Lecture 15-18 Heart Failure Flashcards
What is heart failure
Complex clinical syndrome
Any structural or functional disorder that impairs ventricular filling or ejection of blood
Results in decrease cardiac output
Most common cause of mortality rate in HF
Progressive pump failure
Sudden cardiac death
Pathophysiology in heart failure
Myocardial dysfunction: left ventricular, LowSV, Low CO, Low BP
Important equation for heart failure
BP = CO x SVR
CO= Cardiac out
SVR: Systemic vascular resistance
CO = SV x HR
SV= Stroke volume (amount of blood heart pumps with every beat)
Stroke volume is affected by 3 factors
- Pre load ( end diastolic volume)
- Afterload ( resistance to LV ejection)
- Contractility (inherent strength of contraction of LV myocytes)
Definite pre load and after load
Pre load: volume of blood in the ventricles at end of diastole)
After load: pressure required to push blood into the arteries)
Define stroke volume
Volume of blood ejected by the left ventricles with each beat
(T/F) Increasing after load will increase stoke volume
False
Frank starling curve
Normal
Mild
Severe LV dysfunction
Normal- more filling, greater force
Mild- moderate LV dysfunction: more filling, no more force
Severe LV dysfunction: more filling, less force
Acute compensatory mechanisms aims to maintain:
BP and CO
risk factors for Heart failure
IHD
Hypertension
Valvular disease
Atrial fibrillation
Diabetes
Heavy alcohol or substance use
Chemotherapy or radiation therapy
Family hx of cardiomyopathy
Smoking
Hyperlipidemia
Exacerbating factors of HF
ACS
Uncontrolled hypertension
AF and other arrhythmias
Additional cardiac disease
Acute infections
Non adherence to medication regimen
Anemia
Hypo or hyperthyroidism
Medications that increase sodium retention (NSAIDS)
Medications with negative intropic effect
Medications that can cause or worsen HF
Many of them
Medications that can cause fluid retention
Medication that can decrease cardiac output
Oral meds with high sodium content
Medications with miscellaneous mechanisms of cardiotoxicity
Oncology drugs
LICORICE, NSAID (DOSE DEPENDANT)**
Natriuretic peptides in heart failure: Counter regulation
Should not be used independent of signs, symptoms and other diagnostic info
Gold standard biomarkers in HF
- B-type natriuretic peptide (BNP)
-NTproBNP (N terminal pro-hormone BNP)
Elevated plasma concentrations can be used to in:
- diagnosis
- prognosis
-risk stratification - monitor heart failure
Echocardiogram
Gives info on…..
Quality is dependent on
Size and shape of heart
Pumping capacity (ejection fraction)
Structures
Pressure estimates
Dependent on type of echocardiogram, who is conducting, reading results and patient anatomy + comorbidities
What is a normal left ventricular ejection fraction (LVEF)
Normal = 50-70%
Universally definition and classification of heart failure
Stage C
Stage D
HF (Stage C) = patient with current or prior symptoms and or/signs of HF caused by a structural and/or functional cardiac abnormality
Advanced HF (Stage D) = severe symptoms and/or signs of HF at rest, recurrent hospitalization despite GDMT, refractory or intolerant to GDMT, requiring advanced therapies transplantation, mechanical circulatory support, or palliative care
Typical features, patient profile for HFrEF
Younger male post MI
Clinical features: AF, CAD, Diabetes, hypertension,
Typical patient profile for HFpEF
Older female
Clinical features: AF, CAD, CKD, Diabetes, HTN
Signs and symptoms of right heart failure
Congestion of peripheral tissues:
- dependent edema and ascites
- liver congestions
- GI tract congestions
Signs and symptoms of left heart failure
Decreased cardiac output:
- activity intolerance and signs of decreased tissue perfusion
Pulmonary congestion:
- impaired gas exchange
- pulmonary edema
HF non pharmacological management
Restrict dietary sodium (2-3 grams/day)
Restrict fluid intake ( 2L a day)
Monitor body weight
Excercise
Alcohol
Smoking
Vaccines
Daily weights
Those prone to fluid retention or difficult to control fluid retention
More than 2 lbs in 24hrs or 5lbs in 1 week = fluid retention
Most commonly used Loop diuretics and what do they do
- Furosemide, bumetanide, ethacrynic acid
- blocks sodium potassium chloride cotransporter
