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1 - Cardiology > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Define heart failure

A

1) Condition in which heart is unable to generate sufficient cardiac output to meet metabolic demands of the body
2) ?without increasing diastolic pressure

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2
Q

List the Framingham clinical criteria for diagnosis of heart failure –> remember heart failure is essentially a clinical diagnosis

A

Meet 2 major or 1 major + 2 minor

Major Criteria

1) Orthopnea (Hx)
2) Paroxysmal nocturnal dyspnea (Hx)
3) Elevated JVP (>16cm water) (PE)
4) S3 gallop rhythm (PE)
5) Basal crepitations (PE)
6) Acute pulmonary edema (PE/Ix)
7) Cardiomegaly (PE/Ix)

Minor Criteria

1) Dyspnea on exertion (Hx)
2) Night cough (Hx)
3) Ankle edema (Hx/PE)
4) Tachycardia >120bpm (PE)
5) Hepatomegaly (PE)
6) Pleural effusion (PE/Ix)
7) Maximum vital capacity 4.5kg in 5d when treated (Mx)

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3
Q

How does one assess the severity of heart failure?

A

New York Heart Association (NYHA) assigns patients 1 of 4 functional classes based on degree of functional limitation imposed by heart failure

I –> asymptomatic heart disease
II –> symptomatic heart disease only on ordinary exertion
III –> symptomatic heart disease w/less than ordinary exertion
IV –> symptomatic heart disease at rest

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4
Q

How can the development of heart failure be staged?

A

American College of Cardiology/American Heart Association (ACC/AHA) guidelines emphasizes progressive nature of heart failure and defines therapy appropriate for each stage from A to D as follows

A –> at high risk for HF but no structural heart disease and asymptomatic
B –> structural heart disease but asymptomatic
C –> structural heart disease but symptomatic (includes NYHA Class 1 w/prior symptoms)
D –> refractory HF requiring specialized interventions

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5
Q

Distinguish between systolic and diastolic heart failure

A

Systolic heart failure has systolic dysfunction in which left ventricular ejection fraction (LVEF) is

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6
Q

Explain the role of neurohormonal activation in heart failure

A

1) Short term neurohormonal activation is beneficial in patients w/heart failure as it restores cardiac output and tissue perfusion to near normal by
1. elevating cardiac contractility
2. increasing vascular resistance
3. increasing renal sodium retention

2) Long term neurohormonal activation is detrimental and leads to many complications
1. pathologic myocardial remodeling
2. increased afterload
3. peripheral edema
4. pulmonary edema

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7
Q

List the neurohormonal pathways involved in heart failure

A

1) Sympathetic nervous system
2) Renin-angiotensin-aldosterone system (RAAS)
3) Antidiuretic hormone (ADH) /Arginine vasopressin (AVP)
4) Atrial and brain natriuretic peptides (ANP and BNP)
5) Endothelin

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8
Q

Outline the sympathetic pathway involved in heart failure

A

1) Earliest response to drop in cardiac output via drop in blood pressure
2) Catecholamines augment cardiac output
1. increasing ventricular contractility
2. increasing heart rate
3) Catecholamines increase ventricular preload and afterload by vasoconstriction (both systemic and pulmonary)
4) Catecholamines constrict efferent arteriole more than afferent to maintain GFR despite renal vasoconstriction
5) Catecholamines stimulate proximal tubular Na reabsorption –> Na retention feature seen in HF

6) Chronic catecholamines causes downregulation of beta adrenoreceptors in the heart thus impairing inotropic and chronotropic responses –> catecholamine level is predictor for survival
7) Chronic catecholamine stimulation of beta adrenoreceptors causes molecular and cellular disturbances that contribute to cardiac myocyte dysfunction

Thus sympathetic outflow blockade by certain beta-blockers alongside ACEIs are beneficial for survival in the long run iin heart failure patients

