Cardiology First Aid Flashcards
(250 cards)
1
Q
Acute coronary syndrome- atypical presentation- what lab/scan/procedure do you order?
A
atypical presentation = abdominal pain, nausea, vomiting = women, ELDERLY, diabetes, hx of smokingorder ECG
2
Q
Aortic dissection- Classic presentation- Highest risk factor
A
Causes chest pain that classically described as sudden, tearing, and radiating to the back. Hypertension is the mostcommon predisposing factor.
3
Q
Renal artery stenosis- Triad of signs/symptoms
A
Systolic-diastolic abdominal bruit in a patient with hypertension and atherosclerosis is strongly suggestive.
4
Q
Beta blocker overdose- Presentation- Complications- Treatments
A
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.
5
Q
Acute cardiac tamponade:- Etiology - Presentation- chest x-ray findings
A
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.
6
Q
Acute coronary syndrome:- How can lidocaine affect the heart?
A
Although it can decrease the risk of ventricular fibrillation, it may increase the risk of asystole.
7
Q
Anterior cerebral artery stroke:- Presentation
A
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.
8
Q
Statin medication recommendation:
A
Primary prevention in patients age 40-75 with a 10-year risk of atherosclerotic disease ≥7.5%.
9
Q
Cushing syndrome:
A
High- dose dexamethasone does not suppress plasma cortisol levels in patients with ectopic ACTH syndrome.
10
Q
Cushing’s Disease
A
ACTH-producing pituitary adenoma. Partially inhibited by high- dose dexamethasone.
11
Q
Potassium sparing diuretics:
A
triamterene and amiloride
12
Q
Stress test for CAD:
A
Beta blockers, calcium channel blockers, and nitrates are antianginal agents that are healed 48 before performing acardiac stress test.
13
Q
Acute decompensated heart failure (ADHF):- Presentation- Treatment
A
Presents with acute pulmonary edema. Tx: Oxygen, assisted ventilation, aggressive intravenous diuresis (furosemide), and possible vasodilator therapy.
14
Q
Torsades de pointes (TdP):- Define- Treatment
A
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.
15
Q
Acute type A aortic dissection:- Diagnosis- Treatment
A
Must get a TEE, so you can rapidly diagnose and treat. Surgical emergency!
16
Q
Single photon emission CT scan:
A
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.
17
Q
Variant Angina (or Prinzmetal’s angina):
A
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.
18
Q
Cerebellar hemorrhage:
A
Patients typically have headache, neck stiffness, gait ataxia, and no hemiparesis
19
Q
Putamen hemorragia:
A
Most common cause is hypertension. Next to internal capsule, so leads to hemiparesis.
20
Q
Thalamic stroke (Dejerine-Roussy syndrome):
A
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.
21
Q
Midbrain and medulla strokes have in common:
A
Classically involve the nuclei of the cranial nerves.
22
Q
Sustained monomorphic ventricular tachycardia (SMVT):
A
Hemodynamically unstable electrical cardioversion. Hemodynamically stable give amiodarone.
23
Q
Cardiac tamponade:
A
Catastrophic complication of acute aortic dissection. Suspected in patients with hypotension, tachycardia, distended neck veins, and pulsus paradoxus.
24
Q
Patients with narrow-QRS-complex tachycardia:
A
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.
25
Hypertension in overweight people:
Weight lose is the most effective nonpharmacologic measure to decrease blood pressure in overweight individuals.
26
Mechanism of pain relief in patient with chest pain treated with nitroglycerin:
Dilation of veins (capacitance vessels) which leads to decrease ventricular preload.
27
Acute arterial occlusion (limb ischemia):
Classically presents with “5 Ps” (pain, pallor, pulselessness, paresthesia, and paralysis). Immediate anticoagulation and referral for vascular surgery.
28
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.
29
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.
30
Symptomatic pulmonary embolism most common cause:
The proximal deep veins (iliac, femoral and politeal veins) are the source of ＞90% of acute PEs.
31
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.
32
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.
33
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.
34
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.
35
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.
36
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.
37
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.
38
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.
