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Med School > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Difference between physiologic vs. pathologic hypertrophy

A
  • physiologic is caused by things such as exercise and pregnancy, and involves myocytes and vasculature
  • pathologic is caused by things such as HTN/MI/ valve disease, and involves the interstitial and vasculature
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2
Q

What physiologic changes lead to cardiac hypertrophy

A
  • pressure overload (HTN, aortic stenosis)
  • volume overload (septal defects, valve regurgitation)
  • loss of contractile mass (MI)
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3
Q

What is the law of La Place

A

wall tension/ stress = (pressure x radius)/ (2x thickness)
- more tension = hypertrophy = more thickness = more tension etc.
- basically a way to approximate afterload or the energy needed to pull cardiac muscle fibres together

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4
Q

Different forms of remodelling

A

concentric - relative wall thickness increases and diameter stays the same, due to pressure overload
- parallel replication of sarcomeres
- myocytes increase in total cross-sectional area
- increased peak systolic stress

eccentric - relative wall thickness decreases and diameter expands, due to volume overload
- series replication of sarcomeres
- myocytes increase in both length and cross-sectional area
- increased end diastolic stress

*these are initially adaptive but eventually become harmful

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5
Q

What other changes occur due to hypertrophy

A
  • ion channels (SR Ca ATPase)
  • endocrine function (ANP/BNP expression)
  • cardiac receptors (NE/EPI)
  • contractile proteins (B-MHC)
  • energy metabolism (glycolysis, FA oxidation)
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6
Q

Different forms of stenosis and their causes

A

Mitral - post-inflammatory scarring (rheumatic heart disease), calcification of the mitral valve annulus

Aortic - same as above and congenital bicuspid aortic valve

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7
Q

Different types of regurgitation and their causes

A

Mitral
- leaflet or commissures (rheumatic, endocarditis, prolapse)
- tensor apparatus (papillary muscle dysfunction, rupture of papillary muscle or chordae)
- LV cavity/ annulus (LV enlargement, calcification)

  • Aortic
  • valve cusps (rheumatic, endocarditis)
  • aortic disease (inflammatory i.e. syphilis, ankylosing spondylitis, RA, Marfan’s, degeneration)
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8
Q

Which valvular diseases are more likely to cause concentric vs eccentric remodelling?

A
  • aortic stenosis - concentric
  • aortic regurgitation - bit of both
  • mitral regurgitation - eccentric
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9
Q

Calcific Aortic Stenosis
- sx

A
  • progressive outflow obstruction leads to increased pressure gradient across the valve (increased afterload)
  • angina, syncope, heart failure, sudden death
  • onset of symptoms points to a poor prognosis
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10
Q

Aortic vs. Mitral Regurgitation
- sx

A

Aortic Regurgitation
- typically a long asx period. The severity of symptoms does not indicate the degree of impairment
- progressive LV dysfunction leading to heart failure, arrythmias, angina, sudden death

Mitral Regurgitation
- can have a long asx period
- progressive LV dysfunction leading to palpitations (a.fib due to LA dilation), dyspnea/orthopnea/ PND, heart failure

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11
Q

what are some tools/ measurements for people with heart problems

A
  • anthropometrics - dry weight, usual body weight, % change in body weight, waist circumference, duration of weight change, etc.
  • subjective global assessment - nutrition assessment tool based on history and physical
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12
Q

Nutrition goals for Heart Failure
- sodium
- fluid restriction
- protein
- calories
- supplements

A
  • Na around 2-3g
  • fluid restriction should be individualized, but around under 2L a day (1.5 is too much)
  • high protein (over 1.4g/kg)
  • 30-35 kcal/kg
  • thiamine (B1) can help LVEF, Mg over 1mmol improves outcomes, iron if ferritin and TSAT low improves functional capacity

*DASH and Mediterranean diet often best
*want small frequent meals and snack, supplements
* malnutrition and cachexia can occur in 50% of people with CHF and can be masked by edema and fat

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13
Q

Is BMI a good measurement for heart failure risk?

