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Professional Development > Part 14 > Flashcards

Part 14 Flashcards

1
Q

Recall the coronary circulation (right and left) of a right dominant heart (the posterior descending artery comes off the right coronary)

A
  • right coronary artery
  • right marginal artery branches off to supply lateral right side of heart,SA node, and AV node
  • right coronary becomes posterior descending artery that goes around the back of the heart
  • near apex anastamoses with anterior interventricular artery
  • left coronary artery
  • left anterior descending artery branches off and supplies the interventricular septum and anterior walls of both left and right ventricles
  • Left anterior descending artery becomes anterior interventricular artery and anastamoses with posterior interventricular artery
  • left coronary becomes circumflex artery and supplies left atrium and posterior wall of left ventricle
  • circum
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2
Q

Angina pectoris definition

A

Chest, jaw, shoulder, back, or arm pain/discomfort sometimes associated with other symptoms such as SOB often due to coronary artery disease ischemia but can be due to ANY imbalance in myocardial o2 supply and demand, many can continue to live with the partial occlusion but coronary artery disease is cause of 1/7 deaths in US

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3
Q

Ischemia vs infarct

A

Ischemia is lack of adequate oxygen supply causing tissue damage, infarct is when tissue has died permanently

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4
Q

3 factors that determine if myocardial ischemia will occur

A
  • O2 carrying capacity of blood
  • coronary artery blood flow
  • myocardial workload
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5
Q

Coronary artery blood flow occurs during which phase of the cardiac cycle?

A

diastole

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6
Q

Postprandial angina

A

Angina that occurs as a result of blood flow being redirected to digest food causing ischemia to the coronary arteries, probably could be mistaken for GERD huh?

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7
Q

Angina pain origin mech of action

A
  • Ischemia reduces formation of ATP
  • causes acidosis
  • loss of membrane integrity of myocardial cells
  • stimulates chemoreceptors and mechanoreceptors in the cardiac vessel
  • release of lactate, seratonin, bradykinin, histamine, and adenosine
  • Afferent nerve fibers that travel along pathways from the heart in the upper thoracic and lower cervical spinal cord causes referred discomfort to dermatomes that supply afferent nerves to the same segments of the spinal cord as the heart
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8
Q

Levine sign

A

Positive when patient places his or her fist on the center of the chest indicative of angina pectoris

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9
Q

Big 5 that must be ruled out when a patient presents with chest pain

A
  • acute coronary syndrome (MI, unstable angina)
  • aortic dissection
  • PE
  • tension pneumothorax
  • esophageal rupture
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10
Q

Stable angina

A

Predictable, usually follows a precipitating event, that is generally the same severity as previous attacks, relieved by rest or by the customary dose of nitroglycerin. Caused by fixed coronary artery obstruction 2ndary to atherosclerosis

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11
Q

Prinzmetals’ variant angina

A

also known as vasospastic angina, Occurs at rest, typically between midnight and 8am, manifests electrocardiographically as episodic ST segment elevations, caused by coronary artery spasms without superimposed CAD (no plaques found in coronary arteries that elicit the symptoms), patients also more likely to develop ventricular arrhythmias, may be triggered by stress, cold, hyperventilation

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12
Q

Microvascular angina - cardiac syndrome X

A

Angina symptoms, positive exercise test (ST segment depression), normal coronary angiograms so no coronary spasm, patient does not have any other cardiac or systemic diseases (hyperension, diabetes) known to influence vascular function. Defective endothelium dependent dilation in the coronary microcirculation contributes to the altered regulation of myocardial perfusion and the ischemic manifestations predominantly in women. 2% risk of death or MI at 30 days of follow up

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13
Q

Unstable angina definition

A

New onset (makes it unstable by definition). Increasing severity, duration, or frequency of chronic angina of another type. Occurs at rest or minimal exertion. Not relieved by typical measures. No release of enzymes and biomarkers of myocardial necrosis.

