Free CMC Exam Flashcards

At a PCI-capable hospital, door-to-device under 90 minutes. If the patient must be transferred, first-medical-contact-to-device within 120 minutes. If neither is achievable, give a fibrinolytic within 30 minutes of arrival.

SCAD mostly strikes women under 50 with few atherosclerotic risk factors, often peripartum or after extreme physical or emotional stress. Most dissections heal on their own and PCI can extend the intramural hematoma, so conservative management is preferred unless there is ongoing ischemia, left main involvement, or hemodynamic instability.

Suspect right ventricular infarction. Obtain right-sided leads: ST elevation in V4R confirms it. The infarcted right ventricle is preload-dependent, so treat with volume loading and avoid nitrates, diuretics, and morphine.

Beck triad - hypotension, jugular venous distention, and muffled heart sounds - plus pulsus paradoxus greater than 10 mmHg and equalization of diastolic pressures, so CVP, PA diastolic, and PAOP converge. Echocardiography confirms it and pericardiocentesis relieves it.

HFrEF is an LVEF of 40% or less, HFmrEF is 41-49%, and HFpEF is 50% or greater. Heart failure with improved EF describes a patient whose EF was once 40% or less and has risen above 40%; guideline-directed therapy is continued rather than withdrawn.

Lower systolic pressure by no more than 25% in the first hour, then toward 160/100 over the next 2-6 hours, and to normal over 24-48 hours, because faster drops risk cerebral, coronary, and renal hypoperfusion. Exceptions needing first-hour lowering: aortic dissection to a systolic below 120 mmHg, and severe preeclampsia, eclampsia, or pheochromocytoma crisis to below 140 mmHg.

Pericarditis produces diffuse, concave-upward ST elevation across several lead territories with PR-segment depression and no reciprocal ST depression except in aVR. STEMI elevation is regional, convex, and paired with reciprocal depression in the opposite leads.

Ventricular fibrillation and pulseless ventricular tachycardia are shockable: defibrillate at the manufacturer's recommended biphasic energy, commonly 120-200 J, and resume compressions immediately. Pulseless electrical activity and asystole are not shockable; give epinephrine 1 mg IV every 3-5 minutes and treat reversible causes.

Type A involves the ascending aorta and is a surgical emergency because of tamponade, aortic regurgitation, and coronary occlusion risk. Uncomplicated type B, distal to the left subclavian, is managed medically: an IV beta blocker first to a heart rate of 60-80, adding a vasodilator if needed, to a systolic pressure below 120 mmHg or the lowest that still perfuses the organs.

Pain, pallor, pulselessness, poikilothermia, paresthesia, and paralysis. Sensory loss extending beyond the toes or any motor weakness marks a threatened limb needing revascularization within hours; complete anesthesia with paralysis suggests irreversible injury.

Retroperitoneal hemorrhage from a high femoral puncture. The classic picture is flank or back pain, tachycardia, hypotension, and a dropping hemoglobin with a deceptively normal-looking groin. Stop anticoagulation, resuscitate with fluids and blood, and obtain a non-contrast CT of the abdomen and pelvis.

Embolism-caused sustained hypotension: systolic pressure below 90 mmHg for at least 15 minutes, a drop of 40 mmHg or more from baseline, or a need for vasopressors. These patients are candidates for systemic thrombolysis, catheter-directed therapy, or embolectomy rather than anticoagulation alone.

By PaO2/FiO2 ratio on PEEP of at least 5 cm H2O: mild 201-300, moderate 101-200, severe 100 or less. Onset must be within one week of a known insult, with bilateral opacities not fully explained by effusion, collapse, or cardiogenic pulmonary edema.

Untreated OSA drives resistant hypertension, raises atrial fibrillation recurrence after cardioversion and ablation, and increases heart failure readmission. Repeated nocturnal desaturations and sympathetic surges are the mechanism, so screening and CPAP adherence are part of cardiac care.

Its high iodine load most often causes hypothyroidism, but it also causes thyrotoxicosis in two forms: type 1 is excess hormone synthesis in an abnormal gland, treated with thionamides, and type 2 is destructive thyroiditis, treated with corticosteroids. Check TSH at baseline and roughly every six months.

A platelet fall of 50% or more from baseline, typically 5-10 days after heparin exposure, often with new thrombosis rather than bleeding. Stop all heparin including line flushes and start a non-heparin anticoagulant such as argatroban or bivalirudin. Do not give prophylactic platelets, and do not start warfarin until the platelet count recovers.

