Congestive Heart Failure Flashcards
(151 cards)
1
Q
What is a palpitation?
A
a noticeably rapid, strong, or irregular heartbeat due to agitation, exertion, or illness
2
Q
What is low CO?
A
Inadequate forward flow
3
Q
What is congestion?
A
excessive fluid back up
4
Q
What is heart failure?
A
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
5
Q
True or False: cardiomyopathy results to heart failure
A
false (it can even lead to HF but the term isnt equivalent)
6
Q
What does heart function depend on?
A
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
7
Q
What is afterload?
A
the resistance the LV must
overcome to eject (adequate stroke volume)
- optimally the vascular resistance should be low
8
Q
What is preload?
A
the amount of stretch the heart experiences during diastole ~LV end-diastolic volume
9
Q
What is a marker of HF-rEF and the causes?
A
- 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
10
Q
What is a marker of HF-pEF and the causes?
A
Diastolic dysfxn –> Decreased filling
– Increased Myocardial Mass
• Hypertrophic cardiomyopathy
– Increased myocardial stiffness
• Infiltrative cardiac disease e.g Amyloidosis
– External compression
• Pericardial tamponade/constriction
11
Q
What happens in systolic HF?
A
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)
12
Q
What happens in diastolic HF?
A
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
13
Q
List the pathophysiological causes of HF:
A
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
14
Q
Pressure overload leads to what kind of wall stress, hypertrophy and is a risk for for what type of HF?
A
systolic wall stress, concentric hypertrophy (parallel sarcomeres) –> risk for HF-pEF (diastolic HF)
15
Q
Volume overload leads to what kind of wall stress, hypertrophy and is a risk for for what type of HF?
A
diastolic wall tress, eccentric (series sarcomeres), HF-rEF (systiolic HF)
16
Q
Whats the problem that leads to concentric hypertrophy (pressure overload) and what is the compensation?
A
prob: increased pressure forward
adapt: increased LV wall thickness, decreased radii
result: decreased tension (ie. Pr/T) and stiffness
17
Q
Whats the problem that leads to eccentric hypertrophy (volume overload) and what is the compensation?
A
prob: increased volume leads to increased radii and then tension
adapt: increased wall thickness
result: decreased tension
18
Q
T or F: with increased heart mass there is also an increase in metabolic demand
A
T
19
Q
How to calculate the transmyocardial pressure gradient?
A
Transmyocardial Pressure Gradient =
Epicardial Coronary Pressures - LV Diastolic Pressures
20
Q
What happens when the trans. p gradient decreases?
A
endocardium ischemia [inner most layer] (because less pressure drive for blood to go)
21
Q
When contractility and SV decreases in HF what happens to preload to compensate and it is maladaptive ?
A
increases preload ( by salt/water retention which increases LVEDV) yes maladaptive --> atrial pressure and LV diastolic pressure/volume goes up --> congestion
22
Q
When contractility and SV decreases in HF what happens to after-load to compensate and why is it maladaptive ?
A
increased afterload (by increasing vascular tone [symp sys] and salt/water retention [right AP]) yes maladaptive --> increase mean arterial pressure and LV cavity size
23
Q
How to caculate MAP?
A
SVR*CO + RAP
24
Q
What can occur from increased peripheral vascular resistance?
A
end organ ischemia
25
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
26
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
27
T or F: there is increase in inotropy (ie. contractility) due to SNS activation in HF
T
28
What are negatives of increased ionotropy?
increased O2 demand, ventricular remodelling, SNS chronic effects
29
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
30
Who are more prone to diastolic dysfunction?
elderly, obese, renal failure patients, diabetics,
| Chronic Obstructive Lung Disease, hypertension
31
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.
32
What happens in diastolic dysfunction?
↓ Ventricular Compliance (increase in Stiffness)
-->
LV fills at lower volume & higher pressure
-->
↓ Stroke Volume (but EF preserved)
33
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
34
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)
35
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)
36
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)
```
37
What are the two natruiretic peptides released by the heart?
ANP (Atrial Natriuretic Peptide) and BNP (Brain Natriuretic Peptide)
38
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
39
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
40
What are some symptoms of congestion in HF?
* SOB and/or SOBOE
* Orthopnea
* Paroxysmal Nocturnal Dyspnea
* Early Satiety
* Abdominal distention
* Nausea/Vomiting
* Edema
41
What are some symptoms of low CO in HF?
