‘A 85-year-old man is brought to the emergency department with shortness of breath and ‘generalized weakness since yesterday. This moming he could not get out of bed. He has also had several episodes of midline chest pain but currently is chest pain free. Medical history includes hypertension, hyperlipidemia, type 2 diabetes melitus, and Peripheral vascular disease. The patient is an active smoker with a 20-pack-year history. He appears to be in respiratory distress, and his extremitles are cold and ‘clammy. Temperature is 37.5 C (99.6 F), blood pressure is 80/60 mm Hg, pulse is 420imin, and respirations ere 30/min. There is visible jugular venous distension with the patient in a siting position. Chest auscultation reveals bileteral crackles. The abdomen is soft and nontender. ECG shows sinus tachycardia with let bundle branch block intial laboratory results are as follows: Completa blood count Leukocytes 12.0001mm Hemoglobin 11 gid Platelets :240,000/mm ‘Serum chemistry Blood urea nitrogen 18 mg/dl. Creatinine 14 mgidl. Lactate 3.5 mgidL. Which of the following sets of parameters is most likely to be seen in this patient? cardiac Pretoad Cit Aftertoad Crea orc ae)history. He eppeers to be in respiratory cistress, and his extremities are cold end clammy. Temperature Is 37.5 C (99.5 F), blood pressure Is 80/50 mm Hg, pulse Is. 420Imin, and respirations are 30/min, There is visible Jugular venous distension with the patient in a siting postion. Chest auscultation reveals bilateral crackies. The abdomen is soft and nontender. ECG shoves sinus tachycardia with let bundle branch block. intial laboratory results are as follows: Complete blood count Leukocytes 12,000/mm Hemoglobin ‘1M adL Platelets :240,000/me Serum chemistry Blood urea nitrogen 18 mg/dL. Creatinine 41.4 mgidL Lactate 3.5 mgiaL ‘Which of the following sets of paramsters is most likely to be seen in this patient? pretend SHH peoad OA 1 1 t oB. Fr 4 v oc. L t tT oD. L t L of 4 1 t OF. nomal normal t Pre aera‘A 85-year-old man is brought to the emergency department with shortness of breath and ‘generalized weakness since yesterday. This moming he could not get out of bed. He has also had several episodes of midline chest pain but currently is chest pain free. Medical history includes hypertension, hyperlipidemia, type 2 diabetes melitus, and Peripheral vascular disease. The patient is an active smoker with a 20-pack-year history. He appears to be in respiratory distress, and his extremitles are cold and ‘clammy. Temperature is 37.5 C (99.6 F), blood pressure is 80/60 mm Hg, pulse is 420imin, and respirations ere 30/min. There is visible jugular venous distension with the patient in a siting position. Chest auscultation reveals bileteral crackles. The abdomen is soft and nontender. ECG shows sinus tachycardia with let bundle branch block intial laboratory results are as follows: Completa blood count Leukocytes 12.0001mm Hemoglobin 11 gid Platelets :240,000/mm ‘Serum chemistry Blood urea nitrogen 18 mg/dl. Creatinine 14 mgidl. Lactate 3.5 mgidL. Which of the following sets of parameters is most likely to be seen in this patient? cardiac ‘output Preload Aftertoad 1 [100%] vo 1 4 1 [100%] G. 1 1 7 (00%) f t 1 [100%] ears‘Which of the following sets of parameters is most lkely to be seen in this patient? cardiac Preoad iar Afterload 1 1 [loos 1 + [100% 1 1 (10086) t 1 (rose 1 + (100%) normal 1 [00% User Ic: Hemodynamic measurements in shock Hypovolemic | cardiogenic | Septic Faremeter Nernel shock shock shock RApressure | Mean ‘Normal (preload) 4mm Hg 1 q or) PCWP ‘Mean Normal (preload) 9mm Hg ‘ q ort Cardiac index | 93.42 (pump 2 1 dt 1 function) ‘Ueninie a0R 1,160 {afterload) ane t t J seciem mr 60%-80% 1 1 1 |Explanation: Users: Hemodynamic measurements in shock Hypovolemic | Cardiogenic | Septic Ememeten | ‘Nernel shock shock ‘shock RApressure | Mean ‘Normal (preload) | 4mmig ‘ ' ory PCWP Mean i ; ‘Normal (prota) | mmHg ory Cardiac index | 95.49 (pump 2 1 a fi function) | Lminint 1.180 sve (afterload) eee t 1 4 seciem mae 80%-80% 1 1 1 ‘MvO., = mixed venous oxygen saturation; PEWP = pulmonary capilery wedge pressure; RA = right atrium; SVR = systemic vascviar resistence. This patient with numerous risk factors for coronary artery disease (eg, hypertension, ‘labetes melitus, active smoking) has likely nad an acute myocardial infarction (Ml). Patients typically have substemal chest pain (sometimes intermittent) as well as ‘dyspnea, fatigue, nausea, andlor diaphoresis. Low-grade fever may be present, and laboratory results can demonstrate mild leukocytosis. A new left bundle branch block on ECG Is suggestive of an acute Ml. ‘Acute Mi can lead to profound impairment in left ventricular contractility, decreased stroke volume, anc cardiogenic shock. Cardiac output (stroke volume heart rate) is low as tachycardia is unable to compensate for the decrease in stroke volume. Left ventricular end-diastolic volume, also knowin as left ventricular preload, is high due to impaired ejection of blood from the left ventricle. Systemic vascular resistance (SVR), iso known as afterload. is high as well due to compensatory peripheral vasoconstriction In an effort to maintain blood pressure. Patients typically have hypotension. jugular