HEMODYNAMI

C DISORDERS
SHOCK
 SHOCK

 Shock is a state in which diminished cardiac output or

reduced effective circulating blood volume impairs
tissue perfusion and leads to cellular hypoxia.

 Characterized by systemic hypoperfusion which may

be due to
• Reduced cardiac output
• Reduced effective circulatory blood volume
 Types of shock
 Hypovolemic Shock: Hemorrhage, vomiting, diarrhea,
severe burns

 Cardiogenic Shock: Myocardial pump failure

 Septic Shock: Bacterial or Fungal infection

 Neurogenic Shock: Anesthetic accident, spinal cord injury

 Anaphylactic Shock: IgE mediated hypersensitivity

 Compensatory Mechanisms
 In shock, the hydrostatic pressure decreases and the oncotic pressure is
constant:
• The fluid exchange from the capillary to the extracellular space decreases.
• The fluid return from the extracellular space to the capillary increases.

 This increases the blood volume, BP and helps to compensate shock

situations.

 Known as the “Fluid shift system.”

 Stages of shock

 Shock is a progressive disorder if uncorrected leads to

death.
 Phases:
• Non-progressive
• Progressive
• Irreversible
 Non progressive phase:
• reflex compensatory mechanism are activated
• Perfusion of vital organs is maintained

 Progressive phase:
• Characterized by tissue hypoperfusion
• Onset of worsening circulatory and metabolic imbalances

 Irreversible stage:
• Body has incurred cellular and tissue injury so severe
• Even if hemodynamic defects are corrected survival is not
possible
Irreversible Shock leads to:

 Renal failure

 Hepatic failure

 Multiple organ systems failure

 Adult respiratory distress syndrome

 Death
 Hypovolemic Shock
 Results from low cardiac output

 Non-hemorrhagic
 Vomiting
 Diarrhea
 Bowel obstruction, pancreatitis
 Burns
 Neglect, environmental (dehydration)

 Hemorrhagic
 GI bleed
 Trauma
 Massive hemoptysis
 AAA rupture
 Ectopic pregnancy, post-partum bleeding
 Cardiogenic Shock
 Results from low cardiac output

 Due to myocardial pump failure

 Inadequate filling of heart, poor contractility or

outflow obstruction

 Seen in clinical settings of MI, ventricular arrhythmias,

left ventricular dysfunction etc.
 Neurogenic Shock
 Spinal cord injury
 Spinal anesthetic
 Results in hypotension
and bradycardia
 Septic shock
 Results from vasodilation and peripheral pooling of
blood
 Systemic immune reaction to bacterial or fungal
infection
 Tachycardia, depressed cardiac contractility
 Vascular leakage and edema- Hypovolemia
 Compromised nutrient blood flow to organs
 DIC
 Abnormal blood gases and acidosis
 Respiratory distress and multiorgan failure
 Anaphylactic shock

 Systemic vasodilation

 Increased vascular permeability

 Caused by an IgE mediated hypersensitivity reaction

 Tissue hypoperfusion and hypoxia

EDEMA
 Definition
 An abnormal increase in interstitial fluid within tissues

 Fluid collection in different body cavities: hydroperitoneum,

hydrothorax, hydropericardium

 Anasarca - generalized edema with widespread Subcutaneous

tissue swelling
 Causes
 Increased hydrostatic pressure

 reduced plasma osmotic pressure

 lymphatic obstruction

 inflammation

 Sodium and water retention

 Transudate & exudate
EXUDATE TRANSUDATE

Increased permeability Increased hydrostatic or

decreased osmotic P
High in proteins low proteins

High specific gravity Low specific gravity

High cell debris Low cell debris

 Morphology
 Pitting &non pitting edema

 Renal disease: initial manifestation periorbital edema

 Pulmonary edema: wt doubled ,frothy ,contain blood

tinged fluid

 Brain: generalized grossly swollen with narrowed sulci &

broad gyri of skull
Pitting edema
 Clinical consequences

 Sub cutaneous edema: signals underlying cardiac or

renal disease & impair healing

 Pulmonary edema: impair O2 exchange &fluid

collection in septa favors infection

 Brain: life threatening ,risk of herniation &death

HEMOSTASIS
 HEMOSTASIS

 Maintain blood - fluid state in normal vessels

 Hemostasis is a precisely orchestrated process
involving platelets, clotting factors, and endothelium
that occurs at the site of vascular injury and
culminates in the formation of a blood clot, which
serves to prevent or limit the extent of bleeding.
 Components Of Haemostasis:
•Vascular wall (endothelium)
•Platelets
•Coagulation cascade
 Normal Haemostasis
Vasoconstriction

Primary hemostasis

Secondary hemostasis

Repair of vessels and

dissolution of clots
THROMBOSIS
 THROMBOSIS
 Formation of blood clot inside blood vessel-
obstructing blood flow

 Virchow's triad:
• Endothelial injury,
• Stasis or turbulent
blood flow and
• Hypercoagulability
of blood.
Stasis or Turbulent Blood Flow
 Normally blood flow is LAMINAR
• central (rapid moving)=leucocytes and RBCs
• adjacent (slow moving)=platelets
• peripheral (most slow moving)=cell free plasma

 Turbulence contributes to arterial and cardiac thrombus.

