Pathophysiology of the most common

symptoms and signs of cardiovascular

diseasesProf. 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 anSensory impulses from the viscera create an irritableirritable focufocus s in thein the

segment at which theysegment at which they enter the spinalenter the spinal cordcord

Afferent impulses from the skin entering the sameAfferent impulses from the skin entering the same

segmentsegment as as sensory inputs sensory inputs (convergence),(convergence), are therebyare thereby facilitated, facilitated, giving rise togiving rise to

true true somatic somatic painpain

•• Senzitization of neurons in dorsal horn – different kinds Senzitization of neurons in dorsal horn – different kinds

of neurons in the dorsal horn are more sensitiveof neurons in the dorsal horn are more sensitive toto

comming afferent impulses (even not painful) – comming afferent impulses (even not painful) – centralcentral

sensitizationsensitization

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 awareness of the heartbeat that occures with 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 – -„skipped“ beats, „flip-flop“ sensation (due to premature beats)

-„the heart stop“, „stopped beating“ – 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 – „holiday-heart syndrome“

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

EEdemas 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

• 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

• Development of cyanosis is less probable in people suffering

from anemia and more probable in people with polycythemia

• 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 Corrigans 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 – 1.3Supranormal: > 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 (Kussmauls

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 pressurea - right atrium contractionc - transmission from right ventricular pressure during its isometric contractionx - TK in atrium during its relaxation and shift of fibrous anulus downwordv – end of atrium fillingy - 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