Transcript Lecture 9 - CVS Disorders

Chapter 9
CARDIOVASCULAR
DISORDERS
BY
Dr. Uche Amaefuna- Obasi
•THERE ARE MORE
TO LECTURES
THAN JUST
SLIDES….   
An Epidemiological Overview
• Cardiovascular disease (CVD) is the leading cause
of death in the U.S.
• In 2005 CVD accounted for approximately 38
percent of all deaths
• CVD has been the number one killer in the U.S.
since 1900 except for 1918 (influenza)
• More that 2,500 Americans die from CVD each
day
• Among women, 1 in 2.6 deaths from CVD
Death Rates for Cardiovascular Disease, Including
CHD and Stroke for Selected Countries
Understanding The Cardiovascular System
• Cardiovascular system includes: the heart,
arteries, arterioles, capillaries, venules, and veins
• The heart
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Muscular, four chambered pump
Contracts 100,000 times per day
Two upper chambers: atria
Two lower chambers: ventricles
Tricuspid, pulmonary, mitral, and aortic valves
Heart Function
• Deoxygenated blood enters the right atrium
• From the right atrium blood moves to the right
ventricle, pumped through the pulmonary artery
to the lungs
• Oxygen blood enters the left atrium
• Blood from the left atrium is forced into the left
ventricle
• The left ventricle pumps blood through the aorta
to various parts of the body
Overview
• Diagnostic Tests for
Cardiovascular Function
• General Treatment
Measures for Cardiac
Disorders
• Coronary Artery Disease
(CAD)
– Arteriosclerosis
– Atherosclerosis
– Myocardial Infarction (MI)
• Cardiac Arrhythmias
– Sinus node abnormalities
– Atrial conduction
abnormalities
– Cardiac arrest
• Congestive Heart Failure
(CHF)
• Arterial Diseases
– Hypertension
• Shock
Diagnostic Tests for Cardiovascular
Function
• ECG
– Monitors arrhythmias, MI, infection, pericarditis
– Studies conduction activation and systemic abnormalities
• Auscultation
– Studies heart sounds using stethoscope
• Exercise stress test
– Assess general cardiovascular function
– Checks for exercise-induced problems
• Chest X-ray Film
– Shows shape, size of heart
– Evidence of pulmonary congestion associated with heart failure
– Nuclear imaging
Diagnostic Tests
• Cardiac Catheterization
– Visualize inside of heart,
measure pressure, assess
valve and heart function
– Determine blood flow to
and from heart
Diagnostic Tests
• Angiography
– Visualization of blood
flow in coronary artery
– Obstruction assessed and
treated
• Basic catheterization
• Balloon angioplasty
Diagnostic Tests
• Doppler Studies
– Assessment of blood flow in peripheral vessels
– Microphone records sounds of blood flow
• Can detect obstruction
• Blood tests
– Assess triglyceride and cholesterol levels
– Electrolytes
– Hb, hematocrit, cbcs
• Arterial Blood Gas Determination
– Essential for pts with shock, MI
– Check current oxygen levels, acid-base balance
General Treatment Measures for
Cardiac Disorders
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Dietary modification
Regular exercise program
Quit smoking
Drug therapy
Drug Therapy
• Vasodilators (Nitroglycerin)
– Provide better balance of oxygen supply and
demand in heart muscle
– May cause low bp
• Beta-blockers (Metoprolol or Atenolol)
– Treats angina, hypertension, arrhythmias
– Blocks beta1-adrenergic receptors in heart
• Prevent epine from increasing heart activity
Drug Therapy
• Calcium ion channel blockers
– Block movement of calcium
– Decrease heart contraction
• Antiarrhytmatic for excessive atrial activity
• Antihypertension and vasodilator
• Digoxin
– Treats heart failure
– Increases efficiency of heart
• Decreases conduction of impulses and HR
• Increases contraction of heart
– Pts must be checked for toxicity
• Antihypertensive drugs
– Decrease bp to normal levels
– Include:
• Adrenergic blocking agents
• Calcium ion blockers
• Diuretics
• Angiotensin-converting enzyme (ACE) inhibitors
– Used to treat hypertension, CHF, after MI
Drug Therapy
• Adrenergic Blocking drugs
– Act on SNS (sympathetic nervous system), block
arteriole alpha adrenergic receptors, or act directly
