3. List of contents
A. Common manifestations of dysfunction
B. Circulatory dysfunction
C. Atherossclerosis (pathogenesis ,risk factors and
complication)
D. Hypertension (pathogenesis,risk factors and stages)
E. Coronary artery disease and MI
F. Congestive heart failure and cardiomyopathis
G. Valvular heart desese and congenital heart desese
H. Common arrhythmias
I. Bloo d disorders
4. Pathophysiology
• Atherosclerosis develops as a chronic
inflammatory response of the arterial wall to
endothelial injury.
• Lesion progression occurs through interactions
of modified lipoproteins, monocyte-derived
macrophages, T-lymphocytes, and the normal
cellular constituent of the arterial wall.
• The contemporary view of atherosclerosis is
expressed by the response-to-injury hypothesis.
5. Cont----
Arteriosclerosis
• Arteriosclerosis (literally, "hardening of the
arteries") is a generic term for thickening and
loss of elasticity of arterial walls.
• Three patterns of arteriosclerosis are
recognized; they vary in pathophysiology and
clinical and pathological consequences.
6. Cont-----
Atherosclerosis, the most frequent and important pattern, will be
discussed first and in detail below.
• Mönckeberg medial calcific sclerosis is characterized
by calcific deposits in muscular arteries in persons older than
age 50.
• Arteriolosclerosis affects small arteries and arterioles.
associated with thickening of vessel walls with luminal
narrowing that may cause downstream ischemic injury.
Most often associated with hypertension and diabetes
mellitus, arteriolosclerosis will be described later in this
chapter in the section on hypertension.
7. Figure 11-5 Schematic summary of the natural history, morphologic features,
main pathogenetic events, and clinical complications of atherosclerosis in the
coronary arteries.
10/28/2023 7
8. Cont----
• Atherosclerosis is characterized by intimal lesions
called atheromas, or atheromatous or fibrofatty
plaques, which protrude into and obstruct
vascular lumens and weaken the underlying
media.
• They may lead to serious complications. Global in
distribution, atherosclerosis overwhelmingly
contributes to more mortality—approximately
half of all deaths—and serious morbidity in the
Western world than any other disorder.
9. Cont-----
• Atherosclerotic plaques develop primarily in
elastic arteries (e.g., aorta, carotid, and iliac
arteries) and large and medium-sized muscular
arteries (e.g., coronary and popliteal arteries).
• Symptomatic atherosclerotic disease most often
involves the arteries supplying the heart, brain,
kidneys, and lower extremities.
• Myocardial infarction (heart attack), cerebral
infarction (stroke), aortic aneurysms, and
peripheral vascular disease (gangrene of the legs)
are the major consequences of atherosclerosis
10. Cont-----
• In small arteries, atheromas can occlude lumens,
compromise blood flow to distal organs, and
cause ischemic injury.
• Plaques can undergo disruption and precipitate
thrombi that further obstruct blood flow.
• In large arteries, plaques encroach on the
subjacent media and weaken the affected vessel
wall, causing aneurysms that may rupture.
• More over, extensive atheromas can be friable,
and shed emboli into the distal circulation.
11. Atherosclerosis is at risk for
A. Focal rupture, ulceration, or erosion of
the luminal surface of atheromatous plaques
may result thrombus formation
B. Hemorrhage into a plaque,
C. Superimposed thrombosis, the most feared
complication
D. Aneurysmal dilation may result from ATH-
induced atrophy of the underlying media
13. 10/28/2023 13
Figure 11-11 Evolution of arterial wall changes in the
response to injury hypothesis.
1, Normal.
2, Endothelial injury with adhesion of monocytes and
platelets (the latter to denuded endothelium).
3, Migration of monocytes (from the lumen) and
smooth muscle cells (from the media) into the intima.
4, Smooth muscle cell proliferation in the intima.
5, Well-developed plaque
16. Categories of BP in Adults
16
Classification SBP (mm Hg) Vs DBP(mm Hg)
Normal <120 and <80
Elevated 120-129 or <80
Hypertension
Stage 1 130-139 or 80-89
Stage 2 ≥140 or ≥90
17. Pathogenesis of Hypertension.
• The multiple mechanisms of hypertension constitute
aberrations of the normal physiologic regulation of blood
pressure.
• Arterial hypertension occurs when the relationship between
cardiac output and total peripheral resistance is altered.
• For many of the secondary forms of hypertension, these
factors are reasonably well understood.
• For example, in renovascular hypertension, renal artery
stenosis causes decreased glomerular flow and pressure in the
afferent arteriole of the glomerulus. This activate RAAS
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18. Classification
• Based on etiology, hypertension is classified into
primary and secondary hypertension.