39
The most common cause of sudden cardiac arrest in the immediate postinfarction period in patients withacute MI:
Reentrant ventricular arrhythmias (ventricular fibrillation).
40
Hypokalemia signs and ECG findings:
Causes weakness, fatigue, and muscle cramps. ECG may show U wave, flat and broad T waves, and prematureventricular beats.
41
Amaurosis fugax:
Characterized by visual loss that is transient and usually monocular. “Curtain falling down.” Most common causeRETINAL EMBOLI from the CAROTID ARTERY.
42
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.
43
Sarcoidosis can have elevated serum:
Angiotensin converting enzyme (ACE) levels.
44
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.
45
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.
46
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.
47
The patient’s pulsatile abdominal mass is most likely: Test:
An abdominal aortic aneurysm (AAA). Abdominal ultrasound is the study of choice for diagnosis.
48
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)).
49
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.
50
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.
51
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).
52
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.
53
Chronic GERD and Barrett's esophagus are at risk for:
Adenocarcinoma of the esophagus.
54
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.
55
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.
56
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)).
57
CHF vs COPD exacerbation: What are differences on auscultation:
CHF: Bibasilar crackles.COPD: Widespread bilateral wheezes.
58
Specific test for CHF:
B-type natriuretic peptide (BNP) or pulmonary capillary wedge pressure.
59
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.
60
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.
61
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).
62
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.
63
Effects of maneuvers on hypertrophic cardiomyopathy: What decreases murmur intensity: Why:
1. Sustained hand grip 2. Squatting (from standing position) 3. Passive leg raisePhysiologic effect: 1. Increase Afterload 2. Increase Afterload & Preload 3. Increase Preload
64
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.
65
Multiple Endocrine Neoplasia (MEN) Type I:
Primary hyper((parathyroid))Entero((pancreatic)) tumors:((Pituitary)) tumors:
66
Multiple Endocrine Neoplasia (MEN) Type 2A:
Medullary ((thyroid)) cancer (MTC)((Pheochromocytoma)):((Parathyroid)) hyperplasia:
67
Multiple Endocrine Neoplasia (MEN) Type 2B:
Medullary ((thyroid)) cancer (MTC)((Pheochromocytoma)):Other: mucosal & interstitial neuromas, ((marfanoid habitus))Kyphoscoliosis and lordosis.
68
MEN 2 A & B genetics:
Autosomal dominant mutations involving RET proto-oncogene located on chromosome 10.
69
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.
70
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.
71
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.
72
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.
73
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.
74
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.
75
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.
76
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.
77
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.
78
Metabolic alkalosis defined as:
pH \>7.45 and serum bicarbonate level \> 24 mEq/L
79
Main causes for saline- responsive Metabolic Alkalosis:
Vomiting/ nasogastric aspiration; Prior diuretic use; Current diuretic use.
80
Main causes of non-saline-responsive Metabolic Alkalosis:
Excess mineralocorticoids activity ( Primary aldosteronism, cushing's disease, ectopic ACTH production); Barter & Gitleman syndrome.
81
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.
82
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.
83
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)).
84
Digoxin is a cardiac glycoside with adverse effects that include:
Nausea, vomiting, diarrhea, vision changes, and arrhythmias. Get a drug level.
85
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.
86
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.
87
Opioid intoxication presents with:
((Miosis)), depressed mental status, decreased respiratory rate, decreased bowel sounds, ((hypotension)), and ((bradycardia)).
88
Sinus pauses on monitor, prolonged PR interval or QRS duration: Differential diagnosis:
Sick sinus syndrome, ((bradyarrhythmias)), atrioventricular block; Can be ((intermittent)).
89
Intraventricular conduction delay refers to:
Prolonged QRS duration.
90
Torsades de Pointes is due to:
Polymorphic ventricular tachycardia in the setting of prolonged QT interval. Long QTc interval
91
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.
92
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.
93
Basal ganglia hemorrhage may present with:
Contralateral hemiparesis and sensory loss. Homonymous hemianopsia, and Gaze palsy.
94
Pons hemorrhage may present with:
Deep coma & total paralysis within minutes, PINPOINT reactive pupils.
95
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.
96
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).
