Exam 2 Flashcards
1
Q
What is the most common cause of right-sided heart failure?
A
Left-sided heart failure
2
Q
What are other causes of right-sided heart failure?
A
- L –> R shunt
2. Chronic lung disease - cor pulmonale
3
Q
How does inc. HR effect CO?
A
Increases then plateaus and drops off - dec. diastolic filling time
4
Q
Impaired contractility leads to an inability to handle ________ and CVP _________.
A
- volume
2. increases
5
Q
Afterload is a fx of what two things?
A
- Vasculature
2. Wall stress (Pxr/2wall thickness)
6
Q
What are symptoms of heart failure?
A
- SOB
- Pitting edema
- Distended jugular vein
- S3 gallop
- Tachypnea
7
Q
What does a crescendo-decrescendo murmur indicate?
A
Aortic stenosis
8
Q
In terms of heart failure what is the PCWP to be considered “wet”
A
PCWP > 18 and RA >8
9
Q
In terms of heart failure what is the CI to be considered “warm”
A
CI > 2.1
10
Q
What are the 3 criteria for using an inotrope for acute heart failure?
A
- Advanced systolic HF + low output + hypotension
- Vasodilators ineffective or CI
- Fluid overloaded and unresponsive to diuretics or deteriorating renal fx
11
Q
Heart failure leads to impaired ___ handling. Inotropes work to __________ calcium.
A
- Ca
2. Increase
12
Q
What is a adverse effect of using an inotrope in AHF?
A
Arrhythmias
13
Q
What are 3 typical inotropes used in AHF?
A
- Dobutamine
- Milrinone
- Dopamine
14
Q
What is the MOA of Milrinone?
A
PDE inhibitor (IV infusion)
Inc. contractility and dec. afterload
** Hypotension, arrhythmia
15
Q
What is the MOA of Dobutamine?
A
B1 agonist with weak B2
Inc. contractility with mild vasodilator
**Arrhythmia, angina, HTN, and tachycardia
16
Q
What is the MOA of Levosimendan?
A
Troponin C to inc. its sensitivity to CA
Ca sensitizer and vasodilator
Dec afterload and LVEDP
***Not in US
17
Q
True or False: Diuretics and Inotropes improve mortality in AHF?
A
False - dec. volume - Inc. sympathetic stimulation
18
Q
What are 4 options for treating chest pain?
A
- Morphine (histamine - hypotensive)
- Oxygen
- Nitrate (hypotensive)
- Aspirin
19
Q
What else is on your differential for cardiogenic shock?
A
SIRS Acute coronary syndrome Aortic regurgitation Dilated cardiomyopathy CHF and Pulmonary edema Mitral regurgitation Pericarditis and cardiac tamponade Hypovolemic shock Papillary muscle rupture Acute valvular dysfunction VSD
20
Q
If you suspect sepsis, what must you do within 3 hours?
A
- Measure lactate
- Obtain blood cultures
- Broad spec antibiotics
- Cristalloid 30 ml/kg
21
Q
What should you do if someone with sepsis hasn’t responded to fluids
A
They are in Septic Shock 1. Vasopressors (target: MAP > 65) Norepinephrine is best Low dose vasopressin can be added Dobutamine if inotropic support is needed
22
Q
Automaticity
A
A cell’s ability to depolarize itself to a threshold voltage to generate a spontaneous AP
23
Q
Cells with natural automaticity do not have a ________________.
A
Static resting voltage
24
Q
What current is largely responsible for Phase 4 depolarization?
A
If - pacemaker current
25
If channels are activated by ____________, and mainly conduct _____.
Hyperpolarization (-50mV)
| Na (influx)
26
Why is the upstroke much steeping in Purkinje cells than in sinus and AV nodal cells?
Sinus and AV nodal cells have less negative max diastolic membrane voltage so a greater number of fast Na channels are inactivated.
27
Overdrive Suppression
Inc. stimulation by adjacent pacemaker cells results in increased intracellular Na.
Inc. Na drives the hyperpolarizing Na/K ATPase that antagonizes the If channels preventing spontaneous depolarization
28
What is an example of altered automaticity
Autonomic Signaling
29
What are two ways that sympathetic stimulation increases sinus node automaticity?
