38 TRAUMA Flashcards

Question

Uma vez que o paciente parou de sangrar, quais os alvos de PA e Lab?

Answer 1

* PAs _>_ 110mmhg

Answer 2

Normal PFC PLT/CRIO Antifibrinolitico

Answer 3

* SSVV estaveis * Vasoconstriccao severa, que segura os SSVV, e que prejudica os orgaos * nao clareia Lactato e BE **A perfusao tecidual depende mais do fluxo do que da pressao**

Answer 4

* **Diferenca Art - EtCO₂**:Quanto menor o DC, maior a distancia. Se >10mmHg, prediz mortalidade. * **Diferenca venoarterial**: se > 6-8mmHg, tem má perfusão e metabolismo anaeróbio.

Answer 5

*Paciente deve estar em VM. Diferenca dividia pela media* Pre-requisitos: 1. VPP 2. VC 8ml/kg 3. sinusal 4. Sincronia (sedado, bnm...)

Answer 6

*Algoritmo varia conforme cada aparelho. Diferenca dividida pela media*. * **Volume sistolico é proporcional a Pressao de Pulso** Calculando a resistencia vascular sistemica: * **RVS = [(PAM-PVC)/DC] x80**

Answer 7

* **RVS = [(PAM-PVC)/DC] x80**

Answer 8

* **Hb x 1,34 x Sat/100 + (PaO₂*0,0031)**

Answer 9

* **DC / Superficie Corporal**

Answer 10

*Se quiser em LITRO, multiplicar por 10*

Answer 11

* **Alvo: SatCentral >70%**. INdice de como esta a extracao de oxigenio no corpo. Se abaixo: estou entregando pouco oxigênio ou a DO₂I esta ruim. * Hb * IC * O₂

Answer 12

Fibrinolysis shutdown in trauma refers to a state where the body's ability to break down blood clots (fibrinolysis) is significantly impaired or suppressed. This condition is observed in a subset of trauma patients and is characterized by an excessive formation of stable blood clots, leading to an increased risk of thrombosis and organ dysfunction. ### Key Points: 1. **Mechanism**: Under normal circumstances, fibrinolysis helps to dissolve clots that are no longer needed, preventing excessive clotting. In fibrinolysis shutdown, this process is inhibited, leading to persistent and potentially harmful clots. 2. **Causes**: The exact mechanisms are not fully understood, but it is believed to be associated with the body's acute inflammatory response to trauma, involving complex interactions between the coagulation and fibrinolytic systems. 3. **Detection**: Fibrinolysis shutdown can be detected using thromboelastography (TEG) or rotational thromboelastometry (ROTEM), which measure the dynamics of clot formation and dissolution. A characteristic finding in fibrinolysis shutdown is reduced or absent fibrinolytic activity on these tests. 4. **Clinical Implications**: Patients with fibrinolysis shutdown are at higher risk of complications such as deep vein thrombosis, pulmonary embolism, and multiple organ failure. It is crucial to identify and manage this condition promptly to improve outcomes. 5. **Management**: Treatment strategies may include careful monitoring, use of anticoagulants, and addressing underlying causes of the shutdown, such as controlling bleeding, managing inflammation, and stabilizing the patient's condition. Understanding fibrinolysis shutdown is important for guiding the management of trauma patients and improving their prognosis.

