheral pulses, cool
extremities, hypotension, heart murmurs
• Clarification: not all heart murmurs are
heralding cardiogenic shock.

71. Congenital Heart Disease
(CHD)
• Refers to a defect in the heart, great
vessels or persistence of a fetal structure
• Occurs in 1% live births
• Higher incidence in still births and
aborted fetuses
• Incidence has declined over past 25 yrs
d/t technological advances in
intrauterine assessment, surgical
techniques and intensive care

72. Factors that increase risk for
having a child with CHD
• Family hx of CHD
• Maternal age >35yr
• Coexisting maternal disease: DM, collagen vascular
disease, PKU
• Exposure to teratogens or rubella infection

73. CHD
• Most CHD develop during first 8 wks of gestation
• Usually result of combined genetic and
environmental interaction
 Fetal exposure to drugs: phenytoin &
lithium
 Maternal viral infections: rubella
 Maternal metabolic disorders: DM, PKU
 Maternal complications of pregnancy
i.e. increased age, antepartum bleeding

74. CHD etiologies cont.
 genetic factors: familial patterns
 chromosomal abnormalities: most
common is Down’s syndrome with 40%
occurrence rate of CHD.
defects are divided into cyanotic and
acyanotic (in pure form).

75. Acyanotic Heart Defects
• Constitutes the majority of heart defects in children
• Two types: obstructive and non-obstructive
• Obstructive: PS, AoS, Coarc.
• Non-obstructive: PDA, ASD, AV canal (endocardial cushion)
defect, VSD.

76. Cyanotic Heart Defects
• Generally caused by a valvular or vascular
formation
• ex: Tetralogy of Fallot, Transposition,
hypoplastic LV, tricuspid atresia,
pulmonary atresia, truncus arteriosus, and
total anomalous venous return.

77. Acyanotic; non-obstructive
lesions
• PDA
• ASD
• AV canal
• VSD

78. Pathophysiology of Acyanotic,
non-obstructive CHD
• openings in the septal wall cause a L to R
shunt
• oxygenated blood mixes with
deoxygenated blood
• volume overload to the pulmonary system
• can cause CHF
• PHT occurs d/t chronic volume overload
to the lungs if uncorrected.

79. Patent Ductus Arteriosus
• common; 9-12% of all CHD
• persistent fetal structure
• when the PDA remains open, blood is shunted from
the Aorta to the Pulmonary artery, therefore
increasing blood flow to the lungs: L to R.
• bounding pulses, dyspnea, tachypnea, FTT.
• at risk for frequent URI and endocarditis, CHF.
• continuous systolic murmur and thrill palpable.

80. PATENT DUCTUS ARTERIOSUS

81. Treatment of a PDA
• surgical ligation; transcatheter closure
>18mos of age.
• Indomethacin may stimulate closure in
premies
• Prostaglandin helps to keep the PDA open
until surgical correction is optimal.
• left untreated, LVH, pulmonary
hypertension (PHT) and vascular
obstructive disease develop.

82. Atrial Septal Defect; ASD
• opening in the atrial shunting
• L to R shunting
• accounts for 6-10% of CHD
• small to moderate size may go undiagnosed
until preschool years or later
• sx of large ASD: CHF, tiring easily, poor
growth
• soft systolic murmur heard in pulmonic
space; wide S2 split.

83. ATRIAL SEPTAL DEFECT

84. Treatment of ASD
• Echo shows RV overload and shunt size
• C-xray and EKG may be normal unless a
large shunt
• surgery to close or a patch via catheter
during Cardiac Cath.
• atrial arrhythmias can be a late sign or
associated with a large ASD involving
conduction system in the septum

85. FIGURE 26–7 A, Septal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect (VSD). B, Coil used to close a
patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when a thrombus forms in the mass of fabric and wire.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.

86. Atrioventricular Canal:
Endocardial Cushion Defect
• accounts for 4-5% of CHD
• partial or complete ASD/VSD with some
degree of involvement of mitral/tricuspid
valves variable
• associated with Down’s syndrome
• severity of sx depends on degree of mitral
regurgitation.
• sx in infants: CHF, tachypnea, tachycardia,
FTT, increased URI, systolic murmur.

