Cardiopulm Flashcards
(325 cards)
1
Q
Arrhythmias
A
Sudden cardiac death
2
Q
Hypertensive heart disease
A
Left sided (systemic) Car pulmonale (right sided or pulmonary)
3
Q
Valvular heart disease
A
Calcific valvular degeneration
- calcific aortic stenosis
- calcific stenosis of bicuspid aortic valve
- mitral annular calcification
Mitral valve prolapse
Rheumatic heart disease
Infective endocarditis
Non-infected endocarditis
- nonbacterial thrombotic endocarditis
- lupus
- carcinoid heart disease
- complications of prosthetic valves
4
Q
Cardiomyopathies
A
Dilated cardiomyopathy
Arrhythmoegnic right ventricular cardiomyopathy
Hypertrophic cardiomyopathy
Myocarditis
Other causes of myocardial disease
5
Q
Pericardial disease
A
Pericardial effusion and hemopericardium
Pericarditis
-acute pericarditis
6
Q
Heart disease associated with rheumatologist
A
Ok
7
Q
Tumors fo the heart
A
Primary cardiac tumors
Cardiac effects of noncardiac neoplasms
8
Q
Cardiac transplantation
A
Discuss major complications
9
Q
Arrhythmia: What is the most common cause of rhythmDOs read pg 550
A
Ischemic injury
10
Q
Sick sinus syndrome
A
SA node damaged->bradycardia
11
Q
Atrial fibrillation
A
Myocytes depolarize independently and sporadically (atrial dilation) with variable transmission thru the AV node-> irregular HR=atrial fib
12
Q
Heart block
A
Dysfunctional AV node
13
Q
First degree block
A
Prolonged PR interval
14
Q
Second degree block
A
Intermittent transmission
15
Q
Third degree block
A
Complete failure
16
Q
Abnormalities in gap junction structure or spatial relationship
A
Ischemic heart disease , dilated cardiomyopathies, myocytes hypertrophy, inflammation (myocarditis or sarcoidosis), amyloid…
17
Q
Hereditary conditions arrhythmias
A
AD
Primary electrical DO, Dx thre genetic testing
Chennelopathies: mutations in genes that are required for NL ion channel function
-can be associated with skeletal muscle DOs and diabetes also; most common isolated to heart
18
Q
Most common inherited arrhythmogenic disease
A
Long QT syndrome
19
Q
Genes of long QT syndrome
A
KCNQ1 (K channel LOF)
, KCNH2 (K channel LOF)
SCN5A (Na channel LOF)
CAV2 (caveolin Na current GOF)
20
Q
Short QT syndrome genes
A
KCNQ1 (K channel GOF)
KCNH2 (K channel GOF)
21
Q
Brigade syndrome genes
A
SCN5A (Na channel)
CACNB2b (Ca channel LOF)
SCN1b (Na channel LOF)*
22
Q
cPVT syndrome
A
RYR2 (diastolic Ca release )
CASQ2 (diastolic Ca release LOF)
23
Q
Sudden cardiac death from cardiac cause
A
Unexpected death from cardiac cause, either
- without symptoms or
- within 1-24 hours of symptom onset
- 80-90% of successively resuscitated pts show no lab or ECG changes
24
Q
Coronary artery disease precipitates sudden cardiac death
A
Usually >75% stenosis or one or more of the 3 main coronary arteries
Unfortunately SCD often the first manifestation of IHD
Healed remote MIs seen in about 40$
25
Other causes of sudden cardiac death
Cardiomyopathies, myocarditis, congenital abnormalities of the conduction system, myocardial hypertrophy
26
SCD due to a fatal arrhythmia
Most often arising from ischemia induced myocardial irritability
27
Hypertensive heart disease: left sided hypertensive disease
Left sided hypertensive disease
- pressure overload results in left ventricular hypertrophy (LVH)
- the LV wall is CONCENTRICALLY thickened >1.5 cck, weight >500 gym
Diastolic dysfunction can result in left atrial enlargement
-can lead to atrial fib
28
Hypertensive left sided heart disease may lead to __- and is a risk factor for ___
CHF
| SCD
29
Hypertensive heart disease: right sided hypertensive
Isolated right sided hypertensive heart disease arises in the setting of pulmonary hypertension
Acute car pulmonale may arise from a large pulmonary embolus
-marked dilation of RV
30
Most common cause of pulmonary hypertension is
Left sided heart disease
31
Left sided hypertensive heart disease
Systemic
Concentric
LVH
Decrease lumen
32
Disease of the pulmonary parenchyma that predispose to Cor Pulmonale
Chronic obstructive pulmonary disease
Diffuse pulmonary interstitial fibrosis
Pneumoconioses
Cystic fibrosis
Bronchiectasis
33
Diseases of pulmonary vessels that predispose to Cor pulmonale
Recurrent pulmonary thromboembolism
Primary pulmonary HTN
Extensive pulmonary arteritis
Drug toxin or radiation induced vascular obstruction
Extensive pulmonary tumor microembolism
34
Disorders affecting chest movement predisposing Cor pulmonale
Kyphoscoliosis
Marked obesity (sleep apnea, pickwickian syndrome)
Neuromuscular diseases
35
Disorders including pulmonary arterial constriction predisposing to Cor pulmonale
Metabolic acidosis
Hypoxemia
Chronic altitude sickness
Obstruction of major airways
36
Valvular heart disease
Valve disease may present with stenosis and/or insuffiency
37
Stenosis
Valve doesn’t open completely, occurs chronically
- impedes forward flow
- chronic stenosis may cause pressure overload hypertrophy->CHF
38
Insuffiency
Valve doesn’t close completely, may occur acutely or chronically
- allows reversed flow
- chronic insuffiency may cause volume overload hypertrophy->CHF
39
Mitral valve stenosis cause
Postinflammatory scarring (rheumatic heart disease)
40
Mitral regurgitation cause
Abnormalities of leaflets and commissures
Abnormalities of tensor apparatus
Abnormalities of left ventricle and/or annulus
41
Abnormalities of leaflets and commissures
Postinflammatory scarring
Infective endocarditis
Mitral valve prolapse
Drugs
42
Aortic stenosis cause
Postinflammatory scarring (rheumatic heart disease)
Senile calcific aortic stenosis
Calcification of congenitally deformed valve
43
Aortic regurgitation cause
Postinflammatory scarring (rheumatic heart disease)
```
Degenerative aortic dilation
*syphilic aortitis
Ankylosis spondylitis
Rheumatoid arthritis
*marfans
```
44
Most common valve abnormality
Calcific aortic stenosis
45
Who gets calcific valvular degeneration
60-80 increases with age
Wear a tear associated with chronic HTN, hyperlipidemia, inflammation
46
In calcific valvular degeneration, ___ valves show na accelerated course
Bicuspid
47
Describe valves in calcific aortic stenosis
Osteoblasts like cells, which deposit an osteodystrophy like substance->ossified
Mounded calcification in cusps prevent complete opening of the valve
48
Symptoms of calcific valvular degeneration
Left ventricular hypertrophy (LVH) develops from increased pressure
Most patients with aortic stenosis will die 5 years after developing angina, within 3 years of developing syncope and within 2 years of CHF onset
49
Mitral annular calcification
Calcific deposits in the fibrous annulus
Normally does not affect valve function
Nodules may become sites for thrombus formation or infective endocarditis
50
Who gets mitral annular calcification
Females over 60 with mitral valve prolapse
51
Bicuspid valve
Prone to calcification. Patients can remain relatively asymptomatic until the stenosis reaches a critical point when congestive heart failure rapidly ensues. The dense white nodules of calcification are present on both valve surfaces
