1
Q
Common causes of acute pericarditis (4)
A
viral illness, connective tissue or autoimmune diseases (lupus), uremia (renal dysfunction), metastatic tumors
2
Q
Presneting symptoms of acute pericarditis (2)
A
- SUDDEN ONSET CP (severe), can be persistent for several days
- CP varies with position and breathing
3
Q
Diagnosis of acute pericarditis (6)
A
- CP varies with position and breathing
- Pericardial rub on exam
- Normal or low levels of indicators of myocardial damage
- EKG = diffuse ST elevation (across ALL leads)
- ECHO = pericardial fluid
- Response to anti-inflammatory agents (ibuprofen, ASA, colchicine)
4
Q
Treatment of acute pericarditis
A
Ibuprofen (NSAIDs)
5
Q
Pericardial effusion is»»
A
Fluid around the sac
6
Q
Common causes of pericardial effusion (5)
A
- Viral or acute idiopathic pericarditis
- Metastatic malignancy - tumor cells invade lymphatics or directly invade pericardium resulting in inflammatory fluid accumulation
- Uremia
- Autoimmune disease
- Hypothyroidism
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
8
Q
Pericardial effusion can result in
A
cardiac tamponade
9
Q
Cardia tamponade
A
excessive pericardial fluid compresses the heart and reduces venous return and thus reduces CO (acute emergency)
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
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
12
Q
Diagnosis of cardiac tamponade (3)
A
- XRAY - enlarged heart, non-congested lung fields
- ECHO - collapse of RA and LV in end diastole
a. Dilation of inferior vena cava and no collapse of IVC during inspiration - ECG
13
Q
Treatment of cardiac tamponade
A
pericardiocentesis
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
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
16
Q
Cardiac tamponade vs CHF:
Similarities (4)
A
a. JVD
b. Tachycardia
c. Low BP
d. Large cardiac silhouette on XR
17
Q
Constrictive pericarditis
A
chronic process, pericardium thickens to the point where it compresses the heart and limits CO
18
Q
Causes of constrictive pericarditis
A
Scarring and loss of elasticity of the pericardium
19
Q
Clinical manifestations of constrictive pericarditis (6)
A
- 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 - Elevated jugular venous pressure
- Hepatomegaly
- Edema
- Ascites
- Tachycardia
20
Q
Diagnosis of constrictive pericarditis
A
XRAY or ECG
21
Q
Treatment of constrictive pericarditis
A
surgical stripping of pericardium
22
Q
Tamponade vs. constrictive pericarditis:
Similarities (4)
A
a. Reduced diastolic function, preserved systolic function
b. JVD
c. Tachycardia
d. Low BP
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
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
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
CVPR
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