Memory questions on the MCAT are exactly what they sound like: They test your knowledge about a specific fact or concept. Aside from requiring memorization, these questions do not generally cause problems for students because they are similar to the types of questions that would appear on a typical college science exam.
Mastery of the basics and the ability to apply those concepts to unfamiliar situations is what will sustain you on the MCAT. This is by no means a definitive list but rather a sampling to jump start your prep. And remember, it's more about application of knowledge, than straight up memorization of knowledge. Go back and review. Mnemonic devices are patterns series of letters, the tune of your favorite song that help you memorize. This mnemonic device involves imagining that you are moving through a familiar route or place, such as the rooms of your childhood home, and at various stops along the way leaving a visual representation of a topic you want to remember.
The act of writing something down goes a long way toward committing it to memory.
Guidelines and guidance
Plus, concise and colorful one-page outlines are great study aids. Flashcards can be beneficial if your basic content knowledge is deficient in some area. In the critically ill patient, depressed consciousness often leads to airway obstruction. Treat airway obstruction as a medical emergency: Obtain expert help immediately.
Untreated, airway obstruction causes hypoxaemia low PaO 2 with the risk of hypoxic injury to the brain, kidneys and heart, cardiac arrest, and even death. In most cases, only simple methods of airway clearance are required e. Tracheal intubation may be required when these fail. Give oxygen at high concentration: Provide high-concentration oxygen using a mask with oxygen reservoir. Ensure that the oxygen flow is sufficient usually 15 L min -1 to prevent collapse of the reservoir during inspiration.
Breathing B During the immediate assessment of breathing, it is vital to diagnose and treat immediately life-threatening conditions e. Look, listen and feel for the general signs of respiratory distress: sweating, central cyanosis, use of the accessory muscles of respiration, and abdominal breathing. Count the respiratory rate.
The normal rate is 12—20 breaths min Assess the depth of each breath, the pattern rhythm of respiration and whether chest expansion is equal on both sides. Note any chest deformity this may increase the risk of deterioration in the ability to breathe normally ; look for a raised jugular venous pulse JVP e. The pulse oximeter does not detect hypercapnia. If the patient is receiving supplemental oxygen, the SpO 2 may be normal in the presence of a very high PaCO 2. Stridor or wheeze suggests partial, but significant, airway obstruction. Percuss the chest: hyper-resonance may suggest a pneumothorax; dullness usually indicates consolidation or pleural fluid.
Auscultate the chest: bronchial breathing indicates lung consolidation with patent airways; absent or reduced sounds suggest a pneumothorax or pleural fluid or lung consolidation caused by complete obstruction. Check the position of the trachea in the suprasternal notch: deviation to one side indicates mediastinal shift e. Feel the chest wall to detect surgical emphysema or crepitus suggesting a pneumothorax until proven otherwise.
The specific treatment of respiratory disorders depends upon the cause. Nevertheless, all critically ill patients should be given oxygen. In a subgroup of patients with COPD, high concentrations of oxygen may depress breathing i. Nevertheless, these patients will also sustain end-organ damage or cardiac arrest if their blood oxygen tensions are allowed to decrease. In this group, aim for a lower than normal PaO 2 and oxygen saturation. Some patients with chronic lung disease carry an oxygen alert card that documents their target saturation and their own appropriate Venturi mask.
In cooperative patients who do not have airway obstruction consider the use of non-invasive ventilation NIV. In patients with an acute exacerbation of COPD, the use of NIV is often helpful and prevents the need for tracheal intubation and invasive ventilation. Circulation C In almost all medical and surgical emergencies, consider hypovolaemia to be the primary cause of shock, until proven otherwise.
Look at the colour of the hands and digits: are they blue, pink, pale or mottled? Measure the capillary refill time CRT. Apply cutaneous pressure for 5 s on a fingertip held at heart level or just above with enough pressure to cause blanching. Time how long it takes for the skin to return to the colour of the surrounding skin after releasing the pressure. A prolonged CRT suggests poor peripheral perfusion.