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14
Q

Acute coronary syndromes

A

-occurs with ST elevation MI, non ST elevation MI, or unstable angina, require immediate catheterization

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15
Q

NY Heart Association Functional Classification of Angina

A

Class 1 - usually only with strenuous activity
Class II - slightly more prolonged or slightly more vigorous activity
Class III - angina with usual daily activity
Class IV - Angina at rest

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16
Q

Stable angina treatment (4)

A
  • Risk factor modification
  • aspirin
  • B blockers
  • nitroglycerin
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17
Q

Stable vs unstable angina

A

Stable angina is predictable and fixed with a known onset and treatment, unstable is new onset and or increasing severity or not responding to treatment

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18
Q

Cardioesophageal reflex

A

A reduction in coronary blood flow by constriciton via a neural reflex when the esophagus is stimulated by acid reflux (in cases of chronic acid reflux could manifest as angina)

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19
Q

Nicotine drug class and mech of action

A
  • Ganglionic stimulant
  • At low doses stimulates nicotine receptors and at high doses inhibits nicotine receptors, easily absorbed and distributed across the body (and across the placenta)
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20
Q

Nicotine effects at low doses (such as smoking) (3)

A
  • cardiovascular stimulation of nicotinic receptors in sympathetic ganglia causes vasoconstriction and elevated BP
  • gastrointestinal stimulation of nicotinic receptors in parasympathtic ganglia results in gastric acid secretion and increased tone and motility of GI smooth muscle, can produce vomiting (tolerance develops)
  • CNS stimulant, moderate doses can cause tremors, high doses can cause convulsions, activates pleasure system in brain
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21
Q

Blocking Ca2+ channels prevents the inward movement of Ca2+ into the cell, preventing ____ in vascular smooth muscle of ___ and therefore causing ____

A

contraction, arteries, vasodilation

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22
Q

Ca2+ channel blocker activity on the heart (3)

A
  • decreases contractile effect
  • decreases speed of conduction of AP in SA and AV node
  • Slow heart rate
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23
Q

Coupling of cardiac ca2+ channels to B1 adrenergic receptors

A

Refers to how in the heart the Ca2+ channels are linked to B1 adrenergic receptors, when B1 receptors are activated, Ca2+ influx is enhanced and when blocked, influx is suppressed, therefore Ca2+ channel blockers and B blockers have identical effects on heart

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24
Q

3 classifications of ca2+ channel blockers and what can they be used on?

A
  • dihydropyridine (only affect blood vessels)
  • phenylakylamine (can be used on blood vessels and heart)
  • benzothiazepine (can be used on blood vessels and heart)
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25
Q

Verapamil (calan, covera HS, verelan) drug class and mech of action

A
  • phenylakylamine Ca2+ channel blocker
  • directly effects heart and blood vessel causing vasodilation, reducing heart rate, AV conduction, and force of contraction, balanced by indirect (reflex) effects of baroreceptors, ultimately resulting in net effect of vasodilation and reduced arterial pressure and increased coronary perfusion
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26
Q

Verapamil (calan, covera HS, verelan) therapeutic uses (3)

A
  • angina pectoris (both vasospastic and effort induced)
  • essential hypertension (1st line treatment)
  • cardiac arrhythmias
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27
Q

Verapamil (calan, covera HS, verelan) ADR’s (4)

A
  • constipation frequently due to Ca2+ blockade in small intestine
  • edema in ankles and feet
  • in cardiac diseased hearts could see bradycardia or AV block (in healthy heart effects are minimal)
  • should not be used in patients with sick sinus syndrome or 2nd/3rd degree AV block
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28
Q

Verapamil (calan, covera HS, verelan) toxicity reversal (2)

A
  • atropine
    • glucagon
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29
Q

Diltiazem (cardizem, dilacor, dilitia XT, tiazac) drug class and therapeutic uses (3)