97
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)
98
Initial stabilization of acute ST-elevation MI: Drug given persistent pain:
Intravenous morphine
99
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)
100
Evaluation of secondary amenorrhea with a negative β-hCG, but increased TSH:
Diagnosis hypothyroidism
101
Aortic valve endocarditis and intravenous drug abuse are associated with an increased risk of:
Periannular extension of endocarditis.
102
Serum Sickness like reaction is most commonly caused by: Presentation: Treatment:
Caused by β-lactams, and sulfa drugs. Symptoms arise 1-2 weeks after exposure and include fever, urticarial rash,polyarthralgia, and lymphadenopathy. Remove offending agent.
103
Congestive heart failure due to left ventricular systolic dysfunction is characterized by:
Decreased cardiac output/index, increased systemic vascular resistance (SVR), and an increase in left ventricularend-diastolic volume (LVEDV).
104
Carcinoid syndrome clinical manifestations: Tests:
Skin: flushing, telangiectasia, cyanosis; GI: diarrhea, cramping; Cardiac: valvular lesions (right\>left); Pulmonary:bronchospasms; Niacin deficiency (dermatitis, diarrhea, & dementia). Diagnosis 24-hour urine 5-hydroxyindoleaceticacid. CT/MRI to localize tumor. OctreoScan to detect metastasis.
105
What is the purpose of diagnostic or prognostic exercise testing? (stress testing)
To localize ischemia or assess viability to recommend exercise
106
Pulmonary embolism, treatment
heparin therapy
107
In patients with neurofibromatosis type 1, what type of hypertension is seen in these patients? What is the pathogenesis?
Essential hypertension, from renal vascular lesions, most commonly in the renal vasculature.
108
Children and adolescents with hypertension. What percentile do you treat?
blood pressure greater than the 95th percentile for age, height, weight.
109
Cardiac auscultation - aortic area - systolic ejection murmur. What's the diagnosis?
Aortic stenosis
110
Cardiac auscultation - pulmonic area - systolic ejection murmur. What's the diagnosis?
Pulmonic stenosis, flow murmur, ASD (atrial septal defect)
111
Cardiac auscultation - pulmonic area - systolic ejection click. What's the diagnosis?
Pulmonic stenosis
112
Cardiac auscultation - left sternal border area - systolic ejection murmur. What's the diagnosis?
Hypertrophic cardiomyopathy
113
Cardiac auscultation - left sternal border area - early diastolic murmur. What's the diagnosis?
Aortic regurgitation, pulmonic regurgitation
114
Cardiac auscultation - mitral area - holostolic murmur. What's the diagnosis?
mitral regurgitation
115
Cardiac auscultation - mitral area - mid/late systolic click. What's the diagnosis?
mitral valve prolapse
116
Cardiac auscultation - mitral area - mid/late diastolic murmur. What's the diagnosis?
mitral stenosis
117
Cardiac auscultation - tricuspid area - holosystolic murmur. What's the diagnosis?
tricuspid regurgitation, ventral septal defect
118
Cardiac auscultation - mitral area - mid/late diastolic murmur. What's the diagnosis?
tricuspid stenosis, ASD (atrial septal defect)
119
Increased blood flow in what areas of the heart cause ASD murmurs?
ASD murmurs caused by increased blood flow across pulmonic valve and tricuspid valve
120
Neurologic complications of endocarditis with replacement valve?
Embolic stroke, brain abscess or cerebritis, meningitis, acute encephalopathy, meningoencephalitis.
121
For left ventricular hypertrophy, what are the Cornell criteria and Sokolow-Lyon criteria?
Cornell criteria: Amplitude of R in aVL + S in V3 \> 28 mm in men or \> 20 mm in women.
■ Sokolow-Lyon criteria: S in V1 + R in V5 or V6 \> 35 mm.
122
For right ventricular hypertrophy, what are the ECG signs regarding axis deviation and R wave?
Right-axis deviation and an R wave in V1 \> 7 mm.
123
Jugular venous distention (JVD, \> 7 cm above sternal angle) is presented in a patient, what is the differential diagnosis?
Suggests right heart failure, pulmonary hypertension, volume overload, tricuspid re- gurgitation, or pericardial disease.
