Congestive Heart Failure Flashcards
What is a palpitation?
a noticeably rapid, strong, or irregular heartbeat due to agitation, exertion, or illness
What is low CO?
Inadequate forward flow
What is congestion?
excessive fluid back up
What is heart failure?
clinical syndrome in which abnormal
heart function results in (or increases the subsequent risk of) symptoms and signs of low cardiac output
and/or pulmonary or systemic congestion
True or False: cardiomyopathy results to heart failure
false (it can even lead to HF but the term isnt equivalent)
What does heart function depend on?
Heart function depends upon:
– Preload: the heart must be able to fill at a low
pressure (too high a pressure will cause congestion)
– Afterload: the resistance against which the heart
contracts should not be too high
– Contractility: the heart must be able to generate an
adequate pressure through actin-myosin shortening
• Appropriate Heart Rate
What is afterload?
the resistance the LV must
overcome to eject (adequate stroke volume)
- optimally the vascular resistance should be low
What is preload?
the amount of stretch the heart experiences during diastole ~LV end-diastolic volume
What is a marker of HF-rEF and the causes?
- decreased emptying of LV (systolic dysfunction)
– Loss of muscle
• Myocardial infarction
– Volume/pressure overload for many years
• Valvular regurgitation or stenosis
– Decreased contractility
• Dilated cardiomyopathy
What is a marker of HF-pEF and the causes?
Diastolic dysfxn –> Decreased filling
– Increased Myocardial Mass
• Hypertrophic cardiomyopathy
– Increased myocardial stiffness
• Infiltrative cardiac disease e.g Amyloidosis
– External compression
• Pericardial tamponade/constriction
What happens in systolic HF?
damaged ventricle –> reduced ejection fraction –> re. stroke volume –> Starling’s law tries to restore stroke volume close to normal BUT requires dilation of heart (ie. eccentric hypertrophy)
What happens in diastolic HF?
stiff ventricle (still able to empty well) –> poor ventricular filling –> reduced stroke volume at normal filling pressures –> increased LV filling pressure to keep normal stroke volume by concentric hypertrophy
List the pathophysiological causes of HF:
Metabolic demands (High Output) – Anemia, infections, hyperthyroidism • increased Preload – Renal failure, increased salt intake, NSAIDs • Increased Afterload – Hypertension • Decreased Contractility – Ischemia, infarction = inadequate blood / O2 • Increased HR (rarely, very slow HR) – Atrial fibrillation, or other atrial / ventricular fast (slow) rhythms
Pressure overload leads to what kind of wall stress, hypertrophy and is a risk for for what type of HF?
systolic wall stress, concentric hypertrophy (parallel sarcomeres) –> risk for HF-pEF (diastolic HF)
Volume overload leads to what kind of wall stress, hypertrophy and is a risk for for what type of HF?
diastolic wall tress, eccentric (series sarcomeres), HF-rEF (systiolic HF)
Whats the problem that leads to concentric hypertrophy (pressure overload) and what is the compensation?
prob: increased pressure forward
adapt: increased LV wall thickness, decreased radii
result: decreased tension (ie. Pr/T) and stiffness
Whats the problem that leads to eccentric hypertrophy (volume overload) and what is the compensation?
prob: increased volume leads to increased radii and then tension
adapt: increased wall thickness
result: decreased tension
T or F: with increased heart mass there is also an increase in metabolic demand
T
How to calculate the transmyocardial pressure gradient?
Transmyocardial Pressure Gradient =
Epicardial Coronary Pressures - LV Diastolic Pressures
What happens when the trans. p gradient decreases?
endocardium ischemia [inner most layer] (because less pressure drive for blood to go)
When contractility and SV decreases in HF what happens to preload to compensate and it is maladaptive ?
increases preload ( by salt/water retention which increases LVEDV) yes maladaptive --> atrial pressure and LV diastolic pressure/volume goes up --> congestion
When contractility and SV decreases in HF what happens to after-load to compensate and why is it maladaptive ?
increased afterload (by increasing vascular tone [symp sys] and salt/water retention [right AP]) yes maladaptive --> increase mean arterial pressure and LV cavity size
How to caculate MAP?
SVR*CO + RAP
What can occur from increased peripheral vascular resistance?
end organ ischemia
Contractility is influenced by what?
