SCAI KERN CHAP 20 Shock and support Flashcards
(8 cards)
Q1: Is any PCI procedure completely free of procedural complications?
Q2: What has enhanced the ability to treat more complex and higher-risk PCI patients?
Q3: Why is understanding clinical and anatomical features important in PCI?
Q4: Name three clinical baseline characteristics associated with increased PCI risk.
Q5: Are all clinical risk factors modifiable before PCI?
Q6: Which preprocedural clinical characteristics can be optimized before PCI?
Q7: Name three anatomical factors associated with increased risk of PCI procedural failure.
Q8: Is left main (LM) stenosis considered a high-risk anatomical feature for PCI?
Q9: What type of lesion is a trifurcation lesion?
Q10: Are saphenous vein graft stenoses high-risk lesions for PCI?
Q11: How does heavy calcification affect PCI risk?
Q12: What is the impact of severe tortuosity on PCI complexity?
Q13: What is aorto-ostial stenosis and why is it complex?
Q14: How do diffusely diseased and narrowed segments distal to the lesion affect PCI?
Q15: Are thrombotic lesions associated with increased PCI risk?
Q16: How does lesion length impact PCI complexity?
Q17: What is the approximate lesion length that increases PCI complexity?
Q18: Can optimized volume status help reduce PCI procedural risk?
Q19: Does renal insufficiency affect PCI risk?
Q20: What is the benefit of appropriate planning and adjunct equipment in high-risk PCI?
A1: No, no PCI is truly free of procedural complications.
A2: Advances in technology and hemodynamic support.
A3: To ensure optimal case management and patient outcomes.
A4: Age, diabetes, prior myocardial infarction (MI). [ Age, gender, diabetes, prior myocardial infarction (MI), left ventricular (LV) dysfunction, peripheral artery disease, and renal insufficiency, have all been associated with increased risk of complications, including death, MI, stroke, and stent thrombosis ]
A5: No, many are not modifiable before the procedure.
A6: Renal function and volume status are **modifiable risk factors **
A7: Left main stenosis, bifurcation disease, chronic total occlusions.
A8: Yes, LM stenosis is a high-risk anatomical feature.
A9: A lesion involving three branches of a coronary artery.
A10: Yes, saphenous vein graft stenoses are high-risk lesions.
A11: It increases procedural risk due to difficulty in lesion preparation and stent deployment.
A12: It increases complexity due to challenging catheter and device navigation.
A13: Stenosis at the origin of a coronary artery, complex due to access and positioning.
A14: They complicate PCI by limiting distal flow and increasing procedural difficulty.
A15: Yes, thrombotic lesions increase PCI risk.
A16: Longer lesions increase procedural complexity and risk.
A17: Lesions longer than 20 mm.
A18: Yes, optimizing volume status can help reduce risk.
A19: Yes, renal insufficiency is associated with increased PCI risk.
A20: It helps mitigate risks and optimize patient care.
Q1: Name two of the best validated and commonly used risk calculators for PCI.
Q2: How many patients were included in the original derivation of the Mayo Clinic Risk Score?
Q3: What registry was used to validate the Mayo Clinic Risk Score in 2007?
Q4: How many patients were analyzed in the New York State PCI Database?
Q5: How many risk factors did the New York State PCI Database identify?
Q6: What outcomes do the Mayo Clinic and NY State risk scores accurately predict?
Q7: What type of risk score is the SYNTAX score?
Q8: In what patient population was the SYNTAX score developed?
Q9: What clinical outcomes does the SYNTAX score predict at 1 year?
Q10: Does the SYNTAX score predict **in-hospital outcomes?
Q11: What additional factors does the SYNTAX II score incorporate beyond the anatomic SYNTAX score?
Q12: How was the SYNTAX II score validated?
Q13: What is a major limitation of any single risk calculator?
Q14: What subset of patients is considered particularly high risk for PCI-related hemodynamic collapse?
Q15: What management strategy is discussed for high-risk PCI patients with cardiogenic shock?