as vasodilator
• ACE Inhibitors
– Treat hypertension, CHF (congestive heart failure)
• Diuretics
– Remove excess water, sodium ions
– Block resorption in kidneys
– Treat high bp, CHF
Drug Therapy
• Anticoagulant
– Decrease risk of blood clot formation
– ASA (acetylsalicylic acid) decreases platelet
adhesion
– Block coagulation process
• Cholesterol or lipid reducing drugs
– When diet and exercise fail
– Decrease LDL and cholesterol
Anatomy of the Heart
Types Of Cardiovascular Disease
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Atherosclerosis
Coronary heart disease (CHD)
Chest pain (angina pectoris)
Irregular heartbeat (arrhythmia)
Congestive heart failure (CHF)
Congenital and rheumatic heart disease
Stroke
CAD—Arteriosclerosis:
Pathophysiology
• General term for all
types of arterial changes
• Best for degeneration in
small arteries and
arterioles
• Loss of elasticity, walls
thick and hard, lumen
narrows
CAD—Atherosclerosis:
Pathophysiology
• Presence of atheromas
– Plaques
• Consist of lipids, cells,
fibrin, cell debris
– Lipids usually
transported with
lipoproteins
Artherosclerosis
• Characterized by deposits of fatty
substances, cholesterol, cellular waste
products, calcium, and fibrin in the inner
lining of the artery
• Hyperlipidemia – abnormally high blood
lipid level
• Plaque – the buildup of deposits in the
arteries
Coronary atherosclerosis
Coronary atherosclerosis
Atherosclerosis--Pathophysiology
• Analysis of serum lipids:
– Total cholesterol, triglycerides, LDL, HDL
• LDL
– High cholesterol content
– Transports cholesterol liver  cells
– Dangerous component
• HDL
– “good”
– Low cholesterol content
– Transports cholesterol cells  liver
Consequences of Atherosclerosis
Atherosclerosis—Etiology
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Age
Gender
Genetic factors
Obesity, diet high in cholesterol, animal fats
Cigarette smoking
Sedentary life style
Diabetes mellitus
Poorly controlled hypertension
Combo of BC pills and smoking
Atherosclerosis—Diagnostic Tests
• Serum lipid levels
• Exercise stress test
• Radioisotope
Atherosclerosis—Treatment
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Decrease cholesterol and LDL
Decrease sodium ion intake
Control primary disorders
Quit smoking
Oral anticoagulant
Surgical intervention
– Percutaneous transluminal coronary angioplasty
(PTCA)
– Cardiac catheterization
– Laser beam technology
– Coronary artery bypass grafting
CABG
Coronary Heart Disease
• Myocardial infarction (MI) or heart attack –
blood supplying the heart is disrupted
• Coronary thrombosis – blood clot in the artery
• Embolus – when the blood clot is dislodged and
moves through the circulatory system
• Collateral circulation - if blockage to the heart is
minor, an alternative blood flow is selected
Angina Pectoris
• Ischemia – reduction of the heart’s blood and
oxygen supply
• The more serious the oxygen deprivation the
more severe the pain
• Nitroglycerin – drug used to relax (dilate) the
veins
• Beta blockers control potential over activity of
the heart muscle
Angina Pectoris
• This is a symptom complex. Symptoms caused
by transient myocardial ischaemia that falls
short of inducing the cellular necrosis that
defines myocardial infarction.
• Three variants:– Stable angina
– Prinzmental angina
– Unstable angina
Angina Pectoris
• Stable Angina – Most common form. Chronic
stenosing coronary atherosclerosis, reaching a
critical level, leaving the heart vulnerable to
increased demand.
• Typically relieved by rest or a vasodilator
Prinzmental Angina
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Uncommon pattern
Occurs at rest
Documented to be due to arterial spasm
Unrelated to physical activity, heart rate or
blood pressure.
• Generally responds to vasodilators.
Unstable Angina
• Pattern here is the pain, occurs with
progressively increasing frequency and
tends to be more prolonged
• Associated with disruption of the
atherosclerotic plaque, with superimposed
thrombosis, embolisation or spasm.