52
Aortic stenosis calcification
An aortic valve need not be bicuspid to calcify. Sometimes older adults , a normal aortic valve (three cusps) will undergo calcification, a so called “senile calcific aortic stenosis” nodules of calcification are seen on the cusps
53
Mitral valve prolapse
Valve leaflets prolapse back into LA during systole
Affects 2-3% of adults, mainly female and incidental (mid systolic click**)
54
Marian syndrome
Loss of connective tissue support in the mitral valve leaflets makes them soft and billowy, creating a so called floppy valve
55
Myxomatosis degeneration
MVP leaflets become thickened and rubbery due to proteoglycan deposits (myxomatosis degeneration) and elastic fiber disruption
56
Why else may MVP occur
Complication of other causes of regurgitation (dilated hypertrophy)
57
Symptoms MVP
Most asymptomatic , a minority may experience:
Pain mimicking angina
Dyspnea
Serious (but rare) complications may include
- infective endocarditis
- mitral insuffiency
- thromboembolism
- arrhythmias
58
Rheumatic fever
Multisystem inflammatory disorder following pharyngeal infection with group A streptococcus
59
Incidence of rheumatic fever has _ with more rapid diagnosis and treatment of strep infections
Decrease
60
Acute rheumatic fever
May include a carditis component, and over time may evolve to chronic rheumatic heart disease
Occurs 10 days to 6 weeks after a group a strep infection
-anti-streptomycin O and anti-DNase B
61
Pathogenesis rheumatic fever
Immune response to streptococcal M proteins cross reacts with cardiac (among other) self -antigen
62
RF can include:
Pancarditis, migratory polyarthritis (large jts), subcutaneous nodules, rash (erythema marginatum)
Sydenham chorea: neurologic disorder with involuntary rapid, purposeless movements
63
Cardiac features of acute RF
Pancarditis, featuring Aschoff bodies
Inflammation and fibrinoid necrosis of endocardium and left sided valves, with verrucae (vegetations)
Repeated streptococcal infections will cause these features to recur
64
Chronic RHD
Mitral leaflet thickening, fusion and shortening of commissures, fusion and thickening of tendinous cords, resultingin mitral
65
Chronic RF and RHF
LA enlargement->atrial fib (arrhythmias), thromboembolic events
Pulmonary congestion/RHF
Infective endocarditis
Surgical repair/prosthetic valve replacement
66
Infective endocarditis
An infection of valves and endocardium, characterized by vegetation’s consisting of microbes and debris, associated with underlying tissue destruction
67
Acute infective endocarditis
Rapidly progressing, destructive infection of a previously normal valve
Requires surgery in addition to antibiotics
68
Subacute infective endocarditis
Slower progressing infection of a previously deformed valve (such as in chronic RHD)
-can often be cured with antibiotics alone
69
Infective endocarditis predisposing conditions
Valvular abnormalities
-HRD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV
Bacteremia
- another site of infection, dental work/surgery
- contaminated needle
- compromised epithelium
70
Classic feature of infective endocarditis
Friable, bulky, destructive valvular vegetation’s
-left sided valves are more commonly affected
—right sided valves often involved in IV drug abusers
-friability leads to septic emboli (PE if right side valve)
-vegetation’s are mixtures of fibrin, inflammatory cells, and organisms
—subacute vegetation’s may have a granulation tissue component
71
Nonspecific symptoms of infective endocarditis
Fever, weight loss, fatigue
72
__ are usually present with left sided lesions
Murmurs
73
Organismsof infective endocarditis
S. Viridans (valve abnormalities)
S aureus (normal valves, abnormal valves, IV drug abusers)
S epidermis (prosthetic valves)
HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
74
Acute bacterial endocarditis
<6 weeks with 50% mortality
Highly virulent organisms
Normal valves
Necrotizing, ulcerative destructive lesions
Micro: fibrin, inflammatory cells and organisms
Rapid onset of symptoms
Difficult to cure: surgery
Aortic and mitral valves
Right heart valves if IV drug user
Ring abscess: vegetation erode into underlying myocardium
Emboli->septic infarcts or mycotic aneurysm
75
Subacute infective endocarditis
>6 weeks, most survive with treatment
Less virulent organisms; insidious
Abnormal valves
Less destructive lesions
Micro: granulation tissue, fibrosis, calcification, chronic inflammatory cells
Vague flu like symptoms
Antibiotics
76
Pathological criteria for diagnostic criteria for infective endocarditis
Microorganisms, demonstrated by culture or histologic examination, in a vegetation, embolus from a vegetation or intracardiac abscess
Histologic confirmation of active endocarditis in vegetation or intracardiac abscess
77
Clinical criteria for endocarditis
Blood culture positive for a characteristic organism or persistently positive for an unusual organism
Echocaridiographic identification of a valve related or implant related mass or abscess, or partial separation of artificial valve
New valvular regurgitation
78
Minor clinical features infective endocarditis
Subungual/splinter hemorrhages
Jane way lesions
Oiler nodes, Roth spots
79
Nonbacterial thrombotic endocarditis
Small, sterile thrombi on cardiac valve leaflets, along the line of closure
-loosely attached, not invasive , do not illicit an inflammatory reaction
May be a source of emboli
Associated with malignancies (espicially mucinous adenocarcinomas), sepsis, or catheter induced endocardial trauma
80
Carcinoid heart syndrome
A systemic disorder marked by flushing, diarrhea, dermatitis, and bronchoconstriction; bioactive compounds such as serotonin released by carcinoid tumors
81
In carcinoid syndrome, what correlates with severely of cardiac lesions
Plasma levels of serotonin and urinary excretion of the serotonin metabolite 5-hydroxyindoleacetic acid correlate with the severity of the cardiac lesions
82
Carcinoid heart disease
50% of patients with systemic sx dev cardiac manifestations
-liver normally catabolizes inculcating mediators before they can affect the heart; this usually massive metastatic hepatic burden
-right endocardium and valves*; left side protected due to pulmonary vascular bed degradation of mediators
83
Carcinoid heart disease similar lesions
As patients taking fenfluramine (appetite suppressant) or ergot alkaloids (migraine); affect systemic serotonin metabolism
84
Complications of cardiac valve prostheses
Thrombosis/thromboembolism
Anticoagulant-related hemorrhage
Prosthetic valve endocarditis
- wear, fracture, poppet failure in ball valves, cuspal tear, calcification
- other forms of dysfunction
Inadequate healing (paravalvular leak), exuberant healing (obstruction), hemolysis
85
Cardiomyopathies
Dilated cardiomyopathy
Takotsubo cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Amyloid
86
Dilated functional pattern
