Heart Failure Flashcards
Difference between physiologic vs. pathologic hypertrophy
- 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
What physiologic changes lead to cardiac hypertrophy
- pressure overload (HTN, aortic stenosis)
- volume overload (septal defects, valve regurgitation)
- loss of contractile mass (MI)
What is the law of La Place
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
Different forms of remodelling
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
What other changes occur due to hypertrophy
- ion channels (SR Ca ATPase)
- endocrine function (ANP/BNP expression)
- cardiac receptors (NE/EPI)
- contractile proteins (B-MHC)
- energy metabolism (glycolysis, FA oxidation)
Different forms of stenosis and their causes
Mitral - post-inflammatory scarring (rheumatic heart disease), calcification of the mitral valve annulus
Aortic - same as above and congenital bicuspid aortic valve
Different types of regurgitation and their causes
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)
Which valvular diseases are more likely to cause concentric vs eccentric remodelling?
- aortic stenosis - concentric
- aortic regurgitation - bit of both
- mitral regurgitation - eccentric
Calcific Aortic Stenosis
- sx
- 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
Aortic vs. Mitral Regurgitation
- sx
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
what are some tools/ measurements for people with heart problems
- 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
Nutrition goals for Heart Failure
- sodium
- fluid restriction
- protein
- calories
- supplements
- 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
Is BMI a good measurement for heart failure risk?
- 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
What occurs during the isovolumetric contraction/ relaxation periods?
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
What is the definition of systole? What are S1 and S2?
- 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
What causes S3 and S4? Ejection click? Opening snap?
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
What can cause an increase in S2 splitting?
- it will increase on inspiration
What is the definition of stroke volume/ ejection time?
- the time between the MX opening and the MV closing
What measurement approximates preload?
- LVEDV
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?
- 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
What are signs of mitral regurgitation?
- 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
What are signs of aortic regurgitation? Signs of it being more severe and chronic? Differences from aortic stenosis?
- 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
Mitral Stenosis
- pathophysiology
- etiology
- signs of severity
- 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
What happens if valvular heart disease is acute? (Regurgitation)
- 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
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)
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)
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
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
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!
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
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%
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
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)
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
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
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)
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
Common investigations for heart failure
- CXR, ECG
- CBC, lytes, renal, thyroid
- BNP and echo if likely
Chemotherapy effects in heart failure
- malignancy, radiation, and chemotherapy can all lead to pericardial effusion/ cardiomyopathy
What does a pansystolic murmur indicate?
- regurgitant flow across the mitral valve inn advanced insufficiency
- best heard at the apical region
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
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)
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
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
Non-pharmacological treatment for heart failure
- supplemental O2/ assisted ventilation
- seated posture
- diet and exercise
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
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
HFrEF
- quadruple standard therapy?
- LVEF under or equal to 40% with symptoms
- ARNI/ACEI/ARB
- ACEi/ARB only targets RAAS
- ARNIs (entresto) inhibit RAAS and increase the NP system by inhibiting neprilysin - B-blockers
- metoprolol, bisoprolol, cardevilol
- dose-related increase in LVEF, may see deterioration before improvement - MRA
- spironolactone, eplerenone
- give if NYHA II-IV, LVEF under 30%, hospitalized
- watch K and Cr while on the drug - 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)
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
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)
Vericiguat
- give if recent HF hospitalization
- SGC stimulator, smooth muscle relaxation, increased NO
Hydralazine-Nitrates
- give if black and on optimal GDMT, cannot tolerate ACEi
Digoxin
- give if suboptimal rate control for afib and on optimal GDMT
What are ECG signs that have a worse prognosis for HF?
- tachy/brady arrythmias
- a fib
- axis deviation
- atrial enlargement
- PVCs, wide QRS complex
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)
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
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
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
What should you suspect if there are conduction abnormalities early on in HF?
- infiltration (sarcoidosis), genetic cardiomyopathies (LBBB is most common)
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
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
Percutaneous Valve Interventions
TAVI/TAVR - transcatheter aortic valve implant or replacement
TMVR - transcatheter mitral valve repair
Signs of Cardiogenic Shock
- marked and persistent hypotension (SBP under 90 for 30 minutes)
- reduction in CO
- elevated PCWP (LVEDP) >18
- elevated SVR
Advanced HF invasive assessment
- arterial line (PaO2)
- central venous line (pulmonary artery) - mixed venous O2, RAP –> RVP –> PAP –> PCWP
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
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
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
