Handbook of critical care (1)
Here’s a link. From the description:
“Written as a teaching aid for residents and fellows in intensive care and emergency medicine, this revised edition of the Handbook of Critical Care is also a valuable reference for all medical professionals in the critical care team. The 15 chapters in this pocket-sized basic intensive care manual include eight substantial sections covering the major organ systems, as well as infection, nutrition, physical injury and toxicology, and brief chapters on scoring systems and obstetrics. The chapters feature numerous pictures, comparative tables, diagrams and lists, and provide essential information for juniors training in intensive care medicine. The definitions, etiology, clinical features and differential diagnoses are well covered, while extensive use of bullet points and numbering increases the clarity of presentation enabling readers to quickly get to the key learning points.”
I’m not a medical professional who’s part of a critical care team (surprise!) and so I don’t understand everything that’s going on in this book, but I still feel like I’m learning quite a bit. I think it’s an interesting book, but I certainly wouldn’t recommend it to someone who’s not spent more time than most obtaining an understanding of the human body, pathophysiology, some pharmacology, etc. – if you’re new to the field of medicine I think you’ll simply get blown away here and you’ll have little clue what’s going on most of the time. Khan Academy has a lot of stuff about the heart, and I’ve watched a lot of the videos dealing with this kind of stuff, though far from all of them – but a couple of textbooks plus learning all the material covered in the lectures I link to above is probably the bare minimum you need in order to understand everything that’s going on in chapter 3 alone. So, yeah…
As pointed out, even though I don’t understand everything doesn’t mean I don’t learn a lot by reading this stuff – that’s not how it works. So so far I’m enjoying this – if I could have been bothered to look up all the new terms I’ve come across here so far, I’d have learned more than I did, but that would have been too much work. I did rewatch a few Khan Academy videos to brush up on some of the concepts, but that’s pretty much all I’ve done, aside from an occasional visit to wikipedia. So I’ve read and understood some of it, and I’ve read and not fully understood other parts. That’s okay.
One thing that I’ve achieved a greater understanding of is how stuff like adverse drug reactions, nosocomial infections etc. may be much harder to avoid and deal with than I’ve tended to believe in the past. All drugs have side effects, and as a general rule I don’t think it’d be wrong to say that the more sick you are, the more extensive health interventions are required to make you better (or simply stop you from getting worse). A patient in the ICU who develops pneumonia as a (more or less direct) consequence of having been on a mechanical ventilator for an extended period of time and dies from it would most likely have died even sooner if he had not been put on a ventilator – he was so sick in the first place that he couldn’t even satisfy his own body’s oxygen demands through breathing… Many treatment options critically ill patients have to choose from (or their medical proxy has to choose from) are quite risky, but it should be kept in mind that the risks associated with not treating the conditions in question are usually much worse. Adding to all of this is the fact that quite a few diseases progress much too fast for treatment to follow diagnosis chronologically; in such cases you need to engage in treatment before you’re even certain what’s wrong. Some drugs will work one way when dosed in a specific manner, but will have more or less the opposite effect if given in a higher dose; now add interpersonal differences in drug metabolism, absorption rates, measurement problems, etc. to the mix… This is not to say that attempts to minimize errors and treatment-associated complications should not be undertaken, far from it, but I think I understand a little better at this point why these problems may sometimes be very hard to address satisfactorily, and why some of these problems are probably even best perceived of as inherent risks which simply cannot be avoided.
I decided to add a few quotes below from the first four chapters (95 pages) of the book. I’ve only added quotes from the stuff I understand. I added some wikipedia links along the way in order to make the stuff a little easier to read.
“Several types of sedative available are commonly used in the ICU […] Drug regimens should of course be matched to the particular needs of individual patients; however, generally speaking, no single drug is ideal and what follows is a summary of the advantages and disadvantages of each drug. […] All sedatives can accumulate in critically ill patients, leading to a prolonged sedative effect. This may increase the duration of mechanical ventilation, length of stay in the ICU, and length of stay in the hospital, and lead to complications such as ventilator-associated pneumonia. A strategy to reduce drug accumulation should be implemented […]
“studies that have failed to demonstrate an improved outcome in critical patients have cast doubt on the clinical value of PACs. [PAC: Pulmonary Artery Catheter, US] Nevertheless, traditional indications include the following: [Long list omitted here] […] To date, the use of PAC monitoring has not been shown to confer a clinical benefit in any of these settings.”
“A wide range of inotropes and vasopressors is available to help support CO [cardiac output] or blood pressure (BP). […] Inotropes that vasodilate and vasoconstrict are known as inodilators and inoconstrictors, respectively. Vasoconstrictors should always increase blood pressure, but may have a variable effect on CO. Many of these drugs have the potential to cause myocardial ischemia due to increases in cardiac workload, tachycarrhythmias, etc, and thus as electrocardiogram (EKG) and (preferably direct) arterial pressure monitoring are mandatory during their use. Vasoconstrictor drugs must be given into a central vein.”
“Hypertension is not uncommon in critically ill patients and may worsen myocardial ischemia and increase oxygen requirements. […] Injudicious use of hypotensive drugs reduces perfusion pressure (eg, kidney, brain, myocardium) and may lead to organ dysfunction.”
Heart failure occurs when the heart fails to maintain a CO sufficient for the metabolic needs of the body, or when it can only do so at the expense of abnormally elevated end-diastolic pressures. Heart failure is not a diagnosis as such, but a clinical syndrome; consequently the underlying disease must always be sought and treated.
