Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_3736_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

31.08.2026

Размер:

27 Мб

Скачать

☆

<<< < Предыдущая 1 2 34 / 384 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 > Следующая >>>

R. Samir, K. Amr. Published 18 February 2020.Medicine.

https://t.me/medicina_free

A. Winiger and G. P. Rodgers

ImagebyMatthew Allshouse

EKGLocation

Anterior-V1-4

Septal-V1-V2

Lateral-I, aVL, V5-V6

Inferior-II, III, aVF

Posteriolateral-V7, V8, V9

Right Ventricle-V1, V4R

adapted from Localizationofthe occluded vessel in acutemyocardialinfar ction.

Fig. 3.1 EKG localization and related coronary distribution. (Image by Matthew Allshouse)

symptoms of myocardial ischemia with an EKG revealing ST elevation with the release of biomarkers, the result of myocardial injury.

As discussed in the introduction, a STEMI describes the rupture of the atherosclerotic plaque in a coronary artery due to disruption of the brous cap and the lipid core becoming exposed to the blood stream [2]. This instantly incites thrombosis, which may completely occlude the lumen of the artery and stop the blood ow and oxygen delivery downstream. This cessation of distal blood ow causes muscle cell death, referred to as myocardial infarction. This is a medical emergency. “Time is muscle” because with every minute that passes, there is more necrosis and progressive permanent injury to the heart muscle.

Coronary Distribution

LAD

Prox. LAD

LCx

RCA(85%) or LCx(15%)

RCA or LCx

RCA

rapid, focused history should be obtained using the OLD CARTS format [3]. Ask about the patient’s symptoms. These include pain Onset, Location, Duration (does it wax and wane?), Character (description of what they feel, “elephant on their chest?”, sharp, dull, heavy), Aggravating/Alleviating Factors (activity, position, medication), Radiation, Timing (when did it start and what were you doing? How long did it last?) and Severity (1–10 with 10 being worst pain ever felt). OPQRST is an alternative way to perform rapid questioning regarding symptoms which includes: Onset, Provoking, Quality, Radiation, Severity, Timing of the pain (see Chap. 31).

Also, the patient’s chart should be reviewed, paying special attention to prior coronary artery bypass surgery or percutaneous revascularization (PCI). The provider should attempt to

Evaluation

obtain past procedure notes to determine grafts and/or stenting previously performed. It is

Any encounter with a patient begins with a history and physical exam. The initial bedside evaluation should occur very quickly in a patient with suspected ACS. The goal should be to complete the interview and evaluation within 5 min. A

important to note if the patient was fully revascularized. Prior testing should be reviewed including echocardiograms, stress tests, MRI/ CTs, etc. Old EKGs and medications should be reviewed.

3 Acute Coronary Syndrome (ACS) ST Segment Elevation Myocardial Infarction

https://t.me/medicina_free

Symptoms

The patient presenting with STEMI will often display classic signs and symptoms including extreme pressure-like chest discomfort that is substernal, associated shortness of breath, diaphoresis, and potential nausea/vomiting on presentation to the emergency department. Differential diagnosis of severe anterior chest pain may include pericarditis, aortic dissection, costochondritis, gastroesophageal reux, peptic ulcer disease, esophageal spasm, pulmonary embolism, biliary colic, pneumonia, or coronary vasospasm (Chap. 31).

Physical Exam

Prior to entering the patient’s room, assess: how does the patient look? Does the patient appear to be in pain (clutching his/her chest with Levine’s sign) [3]? Is the patient diaphoretic, anxious, or nauseous/vomiting [4]? Rapid physical exam should be performed including special focus on heart sounds (are there extra heart sounds indicating valve dysfunction or heart failure), jugular venous distention, or rales [5]. While completing the rapid physical exam, specic questions should tailored to the catheterization lab. These may include whether the patient is followed by a physician for any chronic medical problems such as undergoing treatment for cancer. Do they have any upcoming surgeries which may inuence anticoagulation and antiplatelet decisions? The patient should be asked if they have had any history of bleeding including stroke or GI bleeding, and if so, was this due to dual antiplatelet therapy (DAPT)? If there is any question of whether the patient should be taken to the catheterization lab, communicate with the interventional cardiologist. It is always better to over communicate rather than under communicate. It may also be necessary to take the lead in the ED to coordinate and get the patient to the catheterization lab in an urgent manner. Do not be afraid to direct the healthcare team!