- Circulating catecholamines (adrenal gland)
– Sympathetic nervous system Activation
– Parasympathetic (Vagal) Inhibition
– # of Ca++-binding sites actin-myosin & Ca++
release-dependent
What is End-Systolic Pressure Volume Relationship and what is related to?
End-systolic pressure volume relationship (ESPVR) describes the maximal pressure that can be developed by the ventricle at any given LV volume. This implies that the PV loop cannot cross over the line defining ESPVR for any given contractile state.
Related to contractility
T or F: there is increase in inotropy (ie. contractility) due to SNS activation in HF
T
What are negatives of increased ionotropy?
increased O2 demand, ventricular remodelling, SNS chronic effects
What are causes of diastolic dysfunction (ie. When LV can’t fill at a normal pressure)?
• Decreased chamber compliance
– Hypertrophy
– Fibrosis
– Pericardial constraint
• Poor relaxation
– Ischemia
– Hypertrophy
Who are more prone to diastolic dysfunction?
elderly, obese, renal failure patients, diabetics,
Chronic Obstructive Lung Disease, hypertension
What is the End Diastolic Pressure Volume Relationship?
End Diastolic Pressure Volume Relationship (EDPVR) relates to the passive filling curve of the left ventricle during diastole and is a measure of passive chamber stiffness. The slope of EDPVR is the reciprocal of compliance and is used to measure ventricular stiffness.
What happens in diastolic dysfunction?
↓ Ventricular Compliance (increase in Stiffness)
–>
LV fills at lower volume & higher pressure
–>
↓ Stroke Volume (but EF preserved)
How does SNS get activated and what its adaptive effects in relation to circulatory system?
Reduced effective circulating volume sensed by the central baroreceptors (ie. low CO and lowered BP [ie. BP = CO*SVC)
↑ Heart Rate
• + Chronotropy
↑ Contractility
• + Inotropy
↑Afterload
• Increased arteriolar vasoconstriction
↑Preload
• Enhanced venous tone
• Increased sodium reabsorption in proximal tubule
• Increased renin secretion in the kidney
How does the RAAS get activated and what its adaptive effects in relation to circulatory system?
Trigger:
• ↓ in perfusion pressure (kidney directly senses changes in perfusion pressure through changes in stretch of the renal arterioles)
• ↓ filtrate (chloride) delivery to the distal nephron (macula densa)
• Sympathetic nervous system (β1 adrenergic activity)
Adaptive Effects:
↑Afterload
- A II (Angiotensin II)
• increases arterial vasoconstriction both directly and indirectly (SNS activation)
• regulates the production/secretion of endothelin (ie. potent vasocontrictor)
↑Preload
- A II
• increases sodium reabsorption in proximal tubule
• regulates the production/secretion of ADH
- Aldosterone
• increases sodium reabsorption in distal nephron (cortical collecting duct)
What is maladative about RAAS?
Maladaptive
• Volume overload (PRELOAD)
• vasoconstriction (AFTERLOAD)
• in extracellular matrix in the heart (fibrosis)
–> increase chamber stiffness
• Endothelial dysfunction (higher risk of myocardial infarction)
How does the ADH release get activated and what its adaptive effects in relation to circulatory system?
Trigger:
• Carotid and aortic arch baroreceptors sense decrease in circulating volume
Adaptive Effects: ↑Afterload • increases vascular tone (V1 receptors) ↑Preload • increases water reabsorption in distal nephron (V2 receptors)
What are the two natruiretic peptides released by the heart?
ANP (Atrial Natriuretic Peptide) and BNP (Brain Natriuretic Peptide)
What triggers the release of natriuretic peptides and what are its adaptive effects?
Trigger:
• Atrial and Ventricular Stretch
Effects: ↓Afterload • Induce Arterial Vasodilation ↓Preload • Improve GFR and filtration --> Natriuresis (Na Excretion) --> Diuresis • Venodilation (less venous retrun)
Mixed
• Inhibit Renin release
• ↓Circulating A II and Aldosterone
What is ARNI and how does it work?
ARB/Neprilysin Inhibitors combo
The Neprilysin inhibitor decrease the breakdown of
natriuretic peptides while the ARB mitigate the effects
of resulting increase in ANG II by blocking the AT1
receptor
What are some symptoms of congestion in HF?