A1: Mayo Clinic Risk Score and New York State PCI Database
A2: 7457 patients
A3: NCDR Cath PCI Registry ( based on 300.000 patients between 2004 and 2006 )
A4: 45,000 PCI procedures
A5: Nine risk factors
A6: In-hospital mortality
A7: Anatomic risk score
A8: CABG vs PCI outcome, in patients with left main (LM) or multivessel coronary artery disease
A9: Death, myocardial infarction (MI), stroke, and/or repeat revascularization at 1 year
A10: No. SYNTAX score does not predict in-hospital outcomes, and the score lacks any clinical modifiers of risk.
A11: Clinical predictors of risk: Age, gender, ejection fraction, renal function, peripheral or chronic lung disease ( SYNTAX II incorporates both anatomic i.e. syntax I and clinical predcitors )
A12: In an analysis of 1480 patients from two studies comparing PCI and CABG. Syntax II predicts **BOTH in hospital events and mortality for both PCI and CABG for multivessel or LM disease ( predictive accuracy on mortality for 4 years )
A13: No single calculator captures every variable affecting risk
A14: Patients undergoing PCI targeting an **unprotected LM coronary artery or a *last remaining conduit, especially with complex disease and *reduced ejection fraction
A15: Use of circulatory support devices for management of high-risk PCI and cardiogenic shock
Q1: What is a major cause of global morbidity and mortality related to cardiac function?
Q2: What are the two most common conditions leading to cardiogenic shock (CS)?
Q3: How is shock from any cause characterized?
Q4: How is cardiogenic shock (CS) defined?
Q5: What systolic blood pressure criteria define cardiogenic shock?
Q6: What is the required cardiac index (CI) for diagnosing CS *without hemodynamic support?
Q7: What is the required cardiac index (CI) for diagnosing CS *with hemodynamic support?
Q8: What pulmonary capillary wedge pressure (PCWP) value is associated with CS?
Q9: How many stages are there in the Society for Cardiac Angiography and Interventions (SCAI) shock classification?
Q10: What does Stage A represent in the SCAI shock stages?
A1: Cardiogenic shock (CS)
A2: Acute myocardial infarction (AMI) and advanced heart failure (HF)
A3: Tissue hypoperfusion leading to end-organ damage
A4: Tissue hypoperfusion secondary to cardiac failure despite adequate circulatory volume and LV filling pressure
A5: Systolic blood pressure <90 mm Hg for >30 minutes or a fall in mean arterial pressure >30 mm Hg below baseline with low CI and high PCWP
A6: Cardiac index (CI) <1.8 L/min/m² *without hemodynamic support
A7: Cardiac index (CI) <2.2 L/min/m² *with hemodynamic support
A8: Pulmonary capillary wedge pressure (PCWP) >15 mm Hg
A9: Five stages (A-E)
A10: Patients at risk for cardiogenic shock
Q1: What range of conditions can lead to cardiogenic shock (CS)?
Q2: Can CS develop after both STEMI and NSTEMI?
Q3: What are the two main mechanisms by which CS occurs after AMI?
Q4: What percentage of AMI patients develop clinical manifestations of hemodynamic collapse?
Q5: Approximately what percentage of myocardium must be involved in an AMI to cause CS?
Q6: Name three risk factors for developing CS after AMI.
Q7: What is the approximate in-hospital mortality rate for CS after AMI?
Q8: Name four postmyocardial mechanical complications that can **lead to CS.
Q9: How common are mechanical complications like papillary muscle rupture and ventricular septal or free wall rupture in the revascularization era?
Q10: What risk factors are associated with postmyocardial mechanical complications?
Q11: Which papillary muscle is most commonly involved in rupture after AMI?
Q12: Why is the posteromedial papillary muscle more vulnerable to rupture?
Q13: What clinical manifestations occur with papillary muscle rupture?
Q14: Where does septal rupture typically occur in relation to the infarcted artery?
Q15: What clinical presentation is associated with septal rupture?
Q16: What is the most common clinical manifestation of free wall rupture?
Q17: How does free wall rupture typically present on cardiac monitoring?
Q18: What is the typical cause of tamponade in free wall rupture?
Q19: What role does collateral circulation play in the risk of mechanical complications?
