jp advis dvm, ph.d. bartlett hall, animal sciences, cook...
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Pathophysiology 13 • JP Advis DVM, Ph.D.
Bartlett Hall, Animal Sciences, Cook,
932 - 9240, advis@aesop.rutgers.edu
• Course website: rci.rutgers.edu/~advis
• Lectures, tests, grades, office hours, textbook,
• Material to
be covered:
• About
lecture
slides:
• There are not intended to be the sole source for studying the course material !!!!!!!!!!!!!!!!
• Slides are good to review the course material after you have study your course textbook
• Slides are a good indicator of the relative importance of lecture topics (see slide # per topic
• Group slides by titles when using them to review course material. Match lectures and text.
Lectures 1-2: Introduction to Pathophysiology (2) Lectures 3-4: Mechanisms of Self-Defense and Stress (2)
Lectures 5-8: Endocrine and Nervous System Dysfunctions (4) Lecture 9: Alterations of Skeletal Muscle Function (1)
REVIEW AND TEST #1 Lectures 12-18: Cardiovascular, Respiratory and Renal Dysfunctions (7)
REVIEW AND TEST #2
Lectures 21-24: Alterations of Digestive Function and Intermediary Metabolism (4) Lectures 25-26: Alterations of the Reproductive System (2)
REVIEW AND TEST #3
Arteriosclerosis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Arteriosclerosis, is a chronic disease of the arterial system
characterized by abnormal thickening and hardening of vessel
walls. Smooth muscle cells and collagen fibers migrate into the tunica intima, causing it to stiffen and thicken, thus decreasing
the artery’s ability to change lumen size.
Atherosclerosis, is the common form of arteriosclerosis in
which thickening of vessel walls is caused by hardening of soft deposits of intra-arterial fat and fibrin that reduces lumen size. It
is the leading contributor to coronary artery & cerebrovascular
disease.
The process leading to atherosclerosis (atherogenesis), begins with injury to endothelial cells and their inability to produce anti-
thrombic and vasodilating cytokines. Macrophages adhere to
injured endothelial cells and release O2 radicals that result in
oxidation of LDL. When this are engulfed by macrophages are
called “foam cells”, which accumulate to form the “fatty streak”.
Arteriosclerosis, a chronic disease of arteries is characterized by
abnormal thickening and hardening of vessel walls.
Page 2
Arteriosclerosis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
The lesions of atherosclerosis occur primarily within the tunica
intima or the innermost layer. They include fatty streaks, fibrous
plaquse, and the complicated lesions. The early fatty streak is a flat, yellow, lipid-filled smooth muscle cell that causes no
obstruction of the affected vessel.
Fibrous plaque, the characteristic lesion of advancing athero-
sclerosis consist of lipid-laden smooth muscle cell surrounded by collagen, elastic fibers, and mucoprotein matrix. The lesion is
elevated and protrudes into the lumen of the artery, it fixes to the
inner wall of the tunica intima, and may invade the muscular
tunica media. It probably originates from fatty streaks, and has
lipids and debris from cellular necrosis caused by insufficient blood supply. It occludes arterial lumen at arterial bifurcations,
curves, or regions were arteries taper.
Complicated lesions occurs as fibrous plaques are altered by
hemorrhage, calcification, cell necrosis, and blood clots and the intima layer becomes rigid causing extensive vascular occlusion.
Arteriosclerosis, a chronic disease of arteries is characterized by
abnormal thickening and hardening of vessel walls.
Arteriosclerosis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Arteriosclerosis, a chronic disease of arteries is characterized by
abnormal thickening and hardening of vessel walls.
normal artery diseased occluded artery
adventitia
tunica intima
tunica
media
Page 3
Atherosclerosis Progression
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Atherosclerosis is the most common form of arteriosclerosis
Page 4
Atherosclerosis Progression
Arteriosclerosis arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left
failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Progression of atherosclerosis: Basic physiology on the endo-
thelium regulation of vasomotion (constriction and dilation) and
platelet aggregation
Page 5
Atherosclerosis Progression
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Progression of atherosclerosis: Basic physiology on the factors that
cause endothelium – dependent vasodilation. Injured endothelial
cells do not make normal amounts of antithrombic and vasodilating cytokines.
Smooth muscle relaxation
Smooth muscle relaxation
Page 6
Atherosclerosis Progression
Arteriosclerosis arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left
failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Progression of atherosclerosis: low density lipoprotein (LDL)
enters the arterial intima through an intact endothelium. In hyper-
cholesterolemia, influx of LDL exceeds the eliminating capacity and an ECF pool is formed. Intima LDL is oxidized by action of
free O2 radicals and generate pro-inflammatory lipids.