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9
Q

Outline the RAAS pathway involved in heart failure

A

1) In heart failure 3 occurrences stimulate renin release
1. reduced stretch of afferent arteriole
2. reduced delivery of chloride to macula densa
3. increased beta-1 adrenoreceptor activity
2) Renin release induces angiotensin II and aldosterone release causing similar effects to noradrenaline
1. increased proximal tubular Na reabsorption
2. systemic (including renal vasoconstriction)
3) Aldosterone involvement in heart failure means aldosterone antagonists + ACEI/ARB are beneficial for survival in the long run in heart failure patients

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10
Q

Outline the ADH/AVP pathway involved in heart failure

A

1) In heart failure low CO stimulates baroreceptors in 2 areas which induces ADH release and thirst sensation
1. carotid sinus
2. aortic arch
2) ADH acts on V1A receptor to cause vasoconstriction
3) ADH acts on V2 receptor to enhance water reabsorption in distal collecting tubules
4) Increased thirst + enhanced water reabsorption causes dilutional hyponatremia which usually parallels the severity of heart failure –> degree of hyponatremia is predictor of survival

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11
Q

List the 2 most common pathways causing diastolic heart failure

A

1) Myocardial ischemia i.e. ischemic heart disease (IHD)
2) Left ventricular hypertrophy (LVH) of any cause
1. Chronic HT w/concentric remodeling
2. Aortic stenosis
3. Hypertrophic cardiomyopathy

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12
Q

Explain how ischemia causes diastolic heart failure

A

1) Ischemia causes reversible impairment in myocyte active relaxation preventing normal increase in left ventricular distensibility –> diastolic dysfunction
2) Persisting actin-myosin crossbridges generate tension throughout diastolic creating state of “partial persistent systole”
3) This diastolic dysfunction occurs by 2 types of ischemia –> demand ischemia and supply ischemia

Demand ischemia

  • occurs during exercise or other stress tests (e.g. drugs)
  • leads to increased oxygen demand in setting of limited coronary flow
  • ATP depletion causes rigor bond formation causing failure to relax

Supply ischemia

  • occurs w/marked reduction in coronary flow
  • there is inadequate coronary perfusion even at rest
  • i don’t understand the rest on uptodate…

*just remember diastolic heart failure is caused by failure to relax (which is an ACTIVE process requiring ENERGY (ATP)) + drop in ventricular compliance

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13
Q

Explain the relationship between anginal pain, SOB, and diastolic dysfunction

A

1) Ischemia causes both anginal pain and diastolic dysfunction
2) Diastolic dysfunction is characterized by a stiff non-distensible left ventricle which increases diastolic pressure causing acute pulmonary congestion
3) Acute pulmonary congestion cause SOB
4) Thus anginal pain is accompanied by SOB

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14
Q

Outline the relationship between reperfusion and diastolic dysfunction

A

1) Ischemic diastolic dysfunction can continue after reperfusion
2) Occurs after 2 situations
1. Post reperfusion therapy for STEMI
2. Post cardiac surgery
3) Post ischemic mechanical dysfunction actually affects by systolic and diastolic function but diastolic function is usually a more sensitive parameter of ischemic injury
4) Thus reduced cardiac output (CO) or elevated pulmonary capillary wedge pressure (PCWP) in the early postreperfusion or postoperative period only reflects transient left ventricular thickness rather than loss in contractility (distinguish by echocardiography)

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15
Q

List the pathophysiological structural changes in left ventricular hypertrophy (LVH) causing diastolic dysfunction

A

1) Concentric left ventricular remodeling
2) Cardiomyocyte hypertrophy
3) Altered ECM structure and composition
4) Increased fibrillar collagen

In combination these 4 changes impair cellular and myocardial relaxation

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16
Q

Explain why for a given degree of ischemia that hypertrophied heart have a greater decline in diastolic function

Hint: there are 6 reasons

A

Concentric LVH predisposes to subendocardial ischemia which impairs active relaxation of the left ventricle. The reasons for this include

