CARDIOVASCULAR DISEASES

ACUTE CIRCULATORY FAILURE (Shock)

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 SHOCK
Inadequate organ perfusion (blood flow rate) to
meet the tissues oxygenation demand

Early Signs of Shock in Non-Complicated Patients

Warm early stage / Pre shock stage

High index of suspicion signs
- Tachycardia
- Orthostatic hypotension
- Pulse pressure narrowing
- Restlessness
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 Signs of Late Shock Hypotension

Cold late stage

Cold, clammy and pale skin
Rapid, weak, thready pulse
Cyanosis (bluish discoloration of skin)
Rapid breathing
Altered Mental Status -> Coma
Anuria - Low urine production
 End Stage Clinical effects
GI
Cardiovascular
Ischemic bowel
Myocardial depression
Vasogenic effects
Hepatic
Liver failure
Pulmonary
ARDS (acute respiratory
deficiency syndrome) Hematologic
Neutropenia,
Thrombocytopenia
Renal
ARF (Acute Renal Failure)
CNS
Coma
Multiple Organ Dysfunction Syndrome

Number of Mortality (%)

Organs
0 0.8
1 6.8
2 26.2
3 48.5
4 68.8
5 83.3
 Clinical features of shock
- Drop of systolic blood pressure 50 mm Hg
(In hypertonic patients: decrease of 90 torr)
- Low cardiac output and tachycardia
- Vasoconstriction: skin, visceral and abdominal areas
- Oliguria (< 20 mL/hour)
- Cold wet skin / Fevers or rigors (sepsis)
- Constriction of superficial veins
- Marked muscle weakness and trauma pain
- Wheezing (Anaphylaxis)
- Disorientation / confusion
- Metabolic acidosis
 Cardiovascular dysorders in shock

a) Acute circulatory insufficiency

b) Mismatching between blood volume

and volume of vascular bed

tissue hypoperfusion
Factors determining tissue perfusion
A. cardial: cardiac output
B. vascular: changes in vascular resistance
C. humoral: renin, vazopresin, prostaglandins, kinins,
atrial natriuretic factor
 Classification and Etiology of
Acute circulatory shock

1. Hypovolemic - intravascular fluid volume loss,

hemorrhage, fluid depletion or
sequestration

2. Cardiogenic - impairment of heart pump

myopathic lesions: myocardial
infarction, cardiomyopathies
dysrhythmias, obstructive lesions of
intracardial blood flow mechanics
3. Distributive - pathologic redistribution of intravascular
fluid volume
septicaemia: endotoxic, secondary to
specific infection (acute allergic reaction
to an antigen)

4. Obstructive - factors extrinsic to cardiac valves and

myocardium, vena cava obstruction,
pericardial tamponade (compression of
heart by fluid accumulation,
pulmonary embolism,
coarctation (narrowing) of aorta
 REASONS

1. Haemorrhage (Bleeding Fluid Loss)

- Internal / external / body cavity
Eg:
- Abdominal haemorrhage due to leak aortic aneursym
- Ruptured spleen
- Ectopic pregnancy
- Plasma loss in severe burns
- Acute pancreatitis
- Excess urinary fluid loss (diabetic ketoacidosis)
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2. Left / Right side of heart or Pulmonary circulation
interrupted
- Acute myocardial infarction (AMI)
- Acute massive pulmonary embolism
- Acute pulmonary oedema

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ASSOCIATED CAUSES AND DISORDERS
- Dissecting aneurysm of aorta
- Pericardial tamponade
- Aortic valve disease
- Myocardial infarction
- Progressive myocarditis
- Drugs and alcohol
- Diuresis
- Pulmonary congestion
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IF PROMPT TREATMENT IS NOT GIVEN,
SYSTEMIC CONSEQUENCES OCCUR

- Visual and cerebral impairment

- Renal failure: increase urea, K+, acidosis
- Gut: haemorrhage, decrease absorption
- Muscle: acidosis, K+ release
- Skin: peripheral gangrene

