Download Disorders of blood pressure regulation

Terminology
• Hypertension
Disorders of blood
pressure regulation
– High blood pressure, according to WHO
> 140/90 mm Hg
• Shock
– LifeLife-threatening condition, with
microcirculation failure and severe
disorder of tissue and organ perfusion
Arterial blood pressure
• Is one of the best controlled and
regulated variable of cardiovascular
system
• Normal BP = 120/80 mm Hg
• High limits by WHO = 135/85 mm Hg
Baroreceptors of aortic arch and carotid bodies
BP regulation
• Baroreceptors reflex = main
component of the regulation,
monitors and changes BP immediately,
beat by beat
• Renin – angiotensin – aldosterone
system = longlong-term regulation by
control of circulatory volume
• ADH = increases BP by free water
retention
Chemoreceptors in aortic arch and carotid bodies
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Factors affecting cardiac
performance
Disorders of BP regulation
• Hypertension
• Hypotension
– orthostatic hypotension
– Rapid drop in BP → stress response
activation => circulatory shock
Systemic HTN
Pressure
Systolic
Diastolic
Normal
Normal
<130
<85
Borderline normal
130 - 139
85 - 89
1 degree
140 - 159
90 - 99
2 degree (mild)
mild)
160 - 179
100 - 109
3 degree (severe)
severe)
180 - 209
110 - 119
4 degree (very severe)
severe)
>210
>120
HTN
Essential HTN
~ 95% of patients
• Hemodynamic hypothesis = insufficient Na+
excretion → hypervolemia → ↑ CO → ↑ tissue
perfision → autoregulation vasoconstriction
→ ↑ peripheral resistance
• Vasoconstriction hypothesis = nervous,
hormonal and endothelial regulation
imbalance → IC increase Ca2+ → sustained
vesses wall contraction
• Hypothesis of salt intake influence
(genetically predispose)
• Increased sympathetic activity
Risk factors:
factors: age, sex, increased Na+
intake, family history, obesity
2º hypertension
Renal HTN
Causes:
• Increased RAAS activity (e.g., renal
artery atherosclerosis of
fibromuscular dysplasia)
• Renal parenchyma disorders = volume
HTN (chronic glomerulonephritis,
chronic tubular nephropathy,
autoimmune diseases)
2º hypertension
Endocrine HTN
Neurogenic HTN
Eclampsia, prepre-eclampsia
„White coat hypertension"
hypertension"
HTN in sleep apnea syndrome
Other: coarctation of aorta,
polyarteritis nodosa,
hypercalcemia
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HTN complication
• Vessels – atherosclerosis
• Heart – hypertrophy, endomyocardial
fibrosis, ischemia, heart dilatation, failure
• Brain – disorders of autoregulation (↓
perfusion),
perfusion), stroke
• Kidneys - disorders of perfusion
autoregulation → glomerulosclerosis → ↓
number of functional glomeruli (> 90%) →
ESRD (end stage renal disease)
Pulmonary HTN consequences
• Postcapillary HTN → lung edema →
asthma cardiale
Pulmonary HTN
Increased pressure in in the pulmonary
circulation
• Normal ~ 15 -20 torr
Mechanisms:
• Increased pressure in the left atrium (left(left-heart
failure, mitral valve stenosis) → ↑ BP in the
postcapillary bed → lung edema
• Increase of a blood volume in the pulmonary
circulation = hyperkinetic pulmonary HTN (LR
shunts) → doesn’
doesn’t lead to lung edema = ↑ BP
precapillary
• Increase of pulmonary vessels’
vessels’ resistance
(precapillary pulmonary HTN) –
vasoconstriction, obstruction, obliteration
Shock definition
Acute lifelife-threatening condition
Hemodynamic disorder, which is so extensive,
that delivered oxygen cannot cover tissue demand
Shock = a condition of acute peripheral
circulatory failure due to derangement of
circulatory control or loss of circulating fluid
(Dorland's Medical Dictionary)
• Hyperkinetic, precapillary HTN →
right heart overload → cor
pulmonale
Perfusion depends on:
Sufficient circulatory volume
Ability of the heart to pump blood
State of the vascular bed
Basic disturbance = disorder of perfusion and as
a consequence:
tissue ischemia
metabolism disorder
morphological tissue changes
disorder of
organ function
Main causes of shock
• True loss of intravasal volume
• (bleeding)
• Relative loss of intravasal volume
• (vasodilatation in transversal spinal cord lesion)