A

-Benzothiazepine Ca2+ channel blocker

  • angina pectoris
  • essential HTN
  • cardiac arrhythmias
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30
Q

Diltiazem (cardizem, dilacor, dilitia XT, tiazac) ADR’s (3)

A
  • dizziness
  • edema of ankles and feet
  • exacerbate bradycardia, AV block, CHF
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31
Q

Nifedipine (adalat, nifedical, procardia) drug class and mech of action

A
  • Dihydropyridines Ca2+ channel blocker
  • blocks Ca2+ channels in VSM promoting vasodilation, produces very little blockade of Ca2+ channels in the heart, cannot treat cardiac arrhythmias, increases coronary artery perfusion, but does not affect AV conduction, contractile force, or automaticity reduction, net effect lowers BP, increases HR, increases contractile force
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32
Q

Nifedipine (adalat, nifedical, procardia) therapeutic uses (2)

A
  • angina pectoris (vasospactic and exercise induced) alongside B blocker often to prevent reflex tachycardia
  • essential hypertension
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33
Q

Nimodipine (nymalize, nimotop) function

A

Another type of dihydropyridine that is only capable of producing the Ca2+ blockade in cerebral vessels only approved for prophylaxis of neurologic injury following rupture of intracranial aneurysm

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34
Q

amlodipine vs nifidepine

A

amlodipine is longer acting requirng only dosed once per day

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35
Q

Some angiotensin II is produced without requiring ____, therefore drugs that block this enzyme do not completely stop angiotensin II production

A

ACE

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36
Q

ACE inhibitors mech of action and ADR’s (5)

A

Prevents conversion from angiotensin I to II, major response is vasodilation, reduced aldosterone promoting renal retention of K+ and excretion of Na+ and H2O

  • hypotension
  • cough due to increased bradykinin levels
  • hyperkalemia
  • fetal injury use during 2nd or 3rd trimester
  • neutropenia
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37
Q

ACE is also known as…

A

….Kinase II when it functions on bradykinin metabolism

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38
Q

ACE inhibitors therapuetic uses (4) and administration

A
  • hypertension and reduce risk of cardiovascular mortality caused by HTN
  • heart failure
  • ASAP therapy after MI
  • slow progression of established nephropathy (diabetic and nondiabetic)

Oral administration

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39
Q

ACEI advantages to other antihypertensive agents (4)

A
  • no cardiovascular reflexes
  • used safely with bronchial asthma
  • does not promote hypokalemia or hyperglycemia like seen with thiazide diuretics
  • does not induce lethargy, weakness, or sexual dysnfunciton
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40
Q

Angiotensin II action in the vasculature and at the kidney

A

-constricts afferent arterioles and constricts efferent glomerular arteriole raising glomerular pressure and stasis in high enough conc.

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41
Q

ACEI drug interactions (2)

A
  • hypotensive agents are additive effects
  • hyperkalemia if administered with K+ supplements or K+ sparing diuretics
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42
Q

ARB’s therapeutic uses (4) and mech of action

A
  • hypertension
  • diabetic neuropathy
  • MI
  • prevention of MI, stroke, and death in patients with high CV risk

-block binding of angiotensin II to type 1 angiotensin II receptors in blood vessels and other tissues causing dilation of arterioles and veins, block all angiotensin II regardless of where it is produced, decrease release of aldosterone from adrenals, does not impact bradykinin

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43
Q

ARB vs ACEI

A

ARBs have lower risk of cough/hyperkalemia than ACEI

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44
Q

ARB’s ADR’s (4)

A
  • low incidence of dizziness
  • rare angioedema (discontinue if occurs)
  • hyperkalemia may occur
  • fetal harm in 2nd 3rd trimesters
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45
Q

Aliskiren (tekturna) drug class and mech of action

A
  • Direct renin inhibitor
    • binds renin blocking cleavage of angiotensinogen to angiotensin I leading to decreased levels of II and aldosterone
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46
Q

Spironolactone (aldactone) function

A

Block action of aldosterone at distal tubule causing retention of K+ and increased excretion of Na+ over 48 hr period, has diuretic effects that can treat hypertension or edema (often alongside thiazide or loop diuretic as its weak), can act like progesterone and other steroids and cause gynecomastia or hirsutism (or hyperkalemia obvi!!)