Page 7
Atherosclerosis Progression
Arteriosclerosis arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left
failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Progression of atherosclerosis: a summary, slide
Damaged endothelium:
Chronic endothelial injury
Hypertensiom
Smoking
Hyperlipidemia
Hyperhomocystinemia
Hemodynamic factors Toxins
Viruses
Immune reactions
Fatty streak
Page 8
Fibrous plaque
Complicated
lesion
Coronary Artery Disease
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Coronary artery disease, myocardial ischemia and myocardial
infarction impair heart’s pumping ability by depriving it of O2 &
nutrients
Coronary artery disease (CAD), diminishes myocardial blood
supply until deprivation impairs myocardial metabolism. Myo-
cardial cells remain alive but are unable to function normally. Persistent ischemia or complete occlusion of a coronary artery
causes acute coronary syndromes including infarction or death.
Myocardial ischemia, is due predominantly to atherosclerosis.
The growing mass of plaque, platelets, fibrin, and cellular debris can eventually narrow the coronary artery lumen enough to
impede blood flow. Platelet aggregation release thromboxane
A2, a potent vasoconstrictor capable of causing spasm of
coronary arteries and promote further platelet aggregation.
Myocardial infarction, occurs when coronary arteries can not
compensate for lack of O2 caused by myocardial ischemia. As a
marker of inflammation and thrombosis, C-reactive protein rises
shortly after infarction. A common complication of myocardial
infarction are dysrhythmias, arrhythmias, and sudden death.
Page 9
Coronary Artery Disease
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Cycle of ischemic events
Page 10
Myocardial Ischemia
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
The ischemic cost of aggravation, angiogram of coronary
arteries, electrocardiogram (EKG) and ischemia
Normal
Myocardial
Ischemia
Page 11
Myocardial Ischemia
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathophysiology model of the effects of acute stress
as a trigger of cardiac clinical events
VF = ventricular fibrillation
VT = ventricular tachicardia
MI = Myocardial infarction
VF = ventricular fibrillation
VT = ventricular tachicardia
MI = Myocardial infarction
Page 12
Myocardial Ischemia
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathophysiology of acute coronary syndrome
Page 13
Myocardial Ischemia
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of unstable plaques and thrombus formation
Page 14
Myocardial Infarction
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Plaque disruption and myocardial infarction
Myocardial Infarction
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
EKG alterations associated with the three zones of myocardial
infarction
Page 15
Myocardial Infarction
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Three interacting factors related to sudden cardiac death
Page 16
Pericarditis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Disorders of the pericardium includes acute pericarditis,
pericardial effusion, and constrictive pericarditis
Pericardial disease is often a localized manifestation of another
disorder. Infection, trauma or surgery, neoplasm, or metabolic,
immunologic, or vascular disorders can elicit a pericardial response. Pericarditis, pericardial effusion, and constrictive
pericarditis are the consequences of the elicited response.
Acute pericarditis, although idiopathic, is commonly caused by
infection, connective tissue disease, or radiation therapy. Peri-cardium becomes inflamed, roughened, & exudate may develop.
Among its symptoms are sudden chest pain that worsen with
respiration, dysphagia, restlesness, irritability, weakness, and
malaise. A friction rub or scratchy grating sound in the cardiac
apex and left sternal border is pathognomonic. Its treatment, if uncomplicated, is antiinflammatory drugs to relieve symptoms.
Pericardial effusion, is accumulation of fluid in the pericardial
cavity. It is possible with all type of pericarditis. The fluid might
be transudate or an exudate and suggest an underlying disorder.
Pericarditis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pericardial tamponede is when pericardial fluid creates sufficient
pressure to cause cardiac compression, equal diastolic pressure,
decrease atrial and ventricular filling, SV and CO, and circulatory collapse may develop. The most significant clinical finding of
tamponade is pulsus paradoxus, when arterial pressure during
expiration exceeds that of inspiration by more than 10 mm Hg.
Constrictive pericarditis, is either idiopathic or associated with radiation exposure, rheumatoid arthritis, uremia, or coronary
artery bypass graft. Fibrous scarring & occasional calcification
causes visceral and parietal layers to adhere obliterating the
pericardial cavity and reducing CO. It develops gradually, unlike
the tamponade that has a more sudden onset. Among its symptoms are exercise intolerance, dyspnea on exertion,
anorexia, weight loss, edema, distention of the jugular vein, and
hepatic congestion. Chest X-rays show prominent pulmonary
vessels and pericardium calcification. Therapy involves digitalis
glycosides and even removal of the pericardium.
