Cardiology First Aid Flashcards
Acute coronary syndrome- atypical presentation- what lab/scan/procedure do you order?
atypical presentation = abdominal pain, nausea, vomiting = women, ELDERLY, diabetes, hx of smokingorder ECG
Aortic dissection- Classic presentation- Highest risk factor
Causes chest pain that classically described as sudden, tearing, and radiating to the back. Hypertension is the mostcommon predisposing factor.
Renal artery stenosis- Triad of signs/symptoms
Systolic-diastolic abdominal bruit in a patient with hypertension and atherosclerosis is strongly suggestive.
Beta blocker overdose- Presentation- Complications- Treatments
Presents with bradycardia, hypotension, wheezing, hypoglycemia, delirium, seizures, and cardiogenic shock.Intravenous fluids and atropine are first line treatment options. Intravenous glucagon should beadministered in patients with profound or refractory hypotension.
Acute cardiac tamponade:- Etiology - Presentation- chest x-ray findings
Patient presents with hypotension (UNRESPONSIVE to IV FLUID bolus), tachycardia, and elevated jugular pressure after blunt thoracic trauma. Only takes 100-200mL of fluid, so chest X-ray can sometimes be normal.
Acute coronary syndrome:- How can lidocaine affect the heart?
Although it can decrease the risk of ventricular fibrillation, it may increase the risk of asystole.
Anterior cerebral artery stroke:- Presentation
Characterized by contralateral motor or sensory deficits, which are more pronounced in the lower limb than the upperlimb. Urinary incontinence can also be seen occassionaly.
Statin medication recommendation:
Primary prevention in patients age 40-75 with a 10-year risk of atherosclerotic disease ≥7.5%.
Cushing syndrome:
High- dose dexamethasone does not suppress plasma cortisol levels in patients with ectopic ACTH syndrome.
Cushing’s Disease
ACTH-producing pituitary adenoma. Partially inhibited by high- dose dexamethasone.
Potassium sparing diuretics:
triamterene and amiloride
Stress test for CAD:
Beta blockers, calcium channel blockers, and nitrates are antianginal agents that are healed 48 before performing acardiac stress test.
Acute decompensated heart failure (ADHF):- Presentation- Treatment
Presents with acute pulmonary edema. Tx: Oxygen, assisted ventilation, aggressive intravenous diuresis (furosemide), and possible vasodilator therapy.
Torsades de pointes (TdP):- Define- Treatment
Polymorphic ventricular tachycardia that occurs in the setting of congenital or acquired prolonged QT interval. Tx: Immediate defibrillation is indicated in hemodynamically unstable patients with TdP, while intravenous magnesium is the first-line therapy for stable patients with recurrent episodes of TdP.
Acute type A aortic dissection:- Diagnosis- Treatment
Must get a TEE, so you can rapidly diagnose and treat. Surgical emergency!
Single photon emission CT scan:
Tool to evaluate CAD and indicates inducible ischemia when a reversible defect is noted on stress and rest. Antiplatelet therapy, beta blockers, and life style modification.
Variant Angina (or Prinzmetal’s angina):
Vasospastic disorder that typically occurs in young female smokers. It is similar in mechanism to Raynaudphenomenon. Chest pain usually occurs middle of night, and episodes transient ST elevation.
Cerebellar hemorrhage:
Patients typically have headache, neck stiffness, gait ataxia, and no hemiparesis
Putamen hemorragia:
Most common cause is hypertension. Next to internal capsule, so leads to hemiparesis.
Thalamic stroke (Dejerine-Roussy syndrome):
Caused by a stroke involving the VPL nucleus of the thalamus, which transmits sensory information from thecontralateral side of the body. Classically presents with contralateral hemianesthesia that can be accompanied bytransient hemiparesis, athetosis, or ballistic movements.
Midbrain and medulla strokes have in common:
Classically involve the nuclei of the cranial nerves.
Sustained monomorphic ventricular tachycardia (SMVT):
Hemodynamically unstable electrical cardioversion. Hemodynamically stable give amiodarone.
Cardiac tamponade:
Catastrophic complication of acute aortic dissection. Suspected in patients with hypotension, tachycardia, distended neck veins, and pulsus paradoxus.