1. Inc. the open probability of the pacemaker channels thru which If can flow
2. Shifts the AP threshold more negative - inc. the probability that voltage-sensitive Ca channels are capable of opening
30
What are three ways that parasympathetic stimulation decreases sinus node automaticity?
1. Dec. probability that If channels are open
2. Dec probability that Ca channels are open - inc. threshold
3. Inc. probability that K(ACh) channels are open at rest (K efflux) - drives diastolic potential to be more neg
31
Escape rhythm
Impulse initiated by a latent pacemaker because the SA node rate has persistantly slowed
32
Ectopic beat
A latent pacemaker develops an intrinsic rate of depolarization that is faster than the sinus node
33
When do ectopic beats occur?
High catecholamines concentrations, hypoxemia, ischemia, electrolyte disturbances and digitalis toxicity
34
Abnormal automaticity
Cardiac injury leads to myocardial cells acquiring automaticity - likely due to leaky membranes and less negative resting membrane potential
35
Triggered activity
Early afterdepolarizations and delayed afterdepolarizations
36
Early afterdepolarization
Changes of membrane potential in the + direction that interrupt repolarization and are more likely to develop in conditions that prolong the AP duration
*Initiating mechanism of the polymorphic v tach Torsades de Pointes
37
EADs that occur in phase 2 are likely due to which current?
Inward Ca
38
EADs that occur in phase 3 are likely due to which current
Fast Na - more have recovered from inactive state
39
Delayed afterdepolarizations
May appear shortly after repolarization is complete - develop in states of high intracellular calcium - drive Na-Ca exchanger (brief inward current)
*digitalis toxicity or marked catecholamine stimulation
40
Functional heart block
Block occurs because an impulse encounters cardiac cells that are still refractory i.e. from drugs prolonging AP duration
41
Fixed heart block
Block is caused by a barrier i.e. fibrosis, scarring
42
Unidirectional block
AP can conduct in a retrograde direction, but prevented from doing so in the forward direction - occur w/ cellular dysfunction, different refractory periods and myocardial fibrosis
43
Most clinical cases of reentry occur within ______ regions of tissue because the conduction velocity within the reentrant loop is abnormally _____.
Small
| Slow
44
What are the 2 critical conditions for reentry?
1. Unidirectional block
| 2. Slowed conduction thru reentry path
45
What is he most common mechanism of ventricular tachycardia associated with areas of ventricular scar (prior MI)?
Monomorphic tachycardia
46
Wolff-Parkinson-White Syndrome
An additional connection between the atrium and ventricles (accessory pathway)
1. Shortened PR interval
2. Wide, slurred QRS w/ Delta wave
47
What are 3 ways of treating bradyarrhythmias?
1. Anticholinergic - atropine
2. B1-receptor agonist - isoproterenol
3. Electronic pacemakers
48
What are two reasons bradyarrhythmias develop?
1. decreased impulse formation (sinus bradycardia)
| 2. decreased impulse conduction (AV nodal block)
49
What are three reasons tachyarrhythmias develop?
1. Inc. automaticity (SA node, latent pacemakers or abnormal myocardial sites)
2. Triggered activity
3. Reentry
50
What are three intrinsic factors that can suppress automaticity of SA node?
1. Aging
2. Ischemic heart disease
3. Cardiomyopathy affecting the atrium
51
Sick Sinus Syndrome
SA node dysfunction - periods of inappropriate bradycardia
52
What do junctional escape rhythms (AV node/proximal bundle of His) look like on an EKG?
Normal, narrow QRS (40-60 bpm)
QRS not preceded by P wave
Retrograde P wave may follow QRS (inverted) in II, III and aVF
53
What do ventricular escape rhythms look like on EKG?
Widened QRS (30-40 bpm)
54
What does first degree AV block look like on an EKG?
PR interval is lengthened (> 200ms/5 sm boxes)
| 1:1 P : QRS
55
What causes reversible first degree AV block?
1. Heightened vagal tone
2. Transient AV nodal ischemia
3. Drugs that depress AV nodal conduction - B blockers, Ca channel antagonists, digitalis
56
What causes irreversible first degree AV block?
1. MI, chronic degenerative disease
57
How do you treat first degree AV block
Typically asymptomatic
58
What are the two types of 2nd degree AV block?