Increases Na excretion
Increase K excretion
Increase Cl excretion
Diuretic, indication, considerations, Baseline
Indication: volume overload
Considerations: volume status, renal function, electrolytes, urate/gout, sulfa allergy
Baseline: volume assessment (HF symptoms,weight), labs for K,SCr,Urea
Diuretic monitoring
Symptoms
Vitals/exams
Labs
Drug intx
Symptoms: Hypervolemic, dyspnea, orthopnea, PND, hypovolemia
Vitals/exams: BP, HR, daily weights, ascites, JVP
Labs: SCr, urea, decrease in K, Mg, Ca, Na
Drug intx: digoxin toxicity if hypokalemia occurs, lithium toxicity - reduced lithium clearance
Diuretic monitoring
Caution with over-diuretics ( low cardiac output, renal perfusion, symptoms of volume depletion)
Caution with increasing serum creatinine
Symptoms improve in 1-2 hours
Symptom resolution dependent on degree of fluid retention
Diuretic monitoring
Volume depletion
Euvolemic
Volume overload
volume depletion: reduce or hold diuretic for 2-3 days
Euvolemic: consider stepwise reduction in diuretic dose or frequency
Volume overload: increase dose by 25-50% depending on prior response and scenario
Metolazone
Mechanism
Indication
Dose
Adverse effects
Thiazide like diuretic with long duration of action
Most common adjunct added in diuretic resistance, based on experience, Small RCTs and case series
Inpatient: 5-20mg/d
Outpatient: 2.5-10 daily for q2days
Adverse effects: volume depletion, renal function, hyponatremia, hypokalemia
HF pharmacotherapy
HFrEF
ACEi, ARB or ARNI
Beta blocker
MRA
SGLT2i (Flozin)
Ivabradine
Digoxin
Hydralazine-nitrate
Intravenous iron
Vericiguat
HF pharmacotherapy
HFmrEF
ACEi, ARB or ARNI
Beta blocker
MRA
SGLT2i
HF pharmacotherapy
HFpEF
ARB or ARNI
MRA?
SGLT2i( Flozin)
GLP-1RA
Before starting an ACEi/ARB/ARNI
Indication
Contraindications
Baseline
Drug intx
All patients with HFrEF
Previous angioedema, severe aortic stenosis, bilateral renal artery stenosis, pregnancy, systolic BP <90mm Hg
Serum pottasium > 5.2 mmol/l
BP,labs, cough, if on ARNI: assess fluid status
Lithium: increase in lithium levels
Increase pottasium: k sparing diuretics, potassium supplements
Entresto (Sacubitril/valsartan) doses
24mg/26mg
49mg/51mg
97mg/103mg
Converting to ARNI from ACEi and ARB
ACEi: stop ACEi, wait at least 36 hrs after last dose
ARB: stop ARB, no washout period necessary
ACEi/ARB/ARNI adverse effects and monitoring
Vitals
H&N
RESP
Renal
Vitals: hypotension, monitor BP
H&N: Angioedema, monitor for symptoms
RESP: Dry cough, monitor for symptoms
Renal: Hyperkalemia, Monitor labs K, SCr
Key counseling points in ACE/ARB/ARNI
Lightheadedness is common initially, but often improves over 1-2 weeks
Dry cough usually occurs in first few weeks, but may occur after taking ACEi for years
Before starting a beta-blocker
Indication
Absolute contraindications
Relative contraindications
Baseline
Drug intx
All patients with HFrEF
Cardiogenic shock
Decompensated heart failure
Wolff-Parkinson’s-white syndrome
1st degree Atrioventricular block
Systolic BP <100mmhg
Raynaud’s disease
Severe peripheral arterial disease
Volume assessment ) HF symptoms, weight, physical exam)
Non DHP CCB = lower HR
Digoxin + Amiodarone = Lower Heart rate
Beta blocker dosing and outpatient titrations
Initial dose
Target dose
Mean daily dose achieved in HFrEF RCT
Bisoprolol:
Initial: 1.25mg daily
Target: 10mg daily
Achieved: 8.6mg
Carvedilol:
Initial: 3.125mg
Target: 25 mg bid (<85kg), 50mg BID (>85kg)
Achieved: 37mg
Beta blocker adverse effects
Vitals
CV
RESP
ENDO
Vitals: hypotension, bradycardia
CV: fatigue, claudication, acute worsening HF
RESP: bronchspasm
ENDO: Sexual dysfunction
Key counseling points on Beta blockers
Fatigue is symptoms of both HF and Beta blockers
Start low and go slow
Do not stop beta blocker abruptly
Before starting an MRA
Indications
Contraindications
Baseline
Drug intx
Indications: All patients with HFrEF
Contraindications: eGFR <30, K>5.2 mmol/l, severe hepatic impairment
Baseline: BP, Labs: K, eGFR
Drug intx: increase digoxin levels (spironolactone), eplerenone 3A4 substrate, NSAIDS, Potassium supplements
MRA dosing and titrations
Initial dose
Target
Mean daily dose achieved in HFrEF RCT
Spironolactone:
Initial dose: 12.5-25mg daily
Target dose: 25-50mg daily
Mean daily dose: 26mg
Eplerenone