• Predictor of Myocardial Infarction
Effects of ischaemia on myocytes
• Onset of ATP Depletion
• Loss of contractility
• ATP reduced
– to 50% of normal
– To 10% of normal
• Irreversible injury
• Microvascular injury
• Seconds
• < 2 minutes
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10 minutes
40 minutes
20-40 minutes
> 1 hour
Arrythmias
• An irregularity in heart rhythm
• Tachycardia – racing heart in the absence of
exercise or anxiety
• Bradycardia – abnormally slow heartbeat
• Fibrillation – heart beat is sporadic,
quivering pattern
Cardiac Arrhythmias
• Alteration in HR or rhythm
• ECG monitors
– Holter monitors
• decreases efficiency of heart’s pumping cycle
– Slight increase in HR increases CO
– Very rapid HR prevents adequate filling in diastole
– Very slow HR reduces output to tissues
• Irregular contraction inefficient
– Interferes with normal filling/emptying cycle
CA: Sinus Node Abnormalities
• Brachycardia
– Regular but slow HR
• Less than 60 beats/min
– Results from vagus nerve stimulation or PNS
stimulation
• Tachycardia
– Regular rapid HR
• 100-160 beats/min
– SNS stimulation, exercise, fever, compensation
for low blood volume
CA: Atrial Conduction
Abnormalities
• Premature Atrial Contractions (PAC)
– Extra contraction or ectopic beats of atria
– Irritable atrial muscle cells outside conduction
pathway
• Interfere with timing of next beat
• Atrial flutter
– HR 160-350 beats/min
– AV node delays conduction
• Slower ventricular rate
Treatment of CA
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Cause should be determined and treated
Easiest to treat are those due to meds
SA node problems may require a pacemaker
Some may require defibrillators
Cardiac Arrest
• Cessation of all activity in the heart
• No conduction of impulses (flat line)
• May occur b/c:
– Excessive vagal nerve stimulation (decreases
heart)
– Drug toxicity
– Insufficient oxygen to maintain heart tissue
• Blood flow to heart and brain must be
maintained to resuscitate
Congestive Heart Failure (CHF)
• Damaged or overworked heart muscle is unable
to keep blood circulating normally
• Affects over 5 million Americans
• Damage to heart muscle may result from:
rheumatic fever, pneumonia, heart attack, or
other cardiovascular problem
• Lack of proper circulation may allow blood to
accumulate in the vessels of the legs, ankles, or
lungs
• Diuretics relieve fluid accumulation
Congenital And Rheumatic Heart
Disease
• Congenital heart disease affects 1 out of 125
children born
• May be due to hereditary factors, maternal
diseases, or chemical intake (alcohol)
during fetal development
• Rheumatic heart disease results from
rheumatic fever which affects connective
tissue
Rheumatic fever
• Once the most common cause of valvular heart
disease in Hong Kong.
• It is an acute immunologically mediated ,
multi-system inflammatory disease that occurs
a few weeks after an episode of Group A (ßhemolytic) streptococcal pharyngitis.
Chronic Rheumatic Valvular
Heart Disease
• Most important consequence of rheumatic
fever
• Inflammatory deformity of valves
– Almost always involve the mitral valve
– Involvement of aortic or other valves also
common
Characteristics of rheumatic
valvular disease
• Acute phase
– Foci of fibrinoid degeneration surrounded by
lympocytes – Aschoff bodies
– Most distinctive within the heart, but widely
disseminated.