Hypoactive delirium - the quiet, withdrawn, slowed patient - is the most common and the most frequently overlooked. Screen every shift with a validated tool such as CAM-ICU, which requires an acute or fluctuating change plus inattention, and then either an altered level of consciousness or disorganized thinking.

A serum creatinine rise of at least 0.3 mg/dL within 48 hours, a rise to 1.5 times baseline or more within 7 days, or urine output under 0.5 mL/kg/hr for 6 hours or longer. Any one of the three establishes AKI.

Hypomagnesemia causes renal potassium wasting, so potassium will not correct until magnesium is replaced. It also predisposes to torsades de pointes, which is treated with 1-2 g of IV magnesium sulfate even when the serum magnesium level is reported as normal.

Cardiogenic shock shows a low cardiac index with high filling pressures and high systemic vascular resistance. Hypovolemic shock shows low filling pressures with high SVR. Distributive or septic shock shows a normal-to-high cardiac output with low SVR and warm extremities.

Give benzodiazepines first to reduce sympathetic drive, then nitroglycerin, and phentolamine for refractory hypertension. Beta blockers alone are avoided because unopposed alpha stimulation can worsen coronary vasospasm and blood pressure.

It inflates at the dicrotic notch, when the aortic valve closes, to raise diastolic pressure and coronary perfusion, and deflates just before systole to lower afterload and myocardial oxygen demand. Moderate-to-severe aortic regurgitation and aortic dissection are contraindications.

Most have no palpable pulse and unreliable pulse oximetry, so use a Doppler over the brachial artery with a manual cuff: the first sound heard approximates the mean arterial pressure. Target a MAP of roughly 70-80 mmHg and avoid sustained readings above 80, because higher pressures raise stroke and pump thrombosis risk.

New left bundle branch block and high-grade or complete AV block. Keep continuous ECG monitoring and temporary pacing capability for at least the first 24-48 hours, because a meaningful minority of patients need a permanent pacemaker before discharge.

Cerebral hyperperfusion syndrome: a chronically underperfused hemisphere has lost autoregulation, so restored flow causes edema and risks intracranial hemorrhage. Strict blood pressure control is the central nursing intervention, along with urgent neuroimaging.

Persistent blood flow into the aneurysm sac outside the graft, which keeps the sac pressurized and still able to rupture. Type I seal-zone and type III graft-defect leaks need prompt repair, and new or worsening back or abdominal pain after EVAR is treated as rupture until proven otherwise.

An ARNI (or an ACE inhibitor or ARB when an ARNI is not tolerated), an evidence-based beta blocker - carvedilol, metoprolol succinate, or bisoprolol - a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor. All four are started early and titrated together rather than one class at a time.

Overlapping neprilysin and ACE inhibition raises bradykinin levels and sharply increases angioedema risk. A 36-hour washout is required in both directions, but no washout is needed when switching from an ARB.

Euglycemic diabetic ketoacidosis - ketoacidosis with a glucose that may be under 250 mg/dL, so a normal glucose does not rule it out. Risk rises with surgery, fasting, or acute illness, which is why the drug is held at least 3 days before scheduled surgery (4 days for ertugliflozin).

Verapamil and diltiazem, the non-dihydropyridines, are negative inotropes and are avoided in reduced ejection fraction. Amlodipine and felodipine are hemodynamically neutral and may be used when another indication such as hypertension or angina exists.

Dobutamine is a beta-1 agonist with a roughly 2-minute half-life that raises heart rate and loses potency under heavy beta blockade. Milrinone is a phosphodiesterase-3 inodilator that acts past the beta receptor, lowers pulmonary and systemic vascular resistance, and is renally cleared, so it accumulates in kidney injury.

Norepinephrine. Compared with dopamine and epinephrine it produces fewer arrhythmias and less lactic acidosis while restoring perfusion pressure. An inotrope such as dobutamine or milrinone is added when cardiac output remains low after pressure is restored.

Ticagrelor is a reversible, direct-acting P2Y12 inhibitor given twice daily that needs no CYP2C19 activation, so it still works in poor metabolizers. It requires aspirin maintenance of 100 mg or less, commonly causes dyspnea and ventricular pauses, and is usually held 3-5 days before CABG, versus 5 days for clopidogrel and 7 for prasugrel.

Unfractionated heparin - protamine sulfate, which only partially reverses enoxaparin. Warfarin - vitamin K plus 4-factor prothrombin complex concentrate. Dabigatran - idarucizumab. Apixaban and rivaroxaban - andexanet alfa.