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47
Q

Eplerenone (Inspra)) function

A

Produces blockade of aldosterone receptors with no effect on receptors for other steroid hormones, weak K+ sparing diuretic used to treat HTN with other agents, only ADR is hyperkalemia

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48
Q

White coat hypertension

A

Patient’s tendency to have higher blood pressure in presence of doctor’s office due to nerves, still needs to be treated as hypertension but can be mitigated by having patient rest 5 min prior to taking BP

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49
Q

Physical exam for hypertension

A
  • 2 or more bp measurements separated by 2 min sitting, with arm supported at heart level
  • verification in contralateral arm
  • ocular fundus exam
  • exam neck for carotid bruits, jvd, enlarged thyroid
  • cardiac murmur, s3, s4, PMI, lifts or heaves
  • abdominal bruits
  • do CNS exam checking orientation, mental status, cranial nerve, motor and sensory
  • do skin exam looking for hydration, pallor, hair loss, edema
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50
Q

Kinogen-kallikrein system

A

Stimulates nitric oxide release, bradykinin is an active vasodilator and a natriuretic substance, bradykinin broken down by angiotensin II causing further increase in vasoconstriction in the RA system

51
Q

Thiazide diuretics mechanism of action, relative contraindications (3)

A
  • Works on distal convoluted tubule to prevent reabsorption of Na+, allowing water to follow and increase urine production
  • relatively contraindicated in patients with cardiac arrhythmias, gout, hypokalemia
52
Q

Loop diuretics mech of action, indication, and ADRs (4)

A
  • Works on ascending loop of henle
  • Only indicated to use for Htn associated with renal insufficiency
  • can result in weakness, hypokalemia, hyperlipidemia, hyperglycemia
53
Q

Nebivolol (bystolic) - New B blocker

A

-highest specificity for B1 receptor resulting in no metabolic or sexual side effects unlike current B blockers

54
Q

ACEI, what patient group is it used for and why?

A

inhibits angiotensin I from converting to angiotensin II, slows progression of renal disease so used if a patient has proteinuria or diabetes

55
Q

Malignant hypertension

A

A hypertensive emergency with papilledema due to increased intracranial pressure requiring imediate but controlled decrease of BP

56
Q

Nonblack patient first line of hypertension treatment (5)

A
  • thiazide diuretic
  • Ca2+ channel blocker
  • B blocker
  • ACE inhibitor
  • ARB
57
Q

Black patient first line of hypertension treatment

A
  • thiazide diuretic
    • Ca2+ channel blocker
  • (avoid ACEI and ARB as first line in this population unless kidney diease present
58
Q

Mediastinitis risk factors (4)

A
  • Recent cardiac surgeries
  • Esophageal perforation
  • trauma
  • descending infection from head or neck
59
Q

Acute aortic dissection risk factors (4)

A
  • marfan syndrome
  • hypertension
  • cocaine abuse
  • previous aortic surgery
60
Q

Electrical alternans

A

Classic finding for cardiac tamponade

61
Q

Hampton hump

A

Wedge shaped pleural based defect visible on xray where there is a lack of lung tissue in an area due to PE

62
Q

Westermark sign

A

Absence of vascular markings distal to the embolus in the lung tissue due to PE as evidenced on a chest xray

63
Q

Gold standard imaging for confirming pericardial effusion or tamponade

A

bedside ultrasonography

64
Q

HEART score

A

An algorithm that rates a variety of signs and symptoms to come up with a probability of risk of likelihood of acute coronary syndrome

65
Q

Pain that starts in the chest and radiates down to the abdomen is a sign of these 2 pathologies