Disorders of the pericardium includes acute pericarditis,
pericardial effusion, and constrictive pericarditis
Page 17
Pericarditis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
B
C D
Disorders of the pericardium includes acute pericarditis (B),
pericardial effusion (C), and constrictive pericarditis (D)
Acute
pericarditis
Pericardial
effusion
Constrictive
pericarditis
Page 18
Valvular Dysfunctions
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Disorders of the endocardium includes valvular dysfunctions,
acute rheumatic fever and rheumatic heart disease, and
infective endocarditis
Valvular dysfunctions include stenosis and regurgitation.
In valvular stenosis, the valve orifice is constricted or narrowed. This impedes the forward flow of blood and
increases the workload of the cardiac chamber “in front”
or before the diseased valve. Increased volume and
pressure causes the myocardium to work harder and
myocardial hypertrophy develops.
In valvular regurgitation, also known as insufficiency or
incompetence, the valve leaflets or cusps fail to close
completely. This permits blood to continue even when the
valve should be closed. During systole some blood leaks into the atrium, thus increasing the workload of atrium and
ventricle. Increased volume leads to chamber dilation, and
increased workload leads to hypertrophy. Left valves are
more commonly affected than right valves.
Valvular Dysfunctions
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Valvular stenosis and regurgitation
A
C
B
D
Normal valve
(open)
Page 19
A B
D
Normal
valve
(open)
C
Valvular Dysfunctions
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Mitral stenosis with “fish mouth” and vegetation (V) that (impair
blood flow into left ventricle, and mitral valve prolapse (valve
leaflets billow back into atrium during left ventricular systole)
Page 20
Endocarditis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Disorders of the endocardium includes valvular dysfunctions,
acute rheumatic fever and rheumatic heart disease, and
infective endocarditis
Page 21
Endocarditis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of infective endocarditis
Page 22
ENDOTHELIAL
DAMAGE
DEVELOPMENT OF THROMBI
NON-BACTERIAL THROMBOTIC ENDOCARDITIS
Genito-urinary instrumentation
Dental procedure Skin infection
hemodialysis
Intravenous drug abuse Cardiac surgery
PATHOGEN ENTRY INTO BLOODSTREAM
Failure of platelets
Inhibition causing platelet deposition Failure of mechanisms of self-defense
(serum complement, antibodies)
BACTEREMIA
BACTERIAL INFILTRATION OF PLATELET – FIBRIN THROMBI
COLONIZATION ON ENDOCARDIAL SURFACES
Adherences of more platelets Formation of more fibrin
GROWTH OF VEGATATION
INFECTIVE ENDOCARDITIS
Deposition of immune complex
(systemic lupus erythmatosus,
rheumatic heart disease)
Exposure to cold High altitude
Turbulent blood flow (valvular dysfunctions)
Stress
Cardiac catheterization
Endocarditis
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Rheumatic heart disease (RHD) versus infective endocarditis
Cause Pathophysiology Manifestation Treatment
RHD, sequel to streptococus
pharingeal infection
Carditis of all 3 layers of heart wall,
endocardial inflammation and
vege- tative growth on valves and valvular stenosis
Fever, lymphoadeno-
pathy, acute migrato-ry
polyarthritis, chrea,truncal rush, history of strepto
pharingeal infection
Antibiotics, NSAID,surgical valve
repair, continuos prophy-lactic
antibiotic therapy for as long as 5 years
Infective endocar-ditis,
staphyloco-cus followed by
strepto, virus, fungi, ricketsia
Prior endothelial damage to valves
leads to throm-botic endocarditis, blood-
borne microbes colonize damaged valve and form
endocardial vegetations
Fever, cardiac murmur, petechial
lesions of skin and mucosa,
bacteremia, prolonged PR
Antimicrobial therapy for 4-6
weeks, possible valve replacement
Page 23
Cause Pathophysiology Manifestation Treatment
RHD, sequel
to streptococus
pharingeal infection
Carditis of all 3 layers of
heart wall, endocardial inflammation and
vegetative growth on valves and valvular
stenosis
Fever,
lymphoadeno-pathy, acute
migratory polyarthritis, chrea,
truncal rush, history
of strepto pharingeal infection
Antibiotics,
NSAID, surgical valve repair,
continuos prophy-lactic
antibiotic therapy
for as long as 5 years
Infective
endocarditis, staphylococu
s followed by strepto,
virus, fungi,
ricketsia
Prior endothelial
damage to valves leads to thrombotic
endocarditis, blood-borne microbes colonize
damaged valve and
form endocardial vegetations
Fever, cardiac
murmur, petechial lesions of skin and
mucosa, bacteremia,
prolonged PR
Antimicrobial
therapy for 4-6 weeks, possible
valve replacement
Ventricular Remodeling
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathophysiology of ventricular remodeling
Heart failure are several types of cardiac dysfunction causing an
inadequate perfusion of tissues with vital blood-born nutrients.