Primary (or essential) hypertension (90-95% pts)
a single reversible cause cannot be identified
Secondary hypertension (5-10% pts)
cause can be identified
18
19. risk factors for hypertension
age
ethnicity (black)
family history of
hypertension
genetic factors
lower education and
socioeconomic status
greater weight
lower physical activity
tobacco use
psychosocial stressors
sleep apnea
dietary factors (dietary fats,
higher sodium intake, lower
potassium intake, and
excessive alcohol intake)
19
20. CORONARYARTERY DISEASE
• Coronary artery disease (CAD) is the most
prevalent type of cardiovascular disease in
adults. For this reason, it is important for
nurses to become familiar with various
manifestations of coronary artery conditions
and methods for assessing, preventing, and
treating these disorders.
21. Cont----
• Coronary artery disease is the leading cause of
death in the united state .
• CAD is characterized by the accumulation of
plague within the layers of the coronary arteries .
• The plague progressively enlarge , thicken and
calcify , causing a critical narrowing (70%) of
the coronary artery lumen , resulting in a
decrease in coronary blood flow and an
inadequate supply of oxygen to the heart
muscles.
24. Obstructive coronary artery disease
• Was defeide as any stenosis 50% or greater in
the left
• main coronary artery, 70% or greater in any
other coronary artery, or both.
• Obstructive CAD was defined as any stenosis
50% or greater in the left main coronary artery,
70% or greater in any other coronary artery, or
both.
25. Nonobstructive coronary artery disease
(CAD)
• is atherosclerotic plaque that would not be
expected to obstruct blood flow or result in
anginal symptoms (such as chest pain).
26. Coronary microvascular disease
• (sometimes called small artery disease or small
vessel disease) is heart disease that affects the
walls and inner lining of tiny coronary artery
blood vessels that branch off from the larger
coronary arteries.
28. PATHOPHYSIOLOGY
• Coronary artery cannot supply enough blood to
the heart in
• Within 10 second myocardial cells experience
ischemia
• Ischemia cells cannot get enough oxygen or
glucose
• Ischemic myocardial cells may have decrease
electrical and muscular function
30. Cont---
• Cells convert to anaerobic metabolism
• Cells produce lactic acid as waste
• Pain develops from lactic acid accumulation
• Angina symptoms increase oxygen
requirements of myocardial cells
31. Definition of MI
• Myocardial infarction is an ischemic necrosis of the
myocardium, caused by occlusion of coronary artery and
prolonged myocardial ischemia.
• MI is an extreme consequence of acute coronary
syndromes – the spectrum of clinical states caused by
instability of coronary artery lumen due to plaque instability
and (athero)thrombosis
32. • Most patients who sustain an MI have coronary
atherosclerosis.
• The thrombus formation occurs most often at the site
of an atherosclerotic lesion, thus obstructing blood
flow to the myocardial tissues.
• Plaque rupture is believed to be the triggering
mechanism for the development of the thrombus in
most patients with an MI.
• When the plaques rupture, a thrombus is formed at
the site that can occlude blood flow, thus resulting in
an MI.
33. • Irreversible damage to the myocardium can begin as
early as 20 to 40 minutes after interruption of blood
flow.
• The dynamic process of infarction may not be
completed, however, for several hours.
• Necrosis of tissue appears to occur in a sequential
fashion.
• Cellular death occurs first in the subendocardial layer
and spreads like a “wavefront” throughout the
thickness of the wall of the heart.
• The shorter the time between coronary occlusion and
coronary reperfusion, the greater the amount of
myocardial tissue that could be salvaged.
34. • The cellular changes associated with an MI can be followed
by:
1. the development of infarct extension (new myocardial
necrosis),
2. infarct expansion (a disproportionate thinning and dilation
of the infarct zone), or
3. Ventricular remodeling (a disproportionate thinning and
dilation of the ventricle).
• MIs most often result in damage to the left ventricle,
leading to an alteration in left ventricular function.
• Infarctions can also occur in the right ventricle or in
both ventricles.
35. Symptoms
Chest pain ( typical or typical) (mey be absent in DM)
The typical chest pain of acute MI usually is intense and
unremitting for 30-60 minutes. It is retrosternal and often
radiates up to the neck, shoulder, and jaws, and down to the
left arm. The chest pain is
usually described as a substernal pressure sensation that is
also perceived as squeezing, aching,
burning, or even sharp. In some patients, the symptom is
epigastric, with a feeling of indigestion or of fullness and
gas.