Patients with narrow-QRS-complex tachycardia:
Intravenous adenosine is useful in the initial diagnosis and management. It slows the sinus rate, increasesatrioventricular (AV) nodal conduction delay, or can cause a transient block in AV node conduction. Good foridentifying P waves. Terminates PSVT sometimes.
Hypertension in overweight people:
Weight lose is the most effective nonpharmacologic measure to decrease blood pressure in overweight individuals.
Mechanism of pain relief in patient with chest pain treated with nitroglycerin:
Dilation of veins (capacitance vessels) which leads to decrease ventricular preload.
Acute arterial occlusion (limb ischemia):
Classically presents with “5 Ps” (pain, pallor, pulselessness, paresthesia, and paralysis). Immediate anticoagulation and referral for vascular surgery.
Mitral stenosis characteristics:
Causes pulmonary congestion which leads to symptoms such as exertional dyspnea, nocturnal cough, andhemoptysis. Atrial fibrillation occurs due to atrial dilation. Especially common in patients who had rheumatic fever.
Variant angina (Prinzmetal’s angina):
Causes chest pain by coronary vasospasm. Treatment is calcium channel blocker. Nonselective β-blockers andaspirin should be avoided because they can promote vasoconstriction.
Symptomatic pulmonary embolism most common cause:
The proximal deep veins (iliac, femoral and politeal veins) are the source of ＞90% of acute PEs.
Stab wounds near artery veins can cause:
Arteriovenous fistulas (AVF) which can lead to high-output cardiac failure by shunting the blood from the arterial tovenous side, thereby increasing cardiac preload. Hypoxia of tissues drives this. Doppler ultrasound to diagnose.
Paroxysmal supraventricular tachycardia (PSVT) characterized by:
Heart rates between 160-220 beats per minute. Results from accessory conduction pathways through the AV node. Vagal maneuvers and medication (adenosine) that decrease conduction through the AV node often revolve the PSVT.
Treatment of stable chronic angina:
First line therapy Beta blocker: Metoprolol, decreases myocardial contractility & HR. Improves survival.Calcium channel blockers can be added if angina persists. Causes peripheral & coronary vasodilation.Nitrates, Aspirin, Statin, lifestyle.
Patients with persistent tachyarrhythmia (narrow or wide-complex) causing hemodynamic instabilitymanaged:
Immediate synchronized DC cardioversion. Stable patients get vagal maneuvers (carotid sinus massage) and/oradenosine.
In the treatment of a patient using both sildenafil and an alpha-blocker (doxazosin):
It is important to give the drugs with at least a 4-hour interval to reduce the risk of hypotension.
Tricyclic antidepressant overdose: Treatment: Mechanism:
Can present with CNS, cardiac, and anticholinergic findings. Sodium bicarbonate is used to treat cardaic toxicity (QRS＞100msec and ventricular arrhythmias). Sodium bicarbonate increases serum pH and extracellular sodium, therby alleviating the cardio-depressant action on sodium channels.
First degree AV block:
With normal QRS duration delay at AV node and require no further evaluation. Prolonged QRS duration likely have a conduction delay below the AV node and should have electrophysiology testing.
Hypertensive intracranial hemorrhages occur most commonly:
In the basal ganglia, thalamus, pons, and cerebellum. Evolves over minutes to hours with focal neurologic symptoms compared to subarachnoid hemorrhages complain of severe HA do not have focal deficits.
The most common cause of sudden cardiac arrest in the immediate postinfarction period in patients withacute MI:
Reentrant ventricular arrhythmias (ventricular fibrillation).
Hypokalemia signs and ECG findings:
Causes weakness, fatigue, and muscle cramps. ECG may show U wave, flat and broad T waves, and prematureventricular beats.
Amaurosis fugax:
Characterized by visual loss that is transient and usually monocular. “Curtain falling down.” Most common causeRETINAL EMBOLI from the CAROTID ARTERY.
Aspirin intoxication triad and typical blood gas analysis:
Triad of fever, tinnitus, and tachypnea (stimulates respiratory center in the medulla). Adults with aspirin toxicity develop a mixed respiratory alkalosis and anion gap metabolic acidosis. pH 7.39; PaCO2 20; HCO3 12.
Sarcoidosis can have elevated serum:
Angiotensin converting enzyme (ACE) levels.
Digitalis toxicity causes what type of arrhythmia:
Leads to ectopy and increased vagal tone. Atrial tachycardia with AV block occurs from combination of these two digitalis effects and is relatively specific for digitalis.
