Cardio vascularsystempathophysiology.ppt

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Alterations of Cardiovascular Alterations of Cardiovascular
Function – Part 1Function – Part 1
Chapter 23Chapter 23

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Diseases of the VeinsDiseases of the Veins

Varicose veinsVaricose veins - areas of veins in which blood - areas of veins in which blood
has pooled.has pooled.

Distended, tortuous, and palpable veins.Distended, tortuous, and palpable veins.

Caused by: Caused by:

Damaged valves as a result of trauma to the Damaged valves as a result of trauma to the
valvevalve

Chronic venous distention involving gravity Chronic venous distention involving gravity
and venous constrictionand venous constriction

Usually occurs in the saphenous veins.Usually occurs in the saphenous veins.

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Diseases of the VeinsDiseases of the Veins

Chronic venous insufficiencyChronic venous insufficiency - inadequate - inadequate
venous return over a long period of timevenous return over a long period of time

Due to varicose veins or valvular Due to varicose veins or valvular
incompetence.incompetence.

Causes pathologic ischemic changes in the Causes pathologic ischemic changes in the
vasculature, skin, and supporting tissues. vasculature, skin, and supporting tissues.

Venous stasis ulcersVenous stasis ulcers – ulcerations of skin – ulcerations of skin
that occur due to pressure or trauma.that occur due to pressure or trauma.

Develop as a result of the borderline metabolic Develop as a result of the borderline metabolic
state of the cells in the affected extremities. state of the cells in the affected extremities.

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Venous Stasis UlcerVenous Stasis Ulcer

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Diseases of the VeinsDiseases of the Veins

Deep venous thrombosisDeep venous thrombosis – thrombi in deep – thrombi in deep
veins, often in varicose veins of the legs.veins, often in varicose veins of the legs.

Virchow’s triad Virchow’s triad – describes causes of DVT:– describes causes of DVT:

Venous stasisVenous stasis

Venous endothelial damageVenous endothelial damage

Hypercoagulable statesHypercoagulable states

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Venous ThrombiVenous Thrombi

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Diseases of the VeinsDiseases of the Veins
Deep venous thrombosisDeep venous thrombosis (cont.) (cont.)

Obstruction of venous flow leads to increased Obstruction of venous flow leads to increased
venous pressure, resulting in pain and venous pressure, resulting in pain and
edema.edema.

Pulmonary embolism may result if thrombi Pulmonary embolism may result if thrombi
breaks loose. breaks loose.

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Diseases of the VeinsDiseases of the Veins

Superior vena cava syndromeSuperior vena cava syndrome

Progressive occlusion of the superior vena cava.Progressive occlusion of the superior vena cava.

Leads to venous distention of upper extremities Leads to venous distention of upper extremities
and head.and head.

Usually caused by bronchogenic cancer and Usually caused by bronchogenic cancer and
some other cancers.some other cancers.
•As tumors grow they compress the SVC, As tumors grow they compress the SVC,
decreasing its diameter.decreasing its diameter.

Generally considered an oncologic emergency Generally considered an oncologic emergency
rather than a vascular emergency. rather than a vascular emergency.

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HypertensionHypertension

HypertensionHypertension

Consistent elevation of systemic arterial blood Consistent elevation of systemic arterial blood
pressure resulting from increases in total pressure resulting from increases in total
peripheral resistance, circulating blood peripheral resistance, circulating blood
volume, or both. volume, or both.

Normal blood pressure is defined as systolic Normal blood pressure is defined as systolic
pressure less than 120 mm Hg and diastolic pressure less than 120 mm Hg and diastolic
pressure less than 80 mm Hg.pressure less than 80 mm Hg.

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HypertensionHypertension
Primary HypertensionPrimary Hypertension (essential or idiopathic) (essential or idiopathic)

Hypertension without a known cause.Hypertension without a known cause.

Affects 92% to 95% of individuals with Affects 92% to 95% of individuals with
hypertensionhypertension

Appears to be due to a combination of Appears to be due to a combination of
genetic and environmental factors.genetic and environmental factors.