– Pancarditis
• Pericarditis
• Myocarditis
• Verrucae vegetations (1-2 mm)
Characteristics of rheumatic
valvular disease
• Chronic
– Leaflet thickening
– Commissure fusion
– Shortening, thickening and fusion of chordae
tendinae
Stroke
• Occurs when the blood supply to the brain
is interrupted
• Thrombus – blood clot
• Embolus – free flowing clot
• Aneurysm – bulging or burst blood vessel
• Transient ischemic attack (TIA) – brief
interruptions that cause temporary
impairment
Common Blood Vessel Disorders
CAD: Myocardial Infarction—
Pathophysiology
• Coronary artery completely obstructed
– Prolonged ischemia and cell death of myocardium
• Most common cause is atherosclerosis with
thrombus
• 3 ways it may develop:
– Thrombus obstructs artery
– Vasospasm due to partial occlusion
– Embolus blocks small branch of coronary artery
• Majority involve L ventricle
– Size and location of infarction determine severity of
damage
MI—Signs and Symptoms
• Pain
– Sudden, substernal area
– Radiates to L arm and neck
– Less severe in females
• Pallor, sweating, nausea, dizziness
• Anxiety and fear
• Hypotension, rapid and weak pulse (low
CO)
• Low grade fever
MI—Treatment
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Rest, oxygen therapy, morphine
Anticoagulant
Drugs
Cardiac rehabilitation
Prognosis depends on site/size of infarct, presence
of collateral circulation, time elapsed before
treatment
• Mortality rate in 1st year
– 30-40% due to complications, recurrences
Myocardial Infarction
Transmural Infarction
– The ischaemic necrosis involves the full or nearly
the full thickness of the ventricular wall in the
distribution of a single coronary artery.
– Usually associated with chronic coronary
atherosclerosis, acute plaque change and
superimposed completely obstructive thrombosis.
Myocardial Infarction
• Subendocardial infarct
– Limited to the inner one-third or at most one half of
the ventricular wall
– May extend laterally beyond the perfusion territory
of a single coronary artery
– In a majority of cases, there is diffuse stenosing
coronary atherosclerosis.
Gross changes of myocardial
infarction
• Gross changes
– None to occasional mottling (up to 12 hours)
– Dark mottling (12-24 hours)
– Central yellow tan with hypereamic border (3-7
days)
– Gray white scar (2-8 weeks)
Varying gross
appearance of
myocardial
infarction
Recent and Old Myocardial Infarcts
Microscopic changes of
myocardial infarct
• Early coagulation necrosis and oedema;
haemorrhage (4-12 hours)
• Pyknosis of nucleic, hypereosinophilia,
early neutrophilic infiltrate (12-24 hours)
• Coagulation necrosis, interstitial infiltrate of
neutrophils (1-3 days)
• Dense collagenous scar (> 2 months)
Laboratory detection of myocardial
infarction
• This is based on the measurement of
intracellular macromolecules leaked from the
damaged myocytes into the circulation
• Creatine kinase – particularly the MB
isoenzyme
• Lactate dehydrogenase
• Troponin – Troponin 1 and Troponin T
Other diagnostic tools
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Electrocardiogram – Q waves
Echocardiogram
Radioisotope studies
Magnetic Resonance Imaging
Electrocardiogram (ECG) changes
Acute effects of myocardial
infarction
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Contractile dysfunction
Arrhythmias
Cardiac rupture
Pericarditis
Sudden death
– Invariably this would be due to a lethal arrhythmia
(asystole or ventricular fibrillation)
Pathological complications of
myocardial infarction
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Infarct extension
Mural thrombus
Ventricular aneurysm
Myocardial rupture
– Ventricular free wall
– Septal
– Papillary muscle
Infarct extension
Ruptured
Myocardial
Infarct
Old myocardial infarct showing evidence of
thinning of ventricular wall replaced by fibrous scar
Fibrous scarring with compensatory hypertrophy of
unaffected ventricular wall
Ventricular
wall
aneurysm
Anatomy of Heart Valves
• Aortic valve – Commonly tricuspid semi lunar
valves. Can be congenitally bicuspid.
• Mitral valve – Bi-cuspid flaps supported by
chordae tendinae attached to papillary muscles
• Pulmonary valves – Tricuspid semi lunar valves
• Tricuspid valves – Tri-cuspid flaps supported by
chordae tendinae.
Response to injury
• Mechanical injury – superficial fibrous
thickening over preserved architecture.
• Inflammation – invariably leads to
vascularisation of structure, fibrosis leads to
decrease in size/surface area.
• Degenerative changes – distortion and
increase in size due to deposits of material
such as calcium salts, cholesterol, etc.
Effects of valvular disease
• Stenosis – tightening of the valvular
opening resulting in decreased flow of
blood through the opening.
