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CARDIOVASCULAR
PATHOPHYSIOLOGY
ANATOMY OF THE HEART
• Atria – receiving chambers
• Left Atrium receives blood from
pulmonary veins
• Right Atrium – receives blood
from vena cava
• Ventricles – pumping
chambers
• Left Ventricle – pumps blood
through systemic circulation
• Right Ventricle – sends de-
oxygenated blood to be
oxygenated
• Atrioventricular Valves - b/w the
atria and ventricles
• Bicuspid Valve – b/w left atrium
and left ventricle
• Tricuspid Valve – b/w right atrium
and right ventricle
• Semilunar Valves – b/w great
arteries and the ventricles
• Aortic Valve – b/w aorta and left
ventricle
• Pulmonary Valve – b/w pulmonary
artery and right ventricle
PHYSIOLOGY OF THE HEART
• Atria contract by the pacemaker
• SA Node = pacemaker of the
heart
• Impulse travels down the heart
• AV Node
• Bundle of HIS
• Purkinje Fibers
• Ventricles contract
CARDIOVASCULAR DISEASE
• Generally refers to conditions that
involve narrowed or blocked blood
vessels that can lead to a heart attack,
chest pain, or stroke
• Other heart conditions can affect your
heart’s muscle, the valves, or the heart’s
rhythm
GENERAL TREATMENT FOR
CARDIOVASCULAR DISORDERS
• Lifestyle Interventions
• Low sodium, low fat diet to decrease weight
• Exercise to increase HDL and decrease LDL
• Smoking cessation
• Pharmacotherapy
• Vasodilators
• Beta Blockers
• Calcium Channel Blockers
• Anti-Hypertensives
• Diuretics
• Cholesterol Decreasing Drugs
CHOLESTEROL-RELATED DISORDERS
• Arteriosclerosis
• Hardening and narrowing of the arteries
• Fibrous tissue forms due to growing tunica adventicia
• Caused by hypertension and produces vasoconstriction
• Atherosclerosis
• Plaque build-up in the arteries forms a clot
• Coronary Occlusion: angina, myocardial infarction
• Brain Clot: transient ischemic attack, stroke
• Peripheral Clot: aneurysm
• Dyslipidemia
• High cholesterol
HEART DISEASES AND DISORDERS
• Angina Pectoris
• Oxygen is low in
the heart muscle
and causes a
severe, crushing
chest pain
HEART DISEASES AND DISORDERS
• Myocardial Infarction
• Cell death from
oxygen deprivation
• Replaced with fibrous
tissue
• Majority occur in the
left ventricle of the
heart
HEART DISEASES AND DISORDERS
• Pericarditis
• Effusion leads to fibrous adhesions
• Myocarditis
• Arrhythmias
• Endocarditis
• Infection of heart valves can lead to fibrosis
CONGESTIVE HEART FAILURE
• Forward Effect
• Not enough blood is going out because the pump
failed
• Backward Effect
• Congestion of blood behind the failing ventricle
• Forward & Backward Effect
• One side fails first, ultimately leading to the failure of the
other side
• Right Side Failure
• Systemic congestion
• Left Side Failure
• Pulmonary congestion
CONGESTIVE HEART FAILURE
DIAGNOSTIC TESTS
• Auscultation
• Listening to heart sounds
• Imaging
• MRI, CT, ultrasound
• Doppler Blood Flow
• Noninvasive ultrasound
• Estimates blood flow through blood vessels by bouncing high-frequency sound waves
off circulating red blood vessels
• Blood Tests
• Detects enzyme release from infracted heart cells
• EKG
• A recording of the electrical activity of the heart
COMPONENTS OF EKG
• P wave – atrial depolarization
• QRS Complex – ventricular
depolarization
• T Wave – ventricular repolarization
EKG ABNORMALITIES
• Premature Atrial Contraction
• Slight flutter. Benign.
• Premature Ventricular Contraction
• Usually benign.
• Can lead to ventricular fibrillation, which is
life-threatening.
EKG ABNORMALITIES
• Atrial Flutter
• Atria contract quickly in rhythm.
• P waves are not always followed by QRS
Complex.
• Atrial Fibrillation
• Atria quiver ineffectually.
• Can live without coordinated atrial
contraction.