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Risk Factors for Primary Risk Factors for Primary
HypertensionHypertension

Family history Family history

Advanced age Advanced age

Smoking Smoking

Obesity Obesity

Heavy alcohol Heavy alcohol
consumption (>3 consumption (>3
drinks per day)drinks per day)

Gender (men > Gender (men >
women before age women before age
55, women > men 55, women > men
after 55) after 55)

Black race Black race

High dietary sodium High dietary sodium
intake intake

Low dietary intake of Low dietary intake of
potassium, magnesium, potassium, magnesium,
and calcium and calcium

Glucose Glucose
intolerance/diabetes intolerance/diabetes
mellitusmellitus

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Primary HypertensionPrimary Hypertension
Underlying mechanisms of primary hypertensionUnderlying mechanisms of primary hypertension::
1. Overactivity of the sympathetic nervous system 1. Overactivity of the sympathetic nervous system
(SNS)(SNS)

Causes increased heart rate and peripheral Causes increased heart rate and peripheral
vasoconstriction.vasoconstriction.
2. Overactivity of the renin-angiotensin-aldosterone 2. Overactivity of the renin-angiotensin-aldosterone
(RAA) system(RAA) system

High aldosterone levels cause increased retention of High aldosterone levels cause increased retention of
sodium and water.sodium and water.

Angiotensin II causes vasoconstriction and vascular Angiotensin II causes vasoconstriction and vascular
remodeling which increases peripheral resistance.remodeling which increases peripheral resistance.

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Primary HypertensionPrimary Hypertension
Underlying mechanisms of primary hypertensionUnderlying mechanisms of primary hypertension::
3. Abnormal secretion of natriuretic hormones3. Abnormal secretion of natriuretic hormones

These modulate renal sodium excretion and retention.These modulate renal sodium excretion and retention.

Abnormal levels cause sodium and water retention by Abnormal levels cause sodium and water retention by
the kidneys.the kidneys.
4. Complex interactions involving insulin 4. Complex interactions involving insulin
resistance, inflammation, and endothelial resistance, inflammation, and endothelial
function. function.

Contribute to vascular remodeling, increased sodium Contribute to vascular remodeling, increased sodium
retention, and effects of SNS and RAA.retention, and effects of SNS and RAA.

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Primary HypertensionPrimary Hypertension

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Secondary HypertensionSecondary Hypertension

Caused by a systemic disease process or Caused by a systemic disease process or
medication that raises peripheral vascular medication that raises peripheral vascular
resistance or cardiac output, such as:resistance or cardiac output, such as:

Renal diseaseRenal disease

Adrenocortical tumorsAdrenocortical tumors

Adrenomedullary tumors (pheochromocytoma)Adrenomedullary tumors (pheochromocytoma)

Drugs (oral contraceptives, corticosteroids, Drugs (oral contraceptives, corticosteroids,
antihistamines, etc.). antihistamines, etc.).

If the cause is identified and removed before If the cause is identified and removed before
permanent structural changes occur, blood permanent structural changes occur, blood
pressure returns to normal.pressure returns to normal.

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Isolated Systolic HypertensionIsolated Systolic Hypertension

Defined as a sustained systolic BP that is Defined as a sustained systolic BP that is
≥140mm Hg and diastolic BP that is below ≥140mm Hg and diastolic BP that is below
90mm Hg. 90mm Hg.

Common in older individuals who have Common in older individuals who have
stiffer (noncompliant) blood vessels. stiffer (noncompliant) blood vessels.

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Isolated Systolic HypertensionIsolated Systolic Hypertension

Mechanism:Mechanism:

As the cardiac output is ejected into the As the cardiac output is ejected into the
aorta and its branches, they do not stretch aorta and its branches, they do not stretch
to accept this increased blood volume and to accept this increased blood volume and
pressure rises. pressure rises.

As this volume is distributed to the tissues As this volume is distributed to the tissues
during diastole, pressure falls back to during diastole, pressure falls back to
normal. normal.

ISH is a risk factor for heart attack, ISH is a risk factor for heart attack,
congestive heart failure, and stroke.congestive heart failure, and stroke.

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Complicated HypertensionComplicated Hypertension

Severe or sustained hypertension that begins Severe or sustained hypertension that begins
to affect many other organs in the body.to affect many other organs in the body.

Chronic hypertensive damage occurs in the Chronic hypertensive damage occurs in the
walls of systemic blood vessels.walls of systemic blood vessels.