• Incompetence – incomplete closure of the
valvular opening, allowing backflow of
blood through the valvular opening
• Mixed.
Infective Endocarditis
• Colonisation or invasion of heart valves by
microbiologic agent.
• Formation of friable vegetations (composed
of thrombotic debris and organisms.
• Leads to destruction of underlying cardiac
tissue.
• Source of infective embolisation
Infective endocarditis
• Most common sites involve the left heart
valves
• Tricuspid valves typically involved in
intravenous drug abusers
• Development of infective endocarditis
preventable in patients with valvular
diseases by provision of antibiotic cover for
any surgical or dental procedures.
Bacteria Endocarditis
Arterial Diseases: Hypertension—
Pathophysiology
• Increased bp
• Insidious onset, mild symptoms and signs
• 3 major categories
– Essential (primary)
– Secondary
– Malignant
• Can be classified as diastolic or systolic
• Develops when bp consistently over 140/90
• Diastolic more important
Hypertension—Pathophysiology
• Over long time, high bp damages arterial walls
– Sclerosis, decreased lumen
– Wall may dilate, tear
• Aneurysm
• Areas most frequently damaged:
– Kidneys, brain, retina
• End result of poorly controlled hypertension:
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Chronic renal failure
Stroke
Loss of vision
CHF
Hypertension—Etiology
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Increases with age
Males more freq and severe
Genetic factors
High sodium ion intake
Excessive alcohol
Obesity
Prolonged, recurrent stress
Hypertension—Signs and Symptoms
• Asymptomatic in early stages
• Initial signs vague, nonspecific
– Fatigue, malaise, morning headache
Hypertension—Treatment
• Treated in sequence of steps
– Life style changes
– Mild diuretics, ACE inhibitors
– One or more drugs added
• Pt compliance is an issue
• Prognosis depends on treating underlying
problems and maintaining constant control
of bp
The elements of circulation
An effective pump
(The heart)
An effective return
(No peripheral
pooling)
(Normal blood
vessels)
A clear channel
The elements of circulation
Blood Pressure/Heart Rate
Effective venous and
lymphatic return
Intact and unblocked
blood vessels
The economics of circulation
Distribution of blood volume in
the circulatory system
Heart
7%
Arteries
13%
Arterioles and capillaries 7%
Veins
64%
Pulmonary vessels
9%
Body Fluid Compartments
Plasma
3.0L
Interstitial fluid
11.0L
Intracellular fluid
28.L
Blood volume contains both extracellular fluid (plasma) and
intracellular fluid (fluid in RBC). Average blood volume is about
8% of body weight, approximately 5L (60% plasma 40% RBC)
What is shock?
• A state of generalised hypoperfusion of all cells and
tissues due to reduction in blood volume or cardiac
output or redistribution of blood resulting in an
inadequate effective circulating volume
• A systemic (whole body) event resulting from
failure of the circulatory system
• It is at first reversible, but if protracted leads to
irreversible injury and death.
Causes of shock
• Hypovoleamia
• Cardiogenic (pump failure)
• Anaphylactic (peripheral pooling) (return
failure)
• Septic (Septiceamic) – Complex reasons
Hypovoleamic shock
• Haemorrhage
– External (Chop wounds, Gastro-intestinal
bleeding, etc)
– Internal (Hemoperitoneum due to ruptured
aortic aneurysm, ruptured ectopic pregnancy,
etc.
• Fluid loss
– Dehydration (low intake or excessive loss)
Shock (Hypotension)
• Results from decreased circulating blood
vol
– General hypoxia
– Low CO
Classification and Mechanisms of Shock
Type
Hypovolemic
Cardiogenic
Mechanism
loss of blood or plasma
Decreased pumping
capability of heart
Anaphylactic
Systemic vasodilation due
to severe allergic reaction
Septic
Vasodilation due to
severe infection
Neurogenic
Vasodilation due to loss
of SNS and vaso-motor
tone
External loss
Internal Bleeding
Effect of volume loss on
Cardiac Output and Arterial Pressure
Stages of hypovoleamic shock
• Asymptomatic (< 10%)
• Early stage (15-25% loss)
– Compensated hypotension
• Progressive/Advance Stage
– Results when no therapeutic intervention is given for the
early stage, compensatory mechanisms become harmful.