Ventricular remodeling, a process leading to decrease contractility,
is caused by inflammatory, immune, and neurohumoral changes.
Ventricular remodeling results in hypertrophy and dilation of the
myocardium and causes progressive myocyte contractile dysfunc-tion over time. When contractility is decreased, stroke volume falls
and ventricular end-diastolic volume (VEDV) increases. This cause
dilation of the heart and increase preload, which might temporally
increase CO but eventually leads to sarcomere dysfunction. Most
rises in preload are related to intravenous fluid administration, renal failure, and mitral valvular disease. Increased afterload or
TPR is seen in hypertension, and aortic valvular disease. It also
causes myocardium hypertrophy, increase O2 demand and
ventricular remodeling. It has been linked to failed compensatory
mechanisms involving catecholamines, RAS, ANP, and AVP.
Page 24
Ventricular Remodeling
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathophysiology of ventricular remodeling
Ventricular remodeling
due to myocardial
disfunction
Ventricular remodeling
due to myocardial
disfunction
MYOCARDIAL DYSFUNCTION
RENIN – ANGIOTENSIN – ALDOSTERONE SYSTEM ACTIVATED
VENTRICULAR REMODELING
Decreased perfusion to kidneys
Decreased CO
Decreased systemic BP
Myocardial infarction
Ischemic heart disease
Hypertension, others
Baroreceptors activated Left ventricle
Aotic arch Carotide sinus
Vasomotor regulatory centers in medula stimulated
Sympathetic nervous system activated
Increased Cas (Epi & Norepi)
Vasoconstriction Increased afterload Increased BP & HR
Increased AgII
Increased ALDO
Retain Na and water
AVP, endothelin, cytokines (TNF-alpha)
Hypertrophy & dilated ventricles
Geneticall large cells
Impaired contractility
Page 25
Ventricular Remodeling
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Effect of elevated preload on myocardial O2 demand and supply
Increased preload (LVEDV)
Decreased lumen of
coronary arteries
Myocardial
ischemia
Stretching of
myocardium
Decreased
contractility
Ventricular Remodeling
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Role of increased afterload on yje pathogenesis of heart failure
Page 26
Heart Failure
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
The vicious cycle of systolic heart failure
Renal failure hypertension
Decreased RBF
Increased renin
& AgII
Decreased EF
Increased
LVEDV
Decreased contractility
MYOCARDIAL INFARCTION
Page 27
Right Heart Failure
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Right hjeart failure
Right heart failure
Page 28
Left Heart Failure
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Left side failure (congestive heart disese)
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High Output Heart Failure
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
High output failure, the heart is unable to supply nutrients despite
adequate blood volume and myocardial contractility. Common
causes are anemia, septicemia, hyperthyroidism, and beriberi
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High output failure
Shock
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Shock’s impairment of cellular metabolism
In shock, cardiovascular system fails to perfuse tissues adequately,
resulting in widespread impairment of cellular metabolism.
Tissue perfusion may be disrupted by any factor altering heart
function, thus shock has many causes and clinical manifestations.
Ultimately, shock progress to organ failure and death, unless
compensatory mechanisms reveres it or clinical treatment succeed.
Untreated severe shock overwhelms the body’s compensatory
mechanisms through positive feedback loops that initiate and
maintain a downward physiological spiral.
MODS or multiple organ dysfunction syndrome, describes failure of
two or more organ systems after severe illness and injury. It is a
frequent complication of severe shock. The disease process is
initiated and perpetuated by uncontrolled inflammatory and stress
responses. It is progressive & associated with significant mortality.
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Shock and Cellular Metabolism
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Shock’s impairment of cellular metabolism
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Shock events, signs, symptoms
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Events, signs and symptoms of shock
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MODS
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of multiple organ disfunction syndrome (MODS)
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Cardiogenic Shock
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of multiple organ disfunction syndrome (MODS)
Cardiogenic shock
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Hypovolemic shock
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of multiple organ disfunction syndrome (MODS)
Hypovolemic shock
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Neurogenic Shock
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of multiple organ disfunction syndrome (MODS)
Neurogenic shock
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Anaphylactic Shock
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of multiple organ disfunction syndrome (MODS)
Anaphylactic shock
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Septic Shock
Arteriosclerosis
arteriosclerosis, athero-sclerosis, fibrous plaque
Coronary artery disease myocardial isquemia, myocardial infarction
Heart wall disorders
pericardial, valvular stenosis/regurgitation, rheumatic heart disease, infective endocarditis
Heart failure
congestive heart failure (left failure), cor pulmonale (right failure)
Shock cardiogenic, hypovolemic, neurogenic, anaphylactic, septic, and multiple organ dysfunction (MODS)
Pathogenesis of multiple organ disfunction syndrome (MODS)
Septic shock
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