Answer 13

Trauma-induced coagulopathy is a complex condition characterized by abnormal blood clotting and bleeding following severe trauma. It involves a spectrum of coagulation abnormalities, including hypercoagulability, hypocoagulability, and impaired fibrinolysis. ### Relationship between Fibrinolysis Shutdown and Trauma-Induced Coagulopathy: 1. **Coagulation Abnormalities**: Trauma-induced coagulopathy encompasses various coagulation disturbances, including fibrinolysis shutdown. This shutdown can contribute to the hypercoagulable state seen in some trauma patients, where the formation of stable blood clots is excessive, leading to thrombosis and organ dysfunction. 2. **Pathophysiological Mechanisms**: The interplay between inflammation, endothelial injury, and the activation of the coagulation and fibrinolytic systems plays a critical role in TIC. Severe trauma triggers a systemic inflammatory response, leading to endothelial damage, release of tissue factor, and activation of the coagulation cascade. Simultaneously, the fibrinolytic system may become dysregulated, resulting in either excessive fibrinolysis or fibrinolysis shutdown. 3. **Clinical Presentation**: Patients with TIC can present with a wide range of symptoms, from excessive bleeding to thrombotic events. The presence of fibrinolysis shutdown adds complexity to the clinical picture, as it requires careful management to balance the risk of bleeding and thrombosis. 4. **Diagnostic Tools**: Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are useful in diagnosing TIC and assessing fibrinolytic activity. These tools can help identify patients with fibrinolysis shutdown, allowing for tailored therapeutic interventions. 5. **Management Strategies**: Effective management of TIC and fibrinolysis shutdown involves a multifaceted approach, including: - Rapid control of bleeding through surgical or interventional procedures. - Administration of blood products (e.g., plasma, platelets) and clotting factors. - Use of antifibrinolytic agents (e.g., tranexamic acid) in cases of hyperfibrinolysis. - Monitoring and managing anticoagulation therapy to prevent thrombotic complications. In summary, fibrinolysis shutdown is a critical component of trauma-induced coagulopathy, necessitating prompt identification and appropriate management to improve patient outcomes.

Answer 14

Your professor is referring to a modern understanding of coagulation that emphasizes the interplay and integration of the intrinsic and extrinsic pathways, rather than viewing them as entirely separate entities. This perspective aligns with the cell-based model of hemostasis, which provides a more comprehensive and physiologically relevant understanding of the coagulation process. ### Traditional Model of Coagulation Historically, coagulation was described in terms of two distinct pathways: 1. **Intrinsic Pathway**: Initiated by damage to the blood vessel, this pathway involves the activation of clotting factors present within the blood (such as factors XII, XI, IX, and VIII). 2. **Extrinsic Pathway**: Triggered by external trauma that causes blood to escape from the vessel, this pathway is initiated by tissue factor (TF) released from damaged tissues, leading to the activation of factor VII. Both pathways converge on the activation of factor X, which leads to the common pathway and ultimately the formation of a stable fibrin clot. ### Cell-Based Model of Hemostasis The cell-based model of hemostasis integrates the intrinsic and extrinsic pathways, highlighting the role of cellular surfaces (such as platelets and endothelial cells) and the interactions between various components of the coagulation system. Key points of this model include: 1. **Initiation Phase**: The process begins with the exposure of tissue factor (TF) at the site of injury, leading to the activation of factor VIIa. This complex (TF-VIIa) activates factors IX and X. 2. **Amplification Phase**: Small amounts of thrombin generated in the initiation phase activate platelets and additional coagulation factors (V, VIII, and XI), amplifying the response and localizing it to the site of injury. 3. **Propagation Phase**: The formation of the tenase (IXa-VIIIa) and prothrombinase (Xa-Va) complexes on the surface of activated platelets results in a burst of thrombin generation, leading to the formation of a stable fibrin clot. ### Key Points of the Integrated Approach 1. **Interdependence**: The intrinsic and extrinsic pathways are not entirely separate but interdependent. Factors from each pathway can influence the other, and both are necessary for a robust and effective coagulation response. 2. **Physiological Relevance**: The cell-based model better reflects the physiological conditions under which coagulation occurs, emphasizing the role of cellular surfaces and the interactions between various coagulation factors. 3. **Simplified Understanding**: By focusing on the overall process and interactions rather than distinct pathways, this approach provides a more holistic understanding of hemostasis, which can be more applicable in clinical settings. ### Clinical Implications 1. **Diagnosis and Treatment**: Understanding coagulation as an integrated process can improve the diagnosis and treatment of coagulation disorders. It emphasizes the need to consider the entire coagulation cascade and cellular interactions rather than focusing on isolated pathways. 2. **Therapeutic Interventions**: Treatments can be more effectively targeted by recognizing the interdependent nature of coagulation pathways. For example, anticoagulant therapies may need to address multiple points within the coagulation process to be effective. In summary, the modern tendency to view coagulation as an integrated process rather than distinct intrinsic and extrinsic pathways reflects a more accurate and physiologically relevant understanding of hemostasis. This approach highlights the importance of cellular interactions and the interdependence of various coagulation factors in maintaining hemostasis.