* SOB and/or SOBOE
* Fatigue
* Weakness
* Confusion
* Lightheadness
* Sleepiness
* Anorexia
* Decreased urination
42
What temperature and moisture level indicate congestion and low CO?
Wet --> congestion
| Cold --> low perfusion
43
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
44
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
45
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
46
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)
47
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
48
What physical observations gives an estimation of right atrial pressures?
JVP
49
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
50
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)
51
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
```
52
What are some characteristics of a acutely decompensated HF patient?
over 75, female, prior HF, hypertension, dyspnea, congestion on Chest Xray
53
What are the initial investigations for suspected HF?
- CXR
- electrocardiogram (ie. ECG)
- lab work (CBC, electrolytes, renal function, thyroid, glucose, urinalysis)
54
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)
55
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].***
56
What info does an echocardiogram provide?
```
Provides information about
– chamber size, function
– valvular problems
– pericardial effusion
– intracardiac pressures
```
57
When is BNP analysis useful?
when cause of dyspnea is unclear
58
What BNP level is suggestive of HF?
BNP > 400 - 500 pg/ml suggestive of acute heart failure
59
In asymp patients what is the cut-off of BNP for further investigations?
>50 pg/mL to proceed with echo and HF work up
60
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)
61
What is the prognosis of those diagnosed with HF?
50% death in 5 yrs
62
What are usual causes of death in HF?
Causes of death
– Arrhythmias (ventricular stretch / scar à risk
‘chaos’ from short circuits = sudden death)
– Refractory low output heart failure with multi-organ
dysfunction
63
T or F: there are proven therapies for HF-pEF (ie. diastolic HF)
F
64
What are some non-pharm treatments for HF?
* Fluid and sodium restriction
* Physical activity
* Patient/Family education
65
What pharmaco agents should be considered if ACEi/ARB, BB, diuretics fail to control symptoms of HF?
- Aldosterone antagonist: spironolactone or eplerenone (MRA)
– Digoxin
– Specialist referral for valsartan-sacubitril [ie. ARNI - neprilysin inhibitor sacubitril and ARB valsartan]
OR
ivabradine
66
How does furosemide (ie. diuretic) work?
inhibits chloride (and sodium) reabsorption in the ascending loop of Henle (and causes diuresis as well)
67
Which diuretics are most efficacious?
loop diuretics (ie. furosemide)
68
What is the indication for furosemide?
acute and chronic pulmonary edema
69
What is a typical IV dose of furosemide?
20 - 80 mg
70
What are some adverse effects of diuretics?
dehydration, hypotension, hypokalemia, tinnitus/hearing loss, hyperuricemia (and gout), hypochloremic metabolic
alkalosis
• Contraindications: pregnancy, anuria, hypovolemia
71
What is first line treatment for hypertension?
thiazides and ACEis
72
How do ACEi work?
blocks the formation of angiotensin II (a strong vasoconstrictor)
– result is vasodilation and decreased Na and water
retention (via reduced aldosterone)
– Also reduces cardiac remodeling [chronic RAAS can do this]
73
What is the indication for ACEi?
First-line therapy for HF and asymptomatic left ventricular dysfunction (i.e., prevention) and used as first line treatment in hypertension [along with thiazide]
74
What are some of the adverse effects of ACEi and contraindications?
• Adverse Effects: hypotension, worsening of renal function, hyperkalemia, dry cough, taste disturbances, skin rashes,
angioedema
– additive effects with beta blockers and diuretics
(hypotension)
• Contraindications: previous angioedema, pregnancy
– Use with caution in aortic stenosis or renal artery stenosis [?]
***ACEIs are contraindicated in patients with bilateral renal artery stenosis due to risk of azotemia resulting from preferential efferent arteriolar vasodilation in the renal glomerulus due to inhibition of angiotensin II [remember dilation of efferent decreases GFR and filtration of wastes]***
75
How do Beta-blockers work?
competitively blocks the beta-adrenergic receptor:
– reduction of heart rate, cardiac output [reduces resistance and contractility ie. SV] (short term), blood pressure [reduces resistance]
– Some antiarrhythmic effects
76
What are the indications for BB?
– First-line therapy for HFrEF (along with ACEi)
– therapy for ischemic heart disease (angina) and
hypertension (<60 years of age)
– secondary prevention after myocardial infarction
– antiarrhythmic
– also used for migraines and glaucoma
77
What are some adverse effects of BB?