Diagnostics

A STAT EKG, and labs, including high sensitivity troponin, electrolytes, kidney and liver function, CBC, and INR should be performed. Troponin elevation is very specic for cardiac cellular death. The levels vary based on which type of troponin your facility uses. Any elevation above normal is due to cell death. The more elevated, the more muscle necrosed. The troponin levels may not be elevated initially but will elevate over hours to days, and thus should be trended.

A skillset that is critical to any cardiovascular practitioner is interpretation of acute coronary syndrome locations on the electrocardiogram. Figure3.1 will assist you with remembering what each lead of the 12-lead EKG represents. A STEMI is characterized by one or more millimeters of ST elevation in two or more contiguous leads [6]. Contiguous refers to leads that are assessing a certain territory of the heart. Typically, the contiguous leads are fed by a single coronary artery.

The EKG correlates with the coronary anatomy. The anterior precordial leads V2-V4 correspond to the anteroseptal walls of the heart supplied by the LAD (Fig.3.1). In this example, EKG (Fig. 3.2), urgent cardiac catheterization conrmed type I MI in the LAD distribution (Fig. 3.3) and primary stenting was completed (Fig.3.4).

Limb leads 1 and aVL view the lateral aspect of the heart. This distribution is often perfused by the LCX.The distal anterior precordial leads V5 and V6 correspond with the apex and can be supplied by the LAD, LCX, or PDA.Notice the ST depression of V1-V2 in Fig. 3.5. If these depressions are seen with STEMI in the inferior leads, this is a posterior extension of the STEMI and not reciprocal changes. This is large and high-risk MI and is at risk for decompensation to cardiogenic shock. Figures3.6 and 3.7 show the cardiac catheterization lms of the left circumex occlusion and percutaneous coronary intervention (PCI).

https://t.me/medicina_free

Fig. 3.2 STEMI in anterior leads V1-V5 with reciprocal changes

A. Winiger and G. P. Rodgers

Fig. 3.3 Type I MI in LAD

Limb leads II, III, and aVF are evaluating the inferior portion of the heart corresponding to the posterior descending artery (PDA). Vessel dominance is described as the vessel that gives rise to the PDA.In 80% of patients,

Fig. 3.4 LAD after PCI

this vessel arises from the RCA (right dominant) with 20% arising from the LCX (left dominant). Type I STEMI of the RCA causes ST segment elevation of these inferior leads (Fig.3.8).

3 Acute Coronary Syndrome (ACS) ST Segment Elevation Myocardial Infarction

https://t.me/medicina_free

Fig. 3.5 Inferior and posterolateral STEMI

Fig. 3.6 Left circumex occlusion

Fig. 3.7 Primary PCI of left circumex

https://t.me/medicina_free

Fig. 3.8 STEMI inferior leads

A. Winiger and G. P. Rodgers

Fig. 3.9 RCA occlusion

Fig. 3.10 RCA post intervention

3 Acute Coronary Syndrome (ACS) ST Segment Elevation Myocardial Infarction

https://t.me/medicina_free

Figures 3.9 and 3.10 show the catheterization lms of inferior STEMI.

Imaging/Management

Once the diagnosis of STEMI has been conrmed, the interventional cardiologist should be alerted, and the catheterization laboratory notied. The lab and physician are sometimes activated prior to the patient’s arrival in the ED by EMS if symptoms and EKG are consistent with a STEMI. It has been found that it is critical to open the affected artery and restore blood ow as quickly as possible. Percutaneous coronary intervention (PCI) or coronary balloon angioplasty and stenting is the most effective way to open an occluded artery. Timeliness is critically important with “door to balloon time” used as the metric throughout the world. This is the time from when the patient arrives at the hospital (door time) to when the rst ination of the angioplasty balloon occurs (balloon time). The goal of the “door to balloon time” is to open the artery within 90min. This is derived from an important observational study showing that the best results with the lowest mortality rates for STEMIs occur in patients with a door to balloon time of less than 90min [7]. Nationally, this is the target for any STEMI.After 12 h of total occlusion time of a coronary artery, the myocardial infarction is complete and there is little tissue left to salvage, and late revascularization may be dangerous leading to complications of the STEMI (Table3.2).