87. Treatment of AV Canal
• surgery during infancy to prevent PHT
• patches placed over septal defects; mitral
valve replacement
• arrhythmias and mitral valve insufficiency
occur post/op
• no difference between short term survival
rates in infants with or without Down’s
syndrome.

88. Ventricular Septal Defect; VSD
• opening in the ventricular septum
• shunts L to R; increases pulmonary blood
flow
• most common: accounts for 20% CHD
• only 15% large enough to generate
symptoms: tachypnea, dyspnea, FTT,
reduced fluid intake, CHF, PHT.
• systolic murmur ; LLSB
• most small VSD close spontaneously

89. Treatment of VSD
• if no sx CHF or PHT, treatment is
conservative
• surgical patching during infancy if FTT
• closure by transcatheter device during
Cardiac Cath for some defects:
• prophylaxis for infective endocarditis is
required
• high risk for surgical repair in first few
months of life

90. Acyanotic; obstructive lesions
• PS
• AoS
• Coarctation of the Aorta

91. Pathophysiology of Acyanotic, obstructive CHD
• narrowing across the valves causes
pressure overload and hypertrophy of the
closest ventricle
• child will have a murmur
• some experience fatigue and exercise
intolerance d/t inability to increase CO
• many are asymptomatic and grow normally
• older children: exercise induced dizziness
and syncope: requires immediate attention

92. Pulmonary Stenosis: PS
• narrowing of the pulmonary valve or
valvular area
• obstructs flow to the PA
• increases pre-load; results in RVH
• second most common CHD
• accounts for 8-12% of CHD
• systolic murmur with fixed split S2 in
Pulmonic area.

93. Treatment of PS
• dx usually made at birth with murmur
auscultated
• C-xray may show heart enlargement
• EKG may demonstrate RVH
• echo provides information regarding
pressure gradient across the valve
• may dilate during Cardiac Cath using balloon
valvuloplasty or valvular replacement
• lifelong endocarditis prophylaxis is required

94. Aortic Stenosis: AoS
• narrowing of the aortic valve; obstructs blood
flow to systemic circulation
• accounts for 3-6% of CHD; progressive during
childhood
• often associated with bicuspid rather than normal
tricuspid aortic valve.
• asymptomatic, grow normally; BP wnl but may
have a narrow pulse pressure
• systolic murmur; thrill in Ao; chest pain. after
exercise.

95. Treatment of AoS
• C-xray and EKG are usually normal if mild
• echo can reveal number of valve leaflets,
pressure gradient across the valve, and
size of the aorta.
• surgical valvuloplasty or dilated with
balloon during cardiac cath.
• valvular replacement
• requires lifelong SBE prophylaxis

96. Coarctation of the Aorta
• narrowing or obstruction of descending Ao.
• obstructs systemic blood flow
• accounts for 5-8% CHD
• grow normally but constriction is progressive
• lower BP in LE and higher in UE, neck, head.
• pulse weak or absent in LE; full/bounding in
UE

97. COARCTATION OF AORTA

98. Treatment of Coarctation of
the Aorta
• EKG shows LVH
• c-xray reveals enlargement and pulmonary venous
congestion and constricted aorta
• balloon dilation in cardiac cath or surgical
resection/anastomosis/patch.
• risks of reoccurrence, persistent HTN in
adulthood, 20% develop post-coarctectomy
syndrome (abdominal pain and distention).
• SBE prophylaxis needed.

99. Cyanotic Heart Defects
• Tetralogy of Fallot
• Transposition of the Great Vessels
• caused by malformation or a combination
of defects that prevent adequate level of
oxygenation
• R to L shunt occurs resulting in chronic
hypoxemia and cyanosis.

100. Pathophysiology of Cyanotic
Heart Disease
• P02 is lower than normal; PC02 rises
• hypoxemia becomes progressively worse
as respiratory center overreacts and
increased respiratory effort
• increased respiratory effort attempts to
increase P02
• at risk for thromboembolism d/t
hypoxemia causing polycythemia

101. Clinical Manifestations of
Cyanotic Heart Disease
• chronic hypoxemia causes fatigue, clubbing,
exertional dyspnea, delayed milestones, tire easily
with feeding, reduced growth, CHF
• Hyper-cyanotic (hypoxic) spells: increased rate
and depth of respiration, increased cyanosis,
increased HR, pallor and poor perfusion, agitation
and irritability.