Adverse Effects:
– worsening of HF symptoms
– fatigue, lethargy
– depression
– nightmares
– hypotension
– bradycardia
– AV block
– bronchospasm
– worsening of peripheral arterial disease
– worsening of Raynaud’s disease (vasospasm)
– Erectile dysfunction
– masking of hypoglycemia in diabetics
– Additive effects with digoxin, verapamil, diltiazem (on bradycardia
and AV block) and ACE inhibitors or A-II antagonists (hypotension)
78
True or False: BB may worsen HF initially
T: so start slow and then increase gradually (may take time to see effects)
This is because beta-blockers can cause worsening of heart failure before improvement is seen as it reduces chronotropy and ionotropy. Left ventricular ejection fraction tends to worsen initially but subsequently improves after 6 to 12 months of therapy. But overtime it reduces the SNS system and its detrimental effects on the heart (ie. remodelling and myocyte death)
79
What are the contraindications for BB?
poorly controlled asthma,
| bradycardia, 2nd or 3rd degree AV block
80
How does digoxin work?
inhibits the Na-K ATPase pump in the cardiac cell membrane, leading to increased cytosolic calcium and stronger cardiac myocyte contraction: IONOTROPE
– also may have a neurohormonal effect in HF
– also depresses SA node function (reduces heart rate: NEGATIVE CHRONOTROPE),
and AV node conduction via increased vagal tone
81
What are the indications for digoxin?
adjunctive therapy for symptomatic HFrEF
82
What are some adverse effects of digoxin?
– GI: anorexia, nausea, vomiting
– CNS: confusion, visual disturbances
– CVS: arrhythmias (AV block, PVCs, etc.)
• toxicity enhanced by hypokalemia
– additive effects with beta blockers, diltiazem,
and verapamil (heart rate & AV conduction slowing)
83
What are contraindications for digoxin?
Contraindications: AV conduction disturbances
• Other:
– digoxin is a narrow therapeutic range drug
– digoxin has a long half-life of 1.5 days (about 5 days in renal disease)
– elimination primary by kidney (caution in renal
dysfunction and elderly); hypokalemia from diuretics promotes digoxin toxicity
84
T or F: the mechanism of benefit of aldosterone antagonists (MineralcorticoidReceptorAgonists) in HF is unknown
T
85
What are indications for MRAs?
Use with ACE inhibitors (or A-II
antagonists) and beta blockers
– Generally, try spironolactone first (10-fold lower cost)
• If gynecomastia occurs, switch to eplerenone
86
What are adverse effects and contradincations for MRAs?
hyperkalemia, increased serum
creatinine (worsening of renal function),
hypotension, dehydration, gynecomastia, ammenorhea
– Start with low dose and monitor potassium and creatinine at 1 week, then 1 month
• Contraindications: caution with K supplements
– eplerenone drug interactions (increased effects of eplerenone with CYP3A4 inhibitors: ketoconazole, itraconazole, clarithromycin, ritonavir, nelfinavir)
87
How do Hydralazine/Nitrates work?
– hydralazine - direct arterial vasodilator --> reduces afterload
– nitrates - venous vasodilator (more blood held away from getting to heart --> lowers preload)
Used when ACEi cannot be used or Black patients
88
What is another name for Angiotensin Receptor Blockers?
Angiotensin II Antagonists
89
How do ARBs work?
A-II antagonists block the AT1 receptor, responsible for many of the deleterious actions of A-II.
– Actions similar to ACE inhibitors
90
What are the indications for ARBs?
hypertension, heart failure (2nd line – alternative to ACE inhibitors when patients experience severe cough from ACE inhibitors)
91
What are some adverse effects of ARBs?
as for ACE inhibitors - hypotension, increased serum creatinine (worsening of renal function), hyperkalemia.
92
How does Angiotensin-Neprilysin Inhibitor (ARNI) work?
Neprilysin is responsible for the degradation of several vasodilatory peptides, including natriuretic peptides, bradykinin, and adrenomedullin.
– sacubitril inhibits neprilysin, resulting in vasodilation and sodium excretion. (ANP/BNP goes up and antagonizes RAAS)
93
What caution should be taken if patient is given ARNI but was previously on ACEi?