Lightheadednesswith or without syncope
Anxiety or sense of discomfort
Cough
Nausea / vomiting
Shorteness of breath
Fullness/indigestion/choking feeling
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36. MI Classifications
• MI’s can be subcategorized by anatomy and
clinical diagnostic information.
Anatomic
• Transmural and Subendocardial
Diagnostic
• ST elevations (STEMI) and non ST
elevations (NSTEMI).
37. Subendocardial
• a subendocardial (nontransmural) infarct
constitutes an area of ischemic necrosis limited
to the inner one third or at most one half of the
ventricular wall; under some circumstances, it
may extend laterally beyond the perfusion
territory of a single coronary artery.
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38. Cont----
• The precise location, size, and specific morphologic features
of an acute myocardial infarct depend on:
• The location, severity, and rate of development of
coronary atherosclerotic obstructions
• The size of the vascular bed perfused by the obstructed
vessels
• The duration of the occlusion
• The metabolic/oxygen needs of the myocardium at risk
• The extent of collateral blood vessels
• The presence, site, and severity of coronary arterial
spasm
• Other factors, such as alterations in blood pressure,
heart rate, and cardiac rhythm.
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39. Consequences and Complications of
Myocardial Infarction.
• Contractile dysfunction
• Arrhythmias
• Myocardial rupture
• Pericarditis.
• Infarct extension
• Progressive late heart failure
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40. CONGESTIVE HEART FAILURE
• Congestive heart failure (CHF) is a chronic
progressive condition that affects the pumping
power of heart muscles.
While often referred to simply as “heart
failure,”
41. CAUSES
Coronary artery disease and heart attack
High blood pressure (hypertension).
Faulty heart valves.
Damage to the heart muscle (cardiomyopathy).
Myocarditis.
Heart defects you're born with (congenital heart
defects).
Abnormal heart rhythms (heart arrhythmias).
Other diseases- Chronic diseases such as diabetes, HIV,
hyperthyroidism,hypothyroidism, or a buildup of iron
(hemochromatosis) or protein (amyloidosis)
42. CLINICAL MANIFESTATIONS
Shortness of breath (dyspnea) when you exert
your self or when you lie down
Fatigue and weakness
Swelling (edema) in your legs, ankles and feet
Rapid or irregular heartbeat
Reduced ability to exercise
Persistent cough or wheezing with white or pink
blood-tinged phlegm
Increased need to urinate at night
43. Cont-----
Swelling of your abdomen (ascites)
Sudden weight gain from fluid retention
Lack of appetite and nausea
Difficulty concentrating or decreased alertness
Sudden, severe shortness of breath and
coughing up pink,foamy mucus
Chest pain if your heart failure is caused by a
heart attack.
45. Cardiomyopathies
• The term cardiomyopathy (literally, heart muscle
disease) is used to describe heart disease resulting
from a primary abnormality in the myocardium.
• three clinical, functional, and pathologic patterns:
• Dilated cardiomyopathy
• Hypertrophic cardiomyopathy
• Restrictive cardiomyopathy
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47. Figure 12-31 Graphic representation of the three distinctive and predominant
clinical-pathologic-functional forms of myocardial disease.
10/28/2023 47
48. DILATED CARDIOMYOPATHY
• The term dilated cardiomyopathy (DCM) is
applied to a form of cardiomyopathy
characterized by progressive cardiac dilation
and contractile (systolic) dysfunction, usually
with concomitant hypertrophy.
• It is sometimes called congestive
cardiomyopathy.
• HCM causes primarily diastolic dysfunction.
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49. HYPERTROPHIC CARDIOMYOPATHY
• Hypertrophic cardiomyopathy (HCM) is also known
by such terms as idiopathic hypertrophic subaortic
stenosis and hypertrophic obstructive
cardiomyopathy.
• It is characterized by myocardial hypertrophy,
abnormal diastolic filling and, in about one third of
cases, intermittent ventricular outflow obstruction.
• The heart is thick-walled, heavy, and
hypercontracting
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50. Cont----
• The essential feature of HCM is massive
myocardial hypertrophy without ventricular
dilation.
• The classic pattern is disproportionate thickening
of the ventricular septum as compared with the
free wall of the left ventricle (with a ratio greater
than 1:3), frequently termed asymmetrical septal
hypertrophy.
• Although disproportionate hypertrophy can
involve the entire septum, it is usually most
prominent in the subaortic region.
