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
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)
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
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
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)
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
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)
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
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
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
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
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
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
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
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
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
17
Q
What can cause an increase in S2 splitting?
A
- it will increase on inspiration
18
Q
What is the definition of stroke volume/ ejection time?
A
- the time between the MX opening and the MV closing
19
Q
What measurement approximates preload?
A
- LVEDV
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
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
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
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
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
25
ECG findings for LV hypertrophy
- 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)
26
ECG findings for RV hypertrophy
- 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)
27
ECG findings for LA enlargement
- 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
ECG findings for RA enlargement
- 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
Common symptoms of heart failure
- 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
Systolic vs diastolic heart failure and causes
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
What is considered a reduced EF? Preserved EF? An improved EF?
- 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
NYHA classification (symptom classification)
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
ACC/ AHA Stages (disease classification)
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
Frank -Starling Curve
What do you see in systolic vs diastolic failure?
- 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
Activation of RAAS in Heart Failure
- 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
Activation of SNS in heart failure
- 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
Release of natriuretic peptides in heart failure
- 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
Common investigations for heart failure
- CXR, ECG
- CBC, lytes, renal, thyroid
- BNP and echo if likely
39
Chemotherapy effects in heart failure
- malignancy, radiation, and chemotherapy can all lead to pericardial effusion/ cardiomyopathy
40
What does a pansystolic murmur indicate?
- regurgitant flow across the mitral valve inn advanced insufficiency
- best heard at the apical region
41
Signs and sx of an aortic dissection
- dx
- management
- complications
- 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
Factors that predispose to endocarditis
- cardiac lesions (valve disease, prosthetics, previous endocarditis, hypertrophic obstruction)
- immunocompromised or bacteremia more likely (diabetes, IV drug use, alcohol and cirrhosis, colon cancer)
43
ADHF (Acute decompensated heart failure)
- 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
Pharmacological treatment options for heart failure
- 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
Non-pharmacological treatment for heart failure
- supplemental O2/ assisted ventilation
- seated posture
- diet and exercise
46
Surgical treatment for heart failure
- Intra-aortic balloon pump
- Impella
- ECMO
- LV assist device
- S/E and contraindications
- 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
HFpEF
- tx
- 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
HFrEF
- quadruple standard therapy?
- 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
Contraindications of ACEis/ ARNIs, B-blockers
- 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
Ivrabradine
- 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
Vericiguat
- give if recent HF hospitalization
- SGC stimulator, smooth muscle relaxation, increased NO
52
Hydralazine-Nitrates
- give if black and on optimal GDMT, cannot tolerate ACEi
53
Digoxin
- give if suboptimal rate control for afib and on optimal GDMT
54
What are ECG signs that have a worse prognosis for HF?
- tachy/brady arrythmias
- a fib
- axis deviation
- atrial enlargement
- PVCs, wide QRS complex
55
Sudden Cardiac Death
- most common cause
- risk factors
- 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
Effect of CHF Tx on sudden cardiac death
- 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
ICD (implanted cardioverter-defibrillator)
- what does it do?
- who should get one?
- who should get a subcutaneous one?
- who should not get one?
- risks?
- 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
When (timing) should an ICD be implanted?
- 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
What should you suspect if there are conduction abnormalities early on in HF?
- infiltration (sarcoidosis), genetic cardiomyopathies (LBBB is most common)
60
Atrioventricular dyssynchrony vs. intraventricular
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
Treatments for dyssynchrony
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
Percutaneous Valve Interventions
TAVI/TAVR - transcatheter aortic valve implant or replacement
TMVR - transcatheter mitral valve repair
63
Signs of Cardiogenic Shock
- marked and persistent hypotension (SBP under 90 for 30 minutes)
- reduction in CO
- elevated PCWP (LVEDP) >18
- elevated SVR
64
Advanced HF invasive assessment
- arterial line (PaO2)
- central venous line (pulmonary artery) - mixed venous O2, RAP --> RVP --> PAP --> PCWP
65
Mechanisms of organ dysfunction in HF
- congestion - increased filling pressures, redistribution from venous capacitance beds to central venous system
- organ hypoperfusion - decreased CO, tissue hypoxia, cell death
66
Heart Transplant
- who should get one?
- donor criteria
- immunosuppression
- S/E
- 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
Palliative Care in HF
- 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