Must wait at least 36h before starting if patient was
| receiving an ACE inhibitor previously (due to angioedema risk)
94
What are the adverse effects of ARNI?
as for ACE inhibitors or A-II antagonists: worsening of renal function (increased serum creatinine), hypotension,
hyperkalemia, angioedema (because bradykinin is increased as seen in ACEi too)
95
How does Ivabradine work?
Ivabradine inihibits the depolarizing Ifunny current in the sinoatrial (SA) node (sets the rate of depolarization)
– Does not affect blood pressure or myocardial
contractility (like beta blockers)
***NEGATIVE CHRONOTROPE***
96
What are the adverse effects of Ivabradine?
– Bradycardia
– Visual disturbances: blurred vision, phosphenes
– Atrial fibrillation
97
When to use Ivabradine?
Use in patients with HFrEF who remain symptomatic despite
• Appropriate doses of ACEI/ARB + BB + MRA
• Resting HR >77 in sinus rhythm
• Hospitalized for HF in the past 12 months
98
Why do you see increase in JVP and pulmonary edema with LV HF?
Domino effect:
high LVP --> high LAP --> high Pulmonary capillary pressure (pulmonary edema) --> high PAP --> high RVP --> high RAP --> high CVP --> high femoral pressure --> pitting edema
99
Why does the supine position worsens pulmonary congestion and breathing?
Because supine position increases venous return from lower extremities and splanchnic beds to lungs/heart
Heart cannot tolerate blood volume changes --> worsened state
100
What are some symptoms of LHF?
dyspnea on exertion
paroxysmal nocturnal dyspnea (wake up SOB)
orthopnea (need pillows to behind them while sleeping)
101
What are some symptoms of RHF?
increased JVP
lower extremity edema
liver congestion
102
What is the most common cause of RHF?
LHF
103
When does RHF occur in isolation?
usually with pulmonary HTN or COPD --> high PAP --> high RVP --> high RAP
104
What is classic CXR findings for HF?
Rales --> fluid filled alveoli (they pop open during inspiration)
Fluid congestion (more white in lung area)
105
T or F: in chronic heart failure, a CXR can be clear
T due to increased lymphatic drainage
106
What happens to the hepatojugular reflex in HF?
Increase of the double bounce (more than 3 cm)
107
Which heart sound is associated with a high left atrial pressure?
S3 (indicative of LVF)
108
Which heart sound is associated with a stiff left ventricle?
S4 (most often seen in diastolic heart failure)
109
T or F: total peripheral resistance is always high in HF
T
110
How to calculate BP?
BP = CO x TPR
111
What can cause impaired LV filling?
```
Weak LV (systolic HF)
Stiff LV (diastolic HF)
Mitral stenosis
```
112
What is the most common cause of SHF?
previous MI
113
T or F: chemotherapy can lead to cardiomyopathy and SHF
T
114
T or F: Digoxin raises the resting potential of ventricular and atrial cells
T
So easier to depolarise (closer to threshold); and increased automaciity (as seen as a upslope at phase 4)
YET SLOWS THE HEART VIA AV NODE SLOWING
115
What things can cause concentric hypertrophy (diastolic problem but systolic wall stress)?
- aortic stenosis
- severe untreated HTN
- --> leads to increased afterload and pressure build-up
116
What physiological parameter is decreased in systolic heart failure?
contractility is reduced
117
What physiological parameter is decreased in diastolic heart failure?
compliance (ie. stiffer) and lusitropy are reduced
118
Which two physiologic systems are over-activated in systolic heart failure?
RAAS
| Sympathetics (b1 stimulation)
119
What are some intrinsic causes of heart failure?
Intrinsic disease includes conditions such as dilated cardiomyopathy and hypertrophic cardiomyopathy.
120
What are some extrinsic causes of heart failure?
External factors that can lead to heart failure include long-term, uncontrolled hypertension, increased stroke volume (caused by increased blood volume or arterial-venous shunts), and hormonal disorders (e.g., hyperthyroidism, and pregnancy).
121
What can be a cause of acute heart failure?
Acute failure (hours/days) may result from cardiopulmonary by-pass surgery, acute infection (sepsis), acute myocardial infarction, valve dysfunction, severe arrhythmias.
122
T or F: chronic heart failure goes through heart remodelling
T:
Chronic heart failure is a long-term condition (months/years) that is associated with the heart undergoing adaptive responses (e.g., dilation, hypertrophy) to a precipitating cause.
123
What are the two common diseases that lead to heart failure?
