Download SHOCK and HEART FAILURE

SHOCK and HEART FAILURE
08/12/05
1. Shock (cardiovasc collapse): the final result for many potentially lethal clinical events
including hemorrhage, extensive trauma or burns, large MI, massive pulmonary
embolism, and microbial species
- Shock gives rise to systemic hypoperfusion caused by reduction either in cardiac
output or in the effective circulating blood volume
2. End results of shock: hypotension, followed by impaired tissue perfusion and cellular
hypoxia (initially cellular injury is reversible and after a prolonged period causes
irreversible tissue injury and possibly death of patient)
3. 3 major categories of shock:
Cardiogenic: from myocardial pump failure. Caused by intrinsic myocardial damage
(MI), vent arrhythmia, extrinsic compression (tamponade), or outflow obstruction (pulm
embolism)
Hypovolemic: from blood loss or plasma volume loss. From hemorrhage, fluid loss from
burns, or trauma
Septic: caused by systemic microbial infection. Usually from gram-negative infections
(endotoxic shock), but can occur from gram-positive and fungal infections
4. Neurogenic influences produce shock: anesthetic accident or spinal cord injury = loss
of vascular tone and peripheral pooling of blood
Anaphylactic influences produce shock: initiated by a generalized IgE-mediated
hypersensitivity response = systemic vasodilation and increased vasc permeability
5. Septic Shock: results from spread and expansion of an initially localized infection
(abscess, peritonitis, pneumonia) into the bloodstream
6. Gram-negative bacilli: cause 70% of the cases of septic shock. They produce
endotoxins = endotoxic shock
7. All of the cellular and hemodynamic effects of septic shock can be accounted for by
bacterial wall lipopolysaccharide (LPS) alone.
LPS – are endotoxins released when the cell walls of the bacterium are degraded. It
consists of a toxic fatty acid core and a complex polysaccharide coat unique to each
bacterial species. Causes mononuclear cell activation and production of cytokines =
initiation of innate immune system.
8. Fever and increased acute phase reactants repress the effects of TNF and IL-1
9. The four major attributes of high levels of LPS are:
1. Systemic vasodilation
2. Diminished myocardial contractility
3. Endothelial injury causing activation of systemic leukocyte adhesion and
pulmonary alveolar capillary damage
4. Activation of the coagulation system = DIC
10. In multiple organ system failure, the organs in which cellular changes are most
evident are: liver, kidneys, CNS
11. Toxic Shock Syndrome: caused by staphylococci which cause Superantigens.
Superantigens are polyclonal T-lymphocyte activators than induce systemic inflammatory
cytokine cascades. Can cause diffuse rash to vasodilation, hypotension, and death
12. 3 Stages of Shock:
1. Non-progressive: reflex compensatory mechanisms are activated and
perfusion of vital organs is maintained
2. Progressive: characterized by tissue perfusion and onset of worsening
circulatory and metabolic imbalances, including acidosis
3. Irreversible: when body has incurred cell and tissue injury so severe that even
if the hemodynamic defects are corrected, survival is not possible
13. Differences in skin changes between:
Hypovolemic/Cardiogenic shock: cool and pale skin due to vasoconstriction
Septic Shock: warm and flushed skin due to initial cutaneous vasodilation
14. Mortality rate of gram-negative septic shock: 25-50% = 1st among the cause of
mortality in ICU; over 200,000 deaths annually in US
15. 2 types of cardiac dysfunction that can produce heart failure: dysfunction in
myocardial contraction (systolic) or in ventricular filling (diastolic)
16. Approximate mortality per year for patients with congestive heart failure (CHF):
over 300,000 (affects more than 500,000, and 1 million hospitalizations)
Annual cost in US: $18 billion/year
17. The most important mechanisms for cardiovasc system response to an increased
burden or decreased cardiac contractility:
1. Frank-Starling Mechanism: the increased preload of dilation helps to sustain
cardiac performance by enhancing contractility
2. Myocardial Structural Changes: including augmented muscle mass (hypertrophy)
with or without cardiac chamber dilation- mass of contractile tissue is augmented
3. Activation of neurohumoral systems: 1. release of the NE by adrenergic cardiac
nerves (increases HR and augments myocardial contractility against vascular
resistance), 2. activation of the renin-angio-aldosterone system, and 3. release
of ANP
18. 2 most frequent specific causes of systolic dysfunction:
1. Systolic dysfunction: ischemia, pressure of volume overload, dilated
Cardiomyopathy
2. Diastolic dysfunction: inability of the heart chamber to relax, expand and fill
sufficiently during diastole
19. Difference b/w forward and backward failure (characterize CHF):
Forward failure: diminished cardiac output
Backward failure: damming of blood back in the venous system
20. Relationship of cardiac hypertrophy and the onset of heart failure:
- the molecular and cellular changes in hypertrophied hearts that initially mediates
enhanced function may contribute to the development of heart failure
o proteins related to contractile elements, excitation-contraction coupling,
and energy utilization may be significantly altered through production
different isoforms that either may be less functional than normal or may be
reduced or increased amount
-
pattern of hypertrophy reflects the nature of the stimulus
pressure-overloaded ventricles (HTN or aortic stenosis) develop concentric
hypertrophy of the L ventricle – this increased diameter of the L ventricle may
reduce the cavity diameter
- In pressure overload, the deposition of sarcomeres is parallel to the long axes of
cells (cross-section is larger, length stays the same)
- In volume overload, there is deposition of new sarcomeres and cell length =
dilation of ventricle diameter
21. Cardiac hypertrophy represents a tenuous balance b/w which characteristics and
alterations:
- a tenuous balance b/w adaptive characteristics (new sarcomeres) and potentially
deleterious structural and biochemical/molecular alterations (ex/ decreased
capillary-to-myocyte ratio, increased fibrous tissue, and synthesis of abnormal
proteins)
- therefore sustained cardiac hypertrophy often evolves to cardiac failure due to
decreased stroke volume and cardiac output