Vascular remodeling occurs:Vascular remodeling occurs:

Smooth muscle cells undergo hypertrophy and Smooth muscle cells undergo hypertrophy and
hyperplasia hyperplasia

Fibrosis occurs in the tunica intima and tunica Fibrosis occurs in the tunica intima and tunica
mediamedia

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Complicated HypertensionComplicated Hypertension

Clinical manifestations result from damage of Clinical manifestations result from damage of
organs and tissues (end organ damage): organs and tissues (end organ damage):

Heart diseaseHeart disease

Renal diseaseRenal disease

Cerebrovascular accidentsCerebrovascular accidents

Damage to retina of eyeDamage to retina of eye

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Malignant HypertensionMalignant Hypertension

Rapidly progressive hypertension in which Rapidly progressive hypertension in which
diastolic pressure is usually above 140mm Hgdiastolic pressure is usually above 140mm Hg

Sequelae include:Sequelae include:

Encephalopathy - from profound cerebral edema Encephalopathy - from profound cerebral edema
that disrupts cerebral function and causes loss that disrupts cerebral function and causes loss
of consciousness. of consciousness.

Cardiac failureCardiac failure

UremiaUremia

RetinopathyRetinopathy

Cerebrovascular accidentCerebrovascular accident

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Malignant HypertensionMalignant Hypertension

Organ damage resulting from malignant Organ damage resulting from malignant
hypertension is life threateninghypertension is life threatening

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Treatment for HypertensionTreatment for Hypertension

Behavioral changesBehavioral changes – – weight loss through diet weight loss through diet
and exercise and salt restriction.and exercise and salt restriction.

Antihypertensive drugsAntihypertensive drugs

DiureticsDiuretics – enhance urinary fluid loss to reduce – enhance urinary fluid loss to reduce
blood volume.blood volume.

Beta-blockersBeta-blockers – block sympathetic input to – block sympathetic input to
heart, reducing contraction strength, cardiac heart, reducing contraction strength, cardiac
output, and thus lowering blood pressureoutput, and thus lowering blood pressure..

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Treatment for HypertensionTreatment for Hypertension

Antihypertensive drugsAntihypertensive drugs (cont.) (cont.)

ACE-inhibitorsACE-inhibitors – block angiotensin converting – block angiotensin converting
enzyme in lungs, so less angiotensin II is enzyme in lungs, so less angiotensin II is
formed. Reduces vasoconstriction and formed. Reduces vasoconstriction and
aldosterone release.aldosterone release.

Angiotensin-receptor blockers Angiotensin-receptor blockers - cause - cause
vasodilation, reduced secretion of angiotensin vasodilation, reduced secretion of angiotensin
II, and reduced production and secretion of II, and reduced production and secretion of
aldosterone.aldosterone.

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Treatment for HypertensionTreatment for Hypertension

Antihypertensive drugsAntihypertensive drugs (cont.) (cont.)

Calcium channel blockers Calcium channel blockers – restrict entry of – restrict entry of
calcium into arteriolar smooth muscle, thus calcium into arteriolar smooth muscle, thus
producing vasodilation, and into cardiac muscle, producing vasodilation, and into cardiac muscle,
causing lower cardiac output.causing lower cardiac output.

Multiple types of drugs may be combined to Multiple types of drugs may be combined to
increase effectiveness.increase effectiveness.

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Treatment for HypertensionTreatment for Hypertension

Note:Note: Most of these are antagonists to Most of these are antagonists to
substances that would increase blood substances that would increase blood
pressure. pressure.

Antagonists – act against (oppose)Antagonists – act against (oppose)

Agonists – increase activity of something.Agonists – increase activity of something.

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Treatment for HypertensionTreatment for Hypertension
ACE = angiotensin
converting enzyme
ARB = angiotension
receptor blocker
CCB = calcium channel
blocker

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Orthostatic (Postural) Orthostatic (Postural)
HypotensionHypotension

A significant drop in systolic and diastolic A significant drop in systolic and diastolic
blood pressure upon moving from a lying or blood pressure upon moving from a lying or
sitting position to a standing position. sitting position to a standing position.

Systolic blood pressure decrease of 20 mm Systolic blood pressure decrease of 20 mm
Hg (or greater) or diastolic blood pressure Hg (or greater) or diastolic blood pressure
decrease of 10 mm Hg (or greater) within the decrease of 10 mm Hg (or greater) within the
first 3 minutes of standing. first 3 minutes of standing.