124
Hepatojugular reflux is presented in a patient, what is the differential diagnosis?
Fluid overload; impaired right ventricular compliance.
125
Kussmaul's sign (↑ in JVP with inspiration) is presented in a patient, what is the differential diagnosis?
Right ventricular infarction, postoperative cardiac tamponade, tricuspid regurgitation, constrictive pericarditis.
126
What's the Ddx for a systolic murmur?
■ Aortic stenosis: Harsh systolic ejection murmur; radiation to carotids.
■ Mitral regurgitation: Holosystolic murmur; radiation to axillae or to carotids.
■ Mitral valve prolapse: Midsystolic or late-systolic click.
■ Flow murmur: Very common, and does not imply cardiac disease.
127
What's the Ddx for a diastolic murmur?
■ Aortic regurgitation: Early decrescendo murmur.
■ Mitral stenosis: Mid- to late, low-pitched murmur.
128
What are the 2 types of gallops you can hear in the heart auscultation?
S3 gallop and S4 gallop
129
What is the Ddx for an S3 gallop?
Dilated cardiomyopathy (floppy ventricle), mitral valve disease; often normal in younger patients and in high-output states (e.g.,pregnancy).
130
What is the Ddx for an S4 gallop?
Hypertension, diastolic dysfunction (stiff ventricle), aortic stenosis; often normal in younger patients and athletes.
131
What is the Ddx for pulmonary edema?
Left heart failure
132
What is the Ddx for peripheral edema?
Right heart failure and biventricular failure, peripheral venous disease, constrictive pericarditis, tricuspid regurgitation, hepatic disease, lymphedema; also nephrotic syndrome, hypoalbuminemia, and drugs.
133
What is the Ddx for increased peripheral pulses?
Compensated aortic regurgitation, coarctation (arms \> legs), patent ductus arteriosus.
134
What is the Ddx for decreased peripheral pulses?
Peripheral arterial disease
135
What is the Ddx for pulses paradoxus?
Pericardial tamponade; also asthma and COPD, tension pneumothorax, foreign body in airway.
136
What is the Ddx for Pulsus alternans (alternating weak and strong pulses)?
Cardiac tamponade, impaired left ventricular systolic function; poor prognosis.
137
What is the Ddx for Pulsus parvus et tardus (weak and delayed pulse)
Aortic stenosis
138
Etiology of sinus bradycardia.
Normal response to cardiovascular conditioning; can also result from sinus node dysfunction or from β-blocker or calcium channel blocker (CCB) excess
139
Signs and symptoms of sinus bradycardia.
May be asymptomatic, but may also present with lightheadedness, syncope, chest pain, or hypotension.
140
ECG findings of sinus bradycardia.
Ventricular rate
141
Treatment of sinus bradycardia.
None necessary if asymptomatic; atropine may be used to ↑ heart rate; pacemaker placement is the definitive treatment in severe cases.
142
Etiology of First-degree AV block
Can occur in normal individuals; associated with ↑ vagal tone and with β-blocker or CCB use.
143
Symptoms of First-degree AV block
Asymptomatic
144
ECG findings of First-degree AV block
PR interval \> 200 msec.
145
Treatment of First-degree AV block
None necessary
146
Name the 2 second-degree AV blocks with the same etiology, signs & symptoms, ECG profile and treatment
Mobitz 1 and Wenckebach
147
Etiology of second-degree AV block
Drug effects (digoxin, β-blockers, CCBs) or ↑ vagal tone; sinoatrial conduction disease; right coronary ischemia or infarction.
148
Symptoms of second-degree AV block
usually asymptomatic
149
ECG findings of second-degree AV block
Progressive PR lengthening until a dropped beat occurs; PR interval then resets.
150
Treatment of second-degree AV block
Stop the offending drug. Atropine or pacemaker placement as clinically indicated.
151
In the heart, atrial hypertrophy can be detected on an ECG determining left or right atrium by:
- P-wave amplitude of ______ in lead _____ for right
- P-wave amplitude of ______ in lead _____ for left
Right atrial abnormality if P-wave amplitude in lead II is \< 2.5 mm; left atrial abnormality if P-wave width in lead II is \> 120 msec, or if terminal negative deflection in V1 is \> 1 mm in amplitude and \> 40 msec in duration.
