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Flashcards in CV Week 2a Deck (108):
1

Common causes of acute pericarditis (4)

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

2

Presneting symptoms of acute pericarditis (2)

1. SUDDEN ONSET CP (severe), can be persistent for several days

2.CP varies with position and breathing

3

Diagnosis of acute pericarditis (6)

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)

4

Treatment of acute pericarditis

Ibuprofen (NSAIDs)

5

Pericardial effusion is>>>>

Fluid around the sac

6

Common causes of pericardial effusion (5)

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

7

Diagnosis of pericardial effusion

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

8

Pericardial effusion can result in

cardiac tamponade

9

Cardia tamponade

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

10

Clinical manifestations of cardiac tamponade (3)


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

11

Paradoxical pulse

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

12

Diagnosis of cardiac tamponade (3)

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

13

Treatment of cardiac tamponade

pericardiocentesis

14

Cardiac tamponade vs. CHF:

Distinguishing features of Cardiac tamponade (6)

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

15

Cardiac tamponade vs CHF:

Distinguishing features of CHF (6)

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

16

Cardiac tamponade vs CHF:

Similarities (4)

a. JVD

b.Tachycardia

c.Low BP

d.Large cardiac silhouette on XR

17

Constrictive pericarditis

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

18

Causes of constrictive pericarditis

Scarring and loss of elasticity of the pericardium

19

Clinical manifestations of constrictive pericarditis (6)

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

20

Diagnosis of constrictive pericarditis

XRAY or ECG

21

Treatment of constrictive pericarditis

surgical stripping of pericardium

22

Tamponade vs. constrictive pericarditis:

Similarities (4)

a. Reduced diastolic function, preserved systolic function

b.JVD

c.Tachycardia

d.Low BP

23

Tamponade vs. constrictive pericarditis:

Distinguishing features of constrictive pericarditis (5)

a. Normal heart silhouette

b.Pericardial calcification

c.Pulsus paradoxus uncommon

d.Slow development over time

e.Accompanied by hepatic congestion, ascites, pedal edema

24

Process of cardiac depolarization

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

25

P wave =

atrial depolarization

26

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

AV node conduction time

27

Normal PR interval time

0.12-0.2 seconds

28

QRS complex =

ventricular depolarization

29

Normal duration of QRS complex

0.06-0.10 seconds

30

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

total duration of depolarization and repolarization

31

T wave =

ventricular repolarization

32

Paper speed

25 mm/ Second

33

Thin vertical lines are ____ seconds apart

0.04 seconds

34

Thick vertical lines ___ seconds apart

0.2 seconds

35

How wot calculate heart rate

300/ # of heavy lines OR
1500/ # of light lines

36

Ventricular hypertrophy

L and R ventricular hypertrophy result in greater muscle mass.

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

37

General ECG of ventricular hypertrophy

R wave with greater amplitude

38

ECG of left ventricular hypertrophy

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

39

ECG Right ventricular hypertrophy

high voltage in right sided leads - V1 and V2

40

Myocardial ischemia

insufficient blood supply to meet O2 demand in ventricles

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

41

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

causes depression of ST segment

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

42

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

Cause T wave inversion

a.Normally, T waves are in same direction of QRS complex.

i.Inversion of a T wave→myocardial ischemia

43

ST elevation =

sign of transmural injury in acute coronary syndrome

1.Clot due to platelet aggregation obstructing a coronary artery

2.Acute myocardial infarction

44

Sizeable (>0.04 s) Q waves =

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

Inferior infarcts will be detected by which leads (2)

II, III, aVF

46

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

V1-V4

47

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

I, aVL, V5, and V6

48

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

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

Transmural vs. subendocardial infarction

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

ECG: hypercalcemia (1 feature)

short QT interval
- associated with hyperparathyroidism

51

ECG: Hypocalcemia (1 feature)

Long QT
- associated with life threatening ventricular arrhythmias

52

ECG: hypokalemia (3 features)

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

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

53

ECG: Hyperkalemia (3 features)