Autoregulation mechanisms breakdown.
• Irreversible shock
– Irreversible hypoxic injury to vital organs
Compensated hypotension
• Hypotension (low volume or low cardiac output)
• Sympathetico-adrenal stimulation (fight or fright)
• Release of catecholamines – resulting in peripheral
vasoconstriction – maintain BP
• Activation of renin-angiotensin-aldosterone system and
increased anti-diuretic hormone release
• Fluid retention by kidneys, further vasoconstriction
• Impaired renal perfusion and perfusion to other organs with
every effort made to maintain perfusion to brain and heart (autoregulation)
Shock—Pathophysiology
• Bp decreases when blood vol, heart contraction, or
periph resistance fails
• Low CO, microcirculation
– = decreased oxygen, nutrients for cells
• Compensation mechanism
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SNS, adrenal medulla stimulated
Renin secreted
Increased secretion of ADH
Secretion of glucocorticoids
Acidosis stimulates respiration
Shock—Pathophysiology
• Complications of decompensation of shock
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Acute renal failure
Adult respiratory distress syndrome (ARDS)
Hepatic failures
Hemorrhagic ulcers
Infection of septicemia
Decreased cardiac function
Shock—Etiology
• Hypovolemic shock
– Loss of blood, plasma
• Burn pts, dehydration
• Cardiogenic shock
– Assoc w/ cardiac impairment
• Distributive shock
– Blood relocated b/c vasodilation
• Anaphylactic shock
• Neurogenic shock
• Septic shock
– Severe infection
Shock—Signs and Symptoms
• 1st signs
– Shock, thirst, agitation,
restlessness
– Often missed
• 2nd signs
– Cool, moist, pale skin;
tachycardia; oliguria
– Compensation
– Vasoconstriction
• Direct effects
– Decrease bp and blood flow
– Acidosis
• Prolonged
– Decreased responsiveness
in body
– Compensated metabolic
acidosis progresses to
decompensated
– Acute renal failure
– Monitoring
Shock—Treatment
• Primary problem must be treated
• Hypovolemic shock
– Whole blood, plasma, electrolytes, bicarbonate required
• Anaphylactic shock
– Antihistamines, corticosteroids
• Septic
– Antimicrobials, glucocorticoids
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Maximize oxygen supply
Epine reinforces heart action and vasoconstriction
Dopamine, dubutamine increase heart function
Good prognosis in early stages
Mortality increases as irreversible shock develops
Splenic Infarct
Infarct of kidney
Replaced by
scarred tissue
Haemorrhagic infarct of lung
Cardiogenic shock
• Failure of myocardial pump.
– Intrinsic – due to myocardial damage
– Extrinsic
• Due to external pressure –e.g. cardiac tamponade
• Due to obstructed flow – e.g. thrombosis
Compensated heart failure
• Here the situation is one of a compromised cardiac
pump which has been “compensated” by an increase
in right atrial pressure ( increased blood volume
caused by retention of fluid ). Thus cardiac output is
maintained.
• It may not be noticed as it would have developed
gradually over time. However any strain on the heart,
eg sudden increase in exercise would tip the balance
and lead to a “decompensated heart failure”.
Decompensated heart failure
• The pump is so damaged that no amount of
fluid retention can maintain the cardiac output.
This failure also means that the renal function
cannot return to normal, thus fluid continues to
be retained and the person gets more and more
oedematous with eventual death. In short,
failure of the pump to pump enough blood to
the kidneys.
Anaphylactic shock
• Usually due to prior sensitisation
• Exposure to specific antigens
• Mediated by histamines, complements and
prostaglandins
• Vasodilatation of micro-circulation
associated with pooling and fluid
extravasation.
Septic shock
• Commonly due to gram-negative endotoxin
producing bacteria. May also accompany
gram+ve bacteria.