tension, respiratory cistress (eg, dyspnea, tachypnea) due to pulmonarytem Pressure; RA ysteme vascular essence This patient with numerous risk factors for coronary artery disease (ag, hypertension, diabetes melitus, active smoking) has likely had an acute myocardial infarction (Ml), Patiants typically have substernal chast pain (sometimes intermittent) as well as ‘dyspnea, fatigue, nausea, andlor dlaphoresis. Low-grade fever may be present, and laboratory results can demonstrate mil leukocytosis. A new left bundle Branch block on ECG Is suggestive of an acute Ml, ‘Acute Mi can lead to profound impairment in let veriricular contreciity, decreased stroke volume, and cardiogenic shock. Cardiac output (stroke volume x heart rate) is low as tachycardia is unable to compensate for the decrease in stroke volume. Left ventricular end-diastolic volume, also known as left ventricular preload, is high due to Impaired ejection of blood from the left ventricle, Systemic vasculer resistence (SVR). also known 28 afterload, is high as wall due to compensatory peripheral vasoconstriction in an effort to maintain blood pressure. Patients typically have hypotension, jugular ‘venous distension, respiratory distress (eg, dyspnea, tachypnea) due to pulmonary ‘edema, an cold extremities due to poor tissue perfusion. Laboratory results typically demonstrate elevated lactate, reflective of poor organ and tissue perfusion. (Choice A) High-output heart failure (eg, thyrotoxicosis, beriber, arteriovenous fistula) Is ‘characterized by high cardiac output and low afterload. Cardiac preload is high due to Increased venous return (Choice C) Hypovolemia leads to low cardiac preload and, consequently, low cardiac, ‘output. Afterioad Is high due to compensatory vasoconstriction. (Choice D) Sepsis is characterized by low afterload due to peripheral vasouilation and high cardiac output (hyperdynamic state in the early stages of sepsis). Cardiac preload is normal or low cue to leakage of intravascular fluid volume. (Choice &) Exercise is characterize by high cardiac output and high aterioad due to a ne increase in SVR (vasodilation occurs in skeletal musce, but vasoconstriction occurs in organs and tissues not participating in exercise). Carciac preload is low (Choice F) Cocaine ingestion leads to high afterload due to vasocenstrction from alpha- 1 receptor stimulation. Concomitant beta-1 receptor stimulation causes increased heart rate and contractility and allows for maintenance of normal cardiac output in the setting of Increased afterload. Normal preload is maintained as well. Educational objective: Myocardial infarction can lead to left ventricular systolic dysfunction and cardiogenic shack. Low cardiac output leads to high left ventricular end-diastolic volume (preload) 4 ONECG Is suggestive of an acute Ml, ‘Acute Ml can lead to profound impairment in left ventricular contraciity, decreased ‘stroke volume, an¢ cardiogenic shock. Cardiac output (stroke volume = heart rate) is low as tachycardia is unable to compensaie for the decrease in stroke volume. Left ventricular end-diastolic volume, also known as left ventricular preload, is high due to Impaired ejection cf blood from the left ventricle, Systemic vasculer resistance (SVR). also known 2s afterload, is high 2s well due to compensatory peripheral vasoconstriction in an effort to maintain blood pressure. Patients typically have hypotension, jugular venous distension, respiratory cstress (eg, dyspnea, tachypnea) due to pulmonary ‘edema, and cold extremities due to poor tissue perfusion. Laboratory results typically demonstrate elevated lactate, reflective of poor organ and tissue perfusion. {Choice A) High-output heart failure (eg, thyrotoxicosis, beriber, arteriovenous fistula) is ‘characterized by high cardiac output and low afterload. Cardiac preload is high due to Increased venous return [Choice ¢) Hypovolemia leads to low cardiac preload and, consequently, low cardiac ‘output. Aferioad is high due to compensatory vasoconstriction, (Choice D) Sepsis is characterized by low afterload dus to peripheral vasodilation and high carciac output (hyperdynamic state in the eary stages of sepsis). Cardiac preload is notmal or low cue to leakage of intravascular fluid volume. (Choice E) Exercise is characterized by high cardiac output and high afterioad due to a net increase in SVR (vasodilation occurs in skeletal muscle, but vasoconstriction cecurs In organs and tissues not participating in exercise). Cardiac preload is low. [Choice F) Cocaine ingestion leads to high afterload dus to vasoconstriction from alpha- ‘receptor stimulation. Concomitant beta-1 receptor stimulation causes increased heart rate and contractility and allows for maintenance of normal cardiac output in the setting of Increased afterload. Normal preload is maintained as well. Educational objective: Myocardial infarction can lead te left ventricular systolic dysfunction and cardiogenic ‘shock. Low cardiac output leads to high left ventricular end-diastolic volume (preload) ‘and a compensatory increase in systemic vascular resistance (afterioad), References: 1. Cardiogenie shock: failure of oxygen delivery and oxygen utilization. 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