A
  • obesity increases risk of HF, but there is actually better survival rates with a higher BMI
  • doesn’t indicate fat vs. lean mass
  • waist circumference, exercise tolerance, etc. are better markers
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14
Q

What occurs during the isovolumetric contraction/ relaxation periods?

A

Isovolumetric contraction - time between the mitral valve closing and the aortic valve opening, LVP increases
- c wave occurs - mitral valve bulges into the atria

Isovolumetric relaxation - time between the aortic valve closing and the mitral valve opening, LVP decreases
- dicrotic notch occurs

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15
Q

What is the definition of systole? What are S1 and S2?

A
  • time between the mitral (and tricuspid) valve closing (S1) and the AV (and pulmonary) valve closing (S2)

*the left sided heart valves close first because they are under higher pressure, and the R heart is low resistance due to pulmonary circulation

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16
Q

What causes S3 and S4? Ejection click? Opening snap?

A

S3 - occurs in early diastole, due to a volume overloaded ventricle

S4 - occurs in late diastole, due to a pressure overloaded ventricle

Ejection click - abnormal opening of semilunar valve (i.e. bicuspid aorta)

Opening snap - rheumatic mitral valve stenosis

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17
Q

What can cause an increase in S2 splitting?

A
  • it will increase on inspiration
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18
Q

What is the definition of stroke volume/ ejection time?

A
  • the time between the MX opening and the MV closing
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19
Q

What measurement approximates preload?

A
  • LVEDV
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20
Q

What are signs of WORSE valvular aortic stenosis? What does the resulting concentric hypertrophy result in?
What is the well anticipated mortality curve of aortic stenosis?

A
  • later peak in murmur and carotid pulse, softer 2nd heart sound indicates worse stenosis
  • impaired systolic function, decreased cavity size, decreased ventricular compliance, decreased stroke volume, increased myocardial workload
  • onset of angina = 5y
  • onset of syncope = 3y
  • onset of heart failure = 2y
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21
Q

What are signs of mitral regurgitation?

A
  • increase in the V wave and blunting of the C wave
  • holosystolic murmur that goes beyond S2
  • the resulting eccentric hypertrophy results in impaired systolic function, decreased ventricular compliance, decreased stroke volume, increased myocardial workload
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22
Q

What are signs of aortic regurgitation? Signs of it being more severe and chronic? Differences from aortic stenosis?

A
  • loss of dicrotic notch, high pulse pressure (diff between S/D pressures)
  • diastolic murmur
  • greater pulse pressure (bounding) and louder and longer diastolic murmur indicates it is more severe and chronic
  • tends to compensate better than aortic stenosis, as excess preload is the initial predominant feature instead of only excess afterload
  • however, does have all the same consequences
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23
Q

Mitral Stenosis
- pathophysiology
- etiology
- signs of severity

A
  • spares the LV but has effects on the RV (most common cause of RV dysfunction is left heart disease!)
  • increased LA pressure is transmitted to the RV via pulmonary vasculature and results in increased RV afterload
  • thus, see LA dilation and RV hypertrophy
  • classic etiology is rheumatic heart disease
  • louder and longer diastolic “rumble” indicates it is more severe
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24
Q

What happens if valvular heart disease is acute? (Regurgitation)

A
  • there will be a lack of eccentric hypertrophy to compensate for the sudden increase in volume
  • dramatic hemodynamic effects that can lead to shock, death
  • Acute mitral regurgitation - pulmonary edema and shock, soft and short holosystolic murmur
  • Acute aortic regurgitation - same as above
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25
Q

ECG findings for LV hypertrophy

A
  • increase in impulse amplitude, which is seen as an increase in (+) deflection by L sided leads and an increase in (-) deflection by R sided leads
  • R waves taller than normal in V5/6
  • S waves deeper than normal in V1/2
  • sum of the S wave in V1 and R wave in either V5/6 greater than 35mm OR R wave in aVL greater than 11mm
  • may also see ST depression, T inversion in I, avL, V4-6 (signs of LV strain)
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26
Q