A

esophageal rupture or aortic dissection

66
Q

Per 5 squares of an EKG horizontally, we measure ___mm and ___sec

A

5, .2

67
Q

Quick estimate determination of HR from EKG

A
  • Find an R wave that starts on a heavy dark line
    • Start counting at next black line 300 to 150 to 100 to 75 to 60 to 50 to 43 to 38 until you hit the next R wave
68
Q

6 second strip method of HR from EKG

A
  • Take 2 of the 3 second intervals marked at the top of the ekg page to get a 6 second interval
  • find number of cycles within a 6 sec strip x 10 = cycles per min
69
Q

Axis determination quick method

A

If the QRS is positive in lead I and positive in AVF you have a normal axis

70
Q

QRS up in I and down in AVF means…
QRS down in I and up in AVF means…
QRS down in both I and AVF means…

A

…left axis deviation
…right axis deviation
…extreme right axis deviation

71
Q

Block definition

A

Delay or total failure of impulse conduction thru a part of the heart, NOT arterial blockages but rather electrical

72
Q

Sinus block/pause

A

Occurs when SA node fails to pace for at least one cycle appearing as a “skipped beat” with no evidence for a P wave, QRS complex or T wave, can allow for an ectopic beat to escape and overdrive the suppression

73
Q

AV blocks

A

Where conduction is abnormally slowed thru the AV node beyond the normal PR interval of .12 to .2 sec, either 1st, 2nd (type I or II) or 3rd (complete heart block)

74
Q

1st degree AV block

A

A long PR interval >200ms on all beats, usually asymptomatic and has QRS-T sequence consistently normal, caused by ischemia, drugs, electrolyte imbalance, or vagal tone, not a big deal

75
Q

2nd degree AV block Mobitz/type I Wenckebach

A

Characterized by PR interval that falls in normal range and becomes progressively longer until AV node no longer conducts stimulus, often benign and reversible and caused by medications, ratio determined by how many normal cycles occur before an abnormal one does (e.g. 3:1 or 4:1)

76
Q

2nd degree AV block Mobitz/type II

A

Normal PR intervals with punctual P waves not followed by QRS complex, often concerning for pathologic potential to become a 3rd degree block

77
Q

3rd degree AV

A

Occurs when none of impulses that form above AV node conduct to ventricles, characterized by lack of normal PR interval, P wave not related to QRS complex, indication for a permanent pacemaker to prevent sudden death,

78
Q

Bundle branch block

A

Loss of conduction thru right or left superconducting highway of the bundle branches resulting in one bundle branch depolarizing before the other because the one that has the block has to transmit cell to cell

79
Q

Right bundle branch block

A

Caused when electrical impulses are prevented from entering the right bundle branch of the intraventricular conduction system, now the right ventricle must depolarize by cell to cell conduction which is considerably slower causing the right ventricle to depolarize after the left, visualized in leads V1 and or V2 with increased RSR’ (QRS) greater than .12

80
Q

Left bundle branch block

A

Determined in lateral precordial leads V5 and V6, blocked bundle delays conduction to left ventricle causing slower depoarization than right ventricle with widened QRS (RSR’) >.12 sec, and notched R wave and V5-6, makes diagnosis of MI or LVH nonodiagnostic

81
Q

Atrial hypertrophy

A

Occurs when either V1 has a biphasic P wave with initial positive deflection (right) or neg (left), or when lead II has a peaked P wave>3mm amplitude (right) or a notched P wave >3mm (left)

82
Q

Primary skin lesion vs secondary skin lesion and example of each

A

Primary are physical changes to the skin considered to be directly resultant from the disease process, secondary are evolved from primary lesions or caused by external forces such as scratching, trauma, infection or healing
bug bite is primary scratches of the bite are secondary

83
Q

cyst vs nodule

A

cyst is <1cm and nodule is >1cm, both refer to a closed cavity or sac of fluid or semisolid material

84
Q

Where is scabies often seen, where is it almost never seen?