A cardiac catheterization involves bringing the patient to the catheterization laboratory. Conscious sedation may be administered as per physician preference. Arterial access sites are prepped (radial vs. femoral artery). The interventional cardiologist accesses the artery with a needle, and a sheath is placed in the artery. Since the complication rate of femoral access is higher, radial artery access is preferred. A catheter over a guidewire is advanced to where the coronary arteries originate off the aorta. Contrast dye is injected into the coronary arteries while uoroscopy (x-ray) is used to take pictures of the arter-

ies (angiogram). In a STEMI, the angiogram will show an abrupt cut-off of the coronary artery or complete occlusion. The occlusion can be crossed with a coronary wire and using this wire as a monorail, a balloon is placed at the site of the occlusion and is inated to open the artery. Next, another balloon with a stent crimped on it is brought into the coronary artery over the coronary wire and expanded into the walls of the artery, stenting open the artery. Unfractionated heparin is given during the procedure. This is called primary angioplasty and has been shown to reduce mortality in STEMI (see images of PCI). PCI requires a skilled interventional cardiologist and team of catheterization lab staff to perform the procedure safely. This is usually performed at tertiary hospitals.

In some settings, PCI is not available, and thrombolytic therapy must be used to medically open the coronary artery. The choice between PCI or thrombolytic therapy using tissue plasminogen activator (TPA), or TNK, has been carefully studied. In several head-to-head trials, PCI was shown to be superior to thrombolytics. However, thrombolysis may be more practical in rural settings where PCI is not universally available (greater than 2h away for primary PCI).

After PCI, medical therapy is essential. Dual anti-platelet therapy is essential for reducing thrombosis within the stented artery. Typically, the patient is loaded with antiplatelet medication, which includes a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) as well as low dose aspirin. This dual antiplatelet therapy (DAPT) will be continued for 12 months. High-potency statins (Atorvastatin 40–80 mg daily or Rosuvastatin 20–40mg daily) and beta blockers are prescribed in the post STEMI setting according to the guidelines. If a patient has a reduced ejection fraction (EF), LVEF less than 50 percent, typically an angiotensin converting enzyme inhibitor (ACE inhibitor) or angiotensin receptor blocker (ARB) is added to the regimen. If the LVEF is less than 40 percent, Entresto (angiotensin receptor blocker and neprilysin inhibitor (ARNI), ACE inhibitor or an ARB is used. In addition, Spironolactone, a mineral corticoid receptor antagonist (MRA) might be added to the regi-

https://t.me/medicina_free

A. Winiger and G. P. Rodgers

Table 3.1 Complication of cardiac catheterization and PCI

Hematoma at arteriotomy site Pseudoaneurysm CVA/TIA Retroperitoneal hematoma Local nerve injury at

Vascular compromise distal to arteriotomy Complications of closure device-infection

Bleeding: GI bleeding, intracranial hemorrhage

arteriotomy site Embolization atheromatous material

men. All have been shown to reduce mortality and reduce hospital readmissions in STEMI patients with severe depression of LV systolic function (LVEF <40%) [8].

It is essential that the patient is closely monitored for potential complications post PCI. Complications of cardiac catheterization can include peri-procedural bleeding which is the most frequent complication of PCI and associated with poor clinical outcomes (Table3.1) [9].