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Orthostatic (Postural) Orthostatic (Postural)
HypotensionHypotension

Caused by a failure of sympathetic nervous Caused by a failure of sympathetic nervous
system vasomotor compensatory mechanisms system vasomotor compensatory mechanisms
that cause increased heart rate, that cause increased heart rate,
vasoconstriction, and venous valve closing vasoconstriction, and venous valve closing
upon standing. upon standing.

Essential to maintaining adequate cerebral Essential to maintaining adequate cerebral
perfusion during upright positioning. perfusion during upright positioning.

Clinical manifestations - dizziness, syncope Clinical manifestations - dizziness, syncope
(fainting), or sudden loss of vision or blurred (fainting), or sudden loss of vision or blurred
vision.vision.

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Orthostatic (Postural) Orthostatic (Postural)
HypotensionHypotension

Acute orthostatic hypotensionAcute orthostatic hypotension – caused by – caused by
temporary body alterations like drugs and temporary body alterations like drugs and
medications, dehydration, venous pooling, medications, dehydration, venous pooling,
and prolonged inactivity. and prolonged inactivity.

Chronic orthostatic hypotensionChronic orthostatic hypotension – caused – caused
by underlying diseases like endocrine or by underlying diseases like endocrine or
metabolic disorders. Or it may be a primary metabolic disorders. Or it may be a primary
condition caused by degeneration of the CNS condition caused by degeneration of the CNS
with age.with age.

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AneurysmAneurysm

AneurysmAneurysm – a local dilation or – a local dilation or
outpouching of a vessel wall or cardiac outpouching of a vessel wall or cardiac
chamber.chamber.

Primarily develop in the:Primarily develop in the:

Cerebral arteries (most commonly in the Cerebral arteries (most commonly in the
circle of Willis)circle of Willis)

Thoracic or abdominal aortaThoracic or abdominal aorta

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AneurysmAneurysm

Over time aneurysms grow in size, putting Over time aneurysms grow in size, putting
pressure on neighboring structures.pressure on neighboring structures.

The wall becomes thinner and weaker, and The wall becomes thinner and weaker, and
eventually may rupture, causing stroke or eventually may rupture, causing stroke or
life-threatening hemorrhage. life-threatening hemorrhage.

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AneurysmAneurysm

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AneurysmAneurysm

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AneurysmAneurysm

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Dissecting AneurysmDissecting Aneurysm
Dissecting aneurysmDissecting aneurysm (aortic dissection) (aortic dissection)

Occurs when the tunica media is Occurs when the tunica media is
weakened and the intima is torn, allowing weakened and the intima is torn, allowing
arterial pressure to force blood into the arterial pressure to force blood into the
media, dissecting its layers apart.media, dissecting its layers apart.

The dissection compresses vessels as The dissection compresses vessels as
they leave the aorta, causing acute they leave the aorta, causing acute
ischemia and infarction of vital organs ischemia and infarction of vital organs
such as the brain and kidney. such as the brain and kidney.

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Dissecting AneurysmDissecting Aneurysm

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Dissecting AneurysmDissecting Aneurysm
Dissecting aneurysmDissecting aneurysm (cont.) (cont.)

Aortic dissection most commonly involves Aortic dissection most commonly involves
the thoracic aorta. the thoracic aorta.

Symptoms - abrupt onset of severe chest Symptoms - abrupt onset of severe chest
pain along with syncope and symptoms of pain along with syncope and symptoms of
organ ischemia. organ ischemia.

Aortic dissection has a very high mortality Aortic dissection has a very high mortality
rate and is a surgical emergency.rate and is a surgical emergency.

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Arterial Thrombus FormationArterial Thrombus Formation
ThrombusThrombus – a clot that remains attached to a – a clot that remains attached to a
vascular wall.vascular wall.

Causes are the same as for venous Causes are the same as for venous
thrombi: thrombi:

Intimal injuryIntimal injury

Stasis of flowStasis of flow

Hypercoagulable states (although these Hypercoagulable states (although these
more commonly cause venous thrombosis). more commonly cause venous thrombosis).

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Arterial Thrombus FormationArterial Thrombus Formation
ThrombusThrombus (cont.) (cont.)

Can also form on damaged heart valves and Can also form on damaged heart valves and
in cardiac chambers (atrial fibrillation, in cardiac chambers (atrial fibrillation,
ventricular aneurysms). ventricular aneurysms).

