A high index of suspicion for penetrating cardiac injury and an understanding of the modes of presentation can lead to rapid diagnosis even by inexperienced junior staff. Such a structured approach to patients with penetrating trauma to the chest leads to early definitive management and acceptable results.

The clinical aspects of shock syndromes are described from their inception as compensated physiology to a stage of decompensation. The clinical significance of hypotension, fluid-responsive and non fluid-responsive hypotension, is discussed. Untimely or inadequate treatment leads to persistent subclinical shock despite adjustments of the macrohemodynamic variables, which evolves in a second hit of physiological deterioration if not aggressively managed. Irreversible shock ensues as consequence of direct hit or as result of inadequate or delayed treatment and is characterized by drug-resistant hypotension.

A shift of approach from ‘clinics trying to fit physiology’ to the one of ‘physiology to clinics’, with interpretation of the clinical phenomena from their physiological bases to the tip of the clinical iceberg, and a management exclusively based on modulation of physiology, is finally surging as the safest and most efficacious philosophy in hemorrhagic shock. ATLS® classification and recommendations on hemorrhagic shock are not helpful because antiphysiological and potentially misleading. Hemorrhagic shock needs to be reclassified in the direction of usefulness and timing of intervention: in particular its assessment and management need to be tailored to physiology.

Shock syndromes are of three types: cardiogenic, hemorrhagic and inflammatory. Hemorrhagic shock has its initial deranged macro-hemodynamic variables in the blood volume and venous return. In cardiogenic shock there is a primary pump failure that has cardiac output/mean arterial pressure as initial deranged variables. In Inflammatory Shock it is the microcirculation that is mainly affected, while the initial deranged macrocirculation variable is the total peripheral resistance hit by systemic inflammatory response.

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