• Predisposing factors include:– Debilitating diseases
– Complications of instrumentation and treatment
– Burns
Septic shock
• Pathogenesis include:– Inflammatory reaction – vasodilatation mediated by
histamines and complements
– Disseminated intravascular coagulopathy – activation of
clotting factors and platelets together with consumption of
clotting factors
– Endothelial damage – extensive due to endotoxins
– Release of interleukin-1 and TNF-alpha (Tumor necrosis
factor alpha) from macrophages
Possible mechanisms of septic shock
Pathological changes
• Hypoxic injury to vital organs – infarction
• Necrosis of tissues
• Lysis of cells
• The extent of pathological changes is dependent
on the duration of decompensation before death.
• In acute deaths, often no significant findings are
found.
Pathological changes
• Brain
– Hypoxic and ischaemic damage
– Initially found at “boundary” zones
– May also be associated with marked cerebral
oedema.
Pathological changes
• Heart
– Focal myocardial necrosis
– Subendocardial infarction (vulnerable region of
blood supply)
– If there is pre-existing coronary artery diseases,
may also lead to acute transmural myocardial
infarction
Pathological changes
• In cardiogenic shock
– Due to previous ischaemic heart diseases – the
ventricular chambers may well be dilated and
distended. The walls are often thin and may be
replaced by non-elastic fibrous scars
– In intrinsic myocardial diseases leading to
pump failure, the myocardium may be
unusually thickened and rigid.
Pathological changes
• Lungs
– Diffuse alveolar damage (adult respiratory
distress syndrome)
– Damage to Type 1 pneumocytes and to
endothelial cells – oedema as well as damage to
the hyaline membrane due to decreased
surfactant production
– Haemorrhages, fibrosis, atelectasis and
infection.
Pathological changes
• Kidneys
– Acute tubular necrosis – often associated with
remarkably well preserved glomeruli
Pathophysiology of
Acute Tubular Necrosis
Acute Tubular
Necrosis,
Pathological changes
• Gastrointestinal tract
– Mucosal ischaemia, haemorrhage, necrosis,
gangrene
• Liver
– Centrilobular necrosis, fatty degeneration
• Adrenal glands
– Focal necrosis
– Diffuse haemorrhagic destruction
Pump Failure
Cardiogenic Shock
Vessel injury
Peripheral Pooling
Physical injuries such as wounds,
ruptures of aneurysms, etc
(Hypovoleamic)
Hypoalbumineamia,
Ascites, Renal failure,
Toxins , infection and immunecomplexes (DIC, Anaphylaxis,
Septiceamic)
Septiceamic,
Anaphylaxis
(Hypovoleamic)
(Capillary pooling)
Reducing Your Risk For Cardiovascular
Diseases
• Risks you can control
– Avoid tobacco
– Cut back on saturated fat and cholesterol
– Maintain a healthy weight
– Modify dietary habits
– Exercise regularly
– Control diabetes
– Control blood pressure
• Systolic – upper number
• Diastolic – lower number
– Manage stress
Reducing Your Risk For
Cardiovascular Diseases
• Risks you cannot control
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Heredity
Age
Gender
Race
New Weapons Against Heart
Disease
• Techniques for diagnosing heart disease
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Electrocardiogram (ECG)
Angiography
Positron emission tomography (PET)
Single positron emission color tomography
(SPECT)
Radionuclide imaging
Magnetic resonance imaging (MRI)
Ultrafast CT
Digital cardiac angiography (DSA)
Angioplasty Versus Bypass
Surgery
• Angioplasty – a thin catheter is threaded
through the blocked arteries. The catheter
has a balloon on the tip which is inflated to
flatten the fatty deposits against the wall of
the artery
• Coronary bypass surgery – a blood vessel is
taken from another site and implanted to
bypass blocked arteries and transport blood
Aspirin For Heart Disease?
• Research shows that 81 milligrams of
aspirin every other day is beneficial to heart
patients due to its blood thinning properties
• Some side effects of aspirin: gastrointestinal
intolerance and a tendency for difficulty
with blood clotting
• Should only be taken under the advice of
your physician
Thrombolysis
• If victim reaches an emergency room and is
diagnosed quickly, thrombolysis can be
performed
• Thrombolysis involves injecting an agent
such as tissue plasminogen activator (TPA)
to dissolve the clot and restore some blood
flow
Cardiac Rehabilitation
• Every year, 1 million people survive heart
attacks
• Cardiac rehabilitation exercise training
increases stamina and strength, and
promotes recovery.