• Increased vascular permeability
Type of the shock is defined
by the type of perfusion
disorder
Mnemonic for causes of shock: HEN S2CA2M
Hypovolemia, Endocrine (adrenal, thyroid), Neuropathic
(autonomic), Spinal cord injury/S
injury/Sepsis, Cardiac,
Anaphylaxis/A
naphylaxis/Anaesthesia, Massive PE
• (anaphylactic reaction)
• Decreased ventricular filling
• (pulmonary embolization)
• Decreased cardiac output
• (acute MI)
• Combination
3
Stages of shock
* According to the dynamics of pathophysiologic changes
shock can be divided into three stages:
Compensated stage
Decompensation stage
Irreversible stage
2nd stage = DECOMPENSATION
* Depends on the extent and duration of stress, on
energy resorts of organism and rate of metabolism
A. Tissue hypoxia (and ischemia) → anaerobic
metabolism → m. acidosis
B. Failure of cell membrane transport mechanisms
C. Vasoactive substances release: kallikrein, serotonin,
histamine
D. ↑ permeability of lysosomal membrane → cell damage
Consequences:
Consequences:
Disorders of microcirculation
Disorders of coagulation (DIC
*)
(DIC*)
Disorders of organs function
Signs and Symptoms
• Behavior:
Behavior: restlessness, agitation → apathy,
stupor, coma
• Thirst (↓ circulatory volume, ↑ ADH)
• Skin changes: ↑/↓ t°, sweating, paleness/cyanosis
• BP and HR:
HR: BP is gradually decreases, HR
gradually increases and becomes less palpable
• Urination:
Urination: from the beginning gradually decreases
• ↓ kidney perfusion
• ↑ water reabsorption
Kidney failure
1st stage = COMPENSATED
* Basically, it is normal stress reaction which is aimed to
maintain adequate perfusion of the most important tissues
A. Activation of neurohumoral mechanisms:
a. hypothalamushypothalamus-pituitary axis
b. sympathoadrenal axis (RAAS + ADH)
B. Level changes of glucagon (↑
(↑), insulin (↓
(↓)
Consequences:
Consequences:
↑ myocardium contractility
Centralization of circulation, ↑ peripheral
resistance
↑ kidney resorption of Na+ a H20
↑ glucose concentration, AA, FFA
↑ plasma osmolality and K+ concentration
3rd stage = IRREVERSIBLE
A. Circulatory collapse (paradox vasodilatation)
B. Tachycardia (170(170-180/min)
C. MODS (Multiple Organ Dysfunction Syndrome):
a. “shock kidney”
kidney” – acute tubular necrosis
b. “shock lung”
lung” – acute respiratory distress
syndrome
c. GIT – ulceration, bacterial penetration, fluid
loss
d. CNS:
CNS: cortex = behavioral disorders, agitation;
RF = loss of consciousness; spinal cord = death
Shock classification*
• Hypovolemic shock – decrease of circulatory
volume in relation to vascular capacity
• Cardiogenic shock – failure of heart as a
pump caused by decrease of myocardial
contractility, loss of functional abilities of
myocardium
– Extracardial obstructive shock – restriction
of blood flow by cardiovascular system due to decreased
diastolic filling or increased afterload
• Distributive shock – loss of vasomotor
control with vasodilatation
* pathophysiological
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Hypovolemic shock
• Massive blood loss
• Plasma loss
• Dehydratation
• 10 % loss of circulatory volume is well
tolerated
• 20–
20–25 % loss – compensatory
mechanisms begin to fail
• 40% loss - compensatory mechanisms
have failed
Cardiogenic shock*
shock*
Cardiac output is inadequate to meet
tissue demands
Cause is Primary or Secondary heart failure:
–
–
–
–
–
–
–
acute MI
Decompensated heart failure
Malignant arrhythmia
Cardiomyopathy
Acute valve insufficiency
Large vessel obstruction
Worsening of cardiac fillling (mitral stenosis,
cardiac tamponade, constrictive pericarditis)
* The most common cause of death in the patients with
MI while hospitalization
Distributive shock
• Septic = due to inadequate distribution of
circulatory volume caused by bacterial
toxins, release of vasoactive substances
• Anaphylactic = due to generalized
vasodilatation caused by release of
vasoactive substances primary in antigenantigenantibody reaction
• Neurogenic = due to vasomotor center
failure, which leads to generalized
vasodilatation
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