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51. RESTRICTIVE CARDIOMYOPATHY
• Restrictive cardiomyopathy is a disorder
characterized by a primary decrease in
ventricular compliance, resulting in impaired
ventricular filling during diastole;
• the contractile (systolic) function of the left
ventricle is usually unaffected.[
• Thus, the functional state can be confused with
that of constrictive pericarditis
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52. Valvular Heart Disease
• Defined according to the valve or valves
affected and the type of functional alteration
Includes
- stenosis
- regurgitation
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53.
54. Types
STENOSIS
Valve orifice is smaller, impending the forward
flow of blood and creating a pressure gradient
difference across an open valve
REGURGITATION
Incomplete closure of the valve leaflets results in
the backward flow of blood
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55. MITRAL STENOSIS
most common valvular disorder in rheumatic
fever
may also be caused by bacterial infection,
thrombus formation, calcification
obstruct blood flow from left
atrium to the left ventricle
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56. PATHOPHYSIOLOGY
Narrowing of mitral
valve
left atrial
pressure
blood flow to left
ventricle
Hypertrophy left atrium
pulmonary
pressure
pulmonary
congestion
O2/CO2 exchange
(fatigue, dyspnea,
orthopnea)
Right-sided
failure
CO
Left ventricular
atrophy
Fatigue
57. MITRAL REGURGITATION
incomplete closure of the mitral valve
rheumatic disease is the predominant cause
may also be due to congenital anomaly,
infective endocarditis, rupture of papillary
muscle following MI
60. CAUSE:
• due to an inherited connective tissue disorder
• enlargement of one or both valve leaflets
61. AORTIC STENOSIS
• may be due to rheumatic heart disease,
atherosclerosis, congenital valvular disease or
malformations
• narrowing of the aortic valve
• Decrized flow of blood from the left ventricle to
the aorta
• Incrized blood volume and pressure in the left
ventricle
• Left ventricle hypertrophy develops as a
• compensatory mechanism to continue pumping
blood through the narrowed opening.
63. AORTIC REGURGITATION
• may be due to rheumatic fever most common
cause
• other causes:connective tissue disease
(Marfan’s syndrome), severe hypertension
64. PATHOPHYSIOLOGY
Left ventricular hypertrophy
& dilation
Left atrial pressure
Left-sided heart failure
(late stage)
CO
Left atrium hypertrophy
Pulmonary pressure
Right ventricular pressure
Right-sided heart
failure
Backflow of blood to Left ventricle
Incomplete closure of the aortic valve
65. TRICUSPID STENOSIS
• usually occurs together w/ aortic or mitral
stenosis may be due to rheumatic heart disease
decreased blood flow from right atrium to
right ventricle
• decreased right ventricular output
• decreased left ventricular filling CO
blood accumulates in systemic circulation
• increased systemic pressure
66. TRICUSPID REGURGITATION
• uncommon, may be caused by RF, bacterial
endocarditis
• may also be caused by enlargement of right
ventricle
• an insufficient tricuspid valve allows blood to
flow back
• into the right atrium --- venous congestion &
decrised right ventricular output-- decrised
blood flow towards the lungs
67. CONGENITAL HEART DEFECTS
• The major development of the fetal heart occurs between the
fourth and seventh weeks of gestation, and most congenital
heart defects arise during this time.
• resulting from an interaction between a genetic predisposition
toward development of a heart defect and environmental
influences.
• Approximately 13% of children with congenital heart disease
have an associated chromosomal abnormality.
• maternal conditions and teratogenic influences, including
maternal diabetes, congenital rubella, maternal alcohol
ingestion, and treatment with anticonvulsant drugs.
68. Acyanotic and Cyanotic Disorders
• It is devided into cyanotic and acyanotic disorders .
• Left-to-right shunts commonly are categorized as acyanotic
disorders and right-to left shunts with obstruction as cyanotic
disorders.
• Shunting of blood refers to the diverting of blood flow
from one system to the other from the arterial to the venous
system (i.e., left-to-right shunt) or from the venous to the
arterial system (i.e., right-to-left shunt).
69. CYANOTIC HEART DISEASE
with right-to left shunts
1. Tetralogy of fallots.
2. Transposition of great arteries (TGA).
3. Tricuspid atresia.
4. Truncus arteriosus.
5. Eisenmenger’s syndrome.
70. Acyanotic Disorders
• With left to right shunt :-
1. Atrial septal defect (ASD).
2. Ventricular septal defect (VSD).
3. Patent ductus arteriosis.
• With no shunt :-
1. Coarctation of aorta.
2. Congenital aortic stenosis.
3. Pulmonary stenosis, tricuspid stenosis.
4. Dextrocatdia.
71. MITRAL STENOSIS
• Almost all mitral stenosis is due to rheumatic heart disease .
