Transcript Semestral report exampl

Semestral report from
pathophysiology
Authors, date of
presentation,
patient´s initials
Present disease
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patient has noticed edemas of lower
extremities , in time course of last 2 wks
last 2-3 nights he had dyspnoe at night,
no chest pain, no palpitations
dry non productive cough – 2 wks
he is tired, and does not tolerate physical
activity - no other complaints
History
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7 yrs has problems with heart, and
arrhytimias
2 months ex smoker, quite due to
progressive dyspnoea
Drugs: Isoptin ( for arrhythmias)
- Cynt ( for hypertension)
- Warfarin( as anticoagulant)
Physical examination
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Patient is breathless during examination
Breathing sounds are normal, right lower
segment attenuated
Heart action irregular, rate:100/min, P
frequens, irregullaris et inaequalis
BP:125/75 mm Hg, heart sounds are dull,
holosystolic murmor at the apex with the
propagation to left axilla intensity 2/6
Physical examination
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Hepatojugular reflux
Abdomen above the chest niveau, v.s.
ascites
Liver exceeds right costal arc + 4 cm
Legs: symetric edemas, both sides to the
femoral level, no signs of dep venous
thrombosis, arterial pulsations are present
Lab tests + other exams
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↑liver damage markers, ALT, AST, coagulation: Quick
test 28,2%
Chest X ray: right side basal shadow, v.s. fuidothorax,
left costophrenical angle – small level of fluid, lungs –
no infiltrative changes
Heart SONO: mitral regurgitation
EDV LV 67mm, EF 23%, all heart chambers dilated,
with decreased systolic function and hypokinesis of all
walls
Lab tests + other exams
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Lung functions test: mild restriction
EKG: atrial fibrilation, 110/min, horizontal
axis deviation, TZ V4,V5, voltage criteria
for LV hypertrophy with signs of LV
obverload, no fresh ischemic changes
Based on the symptoms, signs and other
tests we conclude that our patient does
complain with heart failure
Categorization of symptoms and signs
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dyspnoe, paroxysmal nocturnal dyspnoe, night cough
dull chest percussion, attenuated breathing sounds, X ray
proved fluidothorax
symptoms and signs of respiratory dysfunction which are
caused by left heart failure, with pulmonary congestion and
other consequences of pulmonary congestion
however patient is ex smoker, it means some of the
sympotms of signs in this case may be influenced by the
fact patient had been smoking before
Categorization of symptoms and signs
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peripheral edema, anasarca, ascites
increased filling of jugular veins, hepatojugulary
reflux
hepatomegaly
these heart is not able to eject the blood to the
pulmonary artery we can clearly see congestion
of peripheral venous system with edema, ascites
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Mechanisms responsible for
the onset of symptoms and
signs
Muscle weakness and
fatigue
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These are most common, however
nonspecific symptoms of heart failure, bc
the heart is not able to keep the perfusion
for the peripheral organs which are
enough for their metabolic demands –
including muscles, thats why the patiens is
weak and tired after performimg physical
exercise
• Dyspnoe – subjective feeling of air lack
Pathomechanisms
a)- increased distension of capillaries and venules in lungs
- increased amount of fluids in pericapillary space
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- stimulation of J-receptors
- stimulation of RAR in airways
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- increased afferent input to CNS
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dyspnoe
+ increased work of respiratory muscles bc of decreased
lung compliance
b) Lung congestion  disorders of gas exchange
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hypoxemia
Stimulation of perif. chemorecept.
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increased respir. drive
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overoad for muscles
Decrease of ventilation
Hypoxia of muscles
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overoad for muscles
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increased aff. drive to CNY
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dyspnoea
Paroxysmal nocturnal dyspnoe
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– acute attack of dyspnoe during night rest
Pathomechanism
horizontal position when lying in bed, increased
venous return, increased flow in pulmonary
circulation – pulmonary edema
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– sudden decrease of the left ventricle function
due to decrease of sympathetic activity and
dominance of parasympathetic
Anasarca + edemas
Edema is defined as an accumulation of body fluids with
inadequate distribution of lfuids in interstitial space
Generalized edemas are caused by heart failure , renal
failure, or problems with liver
In our patient we suppose cardial background for edema
creation
Liver is also affected by congestive hypoxia so it may
contribute to decrease production of albumine
Same time the break down of aldosteron is reduced by
hypoxic liver cells increasing retention of Na and water
Postcapillary portal hypertension enhances onset of ascites
bc of impaired Starling balance
Pathomechanisms
left heart failure
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reduction of effective arterial volume
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activation of SNS
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decreased renal perfusion
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activation of RAA
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NA + water retention
Pathomechanisms
right heart failure
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increase of hydrostatic pressure in abdomen, legs
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Starling balance shift
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more filtration than resorbtion
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accumulation of fluids in tissues
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failure of lymphatic outflow
Conclusion
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Set your conclusions
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What was your intention to demonstrate and
whether you did it 