Left ventricular ejection fracture, mechanism of heart failure, causes of phenotype, indirect myocardial dysfunction (mimicking cardiomyopathy)
,40%
Impairment of contractility (systolic dysfunction)
Genetic, alcohol, peripartum, myocarditis, hemochromatosis, chronic anemia, doxorubicin (adriamycin) toxicity; sarcoidosis; idiopathic
Ischemic heart disease; valvular heart disease; hypertensive heart disease; congenital heart disease
87
Hypertrophic functional
Left ventricular ejection fraction, mechanism of heart failure, causes of phenotype, indirect myocardial dysfunction (mimicking cardiomyopathy0
50-80%
Impairment of compliance (diastolic dysfunction)
Genetic; friedreich ataxia; storage disease; infants of diabetic mother
Hypertensive heart disease; infants of diabetic mother
Hypertensive heart disease; aortic stenosis
88
Restrictive functional pattern
Left ventricular ejection fraction, mechanism of heart failure
Causes of phenotype
Indirect myocardial dysfunction (mimicking cardiomyopathy0
45-90%
Impairment of compliance (diastolic dysfunction)
Amyloidosis; radiation-induced fibrosis;idiopathic
Pericardial constriction
89
Dilated cardiomyopathy
Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy
90
Pathogenesis dilated cardiomyopathy
Thought to be familial in 30-50% of cases (TTN mutations may account for 20% of all cases); usually AD
Alcohol
Myocarditis
Cardiotoxic drugs
91
Cardiotoxic drugs associated with dilated cardiomyopathy
Doxorubicin, cobalt, IRON overload,
92
Iron overload dilated cardiomyopathy
From hereditary hemochromatosis (HFE mutation) or multiple transfusions
93
Morphology of dilated cardiomyopathy
Dilation of all chambers
Mural thrombi are common
Functional regurgitation of valves
94
Presentation dilated cardiomyopathy
Usually manifests between age 20-50
Progressive CHF ->dyspnea , exertional fatigue, decrease EF (<25% end stage)
- arrhythmias
- embolism
95
Takotsubo cardiomyopathy
Broken heart syndrome
Excess catecholamines following extreme emotional or psychological stress
96
Who gets takotsubo cardiomyopathy
>90% women age 58-75
97
Symptoms takotsubo cardiomyopathy
Similar to acute MI
98
Morph takotsubo cardiomyopathy
Apical ballooning of the left ventricle with abnormal wall motion and contractile dysfunction
99
Hypertrophic cardiomyopathy 1
100% genetic causes
100
Hypertrophic cardiomyopathy phenotype—>leads to heart failure, sudden death, atrial fibrillation, stroke
Hypertrophy, marked
Asymmetrical septal hypertrophy
Myofibroblasts disarray
Fibrosis, interstitial and replacement
LV outflow tract plaque
Thickened septal vessel
101
Arrhythmogenic right ventricular cardiomyopathy
Right ventricular failure and arrhythmias
Familial, AD
Naxos syndrome
102
Right ventricular failure and arrhythmias
Myocardium of the right vertncuarl wall replaced by adipose and fibrosis
Causes ventricular tachycardia or fibrillation->sudden death
103
Familial, autosomal dominant ARVC
Defective cell adhesion proteins in the desmosomes that link adjacent cardiac myocyte
104
Naxos syndrome
Arrhythmogenic right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces
-mutations int he gene encoding the desmoosme-associated protein plakoglobin
105
Hypertrophic cardiomyopathy
A genetic disorder leading to myocardial hypertrophy and diastolic dysfunction leading to reduced stroke volume and often ventricular outflow obstruction
106
Mutations of hypertrophic cardiomyopathy
Numerous..involving sarcomeric proteins
| -most commonly B-myosin heavy chain
107
Morphology hypertrophic cardiomyopathy
Massive myocardial hypertrophy, often with marked septal hypertrophy
Microscopically, myocyte disarray
108
Consequences of extensive hypertrophy in hypertrophic cardiomyopathy
Foci of MI may occur
Left atrial dilation and mural thrombus
Dismissed cardiac output and increased pulmonary congestion leads to exertional dyspnea
Arrhythmias
Sudden death
109
Restrictive cardiomyopathy
Decreased ventricular compliance (increased stiffness), leading to diastolic dysfunction (impaired filling), while systolic function of the LV remains normal
May be secondary to deposition of material with int he wall (amyloid). Or increased fibrosis (radiation)
110
Heart size and restrictive cardiomyopathy
Ventricles are usually of normal size, but both atria can be enlarged
111
Amyloid with restrictive cardiomyopathy
Extracellular deposition of proteins which form an insoluble B pleated sheet
May be systemic (myeloma) or restricted to the heart (usually transthyretin)
- certain mutated versions of transthyretin are more amyloidogenic
- amyloid can involve different parts of the heart, but when deposits are in the interstitiium of the myocardium, a restrictive cardiomyopathy results
112
Amyloid Congo red stain
Apple green birefringence
113
Myocarditis
Inflammation of the myocardium , most commonly due to a virus in the US
114
What viruses cause myocarditis
Coxsackie A and B
115
Infectious causes of myocarditis
Tyrpanosome cruzi (chagas)
Bacteria and fungi
116
Trypanosome cruzi (chagas) and myocarditis
10% die during acute attack
May progress to cardiac insuffiency in 10-20 years
Parasitization of scattered myofibroblasts; mixed inflammatory cell infiltrate (PMB, lymph’s, macrophages, occ eosinophils)
117
Noninfectious causes of myocarditis
Immune mediated reactions including RF, DLE, drug hypersensitivity
118
See table 12-13 p 571
Ok
119
Major causes of myocarditis
Infections
Immune mediated reactions
Unknown-sarcoidosis, giant cell myocarditis
120
Pericardial disease: slow accumulation
Normal<50 mL clear, straw colored fluid
Slow accumulation, <500 mL asymptomatic if slow enough
-globular enlargement of heart shadow on CXR
121
Acute pericardial disease
200-300 mL rapid accumulation
—>cardiac tamponade
Normal<50
122
Fibrinous and serofibrinous pericardial disease most common
-AMI, POSTINFARCTION(dressers),Uremia, chest irradiation, RF, SLE, trauma
123
Fibrinous
Dry, finely granular
124
Serofibrinous
Yellow-brown, turbid fliud with WBC, RBC, and fibrin
125
Symptoms pericardial disease
Pain (sharp, pleuritic and position dependent), fever, +/- CHF
LOUD PERICARDIAL FRICTION RUB MOST STRIKING FEATURE
126
Primary cardiac tumors: top 5
All benign
| -myxomatosis, fibroma, lipomas, papillary fibroelastomas, rhabdomyomas, and angiosarcomas
127
Metastatic tumors to heart occur in _% of people dying from cancer
5
128
My MOA
Most common primary, pedunculated (sessile), usually in region of fossa ovalis
129
Genetics myxoma
Familial syndromes associated with myxoma have activating mutations in GNAS1, encoding a subunit of G protein a(in association with MCCUNE-ALBRIGHT syndrome) or null mutations in PPKAR1A, encoding a regulatory subunit of a cyclic AMP dependent protein kinase (carney complex)
130
Morphology myxoma
Globular hard mass, mottled with hemorrhage to soft, translucent, papillary or villous with a gelatinous appearance
131
Symptoms of myxoma
Ball valve obstruction, embolization or constitutional symptoms (fever malaise)
132