Age, kidney function, and cardiogenic shock increase risk for bleeding complications [10,

11]. Use of multiple antithrombotic and antico-

agulants increase the incidence of periprocedural bleeding. Women have an increased risk of bleeding complications due to the smaller size of the femoral artery [12, 13, 14]. Obesity is also a higher risk due to decreased ability to recognize bleeding. Hematomas at the arteriotomy site may form. The patient may develop a pseudoaneurysm if the site heals inappropriately. The pseudoaneurysm is diagnosed with ultrasound (US) and may require thrombin injection to manage this complication. Retroperitoneal hematoma is a potentially life-threatening complication where bleeding occurs in the retroperitoneal space. Acute lower abdominal pain after femoral access requires consideration for retroperitoneal bleeding, and this is diagnosed with CT scan of the abdomen [15]. Vascular compromise distal to the arterial access may occur, especially in patients who already have a large amount of peripheral vascular disease. This complication would be seen as loss of distal pulses, pain, and pallor and may occur after

Table 3.2 Complications of STEMI

Cardiogenic Shock Arrhythmia (VT, Torsade’s) Ventricular septal defect Ventricular free wall rupture Ischemic cardiomyopathy Pericarditis (Dressler’s syndrome)

Papillary muscle rupture and acute mitral regurgitation Apical ventricular thrombus and embolization Ventricular aneurysm

AV node injury and heart block

deployment of a vascular access occlusion device at the end of the PCI. Urgent Vascular Surgery consultation is needed. Finally, nerve injury may occur following PCI. Less common complications may include GI bleeding evidenced by a drop in Hgb with hematemesis or melena, or intracranial hemorrhage diagnosed with head CT after change in neurologic status is observed due to anticoagulation therapy during the PCI. The APP should evaluate for hematoma or pain at the access site, decreased distal pulses to the access site, abdominal or back pain, if femoral access is used [16]. Vitals must be monitored looking for tachypnea, tachycardia which results from increased oxygen demand in the setting of acute blood loss. The patient may also appear pale, cold, and clammy if they are losing blood and hemorrhagic shock is developing. Rapid and direct communication with the interventionalist and vascular surgeon is essential if bleeding is suspected.

STEMI complications may be signicant (Table 3.2). The rst is impairment of LV function which may be transient or permanent. This occurs due to ischemia or infarction of the muscle tissue of the ventricle. Transmural tissue necrosis complications may present 3–5 days after the myocardial infarction, especially in situations where the patient did not have the benet of early PCI or thrombotic therapy. This necrosis can result in papillary muscle infarction, resulting in severe mitral regurgitation due to a ail mitral valve leaet. This event may lead to ash pulmonary edema due to acute severe mitral regurgitation. If the necrosis occurs within the

3 Acute Coronary Syndrome (ACS) ST Segment Elevation Myocardial Infarction

https://t.me/medicina_free

LV septum, there can be ventricular septal wall rupture resulting in a VSD and heart failure symptoms with a new loud murmur. Ischemic VSD is a surgical emergency. A free wall rupture may result which is usually fatal. Occasionally, blood will ll the pericardium resulting in tamponade without death and is a surgical emergency. A rupture may cause a pseudoaneurysm, and the patient is fortunate to have survived. Severe damage to the heart muscle may result in a permanent reduction in LV function, called ischemic cardiomyopathy. If the infarct is localized to the apex, the patient may develop an LV aneurysm which may cause ventricular arrhythmias. Many of these complications require surgical intervention.

Another signicant complication from acute MI is tachyarrhythmia and bradyarrhythmia. See Part III for arrhythmia details. Ventricular tachycardia, and ventricular brillation may result from acute ischemia and may cause sudden cardiac death (SCD) early in STEMI.

Follow-Up

Post MI, the patient is often admitted to the cardiac ICU for monitoring to include the above stated complications. An echocardiogram will likely be completed to evaluate the heart function and valves. The patient will be on continuous telemetry monitoring for arrhythmias. Assessment for post procedural complications is very important in the rst 24 h after STEMI presentation.

All patients that have suffered acute coronary syndrome, and especially STEMI have a class 1 indication for cardiac rehab. This is a supervised program that is three 1-hour sessions per week for 12 weeks. The intradisciplinary healthcare team of RNs, exercise physiologists, and dieticians educate the patient on their medications, exercise regimen, and Mediterranean diet. The patients also meet others who have coronary artery disease; they form a support system for each other.