152
Describe the etiology of Mobitz II second-degree AV block
Results from fibrotic disease of the conduction system or from acute, subacute, or prior myocardial infarction (MI).
153
What are the symptoms and signs of Mobitz II second-degree AV block
Occasionally syncope; frequent progression to third-degree AV block.
154
What is the ECG finding of Mobitz II second-degree AV block
Unexpected dropped beat(s) without a change in PR interval.
155
What is the treatment of Mobitz II second-degree AV block?
pacemaker placement
156
What is a complete AV block called?
Third-degree AV block
157
What is the etiology of a third-degree AV block?
No electrical communication between the atria and ventricles.
158
What is the symptoms and signs of a third-degree AV block?
Syncope, dizziness, acute heart failure, hypotension, cannon A waves.
159
What is the ECG findings of a third-degree AV block?
No relationship between P waves and QRS complexes.
160
What is the treatment of a third-degree AV block?
pacemaker placement
161
What is another name for sick sinus syndrome (SSS)?
tachycardia-bradycardia syndrome
162
What is the etiology of sick sinus syndrome (SSS) / tachycardia-bradycardia syndrome?
A heterogeneous disorder consisting of abnormalities in supraventricular impulse generation and conduction that lead to intermittent supraventricular tachy- and bradyarrhythmias.
163
What is the signs and symptoms of sick sinus syndrome (SSS) / tachycardia-bradycardia syndrome?
2° to tachycardia or bradycardia; may include syncope, palpitations, dyspnea, chest pain, TIA, and stroke.
164
What is the treatment of sick sinus syndrome (SSS) / tachycardia-bradycardia syndrome?
The most common indication for pacemaker placement.
165
What is the most common indication for pacemaker placement?
sick sinus syndrome (SSS) / tachycardia-bradycardia syndrome
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Name the 7 Supraventricular tachyarrhythmias.
- Atrial sinus tachycardia
- Atrial fibrillation
- Atrial flutter
- Multifocal atrial tachycardia
- Atrioventricular nodal reentry tachycardia
- Atrioventricular reciprocating tachycardia
- Paroxysmal atrial tachycardia
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What is the etiology of Atrial Sinus tachycardia?
Normal physiologic response to fear, pain, and exercise. Can also be 2° to hyperthyroidism, volume contraction, infection, or pulmonary embolism.
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What are the signs & symptoms of Atrial Sinus tachycardia?
Palpitations, shortness of breath.
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What is the ECG findings of Atrial Sinus tachycardia?
Ventricular rate \> 100 bpm; normal P waves before every QRS complex
170
What is the treatment of Atrial Sinus tachycardia?
Treat the underlying cause
171
What is the Ddx / Etiology of Atrial fibrillation (AF)?
Acute AF— PIRATES:
- Pulmonary disease
- Ischemia Rheumatic heart disease
- Anemia/Atrial myxoma
- Thyrotoxicosis
- Ethanol
- Sepsis
Chronic AF—
- hypertension, CHF
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What is the signs and symptoms of Atrial fibrillation (AF)?
Often asymptomatic, but may present with shortness of breath, chest pain, or palpitations. Physical exam reveals irregularly irregular pulse.
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What is the ECG findings of Atrial fibrillation (AF)?
No discernible P waves, with variable and irregular QRS response.
174
What is the treatment of Atrial fibrillation (AF)?
Estimate risk of stroke using CHAD2 score.
Anticoagulation if \> 48 hours (to prevent CVA); rate control (CCBs, β-blockers, digoxin, amiodarone).
Initiate cardioversion only if new onset.
175
What is the etiology of an Atrial flutter?
Circular movement of electrical activity around the atrium at a rate of 300 times per minute.
176
Define restrictive cardiomyopathy. Use the words: myocardium, diastolic and systolic in the definition.
Defined as ↓ elasticity of myocardium leading to impaired diastolic filling without significant systolic dysfunction (a normal or near-normal EF)
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What is the etiologies of restrictive cardiomyopathy?