__ form of myxoma cause intermittent obstruction (position dependent) during systole of AV valve or wrecking ball causing damage to the valve leaflets
Pedunculated
133
Constitutional sx of myxoma
Elaboration by some myxomas of the IL-6 , a major mediator of the acute-phase response
134
Auscultation myxoma
Tumor plop
135
Cardiac transplantation
3000 a year worldwide; DCM and IHD most common
136
Major complication of cardiac transplantation
Allograft rejection
| -routine endomyocardial bx to monitor
137
Allograft arteriopathy
Most impt long term limitation
- late, progressice, diffusely stenosing intima proliferation
- 50% dev in 5 yr, virtually all pt within 10yr
- silent MI: enervated transplanted
138
EBV assoc B cell lymphoma
Due to chronic T cell immunosuppression
139
Overall survival cardiac transplantation
90% at year 1, <60% at 5 year
140
Long QT syndrome
Manifests as arrhythmias associated with excessive prolongation of the cardiac depolarization; patients often present with stress induced syncope or sudden cardiac death and some forms are associated with swimming
141
Short QT syndrome
Patients have arrhythmias associated with abbreviated depolarization intervals; they can present with palpating, syncope and SCD
142
Brigade syndrome
Manifests as ECG abnormalities (ST segment elevations and right bundle branch block) in the absence of structural heart disease; patients classically present with syncope or SCD during rest or sleep or after large meals
143
CPVT
Does not have characteristic ECG changes; patients often present in childhood with life threatening arrhythmias due to adrenergic stimulation (stress related)
144
Systemic left sided hypertensive heart disease
Marked concentric thickening of the left ventricle wall causing reduction in lumen size. The left ventricle and left atrium are not he right in this apical four chamber view of the heart.
145
Pulmonary right sided hypertensive heart disease (Cor pulmonale)
Right ventricle dilated and has a thickened free wall and hypertrophied trabecular. The shape of the left ventricle has been distorted by the enlarged right ventricle
146
Cardiac valvular degeneration
Calcific aortic stenosis
Mitral annular calcification
147
Rheumatic aortic stenosis
Commissural fusion is not usually seen. The mitral valve is generally normal, although some patients may have direct extension of aortic valve calcified deposits onto the anterior mitral leaflet. In contrast, virtually all patients with rheumatic aortic stenosis also have concomitant and characteristic structural abnormalities
148
Acute carditis
Pericardial friction rubs, tachycardia, and arrhythmias
Myocarditis can cause cardiac dilation that may culminate in functional mitral valve insuffiency or even heart failure. Approximately 1% of affected die of fulminant RF involvement of the heart
Arthritis typically begins with migratory polyarthritis in which one large joint after another becomes painful and swollen for a period of days and then subsides spontaneously, leaving no residual disability
149
What are verrucae
Vegetation’s=aggregation of fibrin and platelets
Along mitral and/or aortic valvular lines of closure
150
RF histology
Anitschow cells pathogenoc for Rheumatic fever; may be multinucleated
Nucleus-central round oval
Chromatin
-central wavy ribbon
151
Most consistent sign of infective endocarditis
Fever
152
Acute infective carditis
Pt with left sided lesions, 90 % have murmurs
-microemboli give risk to nail bed (splinter) hemorrhages; painless palm or sole erythematous lesions (Jane way); painful fingertip nodules (Oiler); retinal hemorrhages (Roth spots)
153
Jane way lesions
Small erythematous or hemorrhagic, macular, nontender lesions not he palms and soles; consequence of septic embolic events
154
Oiler nodes
Small tender subcutaneous nodules that develop in the pulp of the digits or occasionally more proximally int he fingers and persists for hours to several days
155
Roth spots
Oval retinal hemorrhages with pale centers
156
Sources of mucinous adenocarcinoma??
Ok
157
Endocardial fibrotic lesion in carcinoid heart disease
Involving the right ventricle and tricuspid valve
158
Dilated cardiomyopathy presentation
With slowly progressive signs and symptoms of CHF including dyspnea, easy fatigability, and poor exertional capacity. At the end stage, ejection fractions are typically less than 25% (normal 50-50)
159
Takotsubo
Left ventricular contractile dysfunction following extremes physchological stress; affected myocardium may be stunned or show multifocal contraction band necrosis. For unclear reasons, the left ventricular apex is most often affected leading to apical ballooning that resembles a takotsubo Japanese fishing pot for trapping octopus
160
Dilated cardiomyopathy histology
Masson trichromatic stain) collagen is highlighted as blue
Four chamber dilation and hypertrophy are evident . No mural thrombus at the apex of the left ventricle the coronary arteries were potent
161
Secondary or primary pericardial disease more common
Secondary . Primary usually viral. Secondary; metz from remote neoplasm, s/p surgery, systemic disease
162
Acute suppurative pericarditis
Acute suppurative pericarditis arising from direct extension of an adjacent pneumonia. Extensive purple NT exudate is evident
163
Pericarditis
Fibrinous/serofibrinous exudate (bread and butter pericarditis) usually resolves
164
Myocarditis
Perivascular Aschoff bodies
165
Endocarditis
Subendocardial inflammatory foci. May lead to formation of maccallum plaques (causes abnormal blood flow)
166
Valvulitis
Inflammation may involve the valves, chordates tendinae
167
Benign masses arising from the mesenchymal components of the atrial wall can produce ___ effect by intermittently occluding the atrioventricular valve orifice. Embolization of tumor fragments may occur. 90% arise from the atrial
Ball valve
168
Rheumatic heart disease histology
Aschoff bodies
Valvular lesions
169
Chronic rheumatic disease histology
Fibrous adhesions
Cardiac valve alterations
Fusion of one or more commissures between adjacent leaflets
170
Mitral stenosis
Stenosis and incompetence of the mitral and aortic valve are produced by obstruction of the orifice and regurgitation of blood across the orifice
Right ventricular hypertrophy and dilation and functional tricuspid regurgitation the characteristic opening snap and diastolic rumbling murmur at the cardiac apex
171
SLE heart
Atypical verrucae s endocarditis of Libyan and sacks
172
Nonbacterial thrombotic endocarditis
Sterile thrombi that form as vegetation’s on the superior surface of the leaflets of the aortic mitral tricuspid and pulmonic valves as a result of mild inflammatory and associated surface endothelial damage
173
Infective endocarditis
Results from direct infection of the valvular or mural endocardium by bacteria or other microorganisms including fungi and rickettsia. The bacteria or other microorganisms enter the bloodstream fromt he site of a local infection of the skin, lungs, GU, or oral cavity.