Initial dose: 12.5-25mg
Target: 50mg daily
Mean daily dose: 42.6mg
MRA adverse Effects
Vitals
Renal
ENDO
Vitals : Hypotension’s
Renal: Hyperkalemia (K > 5.5mmol/l
ENDO: gyneomastia/mastodynia erectile dysfunction
MRA key counselling points
This is not being used as a diuretic in this scenario, make sure patients know which medication is their diuretics
Warn males about gynecomastia and there is alternative if this occurs
Before starting a Flozin
Indication
Absolute contraindications
Caution
Baseline
Indication: HFrEF
Absolute contraindication: type 1 diabetes, prior diabetic ketoacidosis, chronic Limb ishcemia
Caution: using insulin/ sulfonylurea : may need to adjust. Using diuretic: assess volume status
Baseline: volume status, BP, Labs
Flozin dosing and titrations
Initial
Target dose
Mean daily dose achieved in HFrEF RCT
Dapagliflozin
Initial: 10mg daily
Target: 10mg daily
Mean daily: 9,8mg
Empafliflozin:
Initial: 10mg daily
Target: 10mg daily
Flozin adverse effect
vitals
CVS
RENAL
GU
ENDO
Vitals: Hypotension
CVS: hypovolemia
Renal: Acute eGFR
GU: genital my optic infection
ENDO: Euglycemic ketoacidosis
T/F
Flozins acutely decrease eGFR ( usually <10%)
True
ACEi/ARB/ARNI and Flozins and renal function
ACEi and ARB dilate the efferent arteriole = decreases intraglomerular pressure
Flozin may also constrict the afferent arteriole and dilate the efferent arteriole, further decreasing intraglomerular pressure
But if combined with lower afferent arteriole flow, can reduce kidney perfusion and lower eGFR
If SCr high/eGFR low >30%
1. Stop NSAID
2. Correct hypovolemia
3. Lower ACEi/ARB/ARNI/SGLT2i dose
Flozin key counseling points
Sick day management is key
Genital mycotic infections , can be prevented with good genital hygiene
HFrEF pharmacotherapy sequencing what’s the right order ??
Order determined by: Acuity, co-morbidities, ADE profile, Financial considerations, patient preference
Traditional sequence: ARNi, BB, MRA, SGLT2i
Withdrawal of HFrEF pharmacotherapy
Generally should be avoided
Most causes of HFrEF, LVEF improvement is remission, not cure
Exceptions : cardiomyopathies from reversible cause: if NYHA 1 + normal LVEF/LV volumes + control of etiology
Canadian guideline on recommendation for Digoxin
Considered in patients with HFrEF and atrial fibrillation, with poor control of ventricular rate and or persistent symptoms despite optimally tolerated beta blocker therapy, or when beta lower are not tolerated in the setting of chronic HF, new onset HF or HF hospitalization
Before starting digoxin and dosing
Indication
Absolute contraindication
Caution
Baseline
Dose
HFrEF with 1 persistent symptoms despite optimized GDMT or (2) AF with suboptimal rate control
Wolff Parkinson’s white syndrome, 2nd or 3rd degree AV block, sick sinus syndrome
K<3.5mmol/l, eGFR <30
HR,labs, (K,eGFR)
Starting: 62.5-125mcg po daily depending on renal function. Max 250mcg po daily
Digoxin safety and monitoring
Vitals
Gen
Renal
Vitals: bradycardia, monitoring EKG If HR <50
Gen : Toxicity, monitor signs and symptoms, altered level of consciousness, psychosis, visual disturbances, Hyperkalemia, Severe N/V/D
Renal: SCr, K, hypokalemia potentiates digoxin toxicity, digoxin can cause Hyperkalemia
Cardiac resynchronization therapy
Dyssynchronous ventricular contraction impairs cardiac function
Biventricular pacemaker: improves symptoms, survival, EF, and reduce hospitalization
Indications: NYHA-FC II-IV, EF <35%, QRS> 130 msec, LBBB, despite optimal medical therapy
Implantable cardioverter defibrillator (ICD)
Sudden cardiac death is a common mode of death in HF
Monitors rhythm, paces or delivers electrical shock
Indications: primary prevention - non ishemic: NYHA II-III; EF< 35% 3 mos post med optimization
HFpEF and HFmrEF pharmacotherapy bottom line for guidelines and evidence
The 3 major HF guidelines differ in their recommendations for HFpEF and HFmrEF
HFpEF: only SGLT2i clearly reduce HF hospitalizations, but dont reduce death
HFmrEF: SGLT2i and MRA reduce HF hospitilizations, ARBs less likely reduce Hospitilizations, role of ARNI and beta blockers, nothing seems to reduce death
All patients with HFrEF unless contraindicated should be on…
ARNI,ACEi,ARB
Beta blocker
MRA
Flozin
What are the S&S of HF?
