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CVPR > CV Week 2a > Flashcards

CV Week 2a Flashcards

1
Q

Common causes of acute pericarditis (4)

A

viral illness, connective tissue or autoimmune diseases (lupus), uremia (renal dysfunction), metastatic tumors

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2
Q

Presneting symptoms of acute pericarditis (2)

A
  1. SUDDEN ONSET CP (severe), can be persistent for several days
  2. CP varies with position and breathing
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3
Q

Diagnosis of acute pericarditis (6)

A
  1. CP varies with position and breathing
  2. Pericardial rub on exam
  3. Normal or low levels of indicators of myocardial damage
  4. EKG = diffuse ST elevation (across ALL leads)
  5. ECHO = pericardial fluid
  6. Response to anti-inflammatory agents (ibuprofen, ASA, colchicine)
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4
Q

Treatment of acute pericarditis

A

Ibuprofen (NSAIDs)

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5
Q

Pericardial effusion is»»

A

Fluid around the sac

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6
Q

Common causes of pericardial effusion (5)

A
  1. Viral or acute idiopathic pericarditis
  2. Metastatic malignancy - tumor cells invade lymphatics or directly invade pericardium resulting in inflammatory fluid accumulation
  3. Uremia
  4. Autoimmune disease
  5. Hypothyroidism
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7
Q

Diagnosis of pericardial effusion

A

echocardiogram - can observe in RA and LA collapsed due to high intrapericardial pressure and then subsequent RV and LV collapse

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8
Q

Pericardial effusion can result in

A

cardiac tamponade

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9
Q

Cardia tamponade

A

excessive pericardial fluid compresses the heart and reduces venous return and thus reduces CO (acute emergency)

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10
Q

Clinical manifestations of cardiac tamponade (3)

A

Decreased venous return due to high intrapericardial pressure → decreased RV and LV output and impaired diastolic filling

a. Due to chronic or acute pericardial effusions
2. Distended neck veins
3. Paradoxical pulse

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11
Q

Paradoxical pulse

A

inspiration → decrease in arterial systolic pressure >10 mmHg

a. Increased RA/RV filling during inspiration (due to negative pressure created in lungs)
b. RA/RV shifts septum, impinging on LA/LV filling during inspiration → decreased LV filling → decreased LV CO

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12
Q

Diagnosis of cardiac tamponade (3)

A
  1. XRAY - enlarged heart, non-congested lung fields
  2. ECHO - collapse of RA and LV in end diastole
    a. Dilation of inferior vena cava and no collapse of IVC during inspiration
  3. ECG
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13
Q

Treatment of cardiac tamponade

A

pericardiocentesis

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14
Q

Cardiac tamponade vs. CHF:

Distinguishing features of Cardiac tamponade (6)

A

a. Impairment in R heart filling during diastole
b. Lungs are clear
c. Pulsus paradoxus present
d. Distant heart sounds
e. Low voltage and pulsus alternans present
f. ECHO: RA collapse

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15
Q

Cardiac tamponade vs CHF:

Distinguishing features of CHF (6)

A

a. No impairment in right heart filling, but diminished heart function causes pulmonary and systemic congestion
b. Lungs congested (rales)
c. Pulsus paradoxus NOT present
d. Normal heart sounds with murmurs, S3 and ventricular lifts
e. Low voltage and pulsus alternans NOT present
f. ECHO: poor contractile function, dilation of ventricles

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16
Q

Cardiac tamponade vs CHF:

Similarities (4)

A

a. JVD
b. Tachycardia
c. Low BP
d. Large cardiac silhouette on XR

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17
Q

Constrictive pericarditis

A

chronic process, pericardium thickens to the point where it compresses the heart and limits CO

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18
Q

Causes of constrictive pericarditis

A

Scarring and loss of elasticity of the pericardium

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19
Q

Clinical manifestations of constrictive pericarditis (6)