174
Early leasions infective endocarditis
Cardiac valves, unless a congenital cardiac defect which predisposes to mural endocar, is present at the site of a jet lesion. As part of a generalized inflammatory reaction to a. Bacteremia, small thrombi form over foci of endothelial damage on the endocardium, producing lesions similar to those of marantic endocarditis.
175
The heart part 1
Cardiac specialization
Effects of aging
Heart failure
Congenital heart disease
Ischemic heart disease
176
Heart failure
Cardiac hypertrophy
Left sided heart failure
Right sided heart failure
177
Congenital heart disease
Left to right shunts
-ASD, VSF, PDA
Right to left shunts
-TOF and TGA
Obstructive lesions
-coarctation of the aorta, pulmonary stenosis, and aortic stenosis
178
What is the number 1 worldwide cause of mortality
Heart disease 1/3 of death
179
Does heart weight vary
Ya with body habitus, approx .4-.5% body weight
180
Femal heart weight
250-320 GN
181
Male heart weight
300-360 gm
182
RT ventricular thickness
.5-.5 cm thick
183
Left ventricular thickness
1.3-1.5 cm
184
Heart hypertrophy
Increased ventricular thickness
185
Dilation of heart
Enlarged chamber size
186
Cardiomegaly
Increased cardiac weight
187
Myocardium
Atrial myocytes have storage granules that contain atrial natriuretic peptide which promotes arterial vasodilation and stimulates renal salt and water elimination (natriuresis and diuresis) which is beneficial in the setting of HTN and CHF
188
Valves
Due to their thin structure, derive most of their nourishment via diffusion
-normal leaflets and cusps vessels limited to proximal portions
189
3 types of valve damage
Collagen (mitral prolapse)
Nodular calcification (calcific aortic stenosis)
Fibrotic thickening (rheumatic heart disease)
190
Conduction
SA node, AV node, bundle of His, purkinje network
| -normal rate spontaneous depolarization fo SA node (50-100bpm) is faster , thus sets the pace typify
191
Blood supply heart
LAD (diagonal branches), LCX (marginal branches) and RCA
| -ventricular diastole: closure of aortic valve leads to blood flow to myocardium
192
Cardiac stem cells
Bone marrow derived precursors and stem cells present in myocardium; only replaces 1% each year
-no significant recovery in zones of necrosis
193
How does aging effect the myocardium
Increase LV chamber size
Increase pericardial fat
Myocardium changes
-lipofuscin and basophillic degeneration
194
How does aging affect valves
Aortic and mitral valves annular calcification
Fibrous thickening
Mitral leaflets buckle towards lt atrium -> increase left atrium size
Lambal excrescences: small filiform processes form on the closure lines of aortic and mitral valves, probably resulting from the organization of small thrombi
195
Aging and vascular changes
Coronary atherosclerosis
Stiffening of the aorta
196
Lambl excrescences
With time small filiform processes (lambl excrescences) form on the closure lines of aortic and mitral valves., probably resulting from the organization of small thrombi
197
Congestive heart failure
Occurs when the heart is unable to pump blood at a rate to meet peripheral demand , or can only do so with increased filling pressure
198
What causes CHF
Loss of myocardial contractile function (systolic dysfunction)
Loss of ability to fill the ventricles during diastole (diastolic dysfunction)
199
CHF heart on biopsy
Heavy and dilated
200
Cardiac hypertrophy
Cardiac myocytes become hypertrophic when
- sustained pressure or volume overload (systemic HTN or aortic stenosis)
- sustained tropical signals (B adrenergic stimulation)
201
Pressure overload hypertrophy
Myocytes become thicker, and LV increases thickness concentrically
202
Volume overload hypertrophy
Myocytes elongate and ventricular dilation is seen
Heart weight best ensure of hypertrophy in dilated heart (vs wall thickness
203
Despite an increase in energy deman, hypertrophy of myocytes is not accompanied by ___
Increase in blood supple
204
The hypertrophied hear is vulnerable to what
Ischemia related decompensation
205
Pressure overload
Sarcomeres assemble in parallel
206
Volume overload
Sarcomerss arange in series
207
Left sided heart failure
Can be systolic do diastolic
208
Most common causes of left sided heart failure
Myocardial ischemia
Hypertension
Left sided valve disease
Primary myocardial disease
209
Clinical effects of lest sided heart failure are due to what
Congestion in the pulmonary circulation
Decreased tissue perfusion
210
With left sided heart failure there is _ ventricular hypertrophy
Left
211
Morphology left sided heart failure
Heart failure cells
Some red cells and plasma proteins extravasated into the edema fluids within the alveolar spaces, where they are phagocytosed and digested by macrophages, which store the iron recovered from hemoglobin in the form of hemosiderin. These hemosiderin laden macrophages are called heart failure cells and are telltale signs of precious episodes of pulmonary edema
212
In left sided heart failure, what does left ventricular dysfunction lead to
Left atrial dilation
213
In left sided heart failure what does left atrial dilation lead to
Atrial fibrillation, stasis, thrombus
214
Pulmonary congestion and edema with left sided heart failure
Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea
215
Decreased ejection fraction with left sided heart failure results in what
Decreased glomerular perfusion
Stimulating release of renin->increased volume
Prerenal azotemia
216
Advanced left sided heart failure may lead to what
Decreased cerebral perfusion and hypoxic encephalopathy
217
Is right or left sided heart failure more common
Right
218
What is right sided heart failure from
Isolated right sided heart failure results from any cause of pulmonary hypertension
- parenchymal lung disease
- primary pulmonary HTN
- pulmonary vasoconstriction
219
What happens with right sided heart failure
Pulmonary congestion is minimal
The venous system is markedly congested
—liver congestion (nutmeg liver)
—splenic congestion-> splenomegaly
—effusions involving peritoneal, pleural and pericardial spaces
—edema, espicially in dependent areas (ankles)
—renal congestion
220
N*congenital heart disease
Sporadic genetic abnormalities are the major causes of congenital heart disease
Turner syndrome and trisomies 13, 18, and 21
221
Most common genetic cause of congenital heart disease
Trisomy 21
40% of patients with Down syndrome have at least one heart defect