1. Mobitz type I (Wenckebach block)
| 2. Mobitz type II
59
Mobitz type I (Wenckebach block)
Impaired conduction thru AV node, benign
| Gradually inc. PR until QRS is blocked
60
What groups of people have Mobitz type I block and how do you treat them?
Children, athletes, people w/ high vagal tone, sleep
Can occur in acute MI due to inc. vagal tone/ischemia
Typically not necessary, normally benign
61
Mobitz type II
Conduction block in bundles of His or Purkinje system
Sudden, intermittent loss of QRS w/o PR interval lengthening
QRS is often widened
62
What causes Mobitz type II and do you need to treat it?
1. Extensive MI involving septum
2. Degeneration of His-Purkinje system
3. Yes. May progress to 3rd degree block w/o warning - pacemaker
63
3rd degree AV block
Complete failure of conduction between atrial and ventricles
64
What causes 3rd degree AV block?
MI and chronic degeneration of pathway with age
65
What does 3rd degree AV block look like on EKG?
P wave march out
| QRS: may be normal (40-60bpm) or widened at slower rates if escape rhythm comes from His-Purkinje
66
How do you treat third degree AV block
Pacemaker
67
Sinus tachycardia
SA discharge > 100bpm
Inc sympathetic tone/dec vagal tone
Fever, hypoxemia, hyperthyroidism, hypovolemia, anemia
68
Atrial premature beats (APB) are caused by ______________ and exacerbated by _________________.
1. Automaticity or reentry in an atrial focus outside SA node
2. Sympathetic simtulation
69
What do APBs look like on an EKG?
Early P wave with an abnormal shape
| May be conducted or blocked
70
How do you treat APBs?
Normally asymptomatic, may cause palpitations
| B-blockers
71
Atrial flutter
```
Atrial activity (180-300bpm) - do not all conduct to ventricles
Caused by reentry over a large anatomically fixed circuit
```
72
What does atrial flutter look like on an EKG
Sawtooth P waves
73
What are predisposing factors for atrial flutter?
1. Prior heart surgery
2. Coronary disease - atrial scarring
3. Cardiomyopathy
4. Ablation procedures
74
True or False: Atrial flutter generally occurs in patients with preexisting heart disease?
True
75
What are people with atrial flutter at high risk for?
Stroke (thrombus) - anticoagulate before cardioversion
76
How do you treat atrial flutter
1. Beta blockers, Ca channel blockers, digoxin
| 2. Catheter ablation of tricuspid valve isthmus - curative 95%
77
Atrial fibrillation
Chaotic rhythm w/ atrial rate of 350-600/min - irregularly irregular ventricular rhythm (140-160bpm)
78
Rapid firing from atrial foci localized to atrial muscle extending into ______________.
Pulmonary veins
79
What factors predispose to AF?
EtOH, CHF, valvular disease, HTN, coronary disease, pulmonary disease, sleep apnea, hyperthyroidism, cardiothoracic surgery -- anything that inc. the size of the atria
80
How can AF present clinically?
Dizziness, hypotension, HF
81
How do you treat AF?
1. Anticoagulation
2. Rate control: AV nodal blockade (B-blockers, Ca channel blocker, digoxin)
3. Restore sinus rhythm (cardioversion, antiarrhythmic drugs, catheter ablation)
82
In AF where are clots most likely to form?
Left atrial appendage
83
AV Nodal Reentrant Tachycardia
Most common form of paroxysmal SVT
| Travels down slow pathway and up fast
84
How does AVNRT present?
Young adults
| Palpitation, dizziness, chest pain, dyspnea
85
How do you acutely treat AVNRT
```
IV adenosine
or
IV verapamil/diltiazem
or
B-blockers
```
86
In a person with AVNRT with frequent episodes how can ou treat them?
1. Oral B-blockers, Ca channel blockers, digoxin
| 2. Catheter ablation of slow AV nodal pathway
87
A patient with AVNRT is undergoing catheter ablation of their slow AV nodal pathway, what would happen if the fast pathway is ablated?
Heart block
88
Atrioventricular Reentrant Tachycardias
Reentry using bypass tract or accessory pathway
89
If the tract in AVRT only conducts retrograde it can promote _________________.