Activation of the clotting cascade leads to Activation of the clotting cascade leads to
platelet aggregation and formation of a clot platelet aggregation and formation of a clot
(thrombus) within a vessel, on a cardiac (thrombus) within a vessel, on a cardiac
valve, or along the wall of a cardiac valve, or along the wall of a cardiac
chamber.chamber.

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Arterial Thrombus FormationArterial Thrombus Formation
ThromboembolusThromboembolus – detached portion of a – detached portion of a
thrombus that travels through the bloodstream.thrombus that travels through the bloodstream.

If the thrombus or embolus blocks a part of the If the thrombus or embolus blocks a part of the
peripheral circulation, this will cause limb ischemia peripheral circulation, this will cause limb ischemia
and tissue infarction (tissue death).and tissue infarction (tissue death).

If the thrombus or embolus blocks one of the If the thrombus or embolus blocks one of the
central arteries, stroke and other types of vital central arteries, stroke and other types of vital
organ infarctions may occur.organ infarctions may occur.

Thromboemboli from the heart valves or chambers Thromboemboli from the heart valves or chambers
frequently travel to the brain, causing stroke.frequently travel to the brain, causing stroke.

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Peripheral Vascular DiseasePeripheral Vascular Disease
Raynaud phenomenon and Raynaud diseaseRaynaud phenomenon and Raynaud disease

Episodic vasospasm in arteries and arterioles Episodic vasospasm in arteries and arterioles
of the fingers, and less commonly the toes.of the fingers, and less commonly the toes.

Raynaud disease Raynaud disease – a primary vasospastic – a primary vasospastic
disorder related to an imbalance of disorder related to an imbalance of
endothelium-derived vasodilators and endothelium-derived vasodilators and
vasoconstrictors.vasoconstrictors.

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Peripheral Vascular DiseasePeripheral Vascular Disease
Raynaud phenomenon and Raynaud diseaseRaynaud phenomenon and Raynaud disease

Raynaud phenomenon Raynaud phenomenon – occurs – occurs
secondary to other systemic diseases or secondary to other systemic diseases or
conditions such as:conditions such as:

Scleroderma, smoking, pulmonary Scleroderma, smoking, pulmonary
hypertension, myxedema, and hypertension, myxedema, and
environmental factors environmental factors

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Peripheral Vascular DiseasePeripheral Vascular Disease
Raynaud phenomenon and Raynaud diseaseRaynaud phenomenon and Raynaud disease

Vasospasm causes pain and color changes Vasospasm causes pain and color changes
in the skin, especially involving the fingers in the skin, especially involving the fingers
and toes. and toes.

Can occur on exposure to even a small drop Can occur on exposure to even a small drop
in room temperature, or occasionally with in room temperature, or occasionally with
vibration or repetitive motion.vibration or repetitive motion.

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ArteriosclerosisArteriosclerosis

Chronic disease of the arterial system Chronic disease of the arterial system
characterized by abnormal thickening and characterized by abnormal thickening and
hardening of the vessel walls.hardening of the vessel walls.

Smooth muscle cells and collagen fibers Smooth muscle cells and collagen fibers
migrate to the tunica intima, gradually migrate to the tunica intima, gradually
narrowing the arterial lumen.narrowing the arterial lumen.

Part of the normal aging process, but it is a Part of the normal aging process, but it is a
disease state when it occurs to the point of disease state when it occurs to the point of
symptom development.symptom development.

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ArteriosclerosisArteriosclerosis

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AtherosclerosisAtherosclerosis

Most common form of arteriosclerosis.Most common form of arteriosclerosis.

Characterized by soft deposits of fat and fibrin in the Characterized by soft deposits of fat and fibrin in the
arterial wall that harden over time (plaques).arterial wall that harden over time (plaques).

Plaque development begins when there is Plaque development begins when there is
endothelial injury and inflammation, caused by:endothelial injury and inflammation, caused by:

Hypertension, diabetes, smoking, high LDL levels, Hypertension, diabetes, smoking, high LDL levels,
aging, autoimmune injury, and possibly bacterial aging, autoimmune injury, and possibly bacterial
infection by infection by Chlamydia pneumoniaeChlamydia pneumoniae..
Biology of progression of atherosclerosis
http://
www.youtube.com/watch?v=mCYAOeEe6-w&feature
=related

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AtherosclerosisAtherosclerosis

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AtherosclerosisAtherosclerosis
ProgressionProgression::

Endothelial injury causes inflammation.Endothelial injury causes inflammation.

