Transcript Prezentace aplikace PowerPoint

Pathophysiology
of the most common symptoms
and signs of cardiovascular
diseases
Prof. Jan Hanacek, MD, PhD
I. Main symptoms and signs of heart diseases
 chest pain/discomfort, dyspnoea, palpitations, cyanosis,
dizziness and syncope, edema, cough, hemoptysis,
fatigue and tiredness, puls changes, urination during
day, urination during night (nocturia)
Chest pain and/or discomfort
• Angina pectoris – consequence of myocardial oxygen lack
Character: dull and deep (sometimes sharp and superficial)
Pathomechanisms:
– change of oxidative to unoxidative metabolism
– overproduction of toxic metabolites and their accumulation
in myocardium and coronary vessel wall (K+, adenosin,
lactic acid, bradykinin, PGE2 , histamin, serotonin)
– chemical stimulation of free nerve endings of afferent limb
of sympathetic nerve fibres  activation of the ascending
spinothalamic neurons as part of nociceptive system into
the CNS  development of pain
Visceral pain – pain arising from visceral organs induced by
myocardial ischemia
Pain localisation – behind the sternum (Levine's sign)
– in epigastrium
• Referred visceral pain (transferred pain)
– pain is feeling in places which are remoted from the place of its
origin, e.g. pain referred to neck, left arm, back, right arm...
Pathomechanism:
– when an algogenic process affecting the viscus recurs frequently or
becomes more intense and prolonged the painful sensation is
progressively felt in more superficial structures (its localisation
becomes more exact)
– convergence of sensitive informations comming from viscera and
from skin – both converge into the same spinothalamic neurons in
segment of spinal cord  transport into region of CNS responsible for
pain processing
 Sensory impulses from the viscera create an irritable focus in the
segment at which they enter the spinal cord
 Afferent impulses from the skin entering the same segment as
sensory inputs (convergence), are thereby facilitated, giving rise to
true somatic pain
• Senzitization of neurons in dorsal horn – different kinds
of neurons in the dorsal horn are more sensitive to
comming afferent impulses (even not painful) – central
sensitization
Abdominal pain/dyscomfort in right heart failure
– expansion of fluid in the liver  liver capsula distension 
 pain (feeling of pressure) in upper right abdominal quadrant
– feeling dyscomfort in abdomen – it is a result of disturbed
digestion due to GIT congestion
• Dyspnoea – difficulty in breathing, due to different pathomechanisms
activated by disturbances associated with pulmonary
vascular congestion (LV failure)
Pathomechanisms:
a) – overdistension of capilaries and venules in the lung
– incresed amount of fluid in pericapilary space

– stimulation of J-receptors in the lung (rapid shallow breathing)
– stimulation of RAR in the mucous membrane of small
airways (cough)

 aferentation to CNS  activatin of system involved
in development of dyspnea
b) Pulmonary vascular congestion  disturbances of gas exchange in
the lung  hypoxemia  hypoxia of respiratory muscles 
 decreased strength of muscles  decresed pulmonary
ventilation  overburden of respiratory muscles