It is caused by infiltrative disease (amyloidosis, sarcoidosis, hemochromatosis) or by scarring and fibrosis (2° to radiation or doxorubicin).
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What is the History / PE of restrictive cardiomyopathy?
Signs and symptoms of left-sided and right-sided heart failure occur, but symptoms of right-sided heart failure (JVD, peripheral edema) often predominate.
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How do you diagnose restrictive cardiomyopathy?
■ Echocardiography is key to diagnosis and reveals rapid early filling with a normal or near-normal EF.
■ Cardiac biopsy may reveal fibrosis or evidence of infiltration.
■ ECG frequently shows LBBB.
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How do you treat restrictive cardiomyopathy?
Therapeutic options are limited and generally are palliative only. Medical treatment includes cautious use of diuretics for fluid overload, vasodilators to ↓ filling pressure, and anticoagulation if not contraindicated.
181
What are the major risk factors for coronary artery disease (CAD)?
Major risk factors for CAD include age, male gender, hyperlipidemia, DM, hypertension, obesity, a family history, and smoking.
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What are the clinical manifestations of coronary artery disease (CAD)?
Clinical manifestations of CAD include stable and unstable angina, shortness of breath, dyspnea on exertion, arrhythmias, MI, heart failure, and sudden death.
183
Define angina pectoris and what causes it?
Substernal chest pain 2° to myocardial ischemia (O2 supply and demand mis- match).
184
Variant Angina (or Prinzmetal's angina):
Vasospastic disorder that typically occurs in young female smokers. It is similar in mechanism to Raynaud phenomenon. Chest pain usually occurs middle of night, and episodes transient ST elevation.
185
Cardiac auscultation - aortic area - systolic ejection murmur. What's the diagnosis?
Aortic stenosis
186
What are the signs and symptoms of an Atrial flutter?
Usually asymptomatic, but can present with palpitations, syncope, and lightheadedness.
187
What are the ECG findings of and Atrial flutter?
Regular rhythm; “sawtooth” appearance of P waves can be seen. Atrial rate is usually 240–320 bpm with varying degrees of blockade.
188
What is the treatment of an Atrial flutter?
Anticoagulation and rate control. Cardiovert according to AF criteria.
189
What is the etiology of Multifocal atrial tachycardia?
Multiple atrial pacemakers or reentrant pathways; COPD, hypoxemia.
190
What are the symptoms of Multifocal atrial tachycardia?
may be asymptomatic
191
What are the ECG findings of Multifocal atrial tachycardia?
Three or more unique P-wave morphologies; rate \> 100 bpm.
192
How do you treat Multifocal atrial tachycardia?
Treat the underlying disorder; verapamil or β-blockers for rate control and suppression of atrial pacemakers (not very effective).
193
Name 3 supraventricular tachyarrhythmias of the AV junction.
Atrioventricular nodal reentry tachycardia (AVNRT)
Atrioventricular reciprocating tachycardia (AVRT)
Paroxysmal atrial tachycardia
194
What is the etiology of Atrioventricular nodal reentry tachycardia (AVNRT)?
A reentry circuit in the AV node depolarizes
the atrium and ventricle nearly simultaneously.
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What is the signs and symptoms of Atrioventricular nodal reentry tachycardia (AVNRT)?
Palpitations, shortness of breath, angina, syncope, lightheadedness.
196
What are the ECG findings of Atrioventricular nodal reentry tachycardia (AVNRT)?
Rate 150–250 bpm; P wave is often buried in QRS or shortly after.
197
What is the treatment of Atrioventricular nodal reentry tachycardia (AVNRT)?
Carotid massage, Valsalva, or adenosine can stop the arrhythmia. Cardiovert if hemodynamically unstable.
198
What is the etiology of Atrioventricular reciprocating tachycardia (AVRT)?
Circular movement of an impulse between the AV node and the atrium through a bypass tract. Seen in Wolff-Parkinson- White syndrome.
199
What is the signs and symptoms of Atrioventricular reciprocating tachycardia (AVRT)?
Palpitations, shortness of breath, angina, syncope, lightheadedness.
200
What is the ECG findings of Atrioventricular reciprocating tachycardia (AVRT)?