ECG findings for RV hypertrophy

A
  • increase in impulse amplitude, which is seen as an increase in (+) deflection by R sided leads and an increase in (-) deflection by L sided leads
  • R waves taller than normal in V1/2
  • S waves deeper than normal in V5/6
  • predominant R wave in V1 over 7mm
  • R wave may get progressively smaller from V2-V4
  • may also see R axis deviation, ST depression, T inversion in V1-V3 (signs of RV strain)
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27
Q

ECG findings for LA enlargement

A
  • want to look at P waves in leads II (points away from SA node), avR (points at the SA node), and V1 (R sided)
  • will see large and prolonged deflection (goes down more and over 40msec) of the P wave in V1
  • will see large and prolonged deflection (notched double peak and over 120msec) of the P wave in lead II
28
Q

ECG findings for RA enlargement

A
  • want to look at P waves in leads II (points away from SA node), avR (points at the SA node), and V1 (R sided)
  • will see large and prolonged deflection (goes up more than 1.5mm and over 40msec) of the P wave in V1
  • will see large and prolonged deflection (much taller, more than 2.5mm) of the P wave in lead II
29
Q

Common symptoms of heart failure

A
  • signs and symptoms of decreased cardiac output and/or volume overload
  • decreased CO - decreased tissue perfusion aka cool extremities, fatigue, decreased exercise capacity, confusion
  • hypotension, tachycardia, mottled skin, narrow pulse pressure, pulses alternates
  • volume overload - edema, dyspnea, orthopnea, PND, nocturnal cough, angina, bloating
  • increased JVP, S3+S4, ascites, hepatosplenomegaly, crackles and rales, pleural effusion
  • idk - early satiety
  • heart failure is a clinical diagnosis!
30
Q

Systolic vs diastolic heart failure and causes

A

Systolic - decreased CO, increased venous pressures, usually associated with impaired LV systolic function
- ischemic heart disease (MI) can decrease contractility
- dilated cardiomyopathy can decrease contractility
- valve regurgitation (eccentric) can decrease contractility

Diastolic - decreased LVEDV/SV, increased venous pressures, sometimes decreased CO, can be associated with preserved or decreased LV function
- chronic HTN/ aortic stenosis/ hypertrophic cardiomyopathy (concentric) can lead to less filling
- restrictive cardiomyopathy (radiation, sarcoidosis, hemochromatosis) can lead to less filling

  • often co-exist together
31
Q

What is considered a reduced EF? Preserved EF? An improved EF?

A
  • Reduced - under or equal to 40%
  • Preserved - over or equal to 50%, increased BNP, either structural changes or diastolic dysfunction
  • Improved - baseline of equal/under 40% and then at least 10% improvement that must be over 40%
32
Q

NYHA classification (symptom classification)

A

Class I - no sx or limitations, 95%+ 1 year survival

Class II - mild symptoms and limitations with ordinary activity, 80-90% 1 year survival

Class III - marked limitations and symptoms with less than ordinary activity, only comfortable at rest, 55-65% 1 year survival

Class IV - severe limitations and symptoms even at rest, bed bound, 5-15% 1 year survival

33
Q

ACC/ AHA Stages (disease classification)

A

A - high risk of developing the disease but no symptoms
B - no symptoms but structural disease (NYHA I)
C - past or current symptoms, structural disease
D - refractory, may need advanced Tx (NYHA IV)

34
Q

Frank -Starling Curve
What do you see in systolic vs diastolic failure?

A
  • x axis is LVEDP, y axis is SV
  • too low SV results in hypotension
  • too much LVEDP results in pulmonary congestion

Systolic - decreased contractility, decreased ESPVR slope
Diastolic - decreased compliance and LV filling, any increase in volume will shift EDPVR higher

35
Q

Activation of RAAS in Heart Failure

A
  • activated due to impaired renal perfusion
  • Na and water retention leads to ventricular dilation, venous congestion, renal edema (decreased CO)
  • vasoncstriction (ang II) results in increase afterload and SVR leading to decreased SV and CO (diastolic dysfunction)
  • myocardial fibrosis
36
Q