- SOB and/or SOBOE
- Orthopnea
- Paroxysmal Nocturnal Dyspnea
- Early Satiety
- Abdominal distention
- Nausea/Vomiting
- Edema
What are some symptoms of low CO in HF?
- SOB and/or SOBOE
- Fatigue
- Weakness
- Confusion
- Lightheadness
- Sleepiness
- Anorexia
- Decreased urination
What temperature and moisture level indicate congestion and low CO?
Wet –> congestion
Cold –> low perfusion
Why HF patient experience SOB?
Lungs stiff
• fluid in capillary bed secondary to backup- pressure (LV diastolic pressure > 18 mm Hg)
Hypoxemia
• (reduced Oxygen Exchange)
Impaired respiratory muscles
• reduced cardiac output and blood flow
What’s the difference between orthopnea and PND [Paroxysmal nocturnal dyspnea]?
Orthopnea - SOB occurs immediately after laying down
PND - SOB occurs some time after laying down
Why is orthopnea/PND observed in HF?
Lying down increases venous return –> increases filling pressures –> blood pools up as it cannot pump it –> backward congestion –> othopnea and PND
What are some congestive signs of HF?
- Elevated JVP (esp right heart failure)
- Lung crackles
- Dependent Edema (esp right heart failure)
- Ascites
- Cachexia (“wasting” disorder that causes extreme weight loss and muscle wasting)
- Third Heart Sound (S3)
- Enlarged heart
- Hepatomegaly (esp right heart failure)
What are some low CO signs of HF?
- Tachycardia
- Low blood Pressure
- Pallor (ie. pale appearance)
- Cool extremities
- Cachexia (“wasting” disorder that causes extreme weight loss and muscle wasting)
- Acrocyanosis (bluish discoloration of the extremities due to decreased amount of oxygen delivered to the peripheral part
What physical observations gives an estimation of right atrial pressures?
JVP
What are the differences btw S3 and S4?
S3 (after S2) vs S4 (just before S1)
- occurs early diastole / at the end of diastole
- occurs during passive LV filling / active
- may be normal / always abnormal
- requires compliant LV / non-compliant [ie. diastolic HF]
- can be a sign of systolic CHF / diastolic
In edema why is there an increase in venous hydrostatic pressure?
Increased hydrostatic pressure in veins because of:
– Salt and water retention
– High right atrial pressure (JVP)
What are some causes of edema?
Decreased Oncotic pressure in capillaries
• Less albumin synthesis: Liver disease
• Protein loss: Renal disease/diarrhea
Increased Hydrostatic pressure in capillaries
• Increased volume: renal failure, heart failure, pregnancy
• increased venous pressure: heart failure, varicose veins
Increased capillary permeability
• Inflammation, infection
Lymphatic obstruction (impaired drainage) – Post radiation therapy
What are some characteristics of a acutely decompensated HF patient?
over 75, female, prior HF, hypertension, dyspnea, congestion on Chest Xray
What are the initial investigations for suspected HF?
- CXR
- electrocardiogram (ie. ECG)
- lab work (CBC, electrolytes, renal function, thyroid, glucose, urinalysis)
What are the next steps after positive findings in initial investigations for HF?
(Assess natriuretic peptides) –> echocardiogram (for ventricular function) –> (cardiac catherization/cardiopulmonary exercise testing)
What are some clinical findings that are highly specific (but not sensitive) for HF?
- S3, abdominojugular reflex, jugual venous distension, rales (ie. lung crackles)
The S3 sound is actually produced by the large amount of blood striking a very compliant left ventricle [ie. dilated].
What info does an echocardiogram provide?
Provides information about – chamber size, function – valvular problems – pericardial effusion – intracardiac pressures
When is BNP analysis useful?
when cause of dyspnea is unclear
What BNP level is suggestive of HF?
BNP > 400 - 500 pg/ml suggestive of acute heart failure
In asymp patients what is the cut-off of BNP for further investigations?
> 50 pg/mL to proceed with echo and HF work up
What is the initial therapy for those with HF-rEF (ie. EF lower or equal to 40%)
Triple therapy: ACEi/ARB + BB + MRA
+ diuretics (for congestion)
