Transcript ESSENTIALIS HIPERTÓNIA

HYPOTENSION, SHOCK
Kapocsi Judit
Semmelweis University
1st Department of Medicine
REGULATION
SHORT TERM
BAROREFLEX
LONG TERM COMPLEX SYSTEM
CENTRAL MECHANISMS
PERIPHERAL MECHANISMS
HYPOTENSION DEFINITION
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Mean blood pressure (BP)=COxTPR
Normal BP 120/70+-20 mmHg
Hypotension BP<100/70 mmHg
Syndrome
Hypotension Syndrome
• Definition of hypotension based mainly on blood
pressure level
• BUT!!!
• Hypotension represents a complex syndrome in
which hemodynamic, neurohumoral and
metabolic abnormalities influence the
development and progression of blood supply
insufficiency of organs
Shock-definition
• The state in which profound and
widespread reduction of effective tissue
perfusion leads first to reversible, and
then, if prolonged, to irreversible cellular
injury.
Syncope
• Sudden transient loss of consciousness, usually due to
transient cerebral hypoperfusion
Causes:
cardiac: arrhythmias
peripheral vascular:
drugs (increased peripheral vasodilation)
vaso-vagal syncope (stress, pain)
hypersensitive carotid sinus
orthostatic hypotension
other: (volume depletion, bleeding, high temperature,
petit mal, hypoglicemia)
Shock-classification
• Classification:
hypovolemic (dehydration, hemorrhage)
cardiogenic (ischemic myocardial injury, heart failure)
distributive
sepsis (endotoxins)
anaphylaxis (hyper-acut immune response)
extracardiac obstructive
(pericardial tamponade, pulmonary emboli)
Shock-pathomechanism
• CO or circulating blood volume decrease--tissue perfusion decrease---anaerob
metabolic pathway---acidosis--compensatory mechanisms---increased
sympathetic tone---exhaustion---more
severe tissue damage---cardiovascular
insufficiency
Main clinical symptoms
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Hypotension
Tachycardia
Tachypnea
Abnormal mental status
Poor peripheral perfusion
Renal insufficiency
Main clinical symptoms
• Clinical findings seen in shock are
common to all forms
• In certain diseases two forms of shock
may be present
SHOCK
The state in which profound and widespread
reduction of effective tissue perfusion
leads first to reversible, and then, if
prolonged, to irreversible cellular injury.
Life-threatening, high mortality situation
The key of the successful management is
the early recognition
Diagnosis in time!
INVESTGATIONAL METHODS
• Catheter into the pulmonary artery:
measurement of pulmonary artery occlusion
pressure („wedge pressure”)- indirect
measurement of the end diastolic pressure in
the left ventricle, measurement of CO
(calculation of systemic vascular resistace indexSVRI)
• Mixed venous oxygen count (MVO2)
determination
HYPOVOLEMIC SHOCK
• Causes: dehydration or hemorrhage
• Clinical characteristics: pale, cool skin, flat
peripheral veins, collapsed jugular veins,
decreased urine output, altered mental status
• Hemodynamic status: decreased preload,
decreased ventricular diastolic pressure and
volume, hypotension (PCWP low, CI low,
SVRI:high
• MVO2 decreased
CARDIOGENIC SHOCK
Causes:
• ischemic myocardial injury
• acute valvular dysfunction
• acut myocarditis
• rapid and slow cardiac rhythms
• congestive heart failure
• hypertrophic cardiomyopathy with obstruction
• Traumatic myocardial contusion
Damages in the heart
• Acut: myocarditis, valvulitis (left ventricular
dysfunction, dilation, relative mitral and/or
tricuspid valve vitium, heart failure)
• Later: platelet-fibrin thrombi
on the valves, fibrosis,
calcification
Mitral valve stenosis and/or regurgitation
Aortic valve regurgitation and/or stenosis
CARDIOGENIC SHOCK
• Clinical characteristics: jugular and
peripheral veins may be distended, middiastolic galopp sound, pulmonary edema
• Hemodynamic status: increased
ventricular preload (PCWP, CVP,