EKG ABNORMALITIES
• Ventricular Tachycardia
• Very fast rhythm beginning in the ventricles
• Ventricular Fibrillation
• Ventricles quiver uselessly instead of pumping
blood
• Will die without swift intervention
EKG ABNORMALITIES
• Heart Block – fault within the heart’s
natural pacemaker due to obstruction in
the electrical conduction system of the
heart
• First Degree
• Long PR interval
• Second Degree
• Missing QRS complex after P wave
• Third Degree
• 2 consecutive missing QRS complexes
VASCULATURE
• Artery Layers
• Tunica Intima
• Endothelial cells
• Respond to hormones, signal smooth muscle
to contract, and relax muscle
• Tunica Media
• Muscle cells
• Tunica Externa
• Connective tissue
• Veins
• Veins have thinner walls than arteries
• Veins have valves to prevent backflow
RENIN-ANGIOTENSIN-ALDOSTERONE COMPLEX
• Hormone system that regulates blood pressure and fluid balance
• When renal blood flow is reduced, juxtaglomerular cells in the kidney convert the
precursor prorenin, already in the blood, to renin and secrete it directly into the
circulation
• Plasma renin carries out the conversion of angiotensinogen, released by the liver,
to angiotensin I
• Angiotensin I is subsequently converted to angiotensin II by the angiotensin-
converting enzyme (ACE) found in the lungs
• Angiotensin II is a potent vasoconstrictor resulting in increased blood pressure, and
it also stimulates secretion of aldosterone from the adrenal cortex
• Aldosterone causes the renal tubules to increase the reabsorption of sodium and
water in the blood, and increases the excretion of potassium to maintain
electrolyte balance
• This increases volume of extracellular fluid in the body, which also increases blood
HYPERTENSION
• 95% idiopathic
• Can cause endothelial cells to shear off
• Epinephrine in the bloodstream is inhibitory for
endothelial cells and excitatory for the smooth muscle
underneath, so it produces vasoconstriction and
increased blood pressure.
• Fat deposits in a hole in the tunica intima to produce
atheroma.
• Blood can begin running between tunica intima and
tunica media.
ANEURYSMS
• Fusiform Aneurysm
• Bulge in all directions
• Dissecting Aortic Aneurysm
• Ticking time bomb
• Saccular Aneurysm
• Sacs form on one side
• Blood pooling causes clotting and forms a
thrombus
• Dissecting Aneurysm
• Most dangerous aneurysm
• Blood runs between the tunica intima and tunica
CIRCULATORY SHOCK
• Life-threatening condition of low blood
perfusion to tissues resulting in cellular injury
and inadequate tissue function
• Causes
• Hypovolemia
• Cardiogenic Shock, Septic Shock, Vasogenic
Shock
• Neurogenic Shock, Anaphylactic Shock
• Compensation
• SNS increases heart rate and force of
contraction
DIFFERENTIAL DIAGNOSIS
• Kawasaki’s Disease
• Antibodies are produced against
endothelial cells and smooth muscle
• Presents as a red tongue, distal
extremity rash, skin sloughing, or
edema
• Recovery is usually spontaneous
• Raynaud’s Disease
• Insufficient blood supplied to distal
phalanges
• More common in women than men
• Prolonged ischemia can lead to
gangrene
• Venous Insufficiency
• Valves can fail due to age, injury, lifestyle, or
obesity
• Failure of valves causes chronic pooling of blood
in lower extremities
• Brown, blue, and purple skin color changes in
feet and toes due to waste accumulation
• Minor trauma – harder to treat because it’s a
large wound
• Lymphomas
• Hodgkin’s Lymphoma affects T cells
• Non-Hodgkin’s Lymphoma affects B cells

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Cardiovascular Pathophysiology

  • 2. ANATOMY OF THE HEART • Atria – receiving chambers • Left Atrium receives blood from pulmonary veins • Right Atrium – receives blood from vena cava • Ventricles – pumping chambers • Left Ventricle – pumps blood through systemic circulation • Right Ventricle – sends de- oxygenated blood to be oxygenated • Atrioventricular Valves - b/w the atria and ventricles • Bicuspid Valve – b/w left atrium and left ventricle • Tricuspid Valve – b/w right atrium and right ventricle • Semilunar Valves – b/w great arteries and the ventricles • Aortic Valve – b/w aorta and left ventricle • Pulmonary Valve – b/w pulmonary artery and right ventricle
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  • 4. PHYSIOLOGY OF THE HEART • Atria contract by the pacemaker • SA Node = pacemaker of the heart • Impulse travels down the heart • AV Node • Bundle of HIS • Purkinje Fibers • Ventricles contract
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  • 6. CARDIOVASCULAR DISEASE • Generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain, or stroke • Other heart conditions can affect your heart’s muscle, the valves, or the heart’s rhythm
  • 7. GENERAL TREATMENT FOR CARDIOVASCULAR DISORDERS • Lifestyle Interventions • Low sodium, low fat diet to decrease weight • Exercise to increase HDL and decrease LDL • Smoking cessation • Pharmacotherapy • Vasodilators • Beta Blockers • Calcium Channel Blockers • Anti-Hypertensives • Diuretics • Cholesterol Decreasing Drugs
  • 8. CHOLESTEROL-RELATED DISORDERS • Arteriosclerosis • Hardening and narrowing of the arteries • Fibrous tissue forms due to growing tunica adventicia • Caused by hypertension and produces vasoconstriction • Atherosclerosis • Plaque build-up in the arteries forms a clot • Coronary Occlusion: angina, myocardial infarction • Brain Clot: transient ischemic attack, stroke • Peripheral Clot: aneurysm • Dyslipidemia • High cholesterol
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  • 10. HEART DISEASES AND DISORDERS • Angina Pectoris • Oxygen is low in the heart muscle and causes a severe, crushing chest pain
  • 11. HEART DISEASES AND DISORDERS • Myocardial Infarction • Cell death from oxygen deprivation • Replaced with fibrous tissue • Majority occur in the left ventricle of the heart
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  • 13. HEART DISEASES AND DISORDERS • Pericarditis • Effusion leads to fibrous adhesions • Myocarditis • Arrhythmias • Endocarditis • Infection of heart valves can lead to fibrosis
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  • 15. CONGESTIVE HEART FAILURE • Forward Effect • Not enough blood is going out because the pump failed • Backward Effect • Congestion of blood behind the failing ventricle • Forward & Backward Effect • One side fails first, ultimately leading to the failure of the other side • Right Side Failure • Systemic congestion • Left Side Failure • Pulmonary congestion
  • 17. DIAGNOSTIC TESTS • Auscultation • Listening to heart sounds • Imaging • MRI, CT, ultrasound • Doppler Blood Flow • Noninvasive ultrasound • Estimates blood flow through blood vessels by bouncing high-frequency sound waves off circulating red blood vessels • Blood Tests • Detects enzyme release from infracted heart cells • EKG • A recording of the electrical activity of the heart
  • 18. COMPONENTS OF EKG • P wave – atrial depolarization • QRS Complex – ventricular depolarization • T Wave – ventricular repolarization
  • 19. EKG ABNORMALITIES • Premature Atrial Contraction • Slight flutter. Benign. • Premature Ventricular Contraction • Usually benign. • Can lead to ventricular fibrillation, which is life-threatening.
