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

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