Activation of SNS in heart failure

A
  • increased HR leads to risk of arrythmias and death
  • increased contractility can lead to cardiomyopathy/ apoptosis (b-receptor down regulation)
  • vasoconstriction increases afterload and thus decreases SV and CO (diastolic dysfunction)
37
Q

Release of natriuretic peptides in heart failure

A
  • due to increased intra-cardiac filling pressures and thus atrial and ventricular distension
  • a good thing!
  • decrease arterial pressure by lowering BP and SVR
  • promote natriuresis, increase GFR, inhibit renin, decrease ang II and aldosterone, vasodilator, lower SNS, lower fibrosis, lower hypertrophy
38
Q

Common investigations for heart failure

A
  • CXR, ECG
  • CBC, lytes, renal, thyroid
  • BNP and echo if likely
39
Q

Chemotherapy effects in heart failure

A
  • malignancy, radiation, and chemotherapy can all lead to pericardial effusion/ cardiomyopathy
40
Q

What does a pansystolic murmur indicate?

A
  • regurgitant flow across the mitral valve inn advanced insufficiency
  • best heard at the apical region
41
Q

Signs and sx of an aortic dissection
- dx
- management
- complications

A
  • difference in blood pressure between L and R arm
  • diaphoresis, nausea
  • diffusion of pain to interscapular area
  • confirm with CXR/CT/echo/MRI
  • manage - decrease pain, decrease BP and contractility with B-blockers and sodium nitroprusside, surgery
  • rupture (tamponade, hemothroax, hemomediastinum)
  • occlusion of aortic branches (carotid - stroke,
    coronary - MI, renal - renal failure, visceral - organ infarct)
  • distortion of aortic annulus (aortic valve insufficiency)
  • confusion, agitation, extreme hypotension, quiet heart sounds and sudden death all suggest the dissection has progressed to a tamponade
42
Q

Factors that predispose to endocarditis

A
  • cardiac lesions (valve disease, prosthetics, previous endocarditis, hypertrophic obstruction)
  • immunocompromised or bacteremia more likely (diabetes, IV drug use, alcohol and cirrhosis, colon cancer)
43
Q

ADHF (Acute decompensated heart failure)

A
  • dyspnea, rapid accumulation of fluid in lung interstitial and alveolar spaces
  • hypoxemia, orthopnea, tachypnea, tachycardia
  • can be hyper or hypotensive (hypo suggests cardiogenic shock)
  • most commonly due to LV dysfxn with or without cardiac pathology
44
Q

Pharmacological treatment options for heart failure

A
  • Diuretics - loop diuretics (IV Lasix)
  • sx relief, decreased central venous and cap wedge pressure
  • use lowest dose possible once cleared up
  • Vasodilators - nitroglycerine/ nitroprusside
  • decreases preload via venodilation, lowers SVR and increases CO
  • ONLY give if normal-high BP
  • Inotropes - dobutamine (B-receptor agonist), milrinone (PDE3 inhibitor)
  • increase contractility, CO, SV
  • use if severe or refractory LV dysfxn/ low BP
  • can cause hypotension and arrythmias
  • Morphine - decrease anxiety, work of breathing, SNS, cardiac filling pressures, increases vessel dilation
  • HOWEVER higher mortality rate due to respiratory depression and hypotension
45
Q

Non-pharmacological treatment for heart failure

A
  • supplemental O2/ assisted ventilation
  • seated posture
  • diet and exercise
46
Q

Surgical treatment for heart failure
- Intra-aortic balloon pump
- Impella
- ECMO
- LV assist device