-usually derived fromt he second heart field (arterioventricular septae)
—most commmonly defects the endocardial cushion, including ostium, ASDs, AV valve malformations, and VSDs
222
Notch pathway and congenital heart disease
Associated with a variety of congenital heart defects
-bicuspid aortic valve (NOTCH1)
Tetralogy of fallot (JAH1 and NOTCH2)
223
Why marfans get congenital heart disease
Fibrillin mutations underlie marfans-associated with valvular defects and aortic aneurysms
224
Name congenital heart diseases
Left to right shunts
Atrial septal defects
Ventricular septal defects
Patent ductus arteriosus (PDA)
Right to left shunts
Obstructive lesions
225
Most commmon heart defects in downs
Atrioventricular septal defects, or AV canal defects (45%)
Ventricular septal defects (35%)
Secundum atrial septal defects (8%)
Patent ductus arteriosus (7%)
226
What does fibrill do
Structural protein in ECM, also an important negative regulator of TGF-B signaling and hyperactive TGF-B signaling contributes to the cardiovascular abnormalities in marfan and loeys-diets
227
Most common congenital cardiac malformation
Ventricular septal defect
228
Genes associated with ASD or conduction defects
NKX2.5 transcription factor
229
Genes associated with ASD or VSD
GATA4 transcription factor
230
Tetralogy of fallot genes
Zfpm2 or NKX2.5 transcription factor
231
Alagille syndrome
Pulmonary artery stenosis or tetralogy of fallot
JAG1 or NOTCH2 signaling proteins or receptors
232
Char syndrome
PDA
TFAP2B transcription factor
233
CHARGE syndrome
ASD, VSD, PDA, or hypoplasia right side of the heart
CHD7 helices binding protein
234
DiGeorge syndrome
ASD VAD or outflow tract obstruction
| TBX1 transcription factor
235
Holt roam syndrome
ASD, VSD, or conduction defect
TBX5 transcription factor
236
Noonan syndome
Pulmonary valve stenosis , VSD, or hypertrophiccardiomyopathy
PTPN1, KRAS, SOS1
Signaling proteins
237
Most common congenital heart disease
Left to right
- ASD
- VSD
- PDA
238
Presntation of atrial septal defect
Asymptomatic until adulthood
But get left to right shunting causing volume overload on the right side, which leads to
- pulmonary HTN
- right heart failure
- paradoxical embolization
- may be closed surgically , with normal survival
239
What are the atrial septal defects
Secundum ASD
Primum anomalies
Sinus venosus defects
240
Secundum ASD
90% of all asd; center of atrial septum ; may be multiple of fenestrated
241
Primum anomalies
5% of all ASD
Adjacent to AV valves
Often associated with AV valve abnormalities and/or VSD
242
Sinus venosus defects
5% of all ASD
Near entrance of SVD
Can be associated with anomalous pulmonary venous return to the R atrium
243
Patent foramen oval
80% close by 2
Remaining 20% the flap can open if increase right side pressure
-thus even temporary increase in pressure can produce brief periods of R-L shunting
—pulmonary HTN, bowel movement, coughing, sneezing
Paradoxical embolus
244
Most common congenital heart disease
Ventricular septal defect
245
VSD types
90% membranous
Infundibulad VSD: below pulmonary cancer or within muscular septum
246
Effects of VSD depend on what
Size, and presence of other heart defects
| -those that manifest with SX as childre, often associated with other cardiac anomalies
247
Many small VSD do what
Close sponataneously
248
Large VSD
May cause significant shunting, leading to
- right ventricular hypertrophy
- pulmonary HTN, which can ultimately reverse flow through the shunt, leading to cyanosis
249
If VSD symptoms manifest in adulthood
Usually a single defect
250
Patent ductus arteriosus
May fail to close when infants are hypoxic and/or have defects associated with increased pulmonary vascular reassure
PDA produces a harsh , machinery like murmur
251
Effect of PDA is determined by what
Shunts diameter
| -large shunts can increase pulmonary pressure and eventually shunt reversal and cyanosis
252
Right to left shunt presentation
Cyanosis early in postnatal life (cyanosis congenital heart disease)
253
What causes R to L shunt
Tetralogy of fallot, most common
Transposition of great arteries
Persistent truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous connection
254
Tetralogy of fallot features
```
FOUR
VSD
Obstruction of RV outflow tract
Aorta overrides the VSD
RV hypertrophy
```
255
What does heart look like in TOF
Enlarged and boot shaped because of the right ventricular hypertrophy
256
Linical severity of TOF depends on what
Degree of subpulmonary stenosis
-mild stenosis: L to R shunt
Classic TOF is R to L shunting with cyanosis
-mst infants cyanosis from birth, or soon after
257
Trnaposion of great vessels results in
Two separate circuits, incompatible with life after birth unless a shunt is present for mixing of blood form the two circuits
- approximately one third have VSD
- 2/3 have a patent foramen ovale or PSA
- right ventricle becomes hypertrophic (supports systemic circulation) and the left ventricle atrophied
- without surgery, patients will die within a few months
258
Coarctation of the aorta
Narrowing of the aorta, generally seen with a PDA (infantile) or without a PDA (adult form )
259
Who gets coarctation of aorta
Males 2x, Turner syndrome 45 XO
260
Clinical severity of coarctation of the aorta depends on what
Clinical severity depends on the degree of stenosis and potency of the ductus arteriosus
261
Coarctation with PDA manifests when
At birth; may produce cyanosis in the lower half of the body
262
Coarctation it’s out PDA presented
Usually asymptomatic
- HTN in UE; hypotension in LE
- claudication and cold lower extremities
- may eventually see concentric LV hypertrophy
263
What can get from coarctation of aorta
Pulmonary stenosis and atresia
Aortic stenosis and atresia
264
Turner syndrome
Complete or partial monosomy of the X chromosome and is characterized primarily by hypogonadism in the phenotypic females. Bilateral neck webbing and persistent looseness of skin on the back of the neck, left sided cardiovascular abnormalities, particularly predictable coarctation of the aorta an bicuspid aortic calve, are seen most frequently. Cardiovascular abnormalities are the most important cause of increased mortality in kids with turner
265
Ischemic heart disease results from
Insufficient perfusion to meet the metabolic of the myocardium
266
Blood to the myocardium is supplied by what
Coronary arteries, so any disruption of coronary flow may result in ischemia
267
Ischemia results in what
Myocardial infarction