Q20: Is female gender a risk factor for postmyocardial mechanical complications?
A1: A wide range of conditions including acute myocardial infarction (AMI) and mechanical complications.
A2: Yes, CS can develop after both STEMI and NSTEMI.
A3: Primary pump failure and mechanical complications.
A4: Approximately 5% to 8% ( thrombotic coronary occlusion is usually well tolerated )
A5: Approximately 40% of the myocardium ( almost half )
A6: Occlusion of the left anterior descending (LAD) artery, age over 65, hypertension, prior infarction, multivessel disease.
A7: In-hospital mortality approaches 60% ( very high +++++ )
A8: Acute mitral regurgitation, papillary muscle rupture, ventricular septal rupture, free wall rupture.
A9: They occur in about 1% of cases ( rare )
A10: Female gender and absence of coronary artery disease ( importance of collaterals in chronic disease )*****
A11: Posteromedial papillary muscle ( PM )
A12: It receives a singular blood supply from the *dominant coronary vessel supplying the posterior descending artery.
A13: Acute, severe mitral regurgitation and heart failure.
A14: Within the territory subtended by the infarct-related artery (anteroapical with LAD occlusion or posterobasal with RCA occlusion) +++
A15: Acute heart failure from a left-right shunt.
A16: Pulseless electrical activity and tamponade.
A17: Pulseless electrical activity.
A18: Accumulation of blood in the pericardial space causing cardiac tamponade.
A19: Collateral circulation reduces risk by providing alternative blood supply.
A20: Yes, it is a risk factor.
Q1: What type of heart failure is cardiogenic shock (CS) following AMI typically related to?
Q2: Can right ventricular myocardial infarction (RVMI) lead to cardiogenic shock?
Q3: What are two complications associated with RVMI?
Q4: Which coronary artery branches supply blood to the right ventricle?
Q5: After occlusion of which artery does RVMI most commonly occur?
Q6: Can RVMI occur after occlusion of the dominant circumflex artery?
Q7: What does RV ischemia lead to in terms of ventricular function?
Q8: How does RVMI induced RV pressure and volume overload affect the left ventricle?
Q9: Name one *hemodynamic index used to assess RV failure in AMI.
Q10: What RA:PCWP ratio suggests RV failure?
Q11: According to the SHOCK registry, what percentage of patients had isolated RV failure as the primary mechanism of CS?
Q12: In the absence of AMI, what condition most commonly causes cardiogenic shock?
Q13: How many heart failure hospitalizations were reported in the US in 2017?
Q14: What NYHA class includes cardiogenic shock as a manifestation?
Q15: What does the INTERMACS registry define?
Q16: Which INTERMACS profiles identify patients with cardiogenic shock?
Q17: What does INTERMACS profile 1 indicate?
Q18: What does INTERMACS profile 2 indicate?
Q19: What therapies might be considered for patients with INTERMACS profiles 1 and 2?
Q20: What is the purpose of temporary circulatory support in advanced heart failure patients?
A1: Left-sided heart failure
A2: Yes
A3: Ventricular fibrillation and *high-grade AV-conduction block
A4: Acute marginal branches of the right coronary artery (RCA) and the posterior descending artery
A5: Acute proximal right coronary occlusion
A6: Yes
A7: Right ventricular systolic failure and **reduced left ventricular preload
A8: The interventricular septum shifts toward the left ventricular cavity, reducing stroke volume
A9: Right atrial to pulmonary capillary wedge pressure (RA:PCWP) ratio ( also RV stroke work and PA pulse pressure )
A10: Greater than 0.8
A11: 5.3%
A12: Advanced heart failure
A13: 1.2 million
A14: New York Heart Association (NYHA) Class IV
A15: Seven clinical profiles before left ventricular assist device (LVAD) implantation
A16: INTERMACS profiles 1 and 2
A17: Patients “crashing” despite aggressive therapy
A18: Patients “sliding fast on inotropes”
A19: Temporary circulatory support, surgical LVAD, or cardiac transplantation
A20: To serve as a bridge to recovery or further advanced therapies
primary valvular disease etc