A retrograde P wave is often seen after a normal QRS.
201
What is the treatment of Atrioventricular reciprocating tachycardia (AVRT)?
Same as that for AVNRT.
Carotid massage, Valsalva, or adenosine can stop the arrhythmia. Cardiovert if hemodynamically unstable.
202
What is the etiology of Paroxysmal atrial tachycardia?
Rapid ectopic pacemaker in the atrium (not sinus node).
203
What is the signs and symptoms of Paroxysmal atrial
tachycardia?
Palpitations, shortness of breath, angina, syncope, lightheadedness.
204
What is the ECG findings of Paroxysmal atrial
tachycardia?
Rate \> 100 bpm; P wave with an unusual axis before each normal QRS
205
What is the treatment of Paroxysmal atrial
tachycardia?
Adenosine can be used to unmask underlying atrial activity.
206
Name the 4 ventricular tachyarrhythmias.
- Premature ventricular contraction (PVC)
- Ventricular tachycardia (VT)
- Ventricular fibrillation (VF)
- Torsades de pointes
207
What is the etiology of Premature ventricular contraction (PVC)?
Ectopic beats arise from ventricular foci. Associated with hypoxia, electrolyte abnormalities, and hyperthyroidism.
208
What is the signs and symptoms of Premature ventricular contraction (PVC)?
Usually asymptomatic, but may lead to palpitations.
209
What is the ECG findings of Premature ventricular contraction (PVC)?
Early, wide QRS not preceded by a P wave. PVCs are usually followed by a compensatory pause.
210
What is the treatment of Premature ventricular contraction (PVC)?
Treat the underlying cause. If symptomatic, give β-blockers or occasionally other antiarrhythmics.
211
What is the etiology of Ventricular tachycardia (VT)?
Can be associated with CAD, MI, and structural heart disease.
212
What is the signs and symptoms of Ventricular tachycardia (VT)?
Nonsustained VT is often asymptomatic; sustained ventricular tachycardia can lead to palpitations, hypotension, angina, and syncope. Can progress to VF.
213
What is the ECG findings of Ventricular tachycardia (VT)?
Three or more consecutive PVCs; wide QRS complexes in a regular rapid rhythm; AV dissociation.
214
What is the treatment of Ventricular tachycardia (VT)?
Cardioversion and antiarrhythmics (e.g., amiodarone, lidocaine, procainamide).
215
What is the etiology of Ventricular fibrillation (VF)?
Associated with CAD and structural heart disease.
Also associated with cardiac arrest (together with asystole).
216
What is the signs and symptoms of Ventricular fibrillation (VF)?
Syncope, absence of blood pressure, pulselessness.
217
What is the ECG findings of Ventricular fibrillation (VF)?
Totally erratic wide-complex tracing.
218
What is the treatment of Ventricular fibrillation (VF)?
Immediate electrical cardioversion and ACLS protocol.
219
What is the etiology of Torsades de points?
Associated with long QT syndrome, proarrhythmic response to medications, hypokalemia, and congenital deafness.
220
What is the signs and symptoms of Torsades de points?
Can present with sudden cardiac death; typically associated with palpitations, dizziness, and syncope.
221
What is the ECG findings of Torsades de points?
Polymorphous QRS; VT with rates between 150 and 250 bpm.
222
What is the treatment of Torsades de points?
Correct hypokalemia; withdraw offending drugs. Give magnesium initially and cardiovert if unstable.
223
What are the AHA/ACC Classification of CHF?
Stage A - High risk factors, no S&S of HD or CHF
Stage B - Structural heart disease, no signs of CHF
Stage C - Stage B + signs of CHF
Stage D - Stage C at rest despite max drugs
224
What are the 4 AHA/ACC Classifications and treatments of CHF?
Stage A - Manage risk factors; ACEIs
Stage B - ACEIs, beta blockers
Stage C - diuretics, ACEIs, β-blockers, digitalis, and dietary salt restriction
Stage D - mechanical assist devices, heart transplantation, continuous IV inotropic drugs, and hospice care for end-stage patients.
225
What are the 4 NYHA Functional Classifications of CHF?