• Rheumatic mitral stenosis is much more common in women
(about 1/3 case) .
• Rare causes of mitral stenosis may be congenital, because
calcification and fibrosis of the valve in elderly .
72. PATHOPHYSIOLOGY
• The commisures of mitral valve become adherent and the
chordae tendinae are short and deformed .
• The normal mitral valve orifice is about 4-6 cm² in diastole, it
is reduced to about 1 cm² in severe mitral stenosis.
• ed left atrial , pulmonary venous, pulmonary capillary
pressure.
• Also result in atrial fibrillation pulmonary edema
pulmonary hypertension .
• All cases may develop pulmonary hypertension and right
ventricular hypertrophy .
73. Cont-----
• All patients with mitral stenosis are at risk of left atrial
thrombosis and systemic thromboembolism .
• Mitral stenosis is frequently associated with mitral
regurgitation or disease of the aortic or tricuspid valve .
78. Cardiac Arrhythmias
• An abnormality of the cardiac rhythm is called
a cardiac arrhythmia
• Arrhythmias may cause sudden death,
syncope, heart failure, dizziness, palpitations
or no symptoms at all
• There are two main types of arrhythmia:
– Bradycardia: the heart rate is slow (< 60 b.p.m)
– Tachycardia: the heart rate is fast (> 100 b.p.m)
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79. Mechanisms of cardiac arrhythmias
• Mechanisms of bradicardias
– Sinus bradycardia is a result of abnormally slow
automaticity
– Bradycardia due to AV block is caused by
abnormal conduction within the AV node or the
distal AV conduction system
• Mechanisms generating tachycardias include
– Accelerated automaticity
– Triggered activity
– Re-entry (or circus movements)
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81. Normal Sinus Rhythm
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Implies normal sequence of conduction, originating in the sinus node and proceeding to
the ventricles via the AV node and His-Purkinje system.
EKG Characteristics: Regular narrow-complex rhythm
Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR
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82. Sinus Bradycardia
• HR< 60 bpm; every QRS narrow, preceded by p wave
• Can be normal in well-conditioned athletes
• HR can be<30 bpm in children, young adults during sleep,
with up to 2 sec pauses
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84. Sinus bradycardia--treatment
• No treatment if asymptomatic
• Sxs include chest pain (from coronary
hypoperfusion), syncope, dizziness
• Office: Evaluate medicine regimen—stop all drugs
that may cause
• Bradycardia associated with MI will often resolve as
MI is resolving; will not be the sole sxs of MI
• ER: Atropine if hemodynamic compromise, syncope,
chest pain
• Pacing
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85. Sinus tachycardia
• HR > 100 bpm, regular
• Often difficult to distinguish p and t waves
10/28/2023 85
87. Sinus Tachycardia--treatment
• Office: evaluate/treat potential etiology :check
TSH, CBC, optimize CHF or COPD regimen,
evaluate recent OTC drugs
• Verify it is sinus rhythm
• If no etiology is found and is bothersome to
patients, can treat with beta-blocker
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88. Atrial Fibrillation
• Irregular rhythm
• Absence of definite p waves
• Narrow QRS
• Can be accompanied by rapid ventricular response
10/28/2023 88
89. Atrial Fibrillation—causes and associations
• Hypertension
• Hyperthyroidism and
subclinical
hyperthyroidism
• CHF (10-30%), CAD
• Uncommon presentation of
ACS
• Mitral and tricuspid valve
disease
• Hypertrophic
cardiomyopathy
• COPD
• OSA
• ETOH
• Caffeine
• Digitalis
• Familial
• Congenital (ASD)
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90. Atrial fibrillation--assessment
• H & P—assess heart rate, sxs of SOB, chest pain,
edema (signs of failure)
• If unstable, need to cardiovert
• Echocardiogram to evaluate valvular and overall
function
• Check TSH
• Assess for RVR
• Assess onset of sxs—in the last 24-48 hours? Sudden
onset? Or no sxs?
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91. Atrial fibrillation--management
• Rhythm vs Rate control—if onset is within last 24-48
hours, may be able to arrange cardioversion—use
heparin around procedure
• Need TEE if valvular disease (high risk of thrombus)
• If unable to definitely conclude onset in last 24-48
hours: need 4-6 weeks of anticoagulation prior to
cardioversion, and warfarin for 4-12 weeks after
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92. Atrial Fibrillation
• Cardioversion: synchronized (w/QRS)
delivery of current to heart; depolarizes tissue
in a reentrant circuit; afib involves more
cardiac tissue, but cardiovert
• Defibrillation: non-synchronized delivery of
current
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