1) Inadequate coronary growth relative to muscle mass
2) Coronary arterial circulation includes epicardial vessels which penetrate transmurally to supply thickened left ventricular myocardium BEFORE the subendocardium further increasing subendocardial ischemia
3) Concentric LVH is accompanied by coronary arterial remodeling which impairs coronary arterial vasodilation
4) Reduced coronary flow reserve as vessels are already maximally dilated even at rest
5) Increased left ventricular diastolic pressures cause vascular compression thus reducing subendocardial perfusion which only occurs during diastole
6) Ischemic heart disease is commonly associated with concentric LVH as both are caused by hypertension

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17
Q

List the causes of diastolic heart failure

A

1) Active relaxation failure
1. Ischemia –> IHD
2. Concentric LVH –> HT, AS, HOCM
1) Compliance failure
1. Cardiac fibrosis (aging, IHD, eosinophilic myocarditis
5-HT stimulation [food, drugs, carcinoid tumour])
2. Restrictive cardiomyopathy
3. Constrictive pericarditis
4. Increased intrathoracic pressure

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18
Q

List investigations for heart failure

A

1) CBC –> exclude infection by looking at WCC
2) RFT –> hyponatremia as marker for HF severity
3) LFT –> any hepatic complications from HF
4) TFT –> assess thyroid causes for HF
5) BNP –> interpret based on cutoffs of 100 and 400
- 400 indicates cardiopulmonary pathology

6) CXR for signs of heart failure by ABCDE
https: //medmnemonics.files.wordpress.com/2011/03/heart_failure.gif?w=450

7) ECG for ischemia, R/LVH, arrhythmia
8) Echocardiography for LVEF and valve functional assessment

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19
Q

What are the CXR signs of heart failure?

A

XR for signs of heart failure by ABCDE

  • A –> alveolar edema = bat’s wings
  • B –> kerley B lines = interstitial edema
  • C –> cardiomegaly
  • D –> dilated prominent upper lobe vessels
  • E –> effusion (pleural)

https://medmnemonics.files.wordpress.com/2011/03/heart_failure.gif?w=450

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20
Q

How does one interpret BNP levels?

A

BNP –> interpret based on cutoffs of 100 and 400

  • 400 indicates cardiopulmonary pathology such as
    1. heart failure
    2. pulmonary embolism
    3. pulmonary HT
    4. renal impairment
  • 100-400 tells us there may or may not be a problem
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21
Q

List poor prognostic factors for heart failure

A

1) sinus tachycardia >100bpm
2) low LVEF
3) hyponatremia
4) impaired RFT
5) elevated renin or aldosterone
6) exercise test max oxygen consumption

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22
Q

List causes of heart failure

incomplete

A

Common causes that MUST be mentioned first

1) Ischemic heart disease (now most common)
2) Hypertension (previously most common; well controlled now)
3) Valvular disease
4) Myocarditis

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23
Q

List the aims of pharmacologic therapy in heart failure

A

1) Symptomatic control
2) Slow or reverse deterioration in myocardial function
3) Reduced mortality/improve survival

24
Q

List drugs for symptomatic control in heart failure

List drugs for improving survival in heart failure

A

1) ACEI/ARBs
2) Aldosterone antagonists
3) Beta blockers
4) Hydralazine + nitrate
5) Diuretics [James notes says this doesn’t either…]
6) Digoxin [only digoxin does not improve survival]

25
Q

Outline the order of drug therapy in heart failure

A

1) Loop diuretics –> relieve volume overload (dyspnea, edema)
2) ACEI/ARBs –> titrate up from low dose (lisinopril 2.5mg)
3) Beta-blockers –> after stabilized on ACEI/ARBs; titrate up from low dose (metoprolol controlled release i.e. betaloc zok 3.125mg)

1st diuretics; 2nd ACEI/ARBs; 3rd beta-blockers

4) Add on –> symptomatic despite adequate ACEI/ARBs and beta-blockers
1. aldosterone antagonist
2. hydralazine + nitrate
3. digoxin