Right HF: congestion of peripheral tissues ⇒⇒⇒ dependent edema and ascites, GI tract congestion ⇒ anorexia, GI distress, weight loss
liver congestion ⇒ signs related to impaired liver fxn,, Left HF: decreased CO ⇒ activity intolerance and signs of decreased tissue perfusion
pulmonary congestion ⇒⇒ impaired gas exchange ⇒ cyanosis and signs of hypoxia
pulmonary edema ⇒ orthopnea, cough with frothy sputum, paroxysmal nocturnal dyspnea
How should dyspnea be evaluated in HF?
Step 1: establish baseline activities, think daily activities ⇒ ex. sighing, dressing, bathing, housework, walking, walking uphill/upstairs, strenuous work, aerobic exercise
Step 2: establish a timeline
What symptoms should be assessed in HF patients?
dyspnea, orthopnea, PND (paroxysmal nocturnal dyspnea), general fatigue
What is paroxysmal nocturnal dyspnea (PND)?
sensation of SOB that suddenly awakes a pt often after 1-2 hours of sleep usually relieved in upright position after 10+ min, may be associated with coughing and wheezing
beware of snoring or sleep apnea
How does orthopnea and PND actually occur (MOA)?
pt lies flat ⇒ redistribution of blood from periphery to heart - heart overwhelmed, chamber pressure increase, pressure increase transmitted back into pulmonary circulation ⇒ pulmonary congestion - alveoli surrounded by interstitial fluid leading to decreased lung compliance ⇒ receptors triggered, CNS activated - orthopnea, CND
What is the NYHA classification?
used to class HF ⇒ Class I: no limitation of activity, normal activity doesn’t cause sx
ex. carry objects >/= 80 lbs, shovel snow, play basketball, jog/walk 5 miles/hr
Class II: slight limitation, comfortable at rest
ex. sex without stopping, rake, play golf, walk 4 miles/hr
Class III: marked limitation, comfortable at rest
ex. mop floors, push lawnmower, shower and dress, walk 2.5 miles/hr
Class IV: severe limitation, sx present at rest
ex. cannot perform any activities previously states
How is lung edema in HF assessed?
may be causing dyspnea, cough, cyanosis
Cardiac: signs of fluid overload ⇒ sx - SOB, PND, orthopnea, cough
Percussion - fluid in lungs, pleural effusion, ‘dullness’
Auscultation - crackles, bubbly, rhochi (coarse rattle)
How is abdominal edema in HF assessed?
S&S - bloating, fullness, early satiety
increased girth
gaining weight over short period of time - not eating but still gaining
evaluate GI for other reasons of bloating, etc before
cardiac: signs of fluid overload ⇒ hepatomegaly - percussion of liver border, abnormal > 3 cm below R subcostal border, palpation
ascites - fluid wave, shifting dullness, bulging flanks
How is peripheral edema in HF assessed?
↔Legs: bilateral, pitting, doesn’t resolve overnight, shoes too tight or don’t fit, onset of swelling associated with other CV sx
Steps: use thumb to firmly press for 5 sec over bony prominence ⇒ start behind ankle, move over dorsum, then shins ⇒ rate severity and note distribution ⇒ evaluate skin: tight, shiny, erythematous = acute edema
dry, scaly, hyperpigmented = chronic edema
What is jugular venous pressure (JVP) in HF, how is it measured and what causes its increase?
assessed via the right internal jugular vein, reflects pressure in right atrium, excellent reflector of fx of the right heart, volume status
soft, undulating pulsation, rarely palpable, pulsation eliminated by soft pressure, double vs single waveform (a or v-wave)
Measured: measured from sternal angle (30 degrees) to highest point of the pulse, normally is < 4cm
Causes: hypervolemia/fluid overload, right ventricular dysfunction, pericardial disease, tricuspid valve disease, obstruction of superior vena cava
What are the different cardiac auscultation sounds, what do they represent, when do they occur, location where they are best heard, and how to listen to them?
S1: represents MV and TV closure, LV movement
occurs during beginning of systole
heard best at apex/mitral area (5th ICS)
listen with diaphragm (lying/sitting)
S2: represents AV and PV closure
occurs during end of systole
heard best at aortic area (USRB 2nd ICS)
listen with diaphragm (lying/sitting)
S3: represents rapid ventricular filling
occurs during early diastole
heard best at apex/mitral area (left, 5th ICS), xiphoid process/left LSB (right)
listen with bell (left lateral lying)
S4: represents ‘atrial kick’ (atrial systole)
occurs during late diastole
heard best at apex/mitral area (left, 5th ICS), xiphoid process/left LSB (right)
listen with bell (left lateral lying)
What heart sounds have extra significance in HF?
S3: ventricular gallop, associated with HFrEF + fluid overload - will result with euvolemia, may be normal in children/young adults with HF
S4: aka atrial gallop, associated with long standing HTN, HFpEF
