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HYPOTENSION, SHOCK. Kapocsi Judit Semmelweis University 1 st Department of Medicine. REGULATION. SHORT TERM BAROREFLEX LONG TERM COMPLEX SYSTEM CENTRAL MECHANISMS PERIPHERAL MECHANISMS. HYPOTENSION DEFINITION. Mean blood pressure (BP)=COxTPR Normal BP 120/70 + -20 mmHg

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hypotension shock

HYPOTENSION, SHOCK

Kapocsi Judit

Semmelweis University

1st Department of Medicine

slide3

REGULATION

SHORT TERM BAROREFLEX

LONG TERM COMPLEX SYSTEM

CENTRAL MECHANISMS

PERIPHERAL MECHANISMS

hypotension definition
HYPOTENSION DEFINITION
  • Mean blood pressure (BP)=COxTPR
  • Normal BP 120/70+-20 mmHg
  • Hypotension BP<100/70 mmHg
  • Syndrome
hyp ote nsion 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
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
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
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
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
Main clinical symptoms
  • Hypotension
  • Tachycardia
  • Tachypnea
  • Abnormal mental status
  • Poor peripheral perfusion
  • Renal insufficiency
main clinical symptoms1
Main clinical symptoms
  • Clinical findings seen in shock are common to all forms
  • In certain diseases two forms of shock may be present
shock
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
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 index-SVRI)
  • Mixed venous oxygen count (MVO2) determination
hypovolemic shock
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
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
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 shock1
CARDIOGENIC SHOCK
  • Clinical characteristics: jugular and peripheral veins may be distended, mid-diastolic galopp sound, pulmonary edema
  • Hemodynamic status: increased ventricular preload (PCWP, CVP, ventricular volume, SVRI increased), CI decreased
  • MVO2 reduced
extracardiac obstructive shock
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 shock1
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
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
slide21
MODS
  • Multiple organ dysfunction syndrome
  • Homeostasis can not be maintened without intervention
  • Microcirculation is the primary target of injury
primary mods
Primary MODS

Well- defined insult

  • Hypotension
  • Hypoxemia
acute respiratory failure
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
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
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 diagnosis1
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
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
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
SEPSIS

Caused by bacterial or fungal infection

Mediators of inflammatory response

  • TNF-alpha
  • Interleukin 1,2 and 6
  • Gamma interferon
sepsis syndrome
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
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
slide33

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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