Mobitz Type I vs Mobitz Type II:
Mobitz Type I: Atrioventricular block has PROGRESSIVE PROLONGATION of PR interval leading to a NON-CONDUCTED P WAVE and a dropped QRS complex. Problem is conduction in the AV node.Mobitz Type II: PR interval is always CONSTANT with no progressive prolongation and ((QRS complex drops suddenly)). Due to a block in the His-Purkinje system below AV node. Can lead to third degree block.
Atrial fibrillation (AF) with rapid ventricular response (RVR): Treatment:
Rate control should be attempted initially with beta blockers or calcium channel blockers. Immediate synchronised electrical cardioversion is indicated in hemodynamically unstable patients.
The patient’s pulsatile abdominal mass is most likely: Test:
An abdominal aortic aneurysm (AAA). Abdominal ultrasound is the study of choice for diagnosis.
Hyperkalemia time to treat:
Initial evaluation is with ECG. Acute therapy is given for patients with ((ECG changes, potassium ≥7.0 mEq/L without characteristic ECG changes, or rapidly rising POTASSIUM due to tissue breakdown)).
PVCs are common in patients post-myocardial infarction: Treatment:
Recognized by their widened QRS (>120 msec), bizarre morphology, and compensatory pause. Worse prognosis but no treatment unless symptomatic then Beta blocker.
Diastolic and continuous murmurs as well as loud systolic murmurs revealed on cardiac auscultation should:
Be investigated using transthoracic doppler echocardiography. Midsystolic soft murmurs in asymptomatic young patient require no further work up.
Cor pulmonale: Define: Signs include: What is seen on right heart catheterization:
Impaired function of the right ventricle due to pulmonary hypertension that usually occurs due to chronic lung disease. Signs: Elevated JVP, right ventricle heart sound, tricuspid regurgitation murmur, pulsatile liver, LEE, ascites. Right heart catheterisation shows elevated pulmonary artery systolic pressure (>25 mmHg).
Thyroid-stimulating hormone-secreting pituitary adenoma is characterized:
Central hyperthyroidism with elevated TSH (or inappropriately normal), T3, and T4. Patients have goiter due to TSH effects on tissue growth. VISUAL DISTURBANCES and HA from tumor growth.
Chronic GERD and Barrett’s esophagus are at risk for:
Adenocarcinoma of the esophagus.
Patients with Wolff-Parkinson-White syndrome (WPW): Describe arrhythmia: Treatment unstable vs stable:
An accessory pathway conducts depolarization directly from the atria to the ventricles with traversing the AV node. Hemodynamically unstable require immediate electrocardioversion: Hemodynamically stable patients PROCAINAMIDE (preferred) or ibutilide.
In WPW what agents are not used:
Adenosine, beta blockers, calcium channel blockers and digoxin. These agents may promote conduction across the accessory pathway and lead to degeneration of AF to VF.
CHF vs COPD exacerbation: what are the blood gas differences:
ABG CHF: hypoxia, HYPOCAPNIA, and respiratory alkalosis; example pH 7.46, pO2 73 mmHG, ((pCO2 31 mmHg)).ABG COPD: hypoxia, HYPERCAPNIA, and respiratory acidosis: example pH 7.39, pO2 80 mmHg ((pCO2 50 mmHg)).
CHF vs COPD exacerbation: What are differences on auscultation:
CHF: Bibasilar crackles.COPD: Widespread bilateral wheezes.
Specific test for CHF:
B-type natriuretic peptide (BNP) or pulmonary capillary wedge pressure.
Hypokalemia combined with computed tomography scan showing 3-cm adrenal mass suggests: Lab findings:Causes:
Primary hyperaldosteronism Conn’s disease). Low renin and elevated aldosterone and serum bicarbonate. Causeshypertension, mild hypernatremia, hypokalemia, and metabolic alkalosis.
Patients who undergo central venous catheterization need:
Portable chest x-ray to confirm proper placement of the catheter tip and absence of complications before administering drugs or other agents through the catheter.
Ischemic cardiac pain can sometimes be mistaken for: What test:
Epigastric pain, especially in the setting of symptoms that worsened with exertion. An exercise stress test withoutimaging if the baseline ECG is normal. Stress test positive then Coronary angiography (gold standard for Dx CAD).