26
Q

List requirements and indications for aldosterone antagonists in heart failure

A

Requirements for aldosterone antagonists add on

1) RFT monitoring for impaired renal function
2) RFT monitoring for K+ concentration

Indications for aldosterone antagonists add on

1) NYHA 2 (symptomatic ordinary exertion) + LVEF ≤30%
2) NYHA 3/4 + LVEF

27
Q

List indications for hydralazine + nitrates in heart failure

A

Indication for hydralazine + nitrates add on

1) Reduced LVEF
2) Persistent symptoms despite adequate dose ACEI/ARB and beta blockers
3) May also be used for those who cannot tolerate ACEI/ARB or beta blockers

28
Q

List indications for digoxin in heart failure

A

Indication for digoxin add on

1) Symptomatic relief to reduce hospitalization rates
2) Concomitant atrial fibrillation rate control

REMEMBER NO SURVIVAL BENEFIT!!!
Causes arrhythmias especially if patient hypokalemic

29
Q

List the types of device therapy for heart failure

A

1) Implantable cardiac defibrillator (ICD)
2) Cardiac resynchronization therapy (CRT)

Most patients who satisfy criteria for CRT are also candidates for ICD so they receive a combined device

Mechanical circulatory support

3) Cardiac contractility modulation (CCM)
4) Left ventricle assisting device
- bridging therapy to heart transplant

30
Q

List the types of ventricular arrhythmias heart failure and cardiomyopathy are associated with.

Outline symptom severity and clinical significance

A

1) Ventricular premature beats (VPB)
- asymptomatic to mild symptoms
- usually treated with heart failure beta blockers
- if non-responsive try amiodarone or sotalol

2) Nonsustained ventricular tachycardia (NSVT)
- asymptomatic to mild symptoms
- drug treatment cannot reduce sudden cardiac death (SCD)
- NSVT indication for electrophysiology study to determine if patient is candidate for ICD

3) Accelerated idioventricular rhythm (AIVR)
- asymptomatic to mild symptoms
- benign rhythm that usually resolves spontaneously
- drug treatment contraindicated for some as suppression of escape rhythm pacemaker can cause asystole
- symptomatic AIVR arising due to sinus node dysfunction may benefit from atrial pacing

4) Sustained ventricular arrhythmias
- high risk for SCD –> treat w/ICD

31
Q

Outline the purpose of electrophysiology (EP) testing in patients with heart failure and cardiomyopathy

A

1) EP testing demonstrates mechanism of induced or spontaneous arrhythmias
2) EP testing checks function of SA node, AV node, and His-Purkinje system
3) EP testing assists in diagnosis of unexplained symptoms (e.g. syncope, palpitations) or arrhythmias
4) Determines ability to induce ventricular arrhythmias in selection for suitable candidates to undergo ICD

32
Q

List indications for electrophysiology (EP) study

A

Indications for EP –> assess ability to induce ventricular arrhythmias

1) Sustained palpitations
2) Presyncope or syncope w/out clear explanation
3) Wide QRS complex of uncertain etiology
4) Bundle branch reentrant tachycardia
- confirms diagnosis and guides ablation in cases of non-ischemic cardiomyopathy
5) Post MI LVEF 40-31%

33
Q

What patients can directly receive ICD without EP?

A

Skip EP, directly ICD

1) LVEF≤30%
2) LVEF ≤35% + NYHA 2-3

34
Q

In what patients is EP useless for risk stratification?

A

EP has no role in risk stratification for ICD in any nonischemic cardiomyopathy

35
Q

Based on NYHA grading which patients should or should not undergo ICD therapy

A

NYHA 1-3 die from sudden arrhythmias –> ICD indicated

NYHA 4 die from pump failure –> ICD not indicated

36
Q

What medications must be used with caution in diastolic heart failure?