Other factors e. Assess the state of the veins: they may be underfilled or collapsed when hypovolaemia is present. Palpate peripheral and central pulses, assessing for presence, rate, quality, regularity and equality. Barely palpable central pulses suggest a poor cardiac output, whilst a bounding pulse may indicate sepsis. Even in shock, the blood pressure may be normal, because compensatory mechanisms increase peripheral resistance in response to reduced cardiac output.
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A low diastolic blood pressure suggests arterial vasodilation as in anaphylaxis or sepsis. A narrowed pulse pressure difference between systolic and diastolic pressures; normally 35—45 mmHg suggests arterial vasoconstriction cardiogenic shock or hypovolaemia and may occur with rapid tachyarrhythmia. Auscultate the heart.
Is there a murmur or pericardial rub?
Algorithms for Advanced Cardiac Life Support
Are the heart sounds difficult to hear? Does the audible heart rate correspond to the pulse rate? Ventricular conduction blocks can be described in terms of the number of fascicles that are affected: monofascicular, bifascicular, or trifascicular. Monofascicular blocks are the syndromes described above in isolation; a single fascicle is damaged, but there is still conduction from the atria to the ventricles.
A bifascicular block occurs when two fascicles are impaired.
These are normally well-tolerated and do not require treatment beyond avoiding AV-node-blocking medications if asymptomatic. In the case where the sole remaining fascicle is unhealthy or partially damaged, a Mobitz II block can occur; this is called an incomplete trifascicular block [ 8 , 9 ]. This infra-His block often presents as a bifascicular block with a history of syncope, indicating transient complete block, and is a Class I indication for permanent pacing [ 7 , 9 ]. Bifascicular blocks that coexist with a 1 st degree AV node block are complicated and should be seen by cardiology.
If the patient has experienced symptoms, such as syncope, they should be paced; asymptomatic individuals need not be paced [ 7 ]. Since atrial impulses are no longer conducted to the ventricles, this results in A-V dissociation with a ventricular escape rhythm. This form of block is often symptomatic as it causes profound bradycardia, and the block is low enough in the conduction system that a compensatory junctional escape rhythm does not occur [ 4 ]. This medication can decrease AV-node blockade and hence increase heart rate by decreasing vagal tone.
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In the case of a complete trifascicular block or an incomplete block such as a Mobitz II , the blocking lesion is distal to the AV node, and atropine in unlikely to have any effect. In an unstable patient with a trifascicular block, the most effective option for restoring hemodynamic stability is with electricity. Transcutaneous and transvenous pacing causes the ventricle to beat at a rate of our choosing — one more compatible with life! A new, isolated fascicular block is benign and not uncommon, but should prompt investigation for the underlying cause, which is most often ischemia.
New, asymptomatic bifascicular blocks do not need urgent management though reversible causes should be ruled out , and should be referred to cardiology. Avoid any medications that impair the AV node. Patients with bifascicular block and a 1 st degree heart block technically have an incomplete trifascicular block.
They may not require pacing if asymptomatic, but they do warrant further work-up [ 4 , 7 , 10 ]. They should be referred to cardiology and have their medications reviewed for any AV-node impairing agents. Patients with a new incomplete trifascicular block also need to see an electrophysiologist for pacemaker implantation. The anatomy of the cardiac fascicles is complicated. As emergency room physicians, we need to recognize fascicular blocks on ECG, and implement pacing as therapy for symptomatic bradycardia caused by a trifascicular block,.
Patients with new complete trifascicular blocks or incomplete trifascicular blocks such as a Mobitz II pattern need urgent referral to an electrophysiologist for pacemaker implantation. Figure 1 Figure 1: Stylized schematic of the anterior and posterior fascicles of the heart. Figure 2: Normal cardiac depolarization.
Related Cardiology Mnemonics (Quick Review Notes)
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