Angina pectoris
Chronic ischemic heart disease, with heart failure
Sudden cardiac death
268
Ischemic heart disease is leading cause of death in US and >90% are secondary to ___
Atherosclerosis
-chronic vascular occlusion
-acute plaque change
—thrombus
269
Angina pectoris
Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction
270
Three clinical variants of angina pectoris
Stable angina
Prinzmetal variant angina
Unstable (crescendo) angina
271
Stable angina
Stenosis occlusion of coronary artery
Squeezing or burning sensation, relieved by rest or vasodilator
Induced by physical activity, stress
272
Prinzmetal variant angina
Episodic coronary artery spasm, relieved with vasodilator
Unrelated to physical activity, HR or BP
273
Unstable crescendo angina
Frank pain, increasing in frequency, duration and severity; at progressively lower levels of physical activity, eventually even at rest
Usually rupture of atherosclerotic plaque, with partial thrombus
50% may have evidence of myocardial necrosis, acute MI may be imminent
274
MI
Age distribution and risk factors mirror those atherosclerosis in general, because nearly 90% of infarcts are caused by an atheromatous plaque
Or embolus, vasospasm, ischemia secondary to vasculitis, shock, hematologic abnormalities
275
Classic presentation MI
Prolonged chest pain >30 min
- crushing, stabbing , squeezing, tightness
- radiating down left arm
Diaphoresis
Dyspnea
Nausea-vomiting
Up to 25% are asymptomatic
276
MI the location , size and features of acute MI depend on what
Site, degree and rate of occlusion of artery, size of the area perfused, duration of occlusion, metabolic and oxygen needs of the area at risk, extend of collateral blood flow, presence of arterial spasm
277
Ischemia of myocytes
| Seconds, 2 min, 10 min, 40 min, 20-40 min, >1 hour
Onset of ATP depletion
Loss of contractility
ATP reduced 50%
10%
Irreversible cell injury
Microvascular injury
278
Coronary vessels and areas of infarction
LAD (40-50%)
-apex, LV anterior wall, anterior two thirds of septum
RCA (30-40%)
-RV free wall, LV posterior wall, posterior third of septum
LCX (15-20%)
-LV lateral wall
279
Transmural infarcts RV
Permanent occlusion of the left anterior descending branch
Permanent occlusion of left circumflex
Permanent occlusion of right coronary artery (or its posterior descending branch)
280
Non transmural infarcts LV
Transient/partial obstruction-> regional subendocardial infarct
Global hypotension->circumferential subendocardial infarct
Small intramural vessel occlusions->microinfarcts
281
Distribution of MI necrosis correlated with the location and nature of decreased perfusion. Left, the positions of transmural acute infarcts resulting from occlusions of the major coronary arteries; top to bottom, left anterior descending, left circumflex, and right coronary arteries. IGH, the types of infarcts that result from a partial or transient occlusion, global hypotension, or intramural small vessel occlusion
Ok
282
0-1 hours MI
Reversible..no gross features, no light microscope,
EM relaxation of myofibroblasts, glycogen loss, mitochondrial swelling
283
1/2 4 hours MI
No gross features,
LM variable waviness of fibers at border
EM sarcolemmal disrutpion, mitochondrial amorphous densities
284
4-12 hours MI
Dark mottling
LM early coagulation necrosis; edema, hemorrhage
285
12-24 hours
Dark mottling
LM ongoing coagulation necrosis; pyknosis of nuclei; myocyte hypereosinophilia; marginal contraction band necrosis; early neutrophilic infiltrate
286
1-2 days MI * note after 4 hours irreversible
Mottling with yellow tan infarct
LM coagulation necrosis, with loss of nuclei and striations; brisk interstitial infiltrate of neutrophils
287
3-7 days MI
Hyperemic border; central yellow tan softening
LM beginning disintegration of dead myofibroblasts, with dying neutrophils l early phagocytosis of dead cells by MACROPHAGES at infarct border
288
7-10 days MI
Maximally yellow tan and soft, with depressed red tan margins
LM well developed phagocytosis of dead cells; granulation tissue at margins
289
10-14 days MI
Red gray depressed infarct borders
Well established granulation tissue with new blood vessels and collagen deposition
290
2-8 weeks MI
Gray white scar progressive from border toward core of infarct
LM increased collagen deposition, with decreased callularity
291
>2 months MI
Scarring complete
Dense collagenous scar
292
Acute MI over 24 hours
Coagulation necrosis, pyknotic nuclei, loss of cross striations
293
MI 1-3 days
Loss of striations
Neutrophilic infiltration
294
Repercussion
Restoring blood flow to an area of ischemia and impending infarction
-an attempt to limit the infarct size by rescuing at risk myocardium
Thrombolysis, angioplasty and stent placement, CABG
295
Effects of reperfusion
Following coronary occlusion, contractile function is lost within 2 minutes and viability begins to dismiss after 20 minutes . If perfusion is not restored then nearly all myocardium int he affected region suffers death
If flow is restored, then some necrosis is prevented, myocardium is salvages and at least some function can return. The earlier reperfusion occurs, the greater the degree of salvage. However, the process of reperfusion itself may inducesome damage and return of function of salvaged myocardium may be delayed for hours to days (postischemic ventricular dysfunction or stunning)
296
Release of myocyte proteins in MI
Troponin I or tropoini T, and creatine kinase, MB fraction (CK-MB) are routinely used as diagnostic biomarkers
297
Measuring the blood levels of proteins that leak out of irreversibly damaged myocytes; the most useful are cardiac specific proteins. What are they
Cardiac specific troponin T and I CTnT and CTnI
MB fraction of creatinine kinase CK-MB
298
The most sensitive and specific biomarkers of myocardial damage are what
Cardiac specific proteins, particularly cnTnT and cTnI (proteins that regulate calcium mediated contraction of cardiac and skeletal muscle )
299
Are troponin I and T normally in circulation
No not normally
Following an MI, levels of both begin to rise at 3-12 hours
CTnT levels peak somewhere between 12-48 hours while cTnI levels are maximal at 24 hours
300
Creatine kinase
Enzyme expressed in brain, myocardium and skeletal muscle; it is a dimer composed of two isoforms designated M and B
301
MM and BB diners creatine kinase
