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Anestesiologia SBA - Pontos ME1 > 38 TRAUMA > Flashcards

38 TRAUMA Flashcards

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1
Q

Gatilhos que ativam o SN Autonomico na fisiopatologia do CHOQUE HEMORRAGICO:

A
  • Dor
  • Percepcao do trauma
  • Hipovolemia -> Hipotensao

Geram a descarga cátecoláminergica (Epi + Norepi).

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2
Q

Resposta Endocrino Metabolica e quais hormonios com a liberação aumentada durante o choque hemorrágico:

A
  • Catecolaminas (Nora, Epi)
  • SRAA
  • ADH
  • Hormonios contrareguladores da insulina: GH, Glucagon, Cortisol
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3
Q

Sinal mais precoce na avaliacao de choque hemorrágico/hipovolemico

A

Encurtamento da Pressao de Pulso.

  • A vasoconstriccao aumenta primeiro a pressao diastólica
  • Quando o sangramento progride com >30% do volume intravascular, espera-se a Hipotensao. Logo é um achado tardio.
  • FC é um sinal mais precoce que a hipotensao

Como os achados tem muita variabilidade, considerar Choque quando o paciente apresenta Taquicardia + Pele fria ate que se prove o contrario.

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4
Q

O que é o Shock Index?

A

SI = FC / PAs

  • baixa sensibilidade
  • Idosos nao costumam fazer taquicardia

Como os achados tem muita variabilidade, considerar Choque quando o paciente apresenta Taquicardia + Pele fria ate que se prove o contrario.

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5
Q

Qual a relacao entre palpação de pulsos e PA sistolica?

A
  • Pulso radial nao palpavel: <80mmHg
  • Pulso carotideo nao palpavel: <70mmHg

variabilidade muito grande. Na pratica: muito cuidado
Como os achados tem muita variabilidade, considerar Choque quando o paciente apresenta Taquicardia + Pele fria ate que se prove o contrario.

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6
Q

Principal achado laboratorial para indicar e classificar choque conforme o ATLS

A

Deficit de bases

Quantidade de bases para trazer o pH de uma solucao ao seu valor basal.

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7
Q

Mecanismo fisiopatologico da isquemia intestinal durante choque hemorrágico e o que é o fenomeno de “No Reflow”?

A
  • nao produz ATP
  • Nao elimina o Na pela bomba Na-K-ATPase
  • celula retem Na+H₂O, incha, esmaga vasos sanguíneos e perpetua a isquemia.

No Reflow:

  • Mesmo que conseguir transfundir, restabelecer a PA e DC, esse tecido continua mal perfundido pelo edema. A cascata lesiva de choque continua a avançar mesmo apos a resolucao macrodinamica do problema. É o fenomeno de NO REFLOW.
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8
Q

O que é a segunda onda de lesao do trauma e quais os principais orgaos afetados?

A
  • Celulas isquemicas liberam acido lático, toxinas, radicais livres, mediadores inflamatórios: todos lesivos a elas mesmas. Se ocorrer a reperfusao, essas substancias sao levadas ao resto do corpo levando a injuria de reperfusao sistêmica. É a Segunda onda de Lesao.

Principais órgaos afetados:

  • Fígado sofre mais, perpetuando a hiperglicemia e disglicemia.
  • Pulmao tambem recebe quase todo o DC. É um órgão sentinela da resposta inflamatória. Desenvolve SIRS, disturbio V/Q
  • Coracao desenvolve hipocontratilidade com a inflamacao.
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9
Q

O que é a lesao endotelial do trauma e quais as consequências?

A

Glicocalix:

  • matriz composta de proteoglicanos que reveste o endotélio.
  • Controla muitas funções endoteliais.
  • No trauma e isquemia, se degenera.

Quando se quebra, as consequências sao:

  • Edema Intersticial
  • Hipovolemia
  • ↓Oxido Nitrico
  • Coagulopatia. Libera proteoglicanos, alguns heparinoides, e caem na circulação. Auto heparinizacao.
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10
Q

Como dosar a auto heparinizacao pela lesao do Glicocalix?

A
  • Heparin Sulfato
  • Syndecan-1
  • Acido Hialuronico
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11
Q

Qual a triade letal do trauma?

A
  • Coagulopatia
  • Acidose
  • Hipotermia
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12
Q

O que é a coagulopatia do trauma? (4)

A
  • Lesao do Glicocalix
  • ativacao exagerada de Proteina C - inibe os fatores V e VIII, inibindo a geração de trombina, agravando o sangramento
  • Disfunçao do Inibidor do ativador do Plasminogenio( para de funcionar), aumentando a fibrinolise.
  • Exaustao plaquetaria: menos responsivas aos gatilhos (ADP e colágeno), Coagulos mais frágeis.
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13
Q

Principal medicacao para a Coagulopatia do Trauma:

A

Acido Tranexamico 1g em 10min + 1g 8/8h

  • Idealmente faz tromboelastograma antes, ja que pode ser um “Fibrinolysis Shutdown” e nao ha beneficio com o Acido-Tx
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14
Q

O que é a proteina C e qual o seu papel na coagulopatia do trauma?

A
  • inibidor dos fatores V e VIII,
  • inibe a geração de trombina, agravando o sangramento
  • inibe o “inibidor do ativador de plasminogenio”, provocando fibrinolise.

Na coagulopatia do trauma, ha uma hiperativacao desta proteina, inibindo a formacao de coágulos.