Macrophages adhere and release cytokines that Macrophages adhere and release cytokines that
further injure the wall.further injure the wall.

Low-density lipoprotein (LDL) in the blood is Low-density lipoprotein (LDL) in the blood is
oxidized and engulfed by macrophages (forming oxidized and engulfed by macrophages (forming
foam cellsfoam cells))

AA fatty streak fatty streak forms as foam cells accumulate in forms as foam cells accumulate in
wall of vessel.wall of vessel.

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AtherosclerosisAtherosclerosis

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AtherosclerosisAtherosclerosis
ProgressionProgression (cont.) (cont.)

Fibrous plaqueFibrous plaque - macrophages release growth - macrophages release growth
factors (mitogens) that promote proliferation of factors (mitogens) that promote proliferation of
smooth muscle cells in the tunica media. These smooth muscle cells in the tunica media. These
cells migrate over the fatty streak, produce cells migrate over the fatty streak, produce
collagen, and form a fibrous cap over the plaque.collagen, and form a fibrous cap over the plaque.

Plaques undergo calcification, grow, and protrude Plaques undergo calcification, grow, and protrude
into lumen of vessel, obstructing flow.into lumen of vessel, obstructing flow.

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AtherosclerosisAtherosclerosis
ProgressionProgression (cont.) (cont.)

Complicated plaqueComplicated plaque – a plaque that has – a plaque that has
ruptured. This initiates thrombus formation and ruptured. This initiates thrombus formation and
instability and vasoconstriction leading to instability and vasoconstriction leading to
obstruction of the lumen and inadequate oxygen obstruction of the lumen and inadequate oxygen
delivery to tissues.delivery to tissues.
Atherosclerosis is the primary risk factor for Atherosclerosis is the primary risk factor for
myocardial infarction, stroke, and peripheral myocardial infarction, stroke, and peripheral
artery disease.artery disease.

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Coronary Artery DiseaseCoronary Artery Disease

Coronary artery diseaseCoronary artery disease (CAD) – any (CAD) – any
vascular disorder that narrows or occludes vascular disorder that narrows or occludes
the coronary arteries.the coronary arteries.

Atherosclerosis is the most common cause.Atherosclerosis is the most common cause.

Plaques narrow the coronary arteries.Plaques narrow the coronary arteries.

May rupture and cause sudden thrombus May rupture and cause sudden thrombus
formation and myocardial ischemia and even formation and myocardial ischemia and even
infarction.infarction.

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Risk Factors for CADRisk Factors for CAD

Gender (men > women Gender (men > women
before age 55, women before age 55, women
> men after age 55) > men after age 55)

High cholesterol/LDL High cholesterol/LDL
levelslevels**

Hypertension Hypertension **

Smoking Smoking **

Diabetes mellitus and Diabetes mellitus and
insulin resistance insulin resistance

Obesity Obesity

Sedentary lifestyle Sedentary lifestyle

Metabolic syndrome Metabolic syndrome

Atherogenic diet (high Atherogenic diet (high
in saturated and trans in saturated and trans
fats)fats)
* Most predictive of * Most predictive of
CAD. CAD.
Conventional or major risk factors Conventional or major risk factors

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Risk Factors for CADRisk Factors for CAD

Markers of Markers of
inflammation inflammation

C-reactive protein C-reactive protein
(CRP) (CRP)

Fibrinogen Fibrinogen

Protein C Protein C

Plasminogen Plasminogen
activator inhibitor activator inhibitor

Interleukins Interleukins

Others Others

Hyperhomocysteinemia Hyperhomocysteinemia

Infection Infection
Nontraditional or novel risk factors Nontraditional or novel risk factors

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Myocardial IschemiaMyocardial Ischemia

Ischemic heart diseaseIschemic heart disease – caused by CAD – caused by CAD
and the resultant decrease in blood supply. and the resultant decrease in blood supply.

Local, temporary insufficiency of the coronary Local, temporary insufficiency of the coronary
blood supply and oxygen.blood supply and oxygen.

Usually occurs when demand for oxygen rises Usually occurs when demand for oxygen rises
(increased heart rate)(increased heart rate)

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MyocardialMyocardial
Ischemia Ischemia

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Myocardial IschemiaMyocardial Ischemia

Angina pectorisAngina pectoris - chest pain caused by myocardial - chest pain caused by myocardial
ischemia. ischemia.