A
  1. Impaired diastolic filling with normal systolic function → very high R sided diastolic filling pressure
    - Equalization of diastolic pressures between LV and RV
    - Chronic disease (takes time to develop)
    - Normal heart size with thickened pericardium
    - No lung congestion because constriction selectively impairs filling of RV
  2. Elevated jugular venous pressure
  3. Hepatomegaly
  4. Edema
  5. Ascites
  6. Tachycardia
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20
Q

Diagnosis of constrictive pericarditis

A

XRAY or ECG

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21
Q

Treatment of constrictive pericarditis

A

surgical stripping of pericardium

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22
Q

Tamponade vs. constrictive pericarditis:

Similarities (4)

A

a. Reduced diastolic function, preserved systolic function
b. JVD
c. Tachycardia
d. Low BP

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23
Q

Tamponade vs. constrictive pericarditis:

Distinguishing features of constrictive pericarditis (5)

A

a. Normal heart silhouette
b. Pericardial calcification
c. Pulsus paradoxus uncommon
d. Slow development over time
e. Accompanied by hepatic congestion, ascites, pedal edema

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24
Q

Process of cardiac depolarization

A

SA node = pacemaker, initiates electrical impulses

Impulse sent through internodal tracts → wave of depolarization in atrium

→ converges on AV node → DELAY

→ Bundle of His → right and left (anterior/posterior) bundles in ventricles → Purkinje fibers → activate ventricular myocardial cell depolarization/contraction

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25
Q

P wave =

A

atrial depolarization

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26
Q

PR interval (from beginning of P to beginning of Q)=

A

AV node conduction time

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27
Q

Normal PR interval time

A

0.12-0.2 seconds

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28
Q

QRS complex =

A

ventricular depolarization

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29
Q

Normal duration of QRS complex

A

0.06-0.10 seconds

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30
Q

QT interval (beginning of Q to end of T)=

A

total duration of depolarization and repolarization

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31
Q

T wave =

A

ventricular repolarization

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32
Q

Paper speed

A

25 mm/ Second

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33
Q

Thin vertical lines are ____ seconds apart

A

0.04 seconds

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34
Q

Thick vertical lines ___ seconds apart

A

0.2 seconds

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35
Q

How wot calculate heart rate

A

300/ # of heavy lines OR

1500/ # of light lines

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36
Q

Ventricular hypertrophy

A

L and R ventricular hypertrophy result in greater muscle mass.

i.Greater muscle mass → greater voltage associated with depolarization and repolarization of myocardium

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37
Q

General ECG of ventricular hypertrophy

A

R wave with greater amplitude

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38
Q

ECG of left ventricular hypertrophy

A

large positive deflections (R waves) in left sided leads (I, AVL, V5 and V6) and large negative deflections (S waves) in V1

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39
Q

ECG Right ventricular hypertrophy

A

high voltage in right sided leads - V1 and V2

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40
Q

Myocardial ischemia

A

insufficient blood supply to meet O2 demand in ventricles

i.Ischemic changes in EKG alter ventricular repolarization and affect ST segment and T wave

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41
Q

ECG of ischemia due to sudden high oxygen demands with fixed coronary obstruction

A

causes depression of ST segment

In some patients a resting EKG is normal - ST depression only visible during exercise due to transient ischemia

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42
Q

ECG of Ischemia due to acute coronary artery obstruction during low oxygen demand

A

Cause T wave inversion

a. Normally, T waves are in same direction of QRS complex.
i. Inversion of a T wave→myocardial ischemia

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43
Q

ST elevation =

A

sign of transmural injury in acute coronary syndrome

  1. Clot due to platelet aggregation obstructing a coronary artery
  2. Acute myocardial infarction
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44
Q

Sizeable (>0.04 s) Q waves =

A

sign of transmural necrosis

  1. Area of necrosis/infarct will not transmit signal → negative deflection in leads over infarcted myocardium
    a. Infarcts usually involve only LV
45
Q

Inferior infarcts will be detected by which leads (2)

A

II, III, aVF

46
Q

Anterior wall infarcts will be detected by which leads (4)

A

V1-V4

47
Q

Lateral wall infarcts will be detected by which leads (4)

A

I, aVL, V5, and V6

48
Q

Evolution of transmural acute myocardial infarcts over time on an ECG (early, middle, end)