Supraventricular tachycardia
90
If both the accessory tract and AV node conduct anterograde, what will result?
Ventricular Pre-excitation Syndrome (V contract sooner due to quicker signal thru accessory tract) aka Wolff-Parkinson-White
91
What are patients with WPW syndrome predisposed to and why?
PSVTs - orthodromic AVRT
Impulse travels anterograde down AV node and retrograde up accessory tract
No delta wave, retrograde P waves
92
A wide QRS with retrograde P waves indicates what on ECG?
Antidromic AVRT - anterograde thru accessory pathway and retrograde up AV node
93
Anterograde conduction over the accessory pathway with AF or atrial flutter present can lead to what?
Ventricular rates up to 300 bpm
V fib
Cardiac arrest
94
How do you treat someone with AVRT?
1. Amiodarone or procainamide (Class I and III)
2. If hemodynamically unstable - cardiovert
3. Ablation of accessory pathway
95
If the accessory pathway can only conduct in retrograde what can form?
Orthodromic AVRT - concealed accessory pathway
96
Focal Atrial Tachycardia
Automaticity of atrial ectopic site or reentry
P-wave before each QRS (P-wave morphology is different)
Can be seen in healthy people
97
AT can be caused by __________ toxicity and is also aggravated by elevated ______________ tone.
1. Digitalis
| 2. Sympathetic
98
Multifocal atrial tachycardia
Irregular rhythm w/ at least 3 P-wave morphologies
Average atrial rate > 100 bpm
Occurs w/ severe pulmonary disease or hypoxemia
Verapamil
99
Ventricular premature beats (VPBs)
Ectopic ventricular focus fires an AP (can occur in healthy people)
100
What does VPB look like on an EKG?
Widened QRS
Not related to P wave
Can be repeating or consecutive
101
How do you treat VPBs?
Normally not necessary - observe
| B-blocker for symptomatic relief
102
Ventricular tachycardia is a series of 3 or more _____. Sustained VT must persist for more than ________.
VPBs
| 30 seconds
103
What conditions predispose someone to VT?
1. Structural heart disease
2. MI
3. HF
4. Ventricular hypertrophy
5. Primary electrical disease - long QT syndrome
6. Valvular heart disease
7. Congenital abnormalities
104
What does monomorphic VT look like on an EKG?
QRS complexes are wide and identical from beat to beat w/ regular rate
105
Sustained monomorphic VT usually indicates what?
A structural abnormality supporting a reentry circuit - MI scar or cardiomyopathy
106
What does polymorphic VT look like on an EKG?
QRS continually changes shape and rate - Multiple foci or changing reentrant circuit
107
What are the most common causes of polymorphic VT?
1. Torsade de pointes
| 2. Acute MI
108
How can you distinguish monomorphic VT from SVT?
1. SVT has a narrow QRS (unless theres aberrant ventricular conduction RBBB or LBBB)
2. Monomorphic VT has AV dissociation - no relation between P waves and QRS
109
Torsades de Pointes
Polymorphic VT - varying amplitudes of QRS
Lightheadedness, syncope, sudden cardiac death
Cardiovert and remove stimulus
Treat symptoms with B-stimulating agents isoproterenol (shorten QT)
110
What three things can lead to Torsades de Pointes?
1. EAD in pt w/ long QT interval
2. Hypokalemia or hypomagnesemia
3. Class III drugs
4. A few non-cardiac drugs
111
What are the 3 mutations that cause Congenital Long QT Syndrome?
Enhance depolarizing Na current or impair depolarizing K current
LQT1: dec. outward K+
LQT2: dec. outward K+
LQT3: Inc. inward Na
112
How should you acutely treat someone with VT?
Stable: antiarrhythmic drugs (amiodarone, lidocaine) or sedate and cardiovert
113
Ventricular fibrillation
Immediate life-threatening arrhythmia - disordered rapid stimulation of ventricles
Often initiated by episode of VT which degenerates
114
Dystrophic calcification
Wear and tear complicated by deposits of calcium phosphate - inc. risk with HTN, hyperlipidemia, inflammation
115
Calcific aortic stenosis and mitral annular calcification are examples of what?
Dystrophic calcification
116
Calcific aortic stenosis
Most common - wear and tear
Occurs in 8th-9th decade
Higher risk w/ bicuspid aortic valve (5th-6th decade)
117
What are clinical effects of calcific aortic stenosis?