Effects of maneuvers on hypertrophic cardiomyopathy: What increases murmur intensity: Why:
Valsalva (straining phase), Abrupt standing (from sitting or supine position), Nitroglycerin. Physiologic effect: Decrease in preload.
Effects of maneuvers on hypertrophic cardiomyopathy: What decreases murmur intensity: Why:
- Sustained hand grip 2. Squatting (from standing position) 3. Passive leg raisePhysiologic effect: 1. Increase Afterload 2. Increase Afterload & Preload 3. Increase Preload
Intravenous drug user with bacterial endocarditis with acute embolic stroke: Treatment:
MRI of brain. TEE of heart. Blood cultures and intravenous antibiotic therapy. Then watch. No need for antiplatelettherapy (aspirin) that you normally give in acute ischemic stroke due to atherosclerotic thrombosis or embolism.Medullary thyroid cancer (MTC): Presentation:Hard nodule, elevated calcitonin, malignant cells.
Multiple Endocrine Neoplasia (MEN) Type I:
Primary hyper((parathyroid))Entero((pancreatic)) tumors:((Pituitary)) tumors:
Multiple Endocrine Neoplasia (MEN) Type 2A:
Medullary ((thyroid)) cancer (MTC)((Pheochromocytoma)):((Parathyroid)) hyperplasia:
Multiple Endocrine Neoplasia (MEN) Type 2B:
Medullary ((thyroid)) cancer (MTC)((Pheochromocytoma)):Other: mucosal & interstitial neuromas, ((marfanoid habitus))Kyphoscoliosis and lordosis.
MEN 2 A & B genetics:
Autosomal dominant mutations involving RET proto-oncogene located on chromosome 10.
Acute cocaine toxicity with myocardial ischemia: Signs/symptoms: Treatment:
Psychomotor agitation, dilated pupils, atrophic nasal mucosa, hypertension, ECG changes. Treatment supplemental oxygen and intravenous benzodiazepines.
D-transposition of the great vessels (TGV) is the most common: Presentation:
Congenital cyanotic heart disease in the neonatal period. Presents in the first few hours of life with cyanosis and asingle loud second heart sound, and a narrow mediastinum “egg on a string” x-ray. Treat prostaglandins keep PDA open.
Pheochromocytoma treatment:
Do not give beta blockers without alpha blockers. A beta blocker alone may cause increases in blood pressure due to unopposed alpha- receptors. Remember alpha-1 causes vasoconstriction of peripheral vessels.
Pressors such as norepinephrine can cause:
Ischemia of the distal fingers and toes secondary to vasospasm. Diagnosis is suggested by symmetric duskiness and coolness of all the finger tips. Norepinephrine has alpha-1 agonist properties which cause vasoconstriction. This phenomenon can occur in intestines and kidneys.
Patients with massive pulmonary embolism usually present with: Effects on heart function:
Signs of low arterial perfusion (hypotension, syncope), and acute dyspnea, pleuritic chest pain, and tachycardia. Thrombus increases pulmonary vascular resistance and right ventricular pressure, causing ventricular hypokinesisand dilation, decreased preload, and hypotension.
During an acute phase myocardial infarction what heart sound can be heard:
An abnormal fourth heart sound (atrial gallop) due to left ventricular stiffening and dysfunction induced by myocardial ischemia.
Drug induced interstitial nephritis is usually caused by: Presentation:
Cephalosporins, penicillins, sulfonamides, NSAIDs, rifampin, phenytoin, and allopurinol. Patient present witharthralgias, rash, renal failure, and the urinalysis will show eosinophiluria.
Any male adolescent who presents with epistaxis, a localized mass, and a bony erosion on the back of thenose has:
An angiofibroma until proven otherwise.
Cardiac amyloidosis should be suspected in patients with:
Unexplained congestive heart failure (predominantly diastolic dysfunction), echocardiography findings of increased ventricular wall thickness with normal ventricular cavity dimensions (especially in the absence of hypertension, and low voltage on ECG.
Metabolic alkalosis defined as:
pH >7.45 and serum bicarbonate level > 24 mEq/L
Main causes for saline- responsive Metabolic Alkalosis:
Vomiting/ nasogastric aspiration; Prior diuretic use; Current diuretic use.