A
  1. Early: Giant upright “hyperacute” T wave
  2. Middle: T wave inverts and ST segment rises.
    - ST elevation can precede/occur simultaneously with T inversion
  3. End: Q waves last to develop
49
Q

Transmural vs. subendocardial infarction

A

Transmural: involves entire thickness of LV

a.ST elevation with Q waves

Subendocardial: localized to inner layer of LV wall

a.ST depression, NO Q waves

50
Q

ECG: hypercalcemia (1 feature)

A

short QT interval

- associated with hyperparathyroidism

51
Q

ECG: Hypocalcemia (1 feature)

A

Long QT

- associated with life threatening ventricular arrhythmias

52
Q

ECG: hypokalemia (3 features)

A

1) QT interval prolonged
2) Prominent U waves
3) inverted T waves common

b.Often caused by overuse of diuretics, vomiting, diarrhea

53
Q

ECG: Hyperkalemia (3 features)

A

1) increased T wave voltages with distinctive peaked/symmetrical appearance
2) QRS widened
3) T waves widened

a. Higher levels → P waves may be flattened and QRS and T waves widened
b. Broad S wave often appears.
c. Very high levels → sinusoidal pattern without P or R waves

54
Q

Normal sinus rate is ______ bpm

A

60-100

55
Q

Sinus Tachycardia and sinus bradycardia

A

normal waves but increased/decreased frequency

56
Q

Treat sinus tach with ______ and treat sinus brady with _______ or ________

A

B-blockers

atropine or pacemaker

57
Q

sinus sickness syndrome

A

sinus bradycardia often seen in elderly patients

may require pacing

58
Q

1st degree AV block is often due to _______ or _____ and appears how on an EKG?

A

drugs, conduction system defect

PR > 0.2 sec (all P waves transmit, just have junctional delay)

AV node dysfunction

59
Q

2nd degree AV block can appear what 2 ways on an EKG?

A

Mobitz 1: PR lengthens until a P does not conduct (AV node dysfunction)

Mobitz 2: no change in PR, just some P waves don’t conduct (dysfunction below AV node)

60
Q

3rd degree AV block causes

A

AV node / junctional failure due to aging (dysfunction below AV node)

Infarct

disruption during cardiac surgery

severe conduction disease

rarely drugs

61
Q

3rd degree AV block appearance on EKG

A

junctional failure

-both P waves and QRSs show regular rhythm but they are at different rates

P rate > QRS rate

62
Q

Atrial flutter on EKG

A

P waves normal but (flutter waves) at rate of 240-320 bpm

-pulse varies widely, ventricular rates vary

63
Q

Treatment of atrial flutter (4)

A

1) anticoagulation (risk of embolic stroke due to clot in LA)
2) rate control (B-blockers)
3) rhythm control - cardioversion, antiarrythmic drugs
4) ablation (CURATIVE)

SAME treatment as AFIB
only difference is ablation is NOT curative for AFIB

64
Q

Problems with Atrial Fibrillation (3)

A

rapid heart rate (syncope, ischemia, HF)

Loss of atrial kick = decrease preload –> HF

Atrial thrombi (embolic stroke)

65
Q

A-FIB on EKG

A

NO P WAVES

-irregular ventricular rhythm (QRS waves)

chaotic atrial depolarizations

66
Q

Treatment of AFIB

A

1) anticoagulation
2) CONTROL RATE - Decrease HR (B-blockers, Ca-channel blockers)
3) CONTROL RHYTHM - Cardioversion or antiarrythmic drugs
4) Catheter ablation (non-curative, high incidence of recurrence)

67
Q

Atrial tachycardia on EKG (3)

A

rapid HR
narrow QRS
P waves are present but abnormal

68
Q

Treatment of atrial tachycardia (3)

A

1) adenosine infusion
2) Vagal maneuver
3) ablation to prevent recurrence of reentry pathway

69
Q

Junctional Rhythm

A

when rhythms originate from the area surrounding the AV node

70
Q

Junctional rhythm on EKG (3)