Stable anginaStable angina - occurs with exercise and relieved - occurs with exercise and relieved
with rest.with rest.
•Usually transient, lasting approximately 3 to 5 min.Usually transient, lasting approximately 3 to 5 min.
•Substernal chest discomfort, which may radiate to Substernal chest discomfort, which may radiate to
the neck, lower jaw, left arm, and left shoulder, or the neck, lower jaw, left arm, and left shoulder, or
occasionally, to the back or down the right arm.occasionally, to the back or down the right arm.
•Other symptoms include dizziness, shortness of Other symptoms include dizziness, shortness of
breath, pallor and sweating.breath, pallor and sweating.

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Myocardial IschemiaMyocardial Ischemia

Prinzmetal anginaPrinzmetal angina – due to vasospasm of – due to vasospasm of
coronary vessels without underlying coronary vessels without underlying
atherosclerosis. atherosclerosis.

Myocardial ischemia occurs unpredictably, often Myocardial ischemia occurs unpredictably, often
at rest or during sleep. at rest or during sleep.

May result from hyperactivity of the sympathetic May result from hyperactivity of the sympathetic
nervous system and changes in endogenous nervous system and changes in endogenous
vasodilators and vasoconstrictors.vasodilators and vasoconstrictors.

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Myocardial IschemiaMyocardial Ischemia

Silent ischemiaSilent ischemia – ischemia without symptoms of – ischemia without symptoms of
chest discomfort.chest discomfort.

Can occur with dysfunction of the autonomic Can occur with dysfunction of the autonomic
nerves that bring efferent messages from the nerves that bring efferent messages from the
heart to the brain. heart to the brain.

Common in diabetics, since they often suffer Common in diabetics, since they often suffer
autonomic dysfunction.autonomic dysfunction.

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Myocardial IschemiaMyocardial Ischemia

Acute coronary syndromes Acute coronary syndromes – caused by – caused by
sudden coronary obstruction due to thrombus sudden coronary obstruction due to thrombus
formation.formation.

Unstable anginaUnstable angina – severe chest pain that occurs – severe chest pain that occurs
due to rupture of a plaque in a coronary artery.due to rupture of a plaque in a coronary artery.
•If the ruptured thrombus is labile and occludes If the ruptured thrombus is labile and occludes
the vessel for no more than 10 to 20 minutes, the vessel for no more than 10 to 20 minutes,
myocardial ischemia will be severe but will not myocardial ischemia will be severe but will not
result in infarction of the heart. result in infarction of the heart.

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Acute Coronary SyndromesAcute Coronary Syndromes

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Myocardial IschemiaMyocardial Ischemia

Unstable anginaUnstable angina (cont.) (cont.)

Anaerobic metabolism is able to support cell Anaerobic metabolism is able to support cell
function for about 20 minutes.function for about 20 minutes.

Causes anginal pain that occurs at unpredictable Causes anginal pain that occurs at unpredictable
times (for example, at rest) or with greater times (for example, at rest) or with greater
frequency and severity. frequency and severity.

Unstable angina is a signal of impending Unstable angina is a signal of impending
myocardial infarction. myocardial infarction.

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Myocardial InfarctionMyocardial Infarction

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Myocardial InfarctionMyocardial Infarction

Caused by prolonged, unrelieved ischemia that Caused by prolonged, unrelieved ischemia that
interrupts blood supply to the myocardium. interrupts blood supply to the myocardium.

Usually due to a ruptured thrombus in a coronary Usually due to a ruptured thrombus in a coronary
artery.artery.

After about 20 minutes of myocardial ischemia, After about 20 minutes of myocardial ischemia,
irreversible hypoxic injury causes cellular death irreversible hypoxic injury causes cellular death
and tissue necrosis due to lack of oxygen. and tissue necrosis due to lack of oxygen.
http://www.youtube.com/watch?v=H_VsHmoRQ
Kk&feature=related

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Plaque Disruption and Myocardial Plaque Disruption and Myocardial
InfarctionInfarction

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Myocardial InfarctionMyocardial Infarction
ClassificationsClassifications::

Non-STEMINon-STEMI - only affects the myocardium just - only affects the myocardium just
under the endocardium (subendocardial).under the endocardium (subendocardial).