MM home dimer s are found predominantly inc Adrian and skeletal msucle, and BB home dimer s in brain, lung, and many other tissues. MB heterodimer are principally localized to cardiac muscle (with considerably lesser amounts found in skeletal msucle)
Thus MB form of CK (CK-MB) is sensitive but not specific , since it can also be elevated after skeletal muscle injury
302
CK-MB begins to rise when
Within three to twelve hours of onset of MI, peaks at twenty four hours, and returns to normal within forty eight to seventy two hours
303
Time to elevation of CKMB, CTnT and cTnI
Three to twelve hours
304
CKMB and cTnI peak
Twenty four hours
305
CKMB returns to normal
Forty eight to seventy two hours
Five to ten days
Five to fourteen days
306
Arrhythmia
Half of all MI deaths occur within one hour of onset and are usually secondary to arrhythmia
Arrhythmia can be a longer term complication of MI, depending on the site and extent of the lesion
-can result from permanent damage to the conducting system, or from myocardial irritability following the infarct
307
Contractile dysfunction
Dependent on size of the infarct and associated loss of function
308
Fibrous pericarditis
Ok
309
Myocardial rupture
Typically requires a transmural infarct
2-4 days post MI, when inflammation and necrosis have weakened the wall
310
Risk factors myocardial rupture
Increased age, large transmural anterior MI, first MI, absence of LV hypertrophy
311
Infarct expansio
Muscle necrosis->weakening, stretching and thinning of the wall
Mural thrombus often seen
312
Ventricular aneurysm
Late complication of large transmural infarcts with early expansion
Composed of thinned wall of scarred myocardium
Also associated with mural thrombus
Rupture does not ususallly occur
313
Myocardial necrosis
Being after forty five minutes of severe ischemia and extends from the subendocardium into the subepicardium in a wave front fashion over a period of approximately three to four hours
314
Subendocardial (intramural) myocardial infarcts
Limited to the inner half of the wall
315
Transmural MI
Extend into the outer half of the wall
316
Lesions of the left anterior descending coronary system give rise to what
Anterior and anteromedial MI
317
Lesiosn of the right coronary artery give rise to
Inferior (posteroapical) and posterior MI
318
Lesions of the left circumflex coronary artery give rise to l
Lateral MI
319
Acute MI may result in death due to pump failure or
Ventricular fibrillation
If patient survives, the infarct undergoes organizationa Nd healing. During the first 2-3 weeks, the necrosis myocardium is gradually replaced by granulation tissue; during the nex two to three months, the granulation tissue is converted to fibrous scar.
320
TRANSMURAL MI
MAY RUPTURE DURING FIRST SEVEN TO TEN DAYS AFTER ONSET. PATIENTS AT HIGH RISK ARE THOSE WITH PERSISTENT HTN DURING THEIR INFARCTS AND THOSE WITH INFARCTS IN REGIONS WITHOUT FIBROSIS; DURING THEIR INFARCTS AND THOSE WITH INFARCTS INR EGIONS WITHOUT FIBROSIS; TYPICLLY THESE ARE FIRST INFARCTS. OVER TIME A DISSECTION TRACK DEVELOPS FROM THE LEFT VENTRICULAR CHAMBER THROUGH THE NECROTIC MYOCARDIUM AND THE COMPLETED PROCESS RESULTS IN ABRUPT DEVELOPMENT OF HEMOPERICARDIUM, CARDIAC TAMPONADE, AND ELECTROMECHANICAL DISSOCIATION. THIS GENERALLY FATAL, IN SOME CASES THE INTRAMURAL DISSECTIONR OCCURS SLOWLY ENOUGH FOR A PERICARDIAL INFLAMMATORY RECTION TO OCCUR AND SEAL OFF A REGION OF PERICARDIUM , CONTAINING THE RUPTURE. THIS GIVES RISE TO A WIDE MOUTHED PSEUDOANEURYSM THAT, UNLIKE TRU ANEURYSMS IS PRONE TO LATE RUPTURE. OTHER SEVERE COMPLCIATIONS OF ACUTE MI INVLVE RUPTURE OF INFARCTED INTERVENTRICULAT SEPTUM TO PRODUCE A VSD AND RUPTURE OF THE HEAD OR ENTIRE TRUNK OF AN INFARCTED PAPILALRY MUSCLE. THESE COMPLCIATIONS LEAD TO SYSTOLIC MURMURS AND CARDIAC FIALURE
321
Concentric hypertrophy hypertension
Leads rapidly to cardiac hypertrophy, a compensatory increase of mass of the LV. The typical pattern of concentric hypertrophy of the LV, characterized by a thick wall and a relatively small chamber columns, is produced by a pressure load (afterload) on the ventricle. The heart size on cardiac silhouette is relatively normal, but the ECG shows increased voltage. When the limits of compensation are reached, the patient may have progressive cardiac decompensation accompanied by cardiac dilation. Cardiac hypertrophy is an independent risk factor for ventricular arrhythmias and sudden cardiac death
322
Heart failure
A state in which the heart fails as a pump to provide sufficient volume of circulating blood to meet the metabolic demands of the body. Bc the dominant symptoms usually result from pulmonary or systemic venous congestion, the condition is termed CHF
Most commonly, heart failure is of the low cardiac output , but some including thiamine defiency (beriberi), thyrotoxicosis and severe anemia, produce cardiac failure with an increased circulating blood volume (high output cardiac failure) as shown here. The failure may be left sided right sided, or combined left and right sided heart failure. This illustration shows the major manifestations of failure of the left and right ventricles. Cardiac transplantation or an artificial heart is the last therapeutic option. The most common conditions necessitating cardiac transplantation are end stage ischemic heart disease and dilated cardiomyopathy
323
Eccentric hypertrophy
Heart failure results in progressive ventricular dilation superimposed on the hypertrophy, which produces a pattern of eccentric hypertrophy
Left sided heart failure-most commonly from HTN and CAD
324
Right sided heart failure
Cor pulmonale
Due to HTN int he pulmonary circulation, is caused by pulmonary vascular or parenchymal disease
Thromboembolism -may cause sudden death bc the obstruction of the pulmonary vasculature produces pulmonary HTN and acute right sided failure with an impaired return of blood to the left heart with consequent decreased systemic and coronary perfusion and secondary left sided heart failure
Segmental thromboembolism- do not make infarcts bc dual circulation from th epulmnonary arterues and bronchial arteries. Pulmonary infarcts do occur int he presence of thromboemboli and impaired systemic circulation associated with preexistent CHF
325
Chronic Cor pulmonale
Typically develops in response to recurring pulmonary thromboembolic disease or chronic pulmonary parenchymal diseases, particularly chronic bronchitis and emphysema. The heart exhibits significant hypertrophy and dilation of the RV with a normal sized LV