 afferentation to the central nervous system

development of dyspnea
c) Pulmonary vascular congestion   lung weight lung resistance
to expansion  overburden of respiratory muscles  aferentation
to CNS  development of dyspnoe
d) Edema of small airway wall  obstruction  wheeze  cardial
asthma
e) Developmet of pleural effusions – in congestive heart failure
Pleural fluid is secreted by the parietal
layer of the pleura and reabsorbed by
the visceral layer of the pleura
Pleural effusions appear on chest X-rays
as white space at the base of the lung.
• Orthopnea - difficulty in breathing in the recumbent position releived
by assuming an upright or sitting position
Pathomechanisms:
–  congestion of lung circulation in recumbent position – due to
 blood return to right heart
– decresede activity SNS during sleep 
  heart performance
  congestion of lung circulation
 Paroxysmal nocturnal dyspnea
– sudden attack of dyspnea at rest during the night
Pathomechanism: – result of LV failure due to:
- serious types of dysrhythmias
-  activity of SNS and  activity of PSNS during night
 Dyspnoe in patients with right heart failure
– in serious lung diseases
– when massive pulmonary artery embolisation
– when there is restriction in diaphragm movement due to
ascites and/or liver enlargement
– development of hypoxia and metabolic acidosis due to
right heart failure
• Palpitation – patient s ́ wawenens s f hen enwehenwh hewh fccrens athe
sudden changes in rate, rhythm, and stroke volume
accompanied with unpleasant sensation with the heart beats
Pathomechanisms:
– changes in the heart rate (tachycardia, bradykardia)
– irregularity of the heart beats (PAB, PVB, heart blocks)
– increased force of ventricular contractions (stroke volume)
Main forms of palpitation
- intermittent, irregular, lasting seconds or fractions of seconds –
-„s ktppnd“ enwhs , „ ltp- lfp“ s nes whtfe (due to premature beats)
-„hen enweh s hfp“, „s hfppnd enwhteg“ – due to compensatory pause
following PVB
- slow regular palpitation – due to sinus bradykardia,
– due to junctional rhythm
– due to 3rd degree of AV-block
– abrupt onset and termination of palpitation
– due to paroxysmal supraventricular tachycardia
– fast, irregular palpitations – due to atrial fibrilation
– palpitations induced by specific diseses
– valvular regurgitations, thyreotoxicosis, anemia, hepatal failure
– palpitation associated with the use of tabacco, coffee, tea, alcohol
– „efltdwy-enweh s yedefmn“
Another symptoms and signs associated with
– supraventricular tachykardia:
• dizziness, dyspnea, sweating, chest discomfort, polyuria (due to
ihibition of ADH secretion and stimulaation of ANF secretion)
(during prolonged attack of palpitation)
– ventricular tachycardia:
• nausea, sweating, chest discomfort, dizziness and syncope
• Edema – can be caused by both cardiac and non - cardiac conditions
– accumulation of fluids and swelling of tissues in the lung (lung edema),
and lower part of the body (dependent edema) ankles, feet, legs,
abdominal cavity)
Pathomechanisms:
– left or right heart failure
– fluid accumulation in the interstitial spaces usually in
mentioned areas as a result of bad drenage or gravity, and
preceded by the respiratory symptoms and signs (when LV failure),
and weight gain
Pulmonary edema – accumulation of a fluid in the lung
Causes and pathomechanisms:
 left heart failure, mitral stenosis  accumulation of blood
in front of LV  increased hydrostatic pressure in pulmonary
vessels  development of pulmonary congestion  development
of interstitial pulmonary edema  development of alveolar
pulmonary edema  pulmonary edema
It is facilitated by:
– limited lymphatic drenage of the lung,
– permeability of the alveolo – capillary membrane,
– oncotic pressure of the blood
Symptoms and signs of pulmonary edema
– reduced pulmonary perfusion and decreased transfer factor 
 impaired maximal O2 uptake  hypoxemia  hypoxia of
different tissue in the body  disturbancies of metabolism,
cyanosis
– distension of congested vessels  prevention of enlargement
of alveoli and decrease of lung compliance  dyspnoea
– distention of congested vessels  bronchi are narrowed 
rezistance to breathing  maximal breathing capacity 
progression of dyspnoea on exercise
– rapid shallow breathing
– cough, haemoptysis
E
Edemas
in right heart failure
– accumulation of blood in systemic venous circulation  venous
congestion
– edemas of feet, legs
– congestion of GIT system, ascites
– anasarca (generalized edemas)
Cyanosis – blue or blue-gray discolloration of a mucosa and/or skin due
to an abnormal amount of deoxyganated Hb, metHb and
sulphHb in capillary vascular bed
Mechanisms:
– 5g and more of deoxygenated Hb per 1dl of blood in small superficial
vessels, especially capillaries
– 1.5g/dl of metHb or 0.5g/dl of sulfHb
– slate blue discoloration of the skin – argyria
Cyanosis can be caused by different mechanisms:
- decreased oxygenation of blood in the lungs