A
  • regular rhythm
  • narrow QRS
  • P waves often hidden in QRS (if present, may be inverted because conducted upward from AV node)
71
Q

Premature atrial contractions, 2 EKG features

A

common (single beat palpitations)

  • preceded by abnormal P wave
  • QRS normal or narrow
72
Q

Premature ventricular contractions, 2 EKG features

A

common (single beat palpitations)

  • no P waves
  • QRS widened
73
Q

Ventricular tachycardia EKG features (2)

A

repetitive, WIDE abnormal QRS (100-200 bpm)

no P wave

74
Q

Treatment of V-tach (2)

A

1) cardioversion - especially if UNSTABLE

2) Amiodarone

75
Q

Ventricular fibrillation

A

no P, no QRS, no T waves

chaotic squiggly lines

76
Q

Treatment of v-fib (1)

A

life threatening

requires emergency defribrillation

77
Q

Sinus arrest

A

failure of sinus node discharge → no atrial depolarization, periods of ventricular asystole

Sinus node dysfunction

78
Q

Tachycardia-Bradycardia (Tachy-Brady)

A

Intermittent episodes of slow and fast rates from SA node or atria

Sinus node dysfunction

79
Q

Chronotropic Incompetence

A

inability of heart to regulate rate appropriately in response to physiologic stress

Sinus node dysfunction

80
Q

Indications for treatment of Bradyarrhythmias (2)

A

1) When patient is symptomatic

2) When rhythm is infranodal (below AV node) –> Mobitz 2, 3rd degree AV block

81
Q

treatment of bradyarrhythmias (2)

Acute treatments? (3)

Long-term treatments? (1)

A

1) Find and treat reversible causes (ischemia/infarction, hypothyroidism, neurologic causes, Lyme disease)

2) Stop offending medications:
B-blockers, Ca2+ channel blockers
Antiarrhythmic drugs
Clonidine, Lithium, others

ACUTE TREATMENTS
1) B-agonists (IV dopamine, isoproterenol)

2) Transcutaneous pacing
3) Temporary transvenous pacing

LONGTERM TREATMENTS
1) Permanent pacemaker

82
Q

Difference between tachyarrhythmias originating from dysfunction above the ventricle (SVT) and dysfunction originating in ventricle (v-tach, v-fib)

A

SVT = narrow QRS

VT = wide QRS

83
Q

SVT with irregular rhythm includes…(3)

A

1) AFIB
2) Multifolcal Atrial Tachycardia (MAT)
3) Atrial Flutter

84
Q

SVT with regular rhythm includes…

A

1) Sinus Tachycardia
2) AVNRT (AV nodal reentry tachycardia)
3) AVRT (AV reentry tachycardia)
4) Atrial Flutter
5) Atrial tachycardia
6) Junctional Tachycardia

85
Q

If rhythm is irregular and patient is hemodynamically unstable then…

A

SHOCK

86
Q

Adenosine is used for treatment of…

A

tachyarrythmias at the level of AV node (AVNRT, AVRT)

Temporarily interrupts conduction at AV node

87
Q

AV nodal reentrant tachycardia

How is it initiated?

A

-Atria and ventricles depolarized simultaneously

P wave buried within or at end of QRS (retrograde P waves)

INITIATION:
-caused by extra beat that encounters un-excitable refractory fast pathway and excitable slow pathway at AV node –> then slow pathway excites fast pathway, and this goes around and around sending depolarization to atria and ventricles simultaneously

-terminated by adenosine

88
Q

Treatment of AVNRT

Acute? (2)
Chronic? (2)

A

ACUTE

1) vagal maneuvers
2) adenosine

CHRONIC

1) Meds (suboptimal)
2) Catheter ablation

89
Q

AV Reentrant Tachycardia

How is it initiated?