Clinical Pearls

• Family history of premature CAD is male <55 or rst-degree relative women female <65.

• Time is muscle: the longer an area is ischemic, the more muscle dies.

• It is critical to know if an AMI patient had prior CABG or stents and the location of these.

• Goal door to balloon time is <90min!!

• Review any old EKGs if possible. Pay particular attention to previous LVH with strain, left bundle branch blocks, or Q-waves.

• Quickly assess patients’ history of bleeding (GIB or head bleed) and history of prior TIA or CVA to guide management with antiplatelets.

• Remember to consider alternative causes for ST elevations, particularly if the clinic picture is not consistent with ST-elevation MI, and if indicated rule out dissection or obtain head CT prior to cath lab (aortic dissection, cocaine induced vasospasm, pulmonary embolism, subarachnoid hemorrhage, etc.).

• Patients treated with 324mg aspirin, 80 mg atorvastatin, 4000U IV heparin prior to transfer to PCI facility. Loading with Plavix per PCI center protocol. Caution with nitroglycerin in RCA infarct.

• When discussing patient’s pertinent medical history with referring provider, inquire about any signicant comorbidities that patient is currently being treated for. If the patient is being treated for cancer, review their notes for treatment plan and prognosis. If possible, talk to the provider directly. Overall prognosis can help guide clinical decision making.

• Obtain patient’s EMR and date of birth. If time allows, review previous medical records, including if patient has previous cardiac history, and any previous cardiac imaging. Review of patient’s labs—particularly creatinine prior to taking to cath lab.

• Standard guideline directed medical therapy post intervention includes DAPT (unless patient on systemic OAC), high dose statin

https://t.me/medicina_free

A. Winiger and G. P. Rodgers

therapy, beta-blocker, and when indicated ACE/ ARB/ARNI when LVEF <40% or anterior MI.

• If patient is on novel oral anticoagulation (NOAC), ask rationale for treatment plan. If patient is on NOAC, provide detailed documentation and plan of care for anticoagulation going forward. For example, DAPT therapy for 1month, in addition to NOAC, then discontinue aspirin.

• Arrange follow-up appointments prior to discharge. Include patient in discussion, they are more likely to follow up if ofce is closer to their home. Prescribe enough rells for antiplatelet medication for 1year.

References

1. Kumar V, etal. Robbins and Cotran pathologic basis of disease. 9th ed. Philadelphia, PA: Elsevier.

2. DeLemos J, Omland T.Chronic coronary artery disease. A companion to Braunwald’s heart disease. Philadelphia, PA: Elsevier; 2018.

3. Lilly LS. Pathophysiology of heart disease. 5th ed. Wolters Kluwer; 2021.

4. Benjamin IJ, et al. Andreoli and Carpenter’s Cecil essentials of medicine. 9th ed. Philadelphia, PA: Elsevier.

5. Schiffman FJ, Wing EJ.Cecil essentials of medicine. 10th ed. Elsevier; 2022.

6. Bielinsky J. 2022. Contiguous leads and the EKG.

https://cme4life.com/acute- care- cme/contiguousleads- ekg/.

7. McNamara RL, etal. Effect of door-to-balloon time on mortality in patients with ST segment eleva-

tion myocardial infarction. J Am Coll Cardiol. 2006;47(6):2180–6.

8. O’Gara PT, etal. 2013 AACF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol. 2013;61(4):e78–e140.

9. Ferrante etal. (2016). Radial versus femoral access for coronary interventions across the entire spectrum of patients with coronary artery disease: a meta- analysis of randomized trials. JACC Cardiovasc Interv, 9(14), 1419–1434.

10. Chhatriwalla AK, etal. Association between bleeding events and in-hospital mortality after percutaneous coronary intervention. J Am Med Assoc. 2013;3903(10):1022–9.

11. Kubler P, et al. In patients undergoing percutaneous coronary intervention with rotational atherectomy radial access is safer and as efcient as femoral access. J Interv Cardiol. 2018;31:471–7.