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15
Q

Melhor acesso IV para o paciente vitima de trauma com Choque Hemorrágico:

A
  • 2x Acesso IV calibroso (18-16).

Periferico > Central:

  • facilidade
  • lei de Pousielle (maior tamanho)
  • A resistencia ao fluxo do cateter é diretamente proporcional ao comprimento do cateter, e o central é muito mais comprido.
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16
Q

Qual veia puncionar para acesso central no trauma?

A

Puncionar a que voce estiver com maior familiaridade.

  • Jugular, embora familiar aos anestesistas, exige remoção do colar cervical e manipulação do pescoço (a menos que outras opções tenham sido esgotadas). A hipovolemia tambem dificulta.
  • Subclavia: se paciente ja tem pneumotorax drenado, é a melhor opcao
  • Femoral: nao fazer se fratura de pelve ou MMII ou trauma abdominal. Alto risco de TVP e infeccao.

Se falha: intraósseo, dissecção de veia safena em nivel de tornozelo (leva >10min)

17
Q

Preparacoes invasivas no paciente vitima de trauma com choque hemorrágico:

A
  • Acesso IV (periferico)
  • PAI
  • Debito urinario
18
Q

Como é feita a ressuscitação volêmica do paciente vitima de trauma e desvantagens de cada:

A
  • SF0.9%: acidose hipercloremica
  • RL: incompativel com hemocomponentes, alcalose metabolica (lactato no figado)

Nenhuma mostrou mais beneficio que outra. Alem disso, nao costumam ser utilizadas em quantidades suficientes para causar efeitos adversos.

19
Q

Por que a normalizacao da PA pode ser prejudicial no trauma e qual a PA media recomendada?

Em que momento é possivel normalizar a PA?

A
  • Deslocamento de coagulos
  • Reversão da vasoconstricao
  • Reativacao do sangramento

Enquanto a hemorragia nao for controlada, nao posso normalizar a PA dos pacientes vitimas de trauma

PA alvo:

  • Media: 50-60mmHg
  • Sistolica < 90-100mmHg
  • exceto: idosos e coronariopatas (nao se sabe a PA alvo)
  • Nunca fazer: Neurotrauma
20
Q

Quais hemocomponentes nao podem ser aquecidos?

A
  • Plaquetas

Aquecer CHM e Plasma. Nao fazer no microondas!!

21
Q

O que é o ABC score?

A
  • Avaliacao sonografica
  • Batimentos
  • Blood pressure
  • Corte:

Se mais de 2 pontos, PTM

22
Q

Sinais que indicam PTM no sangramento do trauma (6+2)

A
  • ABC score > 2 pontos
  • PAS < 70mmHg
  • PAS < 90mmHg apos cristaloide
  • RNI > 1.4
  • TP >18s
  • TTPA > 60s

Sinais de gravidade:

  • BE > -10
  • Htc < 30

Nao confiar na Hemoglobina.

23
Q

Quais valores de Calcio aumentam risco de disfunção miocárdica e coagulopatia, e como prevenir durante a transfusao maciça?

A
  • Disf. Miocardica < 1.8mEq/L (0.9mmol/L)
  • Coagulopatia < 1.2mEq/L ou 0.625mmol/L

Prevencao:

  • A cada 2-3 CHM, fazer Cloreto de Cálcio 1g.
  • Mais comum se muitas transfusões rápidas.
24
Q

O que é o controle parcial da hemorragia no trauma e qual a conduta?

A
  • resolvido grande foco, agora com menos sangramento.

Controle:

  • Hemograma
  • Coagulograma
  • Lactato, Deficit Bases (seriar 2/2h)
  • Tromboelastograma, ROTEM
25
Q

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

A
  • PAs > 110mmhg
26
Q

Qual o tratamento no tromboelastograma?

A

Normal

PFC

PLT/CRIO

Antifibrinolitico

27
Q

O que é a sindrome da hipoperfusao oculta?

A
  • 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

28
Q

Estrategias de avaliacao do CO₂ para o paciente após fase critica do Trauma:

A
  • 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.
29
Q

Como calcular a Variacao da Pressao de Pulso e quais os pré- requisitos?

A

Paciente deve estar em VM. Diferenca dividia pela media

Pre-requisitos:

  1. VPP
  2. VC 8ml/kg
  3. sinusal
  4. Sincronia (sedado, bnm…)
30
Q

Como avaliar o volume sistolico e fluidoresponsividade do paciente?

A

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
31
Q

Como calcular a resistencia vascular sistemica?

A
  • RVS = [(PAM-PVC)/DC] x80
32
Q

Como calcular o conteudo arterial de O₂ (ml/dl)?

A
  • Hb x 1,34 x Sat/100 + (PaO₂*0,0031)
33
Q

Como calcular o Indice Cardiaco?

A
  • DC / Superficie Corporal
34
Q

Como calcular o Indice de Entrega de Oxigencio (DO₂I)

A

Se quiser em LITRO, multiplicar por 10

35
Q

Como otimizar a Saturacao Venosa Central?

A
  • 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
36
Q

O que é o “Fibrinolysis Shutdown” do trauma?

A

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.

  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.

37
Q

What is Trauma Coagulopathy?

A

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.

  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.

38
Q

My university professor said there is currently a tendency to not study the coagulation in intrinsic and extrinsic pathways, as both come together and are sometimes indistinguishable. Can you explain this idea further to me?

A

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.

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.

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.
  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.
  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.

39
Q

Temperatura da sala em trauma grave?

A

30 graus

Anestesiologia SBA - Pontos ME1 (85 decks)

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