102. Tetralogy of Fallot
• combination of four defects
pulmonary stenosis: degree determines
severity
VSD
over-riding of the aorta(the aorta is
positioned directly over a ventricular
septal defect, instead of over the left
ventricle)
RVH
• accounts for 10% of CHD
• elevated R sided pressures: R to L shunt
• xray: boot shaped heart d/t RVH
• risk for metabolic acidosis and syncope.

103. TETRALOGY OF FALLOT

104. Treatment of TOF
• total repair is done by 6 mo if cyanotic
spells
• surgery is not necessarily curative, but
most have improved quality of life and
improved longevity
• residual problems: arrhythmias and RV
dysfunction
• lifelong SBE required

105. Transposition of the Great
Arteries: TGA
• position of the PA and Ao are switched
• life threatening at birth; cyanosis,
hypoxia, acidosis
• cyanosis does not improve with 02 admin
• survival depends upon a patent DA and
foramen ovale
• accounts for 5% of CHD
• may be associated with an ASD or VSD

106. TRANSPOSITION OF THE GREAT VESSELS

107. Treatment of TGA
• prostaglandin E1 used to keep PDA open until
palliative procedure
• corrective surgery (artery switch) usually
performed by 1 wk of age
• balloon atrial septostomy during cardiac cath may
be used to open foramen ovale
• survival depends upon surgery; risk for arrhythmia,
SBE, RV failure, sudden death.

108. Pulmonary Artery
Hypertension: PHT
• increased load to the lungs causes
pulmonary vascular changes in an attempt
to decrease the blood flow
• inflammation, hypertrophy of the
pulmonary vessels and fibrosis develop
• pulmonary venous hypertension develops
and leads to R to L shunting, with R sided
heart function impaired.
• life threatening: irreversible

109. GENERAL S & S of CHD in
INFANTS AND CHILDREN
 INFANTS:
 Dyspnea
 Difficulty feeding
 Stridor, choking spells
 Pulse rate over 200
 FTT
 Heart murmurs
 Frequent URI’s
 Anoxic attacks
 CVA
 CHILDREN:
 Exercise intolerance
 Increased BP
 Poor physical development
 Heart murmurs
 Cyanosis
 Recurrent URI
 Clubbing fingers/toes
 squatting

110. Valvular Heart Disease
• STENOSIS:
• heart valve that does not open
properly
• REGURGITATION:
• leaking heart valves

112. Heart failure and
circulatory shock

113. Congestive Heart
Failure

114. Types of Heart Failure
 Low-Output Heart Failure
 Systolic Heart Failure:
 decreased cardiac output
 Decreased Left ventricular ejection fraction
 Diastolic Heart Failure:
 Elevated Left and Right ventricular end-diastolic pressures
 May have normal LVEF
 High-Output Heart Failure
 Seen with peripheral shunting, low-systemic vascular resistance,
hyperthryoidism, beriberi, carcinoid, anemia
 Often have normal cardiac output
 Right-Ventricular Failure
 Seen with pulmonary hypertension, large RV infarctions.

115. Causes of Low-Output Heart Failure
 Systolic Dysfunction
 Coronary Artery Disease
 Idiopathic dilated cardiomyopathy (DCM)
 50% idiopathic (at least 25% familial)
 9 % mycoarditis (viral)
 Ischemic heart disease, perpartum,
hypertension, HIV, connective tissue disease,
substance abuse, doxorubicin
 Hypertension
 Valvular Heart Disease
 Diastolic Dysfunction
 Hypertension
 Coronary artery disease
 Hypertrophic obstructive cardiomyopathy (HCM)
 Restrictive cardiomyopathy

116. Clinical Presentation of Heart Failure
 Due to excess fluid accumulation:
 Dyspnea (most sensitive symptom)
 Edema
 Hepatic congestion
 Ascites
 Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
 Due to reduction in cardiac output:
 Fatigue (especially with exertion)
 Weakness

117. Cardiomegaly

118. Pulmonary vessel congestion

119. Pulmonary Edema due to Heart Failure

120. Classification of Heart Failure
 New York Heart Association (NYHA)
Class I – symptoms of HF only at levels
that would limit normal individuals.
Class II – symptoms of HF with
ordinary exertion
Class III – symptoms of HF on less than
ordinary exertion
Class IV – symptoms of HF at rest