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 Stages of shock
1. Non-progressive stage (compensated)
Compensatory mechanisms (negative feedback) of the
circulation can return CO and BP to normal levels

- Reflex action Sympathetic stimulation arteries

and veins constriction in most parts of the body
protection of coronary and cerebral blood flow

- Angiotensin-aldosterone, Anti Diuretic Hormone

vasoconstriction, water and salt retention by the
kidneys

- Absorption of fluid from body tissues like GIT,

increased thirst
2. Progressive shock
- circulatory system themselves begin to deteriorate, without therapy
shock becomes steadily worse until death

- positive feedback mechanisms are developed and can cause vicious

circle of progressively decreasing CO

Cardiac depression - coronary blood flow, contractility

Vasomotor failure - cerebral blood flow
Release of toxins by ischemic tissues: histamine, serotonin, tissue
enzymes
Intestines hypoperfusion mucosal barrier disturbance
endotoxin formation and absorption
vasodilatation, cardiac depression
Vasodilation in precapillary bed

Generalised cellular deterioration: Signs of multiorgan failure

3. Irreversible shock
- despite therapy circulatory system continues to
deteriorate and death ensures
- marked hypoxic tissue damage
- endothelial dysfunction adhesive molecules,
neutrophils, macrophages inflammation
- progressive acidosis
- microcirculation failure plasma proteins leakage

- advanced intravascular coagulation

 Septic shock

Typical causes: Peritonitis, gangrenous infection, pyelonephritis

Special features:
1. high fever
2. marked vasodilatation (inflammation)
3. or normal CO: vasodilatation, metabolic rate
4. disseminated intravascular coagulation clotting factors to
be used up hemorrhages occur into many tissue in GIT

Bacterial toxins deterioration of circulation end-stage is

similar to hemorrhagic shock
Death: - hypotension
- multiorgan failure
 Cell dysfunction
Prolong tissue hypoperfusion cell membrane lesion,
lack of lysosomal enzymes cell death

mechanisms: hypoxia, inflammatory mediators,

free radical mechanism

Multiorgan failure
Kidney
- blood flow (to 10%) GF oliguria
- ischemia acute tubular necrosis
- countercurrent mechanism failure and lesions
acute renal failure
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TREATMENT
- Restore and maintain cardiac output
- Identify the cause and special treatment for it

During investigation and treatment, patient should be

protected and monitored for:
- Unnecessary disturbance
- Hypothermia
- Anxiety
- Pain
- Oxygen supply
- Urine output (catheter)
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Hypovolemic (Acute) Circulatory Failure
Fluid replacement
- Isotonic saline / plasma / plasma substitutes < 2lit
- Specific fluid lost to be replaces > 2 lit
- Rate of fluid replacement
- Large transfusion warm the fluid to body temp.

Venous pressure checking

- Jugular venous pressure, Central venous pressure,
Pulmonary venous pressure, Left atrial pressure (LAP)
- LAP 5-10 mm Hg is normal, ACF 30 mm Hg,
should be reduced to 14-15 mm Hg
- Swan-Ganz catheter
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Swan-Ganz catheter

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Acute Pulmonary oedema / Left side cardiac
problem
Diuretics
Vasodilators
Morphine (Relieve breathlessness and reverse vaso
constriction, reduce pain)
High concentration of oxygen supply
Ionotropic agents (Stimulate heart functioning)

Eg: Glyceryl trinitrate (sub-lingual / buccal tablet, spray)

Iso-sorbide dinitrate (IV infusion)
Dopamine (IV infusion)
Dobutamine (IV infusion)
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Circulatory Assist Devices
Intra aortic balloon pump (IABP)

Partial cardiac bypass

- Right ventricular assist device (RVAD)
- Left ventricular assist device (LVAD)
- Biventricular assist device (BVAD)

Extra corporeal membrane oxygenator (ECMO)

Supportive treatment for other systems

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