LV hypertroph
Angina, ischemia, CHF
Syncope
118
How do you treat calcific aortic stenosis?
Valve replacement to avoid heart failure
119
What is the morphology of calcific aortic stenosis?
1. Calcified masses in cusps at bases
2. Cusps not fused
3. Free edge not involved
120
Mitral Annular Calcification
Degenerative calcific deposits on fibrous ring at base
Women
Inc. in myxomatous valves or inc. LV pressure
Does NOT affect function
Prime site for thrombi/infection
121
Myxomatous Degeneration of Mitral Valve
```
Mitral valve prolapse (3% of adults)
One or both leaftlets enlarged, hooded, redundant, floppy
Usually no serious complications
Feature of Marfan syndrome
Deposition of mucoid material in valve
```
122
What does a mid systolic click indicate?
Myxomatous Mitral valve
123
What are the rare complications of myxomatous mitral valve?
1. Regurgitation
2. Infective endocarditis
3. Mitral insufficiency
4. Thrombi - atrial surface
5. Arrhythmias -- sudden death
124
Rheumatic Fever occurs following an episode of _____________________.
Group A strep pyrogenes pharyngitis
125
The most important complication of rheumatic fever is _______________.
Chronic valvular dysfunction - mitral stenosis
126
What is morphology of acute rheumatic fever?
Pancarditis
1. Bread and butter pericarditis - fibrin on surface
2. Myocarditis w/ aschoff bodies
3. Endocarditis w/ fibrinoid necrosis and verrucae - causes problems in chronic
127
The classic lesion of Rheumatic Lesion is _____________.
Aschoff body
| Anitschow cells, foci of swollen eosinophilic collagen surrounded by T lymphocytes, large macrophages, and plasma cells
128
Chronic rheumatic heart disease
1. Thickened valve leaflets
2. Fusion of commissures (fishmouth/buttonhole deformities)
3. Fusion/thickening of chordae tendinae
MAJOR EFFECT IS MITRAL STENOSIS
129
Mitral stenosis in chronic rheumatic heart disease can lead to ____________.
```
Atrial dilatation, thrombi
Reduced CO
Pulmonary congestion
RVH
Right-sided HF
```
130
Hypersensitivity induced by group a strep is caused by what?
M protein cross react w/ glycoprotein antigens in heart, joints, etc
131
How is acute rheumatic fever diagnosed?
```
JONES CRITERIA - Major
J - Joint
O - Heart
N - SubQ Nodules
E - Erythema marginatum
S - Sydenham chorea
```
132
When does acute rheumatic fever occur?
1-4 weeks after Group A (B hemolytic) infection
| Check ASO titers and antibodies to DNAase B
133
When does chronic rheumatic carditis occur?
Years or decades after initial episode
134
What is the difference between acute and subacute endocarditis?
1. Acute is highly virulent, w/ normal valve and high mortality - need surgery/new valve
2. Subacute is low virulence w/ deformed valve, responds to antibiotics
135
Nonbacterial thrombotic endocarditis
Deposition of fibrin, platelets and other blood products on leaflets - non-destructive, noninflammatory
cancer, sepsis, hypercoaguable (pancreatic cancer)
Swan-Gatz catheter
136
Libman-Sacks Endocarditis
SLE - Mitral and tricuspid valves
Primary antiphospholipid syndrome
Both sides of leaflet - may be on endocardium - may be verrucae
Intense inflammation
137
Carcinoid Syndrome
Carcinoid tumors produce serotonin or vasoactive amines (bradykinin, histamine, PG)
Flushing, cramps, NVD
138
Carcinoid Heart Disease
Plaque-like fibrosis on right side of heart (gets inactivated by MAO in lung)
SMC and collagen embed in mucopolysaccharide matrix
Tricuspid and pulmonic valves equally affected T. insufficiency and pulmonic stenosis
139
GI carcinoid w/ hepatic mets
Mets to liver - secretion occurs directly to hepatic vein
or
Direct secretion to systemic circulation
140
Artificial valve complications
1. Thromboembolic complications
2. Infective endocarditis (bio/mechanical)
3. Structural deterioration (bioprosthesis)