STEMI STEMI – damage penetrates all the way from – damage penetrates all the way from
the endocardium to the pericardium the endocardium to the pericardium
(transmural MI). [STEMI = ST-elevated (transmural MI). [STEMI = ST-elevated
myocardial infarction.] myocardial infarction.]

Identifies patients at greatest risk for severe Identifies patients at greatest risk for severe
complications and most likely to benefit from complications and most likely to benefit from
rapid intervention. rapid intervention.

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Myocardial InfarctionMyocardial Infarction

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Myocardial InfarctionMyocardial Infarction

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Myocardial InfarctionMyocardial Infarction
Pathophysiology of MIPathophysiology of MI::

Cellular necrosis results in the release of Cellular necrosis results in the release of
intracellular enzymes such as troponin I and intracellular enzymes such as troponin I and
troponin T, creatinine phosphokinase (CPK-troponin T, creatinine phosphokinase (CPK-
MB), and lactate dehydrogenase (LDH). MB), and lactate dehydrogenase (LDH).

Cellular necrosis is accompanied by release of Cellular necrosis is accompanied by release of
inflammatory mediators and infiltration of the inflammatory mediators and infiltration of the
myocardium with inflammatory cells such as myocardium with inflammatory cells such as
polymorphonucleocytes (neutrophils) and polymorphonucleocytes (neutrophils) and
macrophages.macrophages.

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Myocardial InfarctionMyocardial Infarction
Structural and functional changesStructural and functional changes::

Neurohumoral changes cause structural and Neurohumoral changes cause structural and
functional alterations that contribute to further functional alterations that contribute to further
dysfunction of heart muscle surrounding the dysfunction of heart muscle surrounding the
infarction.infarction.

Myocardial stunningMyocardial stunning - toxic oxygen radicals - toxic oxygen radicals
and other inflammatory mediators cause and other inflammatory mediators cause
temporary loss of contractile function that temporary loss of contractile function that
persists for hours or days after perfusion has persists for hours or days after perfusion has
been restored. been restored.

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Myocardial InfarctionMyocardial Infarction
Structural and functional changesStructural and functional changes (cont.) (cont.)

Hibernating myocardiumHibernating myocardium - Tissue that survives - Tissue that survives
persistent ischemia through metabolic adaptation persistent ischemia through metabolic adaptation
to prolong myocyte survival until perfusion can to prolong myocyte survival until perfusion can
be restored. be restored.

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Myocardial InfarctionMyocardial Infarction
Structural and functional changesStructural and functional changes (cont.) (cont.)

Myocardial remodelingMyocardial remodeling - Myocyte hypertrophy - Myocyte hypertrophy
and loss of contractile function of heart muscle and loss of contractile function of heart muscle
distant from the site of infarction. This process is distant from the site of infarction. This process is
mediated by angiotensin II, catecholamines, mediated by angiotensin II, catecholamines,
aldosterone, adenosine, and inflammatory aldosterone, adenosine, and inflammatory
cytokines. cytokines.

Can be inhibited by the use of ACE inhibitors or Can be inhibited by the use of ACE inhibitors or
angiotensin receptor blockers and beta blockers angiotensin receptor blockers and beta blockers
after an MI.after an MI.

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Myocardial InfarctionMyocardial Infarction
Diagnostic serum enzymesDiagnostic serum enzymes::

An increase in plasma enzyme levels is used An increase in plasma enzyme levels is used
to diagnose the occurrence of myocardial to diagnose the occurrence of myocardial
infarction and indicate its severity. infarction and indicate its severity.

Elevations of the isoenzymes creatine kinase Elevations of the isoenzymes creatine kinase
(CK-MB), troponins, and lactic (CK-MB), troponins, and lactic
dehydrogenase (LDH-1) are most predictive dehydrogenase (LDH-1) are most predictive
of a myocardial infarction. of a myocardial infarction.

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Myocardial InfarctionMyocardial Infarction
Treatments includeTreatments include::

Revascularization (with thrombolytics or PCI Revascularization (with thrombolytics or PCI
[percutaneous coronary intervention])[percutaneous coronary intervention])

Antithrombotics, ACE inhibitors, and beta-Antithrombotics, ACE inhibitors, and beta-
blockers. blockers.

Pain relief and fluid management. Pain relief and fluid management.
SequelaeSequelae::

Dysrhythmias and cardiac failure are the most Dysrhythmias and cardiac failure are the most
common complications of acute myocardial common complications of acute myocardial
infarction. infarction.