ventricular volume, SVRI increased), CI
decreased
• MVO2 reduced
EXTRACARDIAC OBSTRUCTIVE SHOCK
• Causes: pericardial tamponade,
constrictive pericarditis, pneumothorax,
intrathoracic tumor, pulmonary emboli,
acut pulmonary hypertension, aortic
dissection
• Diastolic filling of right ventricle impaired
• Ventricular afterload increased
EXTRACARDIAC OBSTRUCTIVE SHOCK
• Clinical characteristics: hypotension,
tachycardia, dyspnea, pale or cyanotic
skin
• Hemodynamic status: is dependent on the
site of obstruction, CI and MVO2 are
usually low, SVRI high, PCWP normal or
low, but in the case of tamponade is high
DISTRIBUTIVE SHOCK
• Causes: anaphylaxis, spinal injury, adrenal
insufficiency, sepsis
• The main characteristics: hypotension
because of loss of peripheral resistance,
tachycardia, tachypnea, extremities are
warm and well perfused
• Hemodynamic status: PCWP normal or
low, CI high (rarely low), SVRI low
MODS
• Multiple organ dysfunction syndrome
• Homeostasis can not be maintened
without intervention
• Microcirculation is the primary target of
injury
Primary MODS
Well- defined insult
• Hypotension
• Hypoxemia
HYPOTENSION and/or HYPOXIA
ACUTE RESPIRATORY FAILURE
• Primary function of the respiratory system:
provide oxygen (O2) to, remove carbon
dioxid (CO2) from the tissues
• Failure of the respiratory system leads to
hypoxemia (decreased PaO2)
• Hypoxemia can occur with or without an
increase in PaCO2
RESPIRATORY FAILURE
Type 1
• Abnormally low PaO2 with low or normal PaCO2
• Caused by lung diseases (eg. ARDS)
Type 2
• Abnormally low PaO2 with high PaCO2
• Caused by central nervous system depression
or COPD acut exacerbation
ACUT RESPIRATORY DISTRESS SYNDROME
(ADRS) Diagnosis
• Evaluation of hemodynamic status
• Exclusion of left ventricular failure and chronic
lung disease
• Diffuse pulmonary infiltrate on chest radiography
• PaO2<50 mm Hg on Fi O2 >0.60
• Decreased respiratory complience<50 ml/cm
H2O
(Fi O2=fraction of inspired oxygen)
ACUT RESPIRATORY DISTRESS SYNDROME
(ADRS) Diagnosis
• PaO2 and Fi O2 ratio is<-200
• Bilateral pulmonary infiltrates on a frontal chest
radiograph
• PCWP<-18
• Can occur as the result of direct lung injury
(aspiration, viral pneumonia), or as a part of
MODS
ACUT RESPIRATORY DISTRESS SYNDROME
(ADRS) Pathomechanism
• Damage of pulmonary capillary endothelium or
epithelial mebrane
• Increased permeability of alveolar-capillary
membrane
• Pulmonary edema and intrapulmonary shunting
• Hypoxemia and tissue hypoxia
Death or survival
Secondary MODS
Result of the host response to an insult
• Systemic inflammatory response diseases
(SIRS)
• Chracteristics of SIRS: body temperature>38 0C
or<36 0C, heart rate>90 beats/min, respiratory
rate>20/min, PaCO2<32 mmHg, white blood cell
count>12.000 4/cu mm, <4000 4/cu mm, or>
10% immature (band) form.
• When SIRS develops in response to infection,
the patient has sepsis syndrome
SEPSIS
Caused by bacterial or fungal infection
Mediators of inflammatory response
• TNF-alpha
• Interleukin 1,2 and 6
• Gamma interferon
SEPSIS SYNDROME
Clinical manifestations
• Fever,chills
• Hyperventillation
• Hypothermia
• Mental status changes
• Hypotension
• Leukopenia, thrombocytopenia
• End-organ failure: lung, kidney, liver, heart,
disseminated intravascular coagulation
Treatment
• Should be focused toward underlying
disease
• Supportive therapy for failing organs
(blood transfusion, fluid, electrolits,
oxygen, mechanical ventillation)
• Drug therapy (vasoactive drugs,
antibiotics, hormones, antibodies)
• Control in the intensive care unit
Vitious circle in the pathomechanism of
circulatory shock
HYPOTENSION, HYPOXIA
IMPAIRED AUTOREGULATION
HUMORAL FACTORS
EXHAUSTION
INCREASING BP
METABOLIC ACIDOSIS
VASOCONSTRICTION
TISSUE
HYPOPERFUSION
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