Main causes of non-saline-responsive Metabolic Alkalosis:
Excess mineralocorticoids activity ( Primary aldosteronism, cushing’s disease, ectopic ACTH production); Barter & Gitleman syndrome.
Situational syncope typical scenario would include: Mechanism:
A middle age or older male, who loses his consciousness immediately after urination, or a man who loses his consciousness during coughing fits. Mechanism includes autonomic dysregulation.
Patient has an episode of massive hemoptysis: Defined: Treatment:
Defined as > 600mL of expectorated blood over 24-hour period or a bleeding rate >100 mL/hour. Greatest danger is aspyxiation due to airway flooding. Patient placed with bleeding lung in the dependent position (lateral position). Bronchoscopy.
Raloxifene first line agent for: Increases the risk of:
Prevention of osteoporosis, and it decreases breast cancer risk. It increase the risk of thromboembolism. Generally women should not get pregnant after rubella vaccination: How long: Recommended waiting time is 28 days, but if women inadvertently get pregnant shortly after vaccination for rubella, they can be reassured that here is little risk to the fetus and they can proceed with ((routine prenatal care)).
Digoxin is a cardiac glycoside with adverse effects that include:
Nausea, vomiting, diarrhea, vision changes, and arrhythmias. Get a drug level.
Key differences in primary hyperparathyroidism (PHPT) and chronic kidney disease (Secondaryhyperparathyroidism):
PTH levels are usually much higher in secondary than primary. In addition, serum calcium levels are low to normal in secondary hyperparathyroidism. Serum phosphorous may be low or normal in PHPT were it tends to be high in kidney disease.
Myotonic muscular dystrophy: Genetics: Presentation:
Autosomal dominant expansion CTG chromosome 19q 13.3. Onset 12-30. Patient with facial weakness, hand grip myotonia, dysphagia. ((Arrhythmias, cataracts, balding, and testicular atrophy/infertility)). Remember Duchenne and Becker have earlier age of onset without underlined.
Opioid intoxication presents with:
((Miosis)), depressed mental status, decreased respiratory rate, decreased bowel sounds, ((hypotension)), and ((bradycardia)).
Sinus pauses on monitor, prolonged PR interval or QRS duration: Differential diagnosis:
Sick sinus syndrome, ((bradyarrhythmias)), atrioventricular block; Can be ((intermittent)).
Intraventricular conduction delay refers to:
Prolonged QRS duration.
Torsades de Pointes is due to:
Polymorphic ventricular tachycardia in the setting of prolonged QT interval. Long QTc interval
When looking at multiple endocrine neoplasia in a patient with HA and HT: If eye exam is normal:
Get plasma free metanephrine or 24-hour urine metanephrines.
Thalamic hemorrhage may present with:
Contralateral hemiparesis and sensory loss. Typically associated with nonreactive miotic pupils and eyes that deviate TOWARD the side of hemiparesis.
Basal ganglia hemorrhage may present with:
Contralateral hemiparesis and sensory loss. Homonymous hemianopsia, and Gaze palsy.
Pons hemorrhage may present with:
Deep coma & total paralysis within minutes, PINPOINT reactive pupils.
Features for ischemic reperfusion syndrome: Mechanism: Diagnosis:
A form of compartment syndrome (CS). Post-ischemic CS is due to interstitial edema and possibly intracellularswelling following tissue ischemia and subsequent reperfusion such as after and embolectomy. Compartmentpressure > 300 mmHg.
Initial stabilization of acute ST-elevation MI: Initial drugs given:
Aspirin, Clopidogrel, Nitrates (sublingual), beta blocker (unless hypotension, bradycardia, CHF, heart block), Highdose statin, anticoagulation (depends on planned revascularization).
Initial stabilization of acute ST-elevation MI: Drug given if patient has persistent pain, hypertension, or heartfailure:
Intravenous nitroglycerin (not if hypotension, right ventricular infarct, or severe aortic stenosis occurs)
Initial stabilization of acute ST-elevation MI: Drug given persistent pain:
Intravenous morphine
Initial stabilization of acute ST-elevation MI: Drug given for unstable sinus bradycardia:
Intravenous atropineInitial stabilization of acute ST-elevation MI: Drug given pulmonary edema:Intravenous furosemide (not if patient is hypotensive or hypovolemic)
Evaluation of secondary amenorrhea with a negative β-hCG, but increased TSH:
Diagnosis hypothyroidism