Chronic heart failure has increased in incidence due to a decline in mortality from acute myocardial infarction, and an increase in the elderly population. It carries a significant mortality risk, with a 5-year survival rate of approximately 30%.
Acute cardiac failure is a medical emergency with a high mortality rate […] in which diagnosis of the cause and empirical treatment may have to be carried out simultaneously.”
“Pathogenesis of AMI
Rupture of an atheromatous plaque within the lumen of a coronary artery, and the subsequent formation of fresh thrombus, leads to vascular occlusion and (total) cessation of blood flow to the region of the myocardium supplied by that artery. Hypotension, hypoxemia, and local vasospasm may extend the size of the resulting infarct by compromising the blood supply of surrounding ischemic muscle. […] There is ischemic pain, typically retrosternal, spreading across the chest, and possibly radiating to the arms, throat, jaw, and back. The pain lasts for more than 20 min and may be atypical (eg, epigastric) which may confuse the diagnosis. A silent (ie, painless) infarction is more common in elderly people and those with diabetes. […] Less than 10% of patients with enzyme-proven infarcts will have two normal EKGs performed 30 min apart in the hyperacute phase. This establishes electrocardiography as an important initial investigation in the patient with a history suggestive of AMI. […] Aspirin combined with streptokinase improves the reduction in mortality rate from 25% to 42% by preventing reocclusion of thrombolyzed arteries. A dose of 150–300 mg should be given as soon as possible after the onset of symptoms […] The in-hospital mortality rate from AMI is now less than 10%, with most deaths occurring within the first few hours, often due to ventricular fibrillation (VF).”
Cardiogenic shock is a low-cardiac output state with clinical evidence of inadequate blood flow. It has been defined clinically as a syndrome characterized by hypotension (eg, systolic blood pressure <90 mmHg or 30 mmHg less than normal) or evidence of reduced tissue blood flow (eg, cold clammy skin, urine output <30 mL/h, confusion). […] Most cases of cardiogenic shock are caused by severe left ventricular failure, and will present with pulmonary edema […] The mortality rate of cardiogenic shock overall is around 80%, although this improves to approximately 50% in patients with a surgically correctable lesion. Many survivors are left with significant cardiac pathology such as angina or limiting heart failure.”
“The lungs have two major functions: to provide adequate arterial oxygenation for tissue needs and to eliminate CO2. These two functions are largely independent of each other. Respiratory failure can be classified according to the underlying pathophysiologic derangement. All types of respiratory failure may present with arterial hypoxemia and/or arterial hypercapnia.”
“In the normal resting state, 1–5% of the cardiac output is delivered to the respiratory muscles. This can increase up to tenfold in patients with shock and respiratory distress. Mechanical ventilation allows resting of the respiratory muscles.”
“Patients who have been ventilated for brief periods of time (eg, overnight ventilation following major surgery) may be liberated from mechanical ventilation rapidly […] This is in marked contrast to patients who have been critically ill for long periods of time (days), in whom the process of withdrawing ventilatory support is often protracted. Day-to-day changes in the patient’s condition during this period of respiratory convalescence often necessitate the temporary reintroduction of more substantial mechanical ventilatory support.”
“ARDS is a syndrome causing acute respiratory failure characterized by severe hypoxemia, poorly compliant (‘stiff ’) lungs, and diffuse patchy infiltration on the chest X-ray in patients in whom cardiogenic pulmonary edema has been excluded. Rather than being an isolated condition, it is recognized as the pulmonary manifestation of systemic inflammation. ARDS is now recognized as the extreme end of a spectrum of ALI [Acute Lung Injury, US – though see also this], and is defined in terms of the severity of the gas exchange defect […] The mortality rate of ARDS ranges from 30% to 40%, and has improved significantly in recent years with the advent of new ventilator strategies.”
“Pneumonia can be defined as an acute lower respiratory tract illness, which is associated with fever, symptoms and signs in the chest, and abnormalities on the chest X-ray. In patients admitted to the hospital, it carries an overall mortality of about 10%. Mortality is strongly correlated with age, chronic comorbidities, severely abnormal vital signs upon presentation, and laboratory abnormalities (eg, pH, blood urea nitrogen, Na+, glucose, hemoglobin, and PaO2).”
“[Hospital-acquired (nosocomial) pneumonia] is defined as pneumonia developing more than 2 days after admission to hospital. It is particularly common in the ICU and postoperative patients, and carries a mortality rate of up to 50%. […] Diagnosis often proves difficult, particularly in ventilated patients, because features are nonspecific and may be confused with other conditions ”
“Pulmonary embolism (PE) occurs in 15–20 patients per 1,000 of the general hospital population, of which 2–5 cases are fatal. At least 50% of patients who die from PE have had some indication of thromboembolism within the preceding 7 days. Failure to diagnose PE has adverse consequences, since 30% of patients with untreated PE die compared with 8% of treated PE. […] Pulmonary emboli usually result from the formation of asymptomatic deep vein thromboses (DVTs) in deep veins of the lower limbs, pelvis, and abdomen. Upper extremity DVTs are usually associated with indwelling catheters and may account for up to 15% of DVTs. […] Factors promoting the formation of thrombi are described by Virchow’s triad of venous stasis, abnormal vessel walls, and increased coagulability […] Thrombolytic therapy is indicated for massive PE with associated shock. Its role in massive PE, with echocardiographic evidence of right heart failure or massive PE with severe pulmonary hypertension, has demonstrated improved secondary outcomes compared with heparin, though no survival benefit has been noted. Allergic reactions and hemorrhage are the principal complications of thrombolytics, and restrict their use considerably.”
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