Failure to capture shows a pacing spike with no resulting P wave or QRS - suspect lead dislodgement, output set too low, electrolyte disturbance, or ischemia. Failure to sense shows spikes falling at inappropriate times, including on the T wave, which can trigger R-on-T ventricular fibrillation.

Synchronize for unstable tachycardias that still have a pulse - atrial fibrillation, atrial flutter, SVT, and monomorphic VT - so the shock lands on the R wave and avoids R-on-T. Use unsynchronized defibrillation for ventricular fibrillation, pulseless VT, and polymorphic VT.

Three or more separate appropriate shocks or sustained ventricular arrhythmia episodes within 24 hours. Treat with IV amiodarone plus beta blockade, sedation to break the sympathetic cycle, and correction of ischemia and electrolytes; refractory cases go to catheter ablation.

Atrioesophageal fistula - rare but usually fatal if missed. Do not pass a nasogastric tube or TEE probe blindly, because insufflated air can embolize to the brain. Obtain CT of the chest with contrast and involve surgery urgently.

Respiratory or cardiac arrest, inability to protect the airway or clear secretions, a depressed or agitated level of consciousness, vomiting or upper GI bleeding, facial trauma or recent facial or upper airway surgery, and untreated hemodynamic instability.

Tidal volume of 4-8 mL/kg of predicted body weight, usually starting at 6, and plateau pressure at or below 30 cm H2O. Predicted body weight is calculated from height and sex, never actual weight, so an obese patient still receives a small tidal volume.

SCUF removes plasma water only, with no dialysate or replacement fluid, for volume overload. CVVH clears solute by convection using replacement fluid. CVVHD clears solute by diffusion using dialysate. With regional citrate anticoagulation, a rising total-to-ionized calcium ratio signals citrate accumulation.

Select a constant temperature between 32 and 37.5 degrees Celsius and maintain it for at least 36 hours, then keep actively preventing fever. Treat shivering, rewarm slowly, and anticipate the potassium shift - hypokalemia during cooling and rebound hyperkalemia during rewarming.

Palliative care can begin at any stage and runs alongside disease-directed therapy, including inotropes, devices, and transplant evaluation. Hospice requires a prognosis of roughly six months or less and a shift away from curative treatment, and it is the setting where ICD shock deactivation is usually addressed.

After a fast flush, one to two sharp oscillations before the tracing settles is optimal. An overdamped waveform with a slurred upstroke underestimates systolic and overestimates diastolic pressure - look for air bubbles, clots, or kinks. An underdamped waveform with many oscillations overestimates systolic pressure.

CVP 2-6 mmHg, pulmonary artery pressure 15-30/8-15 mmHg, pulmonary artery occlusion pressure 6-12 mmHg, cardiac index 2.5-4.0 L/min/m2, and systemic vascular resistance 800-1200 dynes-sec/cm5.

SvO2 is sampled from the pulmonary artery and normally runs 60-80%; ScvO2 comes from a superior vena cava catheter and normally reads a few points higher. A falling value means oxygen delivery has dropped or consumption has risen - think low cardiac output, anemia, hypoxemia, fever, shivering, or pain.

No. A value above the 99th percentile means myocardial injury; infarction also requires a rise or fall on serial testing plus ischemic symptoms, ECG changes, or imaging evidence. Renal failure, heart failure, pulmonary embolism, myocarditis, and sepsis all raise troponin without an acute coronary syndrome.

It reflects pulmonary blood flow, so it is a live measure of compression quality. A value persistently below 10 mmHg after 20 minutes of high-quality CPR is associated with poor outcome but should never end resuscitation on its own, while an abrupt sustained rise, often to 40 mmHg or more, suggests return of spontaneous circulation - confirm at the next rhythm check rather than interrupting compressions.

It transmits daily PA pressures from selected NYHA class II-III heart failure patients who had a heart failure hospitalization in the past year or have elevated natriuretic peptides, so diuretics and vasodilators can be adjusted before congestion becomes symptomatic. Rising pressures precede weight gain and dyspnea by days.

The pattern of myocardial scar. Subendocardial or transmural enhancement in a coronary distribution means infarction, and scar under 50% of wall thickness suggests the segment is still viable; mid-wall enhancement suggests non-ischemic dilated cardiomyopathy, subepicardial suggests myocarditis, and diffuse subendocardial enhancement suggests amyloid. Check renal function before giving gadolinium.