121. Classification of Heart Failure
 ACC/AHA Guidelines
Stage A – High risk of HF, without
structural heart disease or symptoms
Stage B – Heart disease with
asymptomatic left ventricular
dysfunction
Stage C – Prior or current symptoms of
HF
Stage D – Advanced heart disease and
severely symptomatic or refractory HF

122. Chronic Treatment of Systolic Heart Failure
 Correction of systemic factors
 Thyroid dysfunction
 Infections
 Uncontrolled diabetes
 Hypertension
 Lifestyle modification
 Lower salt intake
 Alcohol cessation
 Medication compliance
 Maximize medications
 Discontinue drugs that may contribute to heart
failure (NSAIDS, anti-arrhythmics, calcium
channel blockers)

123. Management of Refractory Heart Failure
 Inotropic drugs:
 Dobutamine, dopamine, milrinone, nitroprusside, nitroglycerin
 Mechanical circulatory support:
 Intra-aortic balloon pump
 Left ventricular assist device (LVAD)
 Cardiac Transplantation
 A history of multiple hospitalizations for HF
 Escalation in the intensity of medical therapy
 A reproducable peak oxygen consumption with
maximal exercise (VO2max) of < 14 mL/kg per min.
(normal is 20 mL/kg per min. or more) is relative
indication, while a VO2max < 10 mL/kg per min is a
stronger indication.

124. Acute Decompensated Heart Failure
• Cardiogenic pulmonary edema is a
common and sometimes fatal cause of
acute respiratory distress.
• Characterized by the transudation of
excess fluid into the lungs secondary to an
increase in left atrial and subsequently
pulmonary venous and pulmonary capillary
pressures.

125. Acute Decompensated Heart Failure
 Causes:
Acute MI
Rupture of chordae tendinae/acute
mitral valve insufficiency
Volume Overload
Transfusions, IV fluids
Non-compliance with diuretics, diet
(high salt intake)
Worsening valvular defect
Aortic stenosis

126. Decompensated Heart Failure
 Symptoms
 Severe dyspnea
 Cough
 Clinical Findings
 Tachypnea
 Tachycardia
 Hypertension/Hypotension
 Crackles on lung exam
 Increased JVD
 S3, S4 or new murmur

127. Decompensated Heart Failure
 Treatment
 Strict I’s and O’s, daily weights
 Oxygen, mechanical ventilation if
needed
 Loop diuretics (Lasix)
 Morphine
 Vasodilator therapy (nitroglycerin)
 Nesiritide (BNP) – can help in acute
setting, for short term therapy

128. Shock

129. Definition of Shock
• Inadequate oxygen delivery to meet
metabolic demands
• Results in global tissue hypoperfusion and
metabolic acidosis
• Shock can occur with a normal blood
pressure and hypotension can occur
without shock

130. Understanding Shock
• Inadequate systemic oxygen delivery activates autonomic
responses to maintain systemic oxygen delivery
• Sympathetic nervous system
• NE, epinephrine, dopamine, and cortisol release
• Causes vasoconstriction, increase in HR, and
increase of cardiac contractility (cardiac output)
• Renin-angiotensin axis
• Water and sodium conservation and vasoconstriction
• Increase in blood volume and blood pressure

131. Understanding Shock
• Cellular responses to decreased systemic oxygen
delivery
• ATP depletion ion pump dysfunction
→
• Cellular edema
• Hydrolysis of cellular membranes and
cellular death
• Goal is to maintain cerebral and cardiac perfusion
• Vasoconstriction of splanchnic,
musculoskeletal, and renal blood flow
• Leads to systemic metabolic lactic acidosis that
overcomes the body’s compensatory mechanisms

132. Global Tissue Hypoxia
• Endothelial inflammation and disruption
• Inability of O2 delivery to meet demand
• Result:
• Lactic acidosis
• Cardiovascular insufficiency
• Increased metabolic demands

133. Multiorgan Dysfunction Syndrome (MODS)
• Progression of physiologic effects as shock ensues
• Cardiac depression
• Respiratory distress
• Renal failure
• DIC
• Result is end organ failure

134. Approach to the Patient in Shock
• History
• Recent illness
• Fever
• Chest pain, SOB
• Abdominal pain
• Comorbidities
• Medications
• Toxins/Ingestions
• Recent hospitalization
or surgery
• Baseline mental status
• Physical examination
• Vital Signs
• CNS – mental status
• Skin – color, temp,
rashes, sores
• CV – JVD, heart sounds
• Resp – lung sounds, RR,
oxygen sat, ABG
• GI – abd pain, rigidity,
guarding, rebound
• Renal – urine output

135. Shock
• Do you remember how to
quickly estimate blood
pressure by pulse?
60
80
70
90
• If you palpate a pulse,
you know SBP is at
least this number.