A

Often seen in skin folds particularly webbing of toes and fingers, almost never seen above the neck except rarely in infants

85
Q

vesicle vs bullae

A

<1cm is vesicle, >1cm is bullae, both rae fluid filled

86
Q

furuncle vs carbuncle

A

carbuncle is a cluster of boiles connected subq

87
Q

How do we tell the difference between erythema and ecchymoses?

A

If it blanches, it is still contained in the vessel and is erythema (increased blood flow), if it doesn’t, it has spilled out of the vessel and is a bruise

88
Q

Telangiectasias defintion

A

Small, permanent dilated superficial blood vessels on the skin, sometimes a sign of hepatic disease but often environmental exposure

89
Q

Henoch-schonlein purpura definition

A

A rare inflammatory disorder of small blood vessels most commonly occuring in children resulting in disseminated purpura in lower extremities

90
Q

Eschar definition

A

Hardened crust and plaque covering an ulcer of necrotic tissue, giving it a characteristic black appearance

91
Q

Keloid definition

A

Exaggerated connective tissue response to injured skin that extends beyond the original wound’s edges, some form them and others do not, recurrent in almost all cases

92
Q

Sodium nitroprusside function and drug class

A

A drug used for hypertensive emergencies to dilate vascular smooth muscle acting almost immediately acting but stops upon cessation
-a 1 adrenergic receptor blocker

93
Q

Potential unfavorable effects of HTN therapy for concomitant diseases (thiazide diuretics, B blockers, ACEI and ARBS, aldosterone antagonists and K+ sparing diuretics)

A
  • thiazide diuretics in pts with gout or hyponatremia
  • B blockers avoided in asthma, 2nd, or 3rd degree heart block
  • ACEI and ARBS contraindicated in pregnancy
  • aldosterone antagonists and K+ sparing diuretics can cause hyperkalemia
94
Q

Labetalol (trandate) function

A

Blocks a1 and B1 adrenergic receptors for hypertensive emergencies that produces arteriolar dilation, safe in pre-eclampisa

95
Q

Nitroglycerin DOC and mech of action

A
  • Drug of choice for acute anginal attacks
  • Acts directly on vascular smooth muscle to promote vasodilation, acts mostly on veins in peripheral vasculature than arteries (reduces O2 need for heart muscle)
96
Q

Nitroglycerin ADR’s (3)

A
  • headache (can be diminished over time)
  • orthostatic hypotension
  • reflex tachycardia (can be prevented by coadministration with B1 receptor or Ca2+ channel blocker)
97
Q

Nitroglycerin drug interactions (2)

A
  • intensifies other hypotensive drugs
    • phosphodiesterase type 5 inhibitors for ED (sildenafil and such) causes drop in blood pressure
98
Q

B blockers should not be used in patients with these 3 conditions

A
  • sick sinus syndrome
  • heart failure
  • 2nd or 3rd degree heart block
99
Q

Ranolazine (ranexa) function

A

Approved for treatment of angina in patients that have not adequately responded to nitrates, BB or CCB’s and should be combined with at least one of these drugs, act by unknown mechanism

100
Q

Torsades de pointes

A

Uncommon and distinctive tachycardia characterized by twisting of QRS complexes often brought on by prolonged QT interval, can resolve spontaneously or develop into ventricular fibrillation and death

101
Q

What is the rate limiting step of cholesterol formation

A

3 hydroxy 3 methylglutaryl coenzyme A (HMG-CoA)

102
Q

Statin mech of action

A

Inhibition of HMG CoA reductase resulting in increase # of LDL cholesterol receptors in the liver ultimately decreasing overall level of LDL in bloodstream

103
Q

Statin use is completely contraindicated in…

A

….pregnancy

104
Q

Ezetimibe (zetia) drug class and mech of action

A
  • Cholesterol absorption inhibitor
  • selectively inhibits intestinal absorption of dietary and biliary choesterol at brush border of small intestine leading to decreased delivery to liver and therefore reducing all overall blood cholesterol levels, recommended typically when max dose of statin already in use
105
Q

Ezetimibe (zetia) ADR’s (3)

A
  • diarrhea
  • rhabdo
  • hepatitis
106
Q

PCSK9 inhibitors mech of action

A

Prevents PCSK 9 proteins from binds to LDL receptors on hepatocytes promoting receptor degradation thereby preventing LDL-C clearance from blood increasing serum LDL-C conc.