 Turbulence contributes to arterial and cardiac

thrombus
 Stasis or Turbulent Blood Flow
 Stasis & turbulence leads to thrombosis by
• laminar flow disruption
• prevent dilution of activated clotting factors
• retards clotting factor inhibitors inflow
• turbulence → endothelial injury or dysfunction.

 Seen in ulcerated atherosclerotic plaques, aneurysms, acute

myocardial infarction etc.
Hypercoagulability

 Following changes seen in composition of blood:

- ↑ coagulation factors e.g., fibrinogen,
prothrombin etc
- ↑ platelet count & their adhesiveness
- ↓ coagulation inhibitors e.g., antithrombin, fibrin
split products.
Classification
 THROMBUS
• A thrombus is a blood clot that forms in a vessel and remains there.
• An embolism is a clot that travels from the site where it formed to
another location in the body.
• Thrombi or emboli can lodge in a blood vessel and block the flow of
blood in that location depriving tissues of normal blood flow and
oxygen.
 Difference
FEATURES ARTERIAL VENOUS
THROMBI THROMBI
1. Blood flow formed in rapidly flowing blood of formed in slow moving blood in veins
arteries & heart

2. Sites coronary, cerebral & femoral artery Superficial veins of lower limbs, deep
veins of lower limbs- femoral,
popliteal &iliac

3. Thrombogenesis due to endothelial injury by due to stasis

turbulence

4. Development Usually mural not occluding the Almost invariably occlusive

lumen completely
 Contd….
5. Propagation retrograde directionn antegrade direction towards
heart

6. Macroscopy grey white red blue

7. Microscopy distinct lines of Zhan composed lines of Zhan not so

of platelets, fibrin, RBCs & WBCs distinct(mainly RBCs)

8. Effects ischemia leading to infarcts edema, ulcer, poor wound healing

e.g., brain, heart

9. Emboli less common more common

 Fate Of The Thrombosis
 Propagation: Thrombi accumulate additional platelets
and fibrin

 Embolization: Thrombi dislodge and travel to other sites

 Dissolution: Result of fibrinolysis, lead to rapid shrinkage

and total disappearance

 Organization: Became organised by the ingrowth of

endothelial cells, smooth muscles cells & fibroblasts&
Recanalization.
EMBOLISM
 EMBOLISM
 Detached intravascular solid, liquid, or gaseous mass i.e., carried by
the blood to a site distant from its point of origin
 Embolus in greek means ‘stopper’ or ‘plug’

 Coined by Rudolf Virchow in 1848

 TYPES
1. Thromboembolism
2. Fat Embolism
3. Air Embolism
4. Cholesterol Embolism
5. Septic Embolism
DIRECTION
1. Anterograde embolus:
Movement of emboli in the direction of
blood flow.

2. Retrograde embolus:
Movement of emboli in opposition to the
blood flow direction.
 ARTERIAL EMBOLISM

 Sudden interruption of blood flow to an organ or

body part due to an embolus adhering to the arterial
wall.

 Sites:
•Common - legs & feet(most often), brain, heart
•Less common – kidneys, intestines and eyes
 Risk Factors:
• advanced age
• cigarette smoking
• hypertension
• obesity
• hyperlipidemia
• diabetes mellitus
• sedentary lifestyle
• stress
• recent surgery
• previous stroke or CVS disease
• h/o long term i.v. therapy
• bone fracture
COMPLICATIONS
1. Coronary - Myocardial infarction (heart attack)
2. Cerebral - Cerebral infarction (stroke)
/ischemic encephalopathy
3. Aorta - Aortic aneurysms
4. LL vessels - Peripheral vascular disease
(gangrene of the legs) :intermittent
claudication
5. Mesenteric -AMesenteric occlusion and bowel
ischemia
VENOUS EMBOLISM
1. Pulmonary Embolism:
 blockage of main artery
of lung or one of its
branches by substance
that travelled from
elsewhere in the body
through the bloodstream
(embolism)

 complication of deep
vein thrombosis.
2. Amniotic Fluid Embolism:
- Complication of labour and immediate postpartum period
- Mortality rate → 80%
- Underlying cause→ Infusion of amniotic fluid or fetal tissue
INFARCTION
 Infarction

 Area of ischemic necrosis caused by occlusion of

arterial blood supply / venous drainage of a particular
tissue
Causes of Infarction
• 99% = thrombus/emboli  arterial occlusion
• Less common causes
• vasospasm
• volvulus
• atheroma swelling (2° haemorrhage in plaque)
• extrinsic vessel compression (tumour)
• edema (constriction of blood supply)
• hernia sac entrapment
• trauma  blood supply rupture
Classification of Infarction
(basis of colour or infection)

Red Infarct
(haemorrhagic)
 venous occlusions
 Loose connective tissue
allows blood to collect
(lungs)
 dual circulation permit flow
of blood into necrotic tissue
(not enough perfusion to
prevent infarction)
 When flow re-established to
previous area of arterial
occlusion & necrosis
Classification of Infarction
(basis of colour or infection)

White Infarct
(anaemic)

• arterial occlusions
• solid organs
(spleen, heart, kidney)
 Morphology
 In spongy organs  extensive hemorrhage  red
infarct  slightly firmer & browner over a few days
(haemosiderin development)

 HPE  ischemic coagulative necrosis dominant

• Inflammatory response
• Followed by reparative response beginning in preserved
margins  infarcts replaced by scar tissue
• Liquefactive necrosis in brain
• Septic infarcts - converted into abscess (with greater
inflammatory response)