A

Due to accessory pathway between atria and ventricles (aside from AV node) → no delay between depolarization of of atria and ventricles in accessory pathway
→ delta wave (slurred upslope)

Accessory pathway can initiate AVRT if extra beat encounters AV node pathway or accessory pathway that is refractory → initiate reentrant loop

90
Q

Treatment of AVRT (2)

A

1) Catheter ablation

2) Adenosine

91
Q

Medications that can control heart RATE (4)

A

1) B-blockers
2) Digoxin
3) non-DHP Ca2+ channel blockers (Verapamil, Diltiazem)
4) Amiodarone

92
Q

Things can control RHYTHM (2)

A

1) Drugs - class III and class IC antiarrhythmic drugs

2) Cardioversion (SHOCK)

93
Q

When is defibrillator needed?

A

1) Structural heart disease

2) high risk of sudden death due to arrhythmia (primary or secondary prevention)

94
Q

Furosemide, Bumetanide, Torsemide are all _________

A

Loop diuretics:

  • High Ceiling Diuretics
  • HIGHEST efficacy
  • used chronically and acutely
  • most commonly used out of all diuretics
95
Q

Loop diuretics mechanism of action

A

inhibit Na+-K+-2Cl- Cotransporter in THICK ASCENDING LIMB of loop of Henle

0Increases Mg2+ and Ca2+ excretion

-Decreases Na+ reabsorption AND thus more K+ and H+ loss

96
Q

Clinical use of loop diuretics (3)

A

1) CHF with volume overload
2) Acute pulmonary edema
3) Hypercalcemia

97
Q

Loop diuretics are used to treat CHF with volume overload. They can be combined with ________ which acts to ________ and ________ which acts to ____________

A

Thiazides - block Na+ reabsorption at distal tubule

Aldosterone Antagonists - enhance diuresis and ameliorate K+ wasting

98
Q

Side effects of loop diuretics (3)

A

1) Hypokalemia (due to enhanced secretion of K+ and H+)
2) Hypomagnesemia
3) Hyperuricemia

99
Q

Hypokalemia impacts on heart function

A

-decreased extracellular K+ decreases conductance → increased pacemaker rate and ectopic pacemaker arrhythmogenesis (torsades)

Prolongs AP (QT prolongation)

More susceptible to digoxin toxicity and Class III action

Causes U waves

100
Q

Thiazides mechanism of action

A

-inhibit Na+/Cl- cotransporter in distal convoluted tubules

→ increase urinary excretion of NaCl (and thus K+ and H+ loss)

Less efficacious than loops because only 5-10% of Na+ left to be reabsorbed → used less than loops

→ increase Ca2+ reabsorption

101
Q

Clinical uses of thiazides (1)

A

CHF in combination with loop diuretics (not usually used alone because not that great of a diuretic)

102
Q

Side effects of thiazides (3)

A

1) Hypokalemia: less K+ loss than loops
2) Hyperuricemia
3) Hyperlipidemia / Hyperglycemia

103
Q

Aldosterone Antagonists include _____ and ______ and are known as ________ diuretics

A

spironolactone, eplerenone

K+ sparing

104
Q

Mechanism of action of aldosterone antagonists

A

competitive antagonist of aldosterone receptor in COLLECTING TUBULES (binds cytosolic receptor) → prevent Na+ reabsorption

-Primary use is for cardiac anti-remodeling actions (acts on aldosterone receptors in heart), NOT diuresis

105
Q

Clinical Uses of aldosterone antagonists

A

1) CHF:
- Blocks aldosterone receptors on heart → prevent cardiac hypertrophy and fibrosis (INCREASES SURVIVAL IN HF)
- Raises serum K+ - counters risk of hypokalemia-induced arrhythmias resulting from loop and thiazides
- must monitor K+ and kidney function

2) PCOS (block androgen receptor)

106
Q

Adverse reactions of aldosterone antagonists

A

1) Hyperkalemia

2) Gynecomastia

107
Q

Effects of hyperkalemia on the heart

A

increased extracellular K+ increases conductance

→ reduced AP duration, slow conduction, decreased pacemaker rate

Increased incidence of bradycardia, conduction disturbances → heart block

EKG changes include peaked T wave

108
Q

_______, _______, and ________ all have anti-remodeling effects on the heart and REDUCE MORTALITY and IMPROVE SURVIVAL

A

ACE inhibitors/ARBs
Aldosterone Antagonists
B-blockers

CVPR (12 decks)

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