136. End Points of Resuscitation
• Goal of resuscitation is to maximize survival
and minimize morbidity
• Use objective hemodynamic and physiologic
values to guide therapy
• Goal directed approach
• Urine output > 0.5 mL/kg/hr
• CVP 8-12 mmHg
• MAP 65 to 90 mmHg
• Central venous oxygen concentration > 70%

137. Persistent Hypotension
• Inadequate volume resuscitation
• Pneumothorax
• Cardiac tamponade
• Hidden bleeding
• Adrenal insufficiency
• Medication allergy

138. Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

139. Hypovolemic Shock

140. Hypovolemic Shock
• Non-hemorrhagic
• Vomiting
• Diarrhea
• Bowel obstruction, pancreatitis
• Burns
• Neglect, environmental (dehydration)
• Hemorrhagic
• GI bleed
• Trauma
• Massive hemoptysis
• AAA rupture
• Ectopic pregnancy, post-partum bleeding

141. Hypovolemic Shock
• ABCs
• Establish 2 large bore IVs or a central line
• Crystalloids
• Normal Saline or Lactate Ringers
• Up to 3 liters
• PRBCs
• O negative or cross matched
• Control any bleeding
• Arrange definitive treatment

142. Evaluation of Hypovolemic Shock
• CBC
• ABG/lactate
• Electrolytes
• BUN, Creatinine
• Coagulation studies
• Type and cross-match
• As indicated
• CXR
• Pelvic x-ray
• Abd/pelvis CT
• Chest CT
• GI endoscopy
• Bronchoscopy
• Vascular radiology

143. Septic Shock

144. Sepsis
• Two or more of SIRS criteria
• Temp > 38 or < 36 C
• HR > 90
• RR > 20
• WBC > 12,000 or < 4,000
• Plus the presumed existence of
infection
• Blood pressure can be normal!

145. Septic Shock
• Sepsis
• Plus refractory hypotension
• After bolus of 20-40 mL/Kg patient
still has one of the following:
• SBP < 90 mm Hg
• MAP < 65 mm Hg
• Decrease of 40 mm Hg from
baseline

146. Pathogenesis of Sepsis
Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.

147. Septic Shock
• Clinical signs:
• Hyperthermia or hypothermia
• Tachycardia
• Wide pulse pressure
• Low blood pressure (SBP<90)
• Mental status changes
• Beware of compensated shock!
• Blood pressure may be “normal”

148. Cardiogenic Shock

149. Cardiogenic Shock
• Signs:
• Cool, mottled
skin
• Tachypnea
• Hypotension
• Altered mental
status
• Narrowed pulse
pressure
• Rales, murmur
• Defined as:
• SBP < 90 mmHg
• CI < 2.2 L/m/m2
• PCWP > 18 mmHg

150. Etiologies
• What are some causes of cardiogenic shock?
• AMI
• Sepsis
• Myocarditis
• Myocardial contusion
• Aortic or mitral stenosis, HCM
• Acute aortic insufficiency

151. Pathophysiology of Cardiogenic Shock
• Often after ischemia, loss of LV function
• Lose 40% of LV clinical shock ensues
• CO reduction = lactic acidosis, hypoxia
• Stroke volume is reduced
• Tachycardia develops as
compensation
• Ischemia and infarction worsens

152. Treatment of Cardiogenic Shock
• Goals- Airway stability and improving
myocardial pump function
• Cardiac monitor, pulse oximetry
• Supplemental oxygen, IV access
• Intubation will decrease preload and result
in hypotension
• Be prepared to give fluid bolus

153. Anaphylactic Shock

154. Anaphylactic Shock
• Anaphylaxis – a severe systemic
hypersensitivity reaction characterized by
multisystem involvement
• IgE mediated
• Anaphylactoid reaction – clinically
indistinguishable from anaphylaxis, do not
require a sensitizing exposure
• Not IgE mediated
• occur through a direct nonimmune-
mediated release of mediators from
mast cells and/or basophils or result
from direct complement activation.