Class I - No limitation of activity; no symptoms with normal activity.
Class II - Slight limitation of activity; comfortable at rest or with mild exertion
Class III - Marked limitation of activity; comfortable only at rest.
Class IV - Confined to complete rest in bed or chair, as any physical activity brings on discomfort; symptoms present at rest.
226
Left-sided CHF symptoms, auscultation, signs.
DYSPNEA predominates
Left-sided S3/S4 gallop
Bilateral basilar rales
Pleural effusions
Pulmonary edema
Orthopnea, paroxysmal nocturnal dyspnea
227
Right-sided CHF symptoms, auscultation, signs.
FLUID RETENTION predominates
Right-sided S3/S4 gallop JVD
Hepatojugular reflex
Peripheral edema
Hepatomegaly, ascites
228
What is the difference between the age of patients with systolic dysfunction vs. diastolic dysfunction?
Systolic dysfunction 65 y/o
229
What is the physical exam heart auscultation findings of systolic dysfunction ?
Displaced PMI, S3 gallop.
230
What is the physical exam heart auscultation findings of diastolic dysfunction ?
Sustained PMI, S4 gallop
231
What is the chest x-ray findings of diastolic dysfunction ? Lungs? heart size?
Pulmonary congestion, normal heart size.
232
What is the chest x-ray findings of systolic dysfunction? Lungs? Heart size?
Pulmonary congestion, cardiomegaly.
233
What is the ECG/echocardiography findings of diastolic dysfunction ?
LVH, normal EF (\> 55%).
234
What is the ECG/echocardiography findings of systolic dysfunction ?
Q waves, ↓ EF (\< 40%).
235
Define the parameters of heart failure caused by systolic dysfunction - use ejection fraction (EF) and end-diastolic volumes in your answer.
Heart failure caused by systolic dysfunction is defined as ↓ EF (\<40%)
236
Heart failure caused by systolic dysfunction is defined as a ↓ EF (\< 40%). What is this ↓EF caused by?
It is caused by inadequate left ventricular contractility or ↑ afterload.
237
What is the pathophysiology of heart failure caused by systolic dysfunction - defined as a ↓ EF (\<40%).
The heart compensates for low EF and ↑ preload through hypertrophy and ventricular dilation (Frank-Starling law), but the compensation ultimately fails, leading to ↑ myocardial work and worsening systolic function.
238
What is the most common cause of right-sided heart failure?
left-sided heart failure
239
How do you diagnose CHF?
CHF is a clinical syndrome whose diagnosis is based on signs and symptoms.
240
What are the heart echo findings of CHF?
↓ EF and ventricular dilation
241
What are the lab abnormalities in CHF?
BNP \> 500, ↑ creatinine, ↓ sodium
242
Define diastolic dysfunction.
Defined by ↓ ventricular compliance with normal systolic function.
243
What are the 2 types of impairment in diastolic dysfunction and what are their causes?
The ventricle has:
- Impaired active relaxation (2° to ischemia, aging, and/or hypertrophy)
- Impaired passive filling (scarring from prior MI; restrictive cardiomyopathy)
244
What is the pathophysiology of diastolic dysfunction?
The ventricle has either impaired active relaxation or scarring leading to impaired passive filling. Left ventricular end-diastolic pressure ↑, cardiac output remains essentially normal, and EF is normal or ↑.
245
What is the first-line therapy for diastolic dysfunction?
Diuretics
246
What is the Hx/PE for patient w/ diastolic dysfunction?
Stable and unstable angina, shortness of breath, dyspnea on exertion, arrhythmias, MI, heart failure, and sudden death.
247
What is cardiomyopathy and what are the 3 categories?
Myocardial disease; categorized as dilated, hypertrophic, or restrictive
248
What is the most common cardiomyopathy?
Dilated cardiomyopathy
249
What features of the heart must be present for diagnosis of dilated cardiomyopathy?
Left ventricular dilation and systolic dysfunction (low EF) must be present for diagnosis
250
Most cases of cardiac myopathy are idiopathic, but what are the 2 most common secondary causes?
The two most common causes of 2° dilated cardiomyopathy are ischemia and long-standing hypertension.