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

Normal sinus rate is ______ bpm

60-100

55

Sinus Tachycardia and sinus bradycardia

normal waves but increased/decreased frequency

56

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

B-blockers

atropine or pacemaker

57

sinus sickness syndrome

sinus bradycardia often seen in elderly patients

may require pacing

58

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

drugs, conduction system defect

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

AV node dysfunction

59

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

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

3rd degree AV block causes

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

Infarct

disruption during cardiac surgery

severe conduction disease

rarely drugs

61

3rd degree AV block appearance on EKG

junctional failure

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

P rate > QRS rate

62

Atrial flutter on EKG

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

-pulse varies widely, ventricular rates vary

63

Treatment of atrial flutter (4)

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

Problems with Atrial Fibrillation (3)

rapid heart rate (syncope, ischemia, HF)

Loss of atrial kick = decrease preload --> HF

Atrial thrombi (embolic stroke)

65

A-FIB on EKG

NO P WAVES

-irregular ventricular rhythm (QRS waves)

chaotic atrial depolarizations

66

Treatment of AFIB

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

Atrial tachycardia on EKG (3)

rapid HR
narrow QRS
P waves are present but abnormal

68

Treatment of atrial tachycardia (3)

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

69

Junctional Rhythm

when rhythms originate from the area surrounding the AV node

70

Junctional rhythm on EKG (3)

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

71

Premature atrial contractions, 2 EKG features

common (single beat palpitations)

-preceded by abnormal P wave
-QRS normal or narrow

72

Premature ventricular contractions, 2 EKG features

common (single beat palpitations)

-no P waves
-QRS widened

73

Ventricular tachycardia EKG features (2)

repetitive, WIDE abnormal QRS (100-200 bpm)

no P wave

74

Treatment of V-tach (2)

1) cardioversion - especially if UNSTABLE

2) Amiodarone

75

Ventricular fibrillation

no P, no QRS, no T waves

chaotic squiggly lines

76

Treatment of v-fib (1)

life threatening

requires emergency defribrillation

77

Sinus arrest

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

Sinus node dysfunction

78

Tachycardia-Bradycardia (Tachy-Brady)

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

Sinus node dysfunction

79

Chronotropic Incompetence

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

Sinus node dysfunction

80

Indications for treatment of Bradyarrhythmias (2)

1) When patient is symptomatic

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

81

treatment of bradyarrhythmias (2)

Acute treatments? (3)

Long-term treatments? (1)

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

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

SVT = narrow QRS

VT = wide QRS

83

SVT with irregular rhythm includes...(3)

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

84

SVT with regular rhythm includes...

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

85

If rhythm is irregular and patient is hemodynamically unstable then...

SHOCK

86

Adenosine is used for treatment of...

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

Temporarily interrupts conduction at AV node

87

AV nodal reentrant tachycardia

How is it initiated?

-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

Treatment of AVNRT

Acute? (2)
Chronic? (2)

ACUTE
1) vagal maneuvers
2) adenosine

CHRONIC
1) Meds (suboptimal)
2) Catheter ablation

89

AV Reentrant Tachycardia

How is it initiated?

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

Treatment of AVRT (2)

1) Catheter ablation
2) Adenosine

91

Medications that can control heart RATE (4)

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

92

Things can control RHYTHM (2)

1) Drugs - class III and class IC antiarrhythmic drugs

2) Cardioversion (SHOCK)

93

When is defibrillator needed?

1) Structural heart disease
2) high risk of sudden death due to arrhythmia (primary or secondary prevention)

94

Furosemide, Bumetanide, Torsemide are all _________

Loop diuretics:
-High Ceiling Diuretics
-HIGHEST efficacy
-used chronically and acutely
-most commonly used out of all diuretics

95

Loop diuretics mechanism of action

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

Clinical use of loop diuretics (3)

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

97

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

Thiazides - block Na+ reabsorption at distal tubule

Aldosterone Antagonists - enhance diuresis and ameliorate K+ wasting

98

Side effects of loop diuretics (3)

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

99

Hypokalemia impacts on heart function

-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

Thiazides mechanism of action

-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

Clinical uses of thiazides (1)

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

102

Side effects of thiazides (3)

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

103

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

spironolactone, eplerenone

K+ sparing

104

Mechanism of action of aldosterone antagonists

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

Clinical Uses of aldosterone antagonists

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

Adverse reactions of aldosterone antagonists

1) Hyperkalemia
2) Gynecomastia

107

Effects of hyperkalemia on the heart

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

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

ACE inhibitors/ARBs
Aldosterone Antagonists
B-blockers