107
Q

Bile acid binding resins function and 3 example agents

A

Were once main drug for decreasing LDL level, today primarily reserved for adjunct therapy with statins that form insoluble complex with bile acids in intestine, relies on liver’s ability to produce LDL receptors

includes cholestyramine, colestipol, and colesvelam

108
Q

Bile binding resins drug interactions (1)

A

-form insoluble complexes with other drugs preventing absorption including statins, require medication be given 2 hours before or 4-6 hrs after

109
Q

Fibrates function and what is it the most effective drug for?

A

Activate nuclear transcription factor peroxisome proliferator activated receptor (PPAR a) which regulates genes that control lipid and glucose metabolism, inflammation, and endothelial function, most effective drug for decreasing triglycerides

110
Q

Gemfibrozil (lopid) therapeutic uses (2)

A
  • lower VLDL and triglycerides
    • raise HDL
111
Q

fenofibrate (tricor, lofibra, triglide, anatara) function

A

Treat hypertriglyceridemia in pts not responding to dietary measurements, lowers triglycerides by decreasing VLDL

112
Q

Most common cause of left atrial enlargement

A

Left ventricular hypertrophy

113
Q

Common causes of sinus bradycardia (4)

A
  • athlete
  • B blockers, Ca2+ channel blockers
  • hypothyroidism
  • electrolyte imbalances
114
Q

How to determine if sinus bradycardia requires treatment

A

Ask if the organs are being perfused (if yes leave it alone or take time to think about pacemaker, if no identify underlying cause and correct)

115
Q

DOC to improve sinus bradycardia

A

atropine IV repeated every 5 min

116
Q

Sick sinus syndrome and 3 subtypes

A

Dysfunctional SA node due to ischemia, fibrous, or fatty infiltration decreasing the cells and the conduction system, can be slow, fast or both (tachy-brady syndrome)

117
Q

Sick sinus syndrome treatment

A

-dual chamber pacemaker (pace SA node and right ventricle)

118
Q

Premature atrial complex and some common causes (5)

A

Irritable atrial foci that fires early and spontaneously occurs when the PR interval is less then .20 sec

very common due to things such as stress, anxiety, drug use, hypoxia, thyroid dysfunction

119
Q

Sinus arrhythmia

A

Normal physiologic response to changes in preload with inspiration due to fluctuations in parasympathetic vagal tone with inspiration increasing rate and expiration decreasing, regularly irregular variation common in young individuals

120
Q

Any arrhythmia that occurs above the bundle of His is a…

A

…supraventricular

121
Q

Paroxysmal supraventricular tachycardia (PSVT)

A

Common episodic tachycardia that has narrow complex except in the setting of bundle branch block

122
Q

4 conditions required for re-entry phenomena

A
  • electrophysiologic inhomogeneity (diff between conduction and refractory period) in 2 or more areas of the heart that are connected by a potentially closed loop
  • unidirectional block in one pathway
  • slow conduction over an alternative pathway allowing for preveiously blocked path to recover excitability
  • reexcitation of the initially blocked pathway to complete the loop
123
Q

AV nodal re-entry tachycardia and how does it present on EKG

A

Most common PSVT that has abrupt onset, narrow complexes usually initiated by PAC, reentrant mechanism, tolerated well by young and heart disease free but not tolerated well in patients with cardiac disease, rate typically >150 bpm, QRS

Professional Development (19 decks)

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