  • S/E and contraindications
A
  • intra-aortic balloon pump - inflates early diastole (positive pressure increases coronary filling), deflates end diastole/systole (negative pressure decreases afterload)
  • use post MI, decompensated HF, CV surgery
  • can lead to bleeds, thromboembolism, infection, vascular injury
  • lowest level of evidence
  • Impella - hook device in LV, direct ventricular decompression
  • can lead to bleeds, limb ischemia, LV perforation, V arrythmias, need anticoagulation
  • cannot give if LV thrombus, mechanical AV, severe PAD
  • ECMO (extracorporeal membran oxygenation) - better outcomes
  • use if acute Mi with shock, decompensated HF, eCPR, post-pericardiotomy
  • can lead to bleeds, infection, limb ischemia
  • Ventricular assist devices - supplement CO, 3rd gen are magnetic centrifugal pumps
  • use if bridging to transplant, possibility of recovery, NYHA III/IV, primarily HFrEF
  • can lead to thromboembolism , bleeds, infection, renal failure, RV failure, hemolysis
  • cannot give if over 80, psychosocial instability, irreversible comorbidities, morbid obesity, active infection, malnourished, increase RA pressure
47
Q

HFpEF
- tx

A
  • symptomatic despite normal LV systolic function
  • high morbidity but lower mortality
  • mostly an issue with low diastolic filling, increased LVEDP, pulmonary congestion
  • no evidence that drugs decrease risk of mortality
  • If volume overloaded, diuretics first
  • Primary therapy if NYHA II-III with increased BNP - SGLT2 inhibitor and MRA after 2 weeks
  • Secondary therapies - consider ARNI if persistent, B-blockers, Ca-blockers
48
Q

HFrEF
- quadruple standard therapy?

A
  • LVEF under or equal to 40% with symptoms
  1. ARNI/ACEI/ARB
    - ACEi/ARB only targets RAAS
    - ARNIs (entresto) inhibit RAAS and increase the NP system by inhibiting neprilysin
  2. B-blockers
    - metoprolol, bisoprolol, cardevilol
    - dose-related increase in LVEF, may see deterioration before improvement
  3. MRA
    - spironolactone, eplerenone
    - give if NYHA II-IV, LVEF under 30%, hospitalized
    - watch K and Cr while on the drug
  4. SGLT2 inhibitor
    - empagliflozin
    - decrease plasma glucose by blocking tubular reabsorption, osmotic diuresis
    - use especially if DM, artheroslcerosis
    - caution when using with ARNIs (both promote diuresis)
49
Q

Contraindications of ACEis/ ARNIs, B-blockers

A
  • ARNI: systolic BP <100, severe renal impairment, hyperkalemia
  • ACEi: severe renal impairment (over 30% increase in Cr), hyperkalemia
  • BB: symptomatic hypotension, bradycardia, significant AV block, severe asthma
50
Q

Ivrabradine

A
  • give if HR over 70, sinus rhythm, GFR over 15
  • blocks the sinus node, decreases HR with no effect on BP or contractility
  • cannot use if afib, SA node dysfxn, use fo CYP3A4 inhibitors (macrolide ABX)
51
Q

Vericiguat

A
  • give if recent HF hospitalization
  • SGC stimulator, smooth muscle relaxation, increased NO
52
Q

Hydralazine-Nitrates

A
  • give if black and on optimal GDMT, cannot tolerate ACEi
53
Q

Digoxin

A
  • give if suboptimal rate control for afib and on optimal GDMT
54
Q

What are ECG signs that have a worse prognosis for HF?

A
  • tachy/brady arrythmias
  • a fib
  • axis deviation
  • atrial enlargement
  • PVCs, wide QRS complex
55
Q

Sudden Cardiac Death
- most common cause
- risk factors

A
  • occurs within 1 hour of the onset of cardiac symptoms
  • asystole/ pulseless electrical activity - primary arrythmia, HF, valve failure
  • VTach (due to scar re-entry)/ fibrillation - primary arrythmia, secondary to MI/drugs/surgery
  • 75% is CAD, next most common is cardiomyopathies
  • now commonly occurs long after discharge
  • risk factors: scars (MIs, cardiomyoptahy), autonomic abnormalities (DM, severe HF, renal failure), repolarization abnormalities (diffuse fibrosis, BBB, ischemia)
56
Q

Effect of CHF Tx on sudden cardiac death

A
  • general tx of CHF/ CAD only has a moderate impact on SCD
  • anti-arrythmic meds (amiodarone) have minimal impact on SCD
  • amiodarone may actually increase non-sudden death, and Na blockers can increase SCD
57
Q

ICD (implanted cardioverter-defibrillator)
- what does it do?
- who should get one?
- who should get a subcutaneous one?
- who should not get one?
- risks?