A

Any preload reduction medications as a stiff heart (no active relaxation + low compliance) is dependent on preload for ventricular filling

1) Diuretics
2) Nitrates
3) Dihydropyridine CCB

So basically only ACEI/ARB and AA used without concern

37
Q

List the causes of sudden cardiac arrest (SCA)/death (SCD)

A

Ischenmic cardiomyopathy

  • coronary artery disease
  • coronary artery embolism
  • non-atherogenic coronary artery disease
    • e.g. dissection, arteritis
  • coronary artery spasm

Nonischemic cardiomyopathy

  • hypertrophic cardiomyopathy
  • arrhythmogenic right ventricular dysplasia
  • restrictive cardiopmyopathy
  • dilated cardiomyopathy
  • valvular heart disease
  • acute pericardial tamponade
  • myocarditis
  • aortic dissection

Rhythm Disease

  • complete heart block
  • long QT syndrome
  • Brugada syndrome
38
Q

List general requirements for ICD implantation

A

General requirements

1) Survival expected to be >1y
2) No complete reversible cause of VT/VF
3) NYHA 4 refractory to medical management
4) VT/VF amenable to catheter or surgical ablation

39
Q

List primary prevention indications for ICD

A

Primary prevention

1) Indicated by EP ability to induce VT/VF
2) NYHA 2-3 + LVEF ≤35%
3) Hx MI >40d + LVEF ≤30%
4) Hypertrophic cardiomyopathy
5) Arrhythmogenic right ventricular cardiomyopathy
6) Long QT syndrome
7) Brugada syndrome

40
Q

List secondary prevention indications for ICD

A

Secondary prevention

1) Hx aborted SCD (VT/VF) in which a reversible cause cannot be identified –> excludes VT/VF occurring in initial 48h post MI
2) Hx spontaneous sustained VT in presence of heart disease (valvular, ischemic, hypertrophic, dilated, infiltrative cardiomyopathies)

41
Q

Outline the problems with right ventricular pacing

A

1) Right ventricular pacing exacerbates heart failure by several mechanisms
2) RV pacing causes RV to contract before LV causing INTERventricular dyssynchrony
3) RV pacing stimulates the effect of left bundle branch block (LBBB) thus causing septal contraction to occur before LV lateral wall contraction causing INTRAventricular dyssynchrony
4) This problem persists despite dual chamber pacing of the RA and RV

It is for these 2 reasons that cardiac resynchronization therapy involves biventricular pacing to avoid dyssynchrony and thus worsen heart failure

42
Q

Define cardiac resynchronization therapy (CRT)

A

Pacemaker that simultaneously paces the RV and LV i.e. biventricular pacing –> avoid exacerbation of heart failure via ventricular dyssynchrony seen in right sided pacing alone

43
Q

Outline the main role of implantable cardioverter defibrillators (ICDs)

A

ICDs are given in selected patients for primary and secondary prevention of sudden cardiac death (SCD)

44
Q

Outline the NBG code for pacing

A 
0 = none
A = atrium
V = ventricle
D = dual (A+V)
T = triggered
I = inhibited
D = dual (T+I)
R = rate modulation
I --> chamber(s) paced (0, A, V, D)
II --> chamber(s) sensed (0, A, V, D)
III --> response to sensing (0, T, I, D)
IV --> rate modulation (0, R)
V --> multisite pacing (0, A, V, D) [really only used in CRT]
45
Q

Explain VVI/VVIR

A

ventricle sensed, ventricle paced, pacemaker inhibited in response to sensed beat

1) VVI/VVIR is a form of single chamber pacing in the RV
2) Most commonly used pacing mode
3) Protects against ventricular bradyarrhythmias w/a single lead
4) Causes ventricular dyssynchrony inducing pacemaker syndrome

46
Q

Explain AAI/AAIR

A

atrium sensed, atrium paced, pacemaker inhibited in response to sensed beat

1) AAI/AAIR is a form of singe chamber pacing in the RA
2) For cases with SA node dysfunction but normal AV node
3) Patients should have retained ability to accelerate HR upon exertion for AAI otherwise AAIR is needed
4) No protection against ventricular bradyarrhythmias
5) Due to this downfall AAI/AAIR is rarely used