155. Anaphylactic Shock
• What are some symptoms of anaphylaxis?
• First- Pruritus, flushing, urticaria appear
• Next- Throat fullness, anxiety, chest tightness,
shortness of breath and
lightheadedness
• Finally- Altered mental status, respiratory
distress and circulatory collapse

156. Anaphylactic Shock
• Risk factors for fatal anaphylaxis
• Poorly controlled asthma
• Previous anaphylaxis
• Reoccurrence rates
• 40-60% for insect stings
• 20-40% for radiocontrast agents
• 10-20% for penicillin
• Most common causes
• Antibiotics
• Insects
• Food

157. Anaphylactic Shock- Diagnosis
• Clinical diagnosis
• Defined by airway compromise,
hypotension, or involvement of
cutaneous, respiratory, or GI systems
• Look for exposure to drug, food, or insect
• Labs have no role

158. Neurogenic Shock

159. Neurogenic Shock
• Occurs after acute spinal cord injury
• Sympathetic outflow is disrupted
leaving unopposed vagal tone
• Results in hypotension and bradycardia
• Spinal shock- temporary loss of spinal
reflex activity below a total or near
total spinal cord injury (not the same
as neurogenic shock, the terms are not
interchangeable)

160. Neurogenic Shock
• Loss of sympathetic tone results in
warm and dry skin
• Shock usually lasts from 1 to 3
weeks
• Any injury above T1 can disrupt the
entire sympathetic system
• Higher injuries = worse
paralysis

161. Neurogenic Shock- Treatment
• A,B,Cs
• Remember c-spine precautions
• Fluid resuscitation
• Keep MAP at 85-90 mm Hg for first
7 days
• Thought to minimize secondary
cord injury
• If crystalloid is insufficient use
vasopressors
• Search for other causes of hypotension
• For bradycardia
• Atropine
• Pacemaker

162. Obstructive Shock

163. Obstructive Shock
• Tension pneumothorax
• Air trapped in pleural space with 1 way
valve, air/pressure builds up
• Mediastinum shifted impeding venous
return
• Chest pain, SOB, decreased breath sounds
• No tests needed!
• Rx: Needle decompression, chest tube

164. Obstructive Shock
• Cardiac tamponade
• Blood in pericardial sac prevents
venous return to and contraction of
heart
• Related to trauma, pericarditis, MI
• Beck’s triad: hypotension, muffled
heart sounds, JVD
• Diagnosis: large heart CXR, echo
• Rx: Pericardiocentisis

165. Obstructive Shock
• Pulmonary embolism
• Virscow triad:
hypercoaguable, venous
injury, venostasis
• Signs: Tachypnea, tachycardia,
hypoxia
• Low risk: D-dimer
• Higher risk: CT chest or VQ
scan
• Rx: Heparin, consider
thrombolytics

166. Obstructive Shock
• Aortic stenosis
• Resistance to systolic ejection
causes decreased cardiac function
• Chest pain with syncope
• Systolic ejection murmur
• Diagnosed with echo
• Vasodilators (NTG) will drop
pressure!
• Rx: Valve surgery

167. Pregnancy
 Physiological edema
 Renin and aldosterone activity are increased by
estrogens, progesterone and prostaglandins, leading to
increased fluid and electrolyte retention.
 Physiological anemia
 The total plasma volume is increase in higher
percentage in comparison to RBC which result in
hemodilution

168.  Decrease blood pressure
 Increase cardiac output leads to decreased arterial
blood pressure by 10%, therefore resistance to flow
must be decreased. In addition this can be result in
decrease in systemic vascular resistance,
particularly in the peripheral vessels. The decrease
begins at 5 weeks' gestation, reaches a nadir in the
second trimester (a 21% reduction) and then
gradually rises as term approaches

169. Supine hypotensive syndrome
 The enlarging uterus compresses both the
inferior vena cava and the lower aorta
when the woman lies in supine position.
This reduces venous return to the heart
this condition happen in 10% of pregnant
women.
 Sign of supine hypotension
• hypotension, bradycardia, dizziness, light-
headedness.