  • 20. EKG ABNORMALITIES • Atrial Flutter • Atria contract quickly in rhythm. • P waves are not always followed by QRS Complex. • Atrial Fibrillation • Atria quiver ineffectually. • Can live without coordinated atrial contraction.
  • 21. EKG ABNORMALITIES • Ventricular Tachycardia • Very fast rhythm beginning in the ventricles • Ventricular Fibrillation • Ventricles quiver uselessly instead of pumping blood • Will die without swift intervention
  • 22. EKG ABNORMALITIES • Heart Block – fault within the heart’s natural pacemaker due to obstruction in the electrical conduction system of the heart • First Degree • Long PR interval • Second Degree • Missing QRS complex after P wave • Third Degree • 2 consecutive missing QRS complexes
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  • 25. VASCULATURE • Artery Layers • Tunica Intima • Endothelial cells • Respond to hormones, signal smooth muscle to contract, and relax muscle • Tunica Media • Muscle cells • Tunica Externa • Connective tissue • Veins • Veins have thinner walls than arteries • Veins have valves to prevent backflow
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  • 27. RENIN-ANGIOTENSIN-ALDOSTERONE COMPLEX • Hormone system that regulates blood pressure and fluid balance • When renal blood flow is reduced, juxtaglomerular cells in the kidney convert the precursor prorenin, already in the blood, to renin and secrete it directly into the circulation • Plasma renin carries out the conversion of angiotensinogen, released by the liver, to angiotensin I • Angiotensin I is subsequently converted to angiotensin II by the angiotensin- converting enzyme (ACE) found in the lungs • Angiotensin II is a potent vasoconstrictor resulting in increased blood pressure, and it also stimulates secretion of aldosterone from the adrenal cortex • Aldosterone causes the renal tubules to increase the reabsorption of sodium and water in the blood, and increases the excretion of potassium to maintain electrolyte balance • This increases volume of extracellular fluid in the body, which also increases blood
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  • 29. HYPERTENSION • 95% idiopathic • Can cause endothelial cells to shear off • Epinephrine in the bloodstream is inhibitory for endothelial cells and excitatory for the smooth muscle underneath, so it produces vasoconstriction and increased blood pressure. • Fat deposits in a hole in the tunica intima to produce atheroma. • Blood can begin running between tunica intima and tunica media.
  • 30. ANEURYSMS • Fusiform Aneurysm • Bulge in all directions • Dissecting Aortic Aneurysm • Ticking time bomb • Saccular Aneurysm • Sacs form on one side • Blood pooling causes clotting and forms a thrombus • Dissecting Aneurysm • Most dangerous aneurysm • Blood runs between the tunica intima and tunica
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  • 32. CIRCULATORY SHOCK • Life-threatening condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function • Causes • Hypovolemia • Cardiogenic Shock, Septic Shock, Vasogenic Shock • Neurogenic Shock, Anaphylactic Shock • Compensation • SNS increases heart rate and force of contraction
  • 33. DIFFERENTIAL DIAGNOSIS • Kawasaki’s Disease • Antibodies are produced against endothelial cells and smooth muscle • Presents as a red tongue, distal extremity rash, skin sloughing, or edema • Recovery is usually spontaneous • Raynaud’s Disease • Insufficient blood supplied to distal phalanges • More common in women than men • Prolonged ischemia can lead to gangrene • Venous Insufficiency • Valves can fail due to age, injury, lifestyle, or obesity • Failure of valves causes chronic pooling of blood in lower extremities • Brown, blue, and purple skin color changes in feet and toes due to waste accumulation • Minor trauma – harder to treat because it’s a large wound • Lymphomas • Hodgkin’s Lymphoma affects T cells • Non-Hodgkin’s Lymphoma affects B cells