2. Hemmorhage is defined as excessiveHemmorhage is defined as excessive
escape of blood outside the blood vessel.escape of blood outside the blood vessel.
Based on vessel bleedingBased on vessel bleeding
Artery veinArtery vein
4. Primary haemorrhagePrimary haemorrhage
It refers to the escape of blood at the timeIt refers to the escape of blood at the time
of injuryof injury
Reactionary haemorrhageReactionary haemorrhage
It occurs with in first 24 hrsIt occurs with in first 24 hrs
It is due to displacement of blood clotIt is due to displacement of blood clot
5. Secondary haemorrhageSecondary haemorrhage
It occurs after 7 to 10 days after injuryIt occurs after 7 to 10 days after injury
It is due to sepsisIt is due to sepsis
acid pusacid pus
Digestion of vessel wallDigestion of vessel wall
6. Clinical signs and symptomsClinical signs and symptoms
DizzinessDizziness
BleedingBleeding
Rapid heart rate and respiratory rateRapid heart rate and respiratory rate
7. INTERNAL BLEEDING- Bleeding with inINTERNAL BLEEDING- Bleeding with in
body cavitybody cavity
EXTERNAL BLEEDING-Blood escapingEXTERNAL BLEEDING-Blood escaping
through wound in skinthrough wound in skin
SPONTANEOUS BLEEDING- patient onSPONTANEOUS BLEEDING- patient on
oral hypoglceamic agents, heriditaryoral hypoglceamic agents, heriditary
coagulopathy.coagulopathy.
8. Steps in haemostasisSteps in haemostasis
vasoconstrictionvasoconstriction
platelet plug &primary haemostasisplatelet plug &primary haemostasis
activation of clotting mechanismactivation of clotting mechanism
secondary haemostasissecondary haemostasis
fibrous organisationfibrous organisation
9. Primary haemostasisPrimary haemostasis
It is a process of platelet plug formationIt is a process of platelet plug formation
It occurs with in seconds of injuryIt occurs with in seconds of injury
important in stopping of blood from vesselimportant in stopping of blood from vessel
Release of granules and plateletRelease of granules and platelet
aggregationaggregation
10. Secondary hemostasisSecondary hemostasis
It occurs via clotting process.It occurs via clotting process.
Reaction 1. intrinsic phaseReaction 1. intrinsic phase
factors 7, 9, 11, 12,along with calcium &factors 7, 9, 11, 12,along with calcium &
plasma protein(PTT)plasma protein(PTT)
Reaction 2. release of tissue thromboplastinReaction 2. release of tissue thromboplastin
(PT)(PT)
Reaction 10. activation of factor 10.Reaction 10. activation of factor 10.
11. Reaction 4. conversion of prothrombin toReaction 4. conversion of prothrombin to
thrombin(factor 5)thrombin(factor 5)
Fibrinogen – fibrin (thrombin)Fibrinogen – fibrin (thrombin)
19. Ligation of major vesselsLigation of major vessels
External carotid and its branchesExternal carotid and its branches
Ligation of greater palatine vesselLigation of greater palatine vessel
20. shockshock
It is a pathophyisiological conditionIt is a pathophyisiological condition
,clinically recogonized as a state of in,clinically recogonized as a state of in
adequate perfusion.adequate perfusion.
24. Basic haemodynamic mechanismBasic haemodynamic mechanism
Reduced circulating blood volumeReduced circulating blood volume
Decreased venous return to heartDecreased venous return to heart
Decreased cardiac out putDecreased cardiac out put
Reduced blood flow through tissuesReduced blood flow through tissues
Tissue hypoxiaTissue hypoxia
AcidosisAcidosis
25. HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK
in circulating blood volumein circulating blood volume
Hypovolemic shockHypovolemic shock
Haemorrhagic Non haemorrhagicHaemorrhagic Non haemorrhagic
Example (fluid loss vomiting burns)Example (fluid loss vomiting burns)
26. Inadequate cardiac outputInadequate cardiac output
Impaired OImpaired O22 delivery and reduced tissue perfusiondelivery and reduced tissue perfusion
Causes-Causes-
Loss of effective contractile function of myocardiumLoss of effective contractile function of myocardium
Reducing adequate forward outputReducing adequate forward output
Cardiogenic shockCardiogenic shock
27. Clinical feature –Clinical feature –
Increase pulmonary artery wedge pressureIncrease pulmonary artery wedge pressure
Decrease cardiac our putDecrease cardiac our put
Increase peripheral vascular resistanceIncrease peripheral vascular resistance
Less mean arterial presser (<60 mmHg)Less mean arterial presser (<60 mmHg)
Management –Management –
Identifying the causeIdentifying the cause
Dopamine (vasopressor), norepinephrine andDopamine (vasopressor), norepinephrine and
doputaminedoputamine
28. Neurogenic shockNeurogenic shock
In neurogenic shock vascular capacity increasesIn neurogenic shock vascular capacity increases
so much that even the normal amount of bloodso much that even the normal amount of blood
becomes incapable of adequately filling thebecomes incapable of adequately filling the
circulatory system.circulatory system.
29. Early Signs and symptoms –Early Signs and symptoms –
Pale skinPale skin
PerspirationPerspiration
NauseaNausea
TachycardiaTachycardia
Feeling of warmth in neck or faceFeeling of warmth in neck or face
30. Late symptoms –Late symptoms –
Coldness in hands and feetColdness in hands and feet
HypotensionHypotension
BradycardiaBradycardia
DizzinessDizziness
Visual disturbanceVisual disturbance
Pupillary dilationPupillary dilation
Hyperpnoea andHyperpnoea and
loss of consciousnessloss of consciousness
31. Septic shockSeptic shock
Due to cell membrane endothelial injuryDue to cell membrane endothelial injury
Peripheral vasodilatationPeripheral vasodilatation
Example Ecoli, klebsiellaExample Ecoli, klebsiella
33. Management –Management –
Early and effective volume replacementEarly and effective volume replacement
Restoration of tissue perfusionRestoration of tissue perfusion
Adequate OAdequate O22 supply to cellssupply to cells
AntibioticsAntibiotics