47
Q

Explain DDD/DDDR

A

A+V sensed, A+V paced, pacemaker triggered and inhibited depending on sensed beats

1) Normal sinus rhythm = pacemaker inhibited if
1. SA rate faster than pacemaker rate
2. AV conduction faster than pacemaker AV interval
2) Atrial pacing if
1. SA rate slower than pacemaker rate
2. AV conduction faster than pacemaker AV interval
3) AV sequential pacing if
1. SA rate slower than pacemaker rate
2. AV conduction slower than pacemaker AV interval
4) Atrial sensing and ventricular pacing
1. SA rate faster than pacemaker rate
2. AV conduction slower than pacemaker AV interval

48
Q

Outline the benefits of physiologic pacing (AAI or DDD) versus VVI

A

1) Reduced incidence of atrial fibrillation
2) Reduced incidence of thromboembolisms
3) Avoid pacemaker syndrome caused by
1. AV dyssyncrhony
2. retrograde ventricular to atrial conduction

49
Q

List indications and contraindications for VVI

A

VVI Indications
1) Atrial fibrillation w/symptomatic bradycardia in chronotropically competent patient

VVI Contraindications

1) Hx pacemaker syndrome
2) Hx hemodynamic deterioration w/ventricular pacing
3) Chronotropic incompetent requiring rate response
4) Hemodynamic need for dual chamber pacing

50
Q

List indications and contraindications for VVIR

A

VVIR Indications
1) Fixed atrial arrhythmias with symptomatic bradycardia in chronotropically incompetent patient

VVIR Contraindications [same as VVI]

1) Hx pacemaker syndrome
2) Hx hemodynamic deterioration w/ventricular pacing
3) Chronotropic incompetent requiring rate response
4) Hemodynamic need for dual chamber pacing

51
Q

List indications and contraindications for AAI

A

AAI Indications

1) Sinus node dysfunction with symptomatic bradycardia in otherwise chronotropically competent patient
2) AV conduction must be proven normal

AAI Contraindications

1) AV conduction block
2) Inadequate atrial sensing

52
Q

List indications and contraindications for AAIR

A

AAIR Indications

1) Sinus node dysfunction with symptomatic bradycardia in otherwise chronotropically incompetent patient
2) AV conduction must be proven normal

AAI Contraindications [same as AAIR]

1) AV conduction block
2) Inadequate atrial sensing

53
Q

Outline the difference between DDD pacing and CRT

A

DDD pacing involves only 2 leads 1 in the RA and 1 in the RV, there remains the issue of ventricular dyssynchrony which impairs ventricular pump function worsening heart failure

CRT involves placement of 3 leads 1 in RA, 1 in RV, and 1 more in the coronary sinus aiming to pace the lateral wall of the left ventricle –> enables synchronized left ventricular contraction improving ventricular pump function thus avoiding exacerbation of heart failure

54
Q

List the benefits of CRT in heart failure

A

1) Improves exercise tolerance
2) Improves NYHA functional class
3) Reduces mortality
4) Reduces hospitalization rates for patients in sinus rhythm

55
Q

List indications for CRT

A

1) prolonged QRS ≥150ms but NOT QRS ≥120-149ms as there may be potential harm for CRT for QRS duration 120-149ms
2) LVEF ≤35% + sinus rhythm
3) NYHA 3
4) NYHA 4 + optimal medical therapy + non-LBBB pattern
5) Anticipated significant ventricular pacing (>40% of the time)
6) AF undergoing AV node ablation

56
Q

Define pacemaker syndrome

A

1) Occurs in VVI due to AV dyssychrony
2) RA and RV contract simultaneously meaning atrium contracts against closed atrioventricular valves –> produces cannon A waves

Signs and symptoms of pacemaker syndrome

1) SOB
2) Dizziness
3) Complaints of neck engorgement
4) Cannon A waves

1 - Cardiology (4 decks)

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