- increased consumption of O2 by tissue
- decresed speed of blood flow
- drug overdose-nitrates, nitrites
- due to deposition of melanin stimulated by silver iodide
• Development of cyanosis is less probable in people suffering
from anemia and more probable in people with polycythemia
• Syncope – transient loss of cosciousness associated with weakness
and inability to maintain an upright position
Pathomechanism:
– result of inadequate cerebral blood flow and reduced perfusion of
the brain
– another symptoms and signs associated with syncope:
loss of vision, aphasia, muscular weakness, confusion,
generalized convulsive movements
• Fatigue and weakness – skeletal muscles indurance
and strength is decreased
Pathomechanism:
– low cardiac output
– redistribution of blood flow peripheral vasoconstriction 
 centralisation of blood flow  oxygen and substrates supply
to the working muscles
Changes of arterial pulse and blood pressure
• Changes of the rate, regularity, amplitude, and quality of arterial pulse
should be taken into account
– radial pulse deficit: the consequence of irregular heart activity  some
diastolic pauses are too short to normal filling of the LV  some LV
contractions are ineffective (no systolic blood ejection)
– weak thready pulse: the consequence of a low stroke volume
or incrased/decreased peripheral arterial resistance
– forceful bounding pulse: consequence of high stroke volume and
reduced peripheral arterial rersistance
– small pulse with a slow upstroke (pulsus tardus):
- result of aortic stenosis
– bounding, rapidly rising and collapsing pulse (reffered to a waterhammer
pulse or Corrigans pulse: result of aortic regurgitation
– pulsus alternans: alterning strong and weak pulses at regular intervals:
- it frequently reflects LVF
– pulsus bigeminus: alterning strong and weak pulses at irregular intervals:
- consequence of extrasystolic bigeminia
– pulsus paradoxus: smaller pulse amplitude during inspirium:
- it is the consequence of exaggerated fall in systolic BP
of greater than 10 mmHg during inspiration – it is
present in heart tamponade and constrictive
pericarditis
Pulsus alternans
 Cosequence of ventricular function changes
a) Mechanical alternans (pusus alternans)
b) Electrical alternans (alternation of tall and short QRS kompexes)
a) Mechanical alternans
– beat-to-beat oscilation in the strength of ventricular myocardium
contraction at a constant rate (sinus rhythm)
Manifestation: - in patients with heart failure
- in patients with aortic or subaortic stenosis
Mechanisms responsible:
1) based on Frank-Starling mechanism
2) based on alternation of myocardial contractility:
- due to alternation of iCa2+ concentration caused by alternation
of Ca2+ release from sarcoplasmatic reticulum (e.g. in hypotermia,
ischemia)
Ankle-brachial index (ABI)
ABI = Ankle systolic BP/ Arm systolic BP
– test comparing the BP in feet to BP in arm
– it is used for diagnosis of peripheral arterial diseases
Normal ABI: 1.0 – 1.3
Supranormal: > 1.30 (OK!)
A normal resting ankle-brachial index is 1.0 to 1.3. This means that your BP
at your ankle is the same or greater than the pressure at your arm, and
suggests that you do not have significant narrowing or blockage of blood flow.
Abnormal
An abnormal resting ankle-brachial index is 0.9 or lower.
If the ABI is 0.91 to 0.99, it is considered borderline abnormal.
Venous pressure and pulsation
Jugular venous pressure and pulsation reflect the function of
the right side of the heart:
– pressure in the internal jugular vein (IJV) is taken as the central
venous pressure(CVP)
– CVP is increased when pulsation in IJA is present higher than 3 cm
over the sternal angle: it is the consequence of right side heart failure
– paradoxic increase in CVP during inspiration (Kussmauls sign):
consequence of venous return impediment to the right heart – it is
present in severe right heart failure
– positive hepatojugular reflux: result of right HF
Pulsation in internal jugular vein
- Norm – up to 7 cm over
- Pathologic – more than 10 cm
Record of Int jug art pressure
a - right atrium contraction
c - transmission from right ventricular
pressure during its isometric
contraction
x - TK in atrium during its relaxation
and shift of fibrous anulus
downword
v – end of atrium filling
y - atrium empties
Precordial movements – sign of ventricular hypertrophy and
incresed myocardial contractility
Pathomechanism:
– LV hypertrophy
 the apical impulse is more sustained, more forceful, and larger
 point of maximal impulse done by LV is displaced laterally to the
left and down-ward
– RV hypertrophy  produces substernal heave or a systolic lift of the
sternum
Abnormal heart sounds
– third heart sound – develops during fast filling of ventricle in early
phase of diastole
– forth heart sound – it is present at the end of ventricular distole
due to pushing the blood from atrium by its
contraction
Abnormal heart sounds