A
  • has full pacemaker abilities (can treat bradycardia)
  • defibrillation terminates refractory VT and VF
  • give if LVEF under 30% or 31-35% with ischemia
  • give if previous cardiac arrest from VF or VT
  • subcutaneous ICDs only defibrillate, better for younger patients with structurally normal hearts, or people with previous infection/ failure, no need for pacing, no vascular access
  • no benefit is life expectancy is under 1 year or do not wish to be resusscitated
  • infection, tamponade, pneumothorax, inappropriate shocks, lead fracture or failure, battery malfunction
58
Q

When (timing) should an ICD be implanted?

A
  • must be implanted after 48 hours if post MI and secondary prevention
  • must be implanted after 4 days if post MI and primary prevention
  • must be implanted after 3 months after stent/surgery
59
Q

What should you suspect if there are conduction abnormalities early on in HF?

A
  • infiltration (sarcoidosis), genetic cardiomyopathies (LBBB is most common)
60
Q

Atrioventricular dyssynchrony vs. intraventricular

A

AV
- if not enough time for A to contract, HR too fast, treat by slowing HR w meds
- if too much time between A and V contraction, passive leak back into A, treat with pacemaker

Intraventricular
- contraction of the lateral wall is delayed compared to the septum, leads to negative remodelling
- LBBB is a good marker of this - wider QRS means more dyssynchrony

61
Q

Treatments for dyssynchrony

A

Standard dual chamber pacemaker
- only fixes AV dyssynchrony

Pacing simultaneously from RV apex and LV lateral wall
- re-coordinates LV contraction

CRT implant
- standard pacing lead in RA, standard pacing lead/ ICD lead in RV apex, LV lead inserted into branch of the coronary sinus
- can be CRT pacemaker alone or with ICD (CRT-D) to treat VF/VT (done if below criteria met)
- best if LVEF under 45% despite meds, LBBB»>RBBB with QRS over 130, dilated non-ischemic CMO, or non LBBB with QRS over 150

ICD
- see other card

62
Q

Percutaneous Valve Interventions

A

TAVI/TAVR - transcatheter aortic valve implant or replacement

TMVR - transcatheter mitral valve repair

63
Q

Signs of Cardiogenic Shock

A
  • marked and persistent hypotension (SBP under 90 for 30 minutes)
  • reduction in CO
  • elevated PCWP (LVEDP) >18
  • elevated SVR
64
Q

Advanced HF invasive assessment

A
  • arterial line (PaO2)
  • central venous line (pulmonary artery) - mixed venous O2, RAP –> RVP –> PAP –> PCWP
65
Q

Mechanisms of organ dysfunction in HF

A
  • congestion - increased filling pressures, redistribution from venous capacitance beds to central venous system
  • organ hypoperfusion - decreased CO, tissue hypoxia, cell death
66
Q

Heart Transplant
- who should get one?
- donor criteria
- immunosuppression
- S/E

A
  • if ACC stage D/ NYHA III/IV, refractory shock/ arrythmias/ angina
  • recipients selected with MOCA, infections, ABO/HLA, absence of irreversible pHTN and malignancy
  • donor criteria - under 55, normal ECG/ echo/angio, no history of CV disease
  • prednisone/ATG to induce
  • calcineurin inhibitors (cyclosporin, tacrolimus) to block T cells
  • antiproliferatives (azathioprine)
  • SE: rejection (graft failure is #1), infection, hypertension, DM, renal disease, malignancy
67
Q

Palliative Care in HF

A
  • survival of HF is similar to malignancy, but less likely to receive palliative care and more likely to die in hospital
  • PCI/TAVI/LVAD/transplant are all considered palliative
  • ICD deactivation is rarely discussed and many people are admitted to hospice with their’s still active
  • SOB, depression, insomnia, confusion, pain are common sx of HF
  • may give opioids if severe dyspnea/ pain (hydromorphone, midazolam, nozinan)
  • early palliative care may increase survival

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