12. Daughtery SL, etal. Patterns of use and comparative effectiveness of bleeding avoidance strategies in men and women following percutaneous coronary interventions. J Am Coll Cardiol. 2013;61(20):2070–8.

13. Kwok CS, et al. Effect of access site, gender, and indication on clinical outcomes after percutaneous coronary intervention: insights from the British Cardiovascular Intervention Society. Am Heart J. 2015;170(1):164–172.e5.

14. Ndrepepa G, etal. Bleeding after percutaneous intervention in women and men matched for age, body mass index, and type of antithrombic therapy. Am Heart J. 2013;166(3):534–40.

15. Sorajja P, Holmes DR. 2021. Periprocedural bleeding in patients undergoing percutaneous coronary intervention. Up to Date.

16. Rodgers GP, et al. 2020 ACC clinical competencies for nurse practitioners and physician assistants in adult cardiovascular medicine: a report of the ACC Competency Management Committee. J Am Coll Cardiol. 2020;2020(75):2483–517.

ACS Non-ST Elevation Myocardial

https://t.me/medicina_free

Infarction (NSTEMI)

MichelleRoss andJohnCedarholm

Introduction

The term acute coronary syndrome (ACS) refers to ST elevation MI (STEMI), NSTEMI, and unstable angina (UA.) STEMI and NSTEMI are caused by acute disruption of a coronary plaque resulting in partial or complete obstruction of ow through a coronary artery by a superimposed thrombus. The diminished blood ow and reduction in oxygen supply results in ischemia and ultimate infarct of myocardium. This usually causes symptoms of angina at rest (unstable angina), may cause ECG changes, and results in elevated troponins. Unstable angina without infarction may have a similar presentation to NSTEMI, but without a troponin release.

Type IandType II Myocardial Infarction

As stated in the Chap. 3, Myocardial infarction can be classied as type I and type II.This is important distinction for patient care and prognosis. An ele-

M. Ross (*) Atrium Health/Sanger Heart & Vascular Institute, Charlotte, NC, USA e-mail: michelle.ross@atriumhealth.org

J. Cedarholm Lake Norman Regional Medical Center, Mooresville, NC, USA e-mail: John_cedarholm@lnrmc.com

vated troponin occurring secondary to plaque rupture or erosion is considered a Type I MI (this includes STEMI and NSTEMI). Myocardial injury occurring due to acute oxygen supply and demand mismatch, without plaque rupture, is dened as a Type II MI. In this case, myocardial cell death occurs because of the inability to meet the oxygen demand of the tissue or in the presence of profound metabolic derangement. The patient may have chest pain, ECG changes with or without the presence of CAD.Examples can be seen in patients presenting with a COPD exacerbation, rapid atrial brillation, severe anemia, along with many other presentations (see Table4.1). It is very important to make this dis- tinction as the mortality rate of type II MI is higher than type I and type II may not require invasive evaluation [1] Treatment of the underlying cause of the Type II MI is the best treatment option, not an invasive evaluation or anticoagulation.

Table 4.1 Etiologies of myocardial cell death in Type II MI

CKD/ESRD Heart failure (acute and/or chronic) Sepsis/critical illness Pulmonary embolism Myocarditis Stress cardiomyopathy (Takotsubo) Cardiotoxic drugs CPR/debrillator shocks Chest trauma (cardiac contusion) Stroke Anemia

https://doi.org/10.1007/978-3-031-35819-7_4

<<< < Предыдущая 1 2 34 / 384 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
31.08.202628 Мб0Книга_3731_Библиотеки_им_академика_М_И_Перельмана.epub
#
31.08.202628 Мб0Книга_3732_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202627 Мб0Книга_3733_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202627 Мб0Книга_3734_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202627 Мб0Книга_3735_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202627 Мб0Книга_3736_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202627 Мб0Книга_3737_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202626 Мб0Книга_3738_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202626 Мб0Книга_3739_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202626 Мб0Книга_3740_Библиотеки_им_академика_М_И_Перельмана.pdf
#
31.08.202626 Мб0Книга_3741_Библиотеки_им_академика_М_И_Перельмана.pdf