The number one cause of heart failure is coronary artery disease (CAD). CAD reduces coronary blood flow and oxygen delivery to the myocardium. This leads to myocardial hypoxia and impaired function.
Another common cause of heart failure is myocardial infarction, which is the final and often fatal culmination of CAD. Infarcted tissue does not contribute to the generation of mechanical activity so overall cardiac performance is diminished. Furthermore, non-infarcted regions must compensate for the loss of function and this extra burden can precipitate changes that lead to failure.
124
The pathophysiology of heart failure involves changes in what parameters?
```
cardiac function
neurohumoral status
systemic vascular function
blood volume
integration of cardiac and vascular changes
```
125
T or F: Both systolic and diastolic dysfunction result in a higher ventricular end-diastolic pressure
T:
| Serves as a compensatory mechanism by utilizing the Frank-Starling mechanism to augment stroke volume.
126
In some types of heart failure, what is the purpose of anatomical dilatation?
the ventricle dilates anatomically, which helps to normalize the preload pressures by accomodating the increase in filled volume.
127
What are the compensatory mechanisms that happen during heart failure?
Cardiac
Frank-Starling mechanism
Chronic ventricular dilation or hypertrophy
Tachycardia
Autonomic Nerves
Increased sympathetic adrenergic activity
Reduced vagal activity to heart
Hormones
Renin-angiotensin-aldosterone system
Vasopressin (antidiuretic hormone)
Circulating catecholamines
Natriuretic peptides
128
What neurohumoral changes occur in heart failure?
Activation of sympathetic nerves and the renin-angiotensin system, and increased release of antidiuretic hormone (vasopressin) and atrial natriuretic peptide.
The net effect of these neurohumoral responses is to produce arterial vasoconstriction (to help maintain arterial pressure), venous constriction (to increase venous pressure), and increased blood volume to increase ventricular filling.
But they can also aggravate heart failure by increasing ventricular afterload (which depresses stroke volume) and increasing preload to the point where pulmonary or systemic congestion and edema occur.
129
What systemic vascular changes occur in heart failure?
In order to compensate for reduced cardiac output during heart failure, feedback mechanisms within the body try to maintain normal arterial pressure by constricting arterial resistance vessels through activation of the sympathetic adrenergic nervous system, thereby increasing systemic vascular resistance.
Veins are also constricted to elevate venous pressure.
Arterial baroreceptors are important components of this feedback system, especially in acute heart failure.
Humoral activation, particularly the renin-angiotensin system and antidiuretic hormone (vasopressin) also contribute to systemic vasoconstriction.
Heightened sympathetic activity, and increased circulating angiotensin II and increased vasopressin contribute to an increase in systemic vascular resistance.
130
What changes in blood occur in heart failure?
There is a compensatory increase in blood volume that serves to increase ventricular preload and thereby enhance stroke volume by the Frank-Starling mechanism.
- Reduced renal perfusion results in decreased urine output and retention of fluid
- Reduced renal perfusion and sympathetic activation of the kidneys stimulates the release of renin, and enhances aldosterone secretion
- Increase in circulating arginine vasopressin (antidiuretic hormone) that contributes to renal retention of water.
---> final outcome is an increase in renal reabsorption of sodium and water. The resultant increase in blood volume helps to maintain cardiac output; however, the increased volume can be deleterious because it raises venous pressures, which can lead to pulmonary and systemic edema (and lead to exertional edema)
131
What is impaired in systolic dysfunction of heart failure?
Systolic dysfunction refers to impaired ventricular contraction (loss of inotropy).
132
What is the cause of systolic dysfunction in chronic heart failure?
In chronic heart failure, this is most likely due to changes in the signal transduction mechanisms regulating cardiac excitation-contraction coupling.
133
What happens to Frank-Starling curve in systolic heart failure?
The loss of cardiac inotropy (i.e., decreased contractility) causes a downward and rightward shift in the Frank-Starling curve.
--> This results in a decrease in stroke volume and a compensatory rise in preload (often measured as ventricular end-diastolic pressure or pulmonary capillary wedge pressure) because of incomplete ventricular emptying, which leads to an increase in ventricular end-diastolic volume and pressure.
134
What kind of ventricular remodelling occurs in chronic systolic HF?
Ventricular remodeling occurs in chronic failure leading to anatomic dilation of the ventricle.
135
What is compensatory mechanism is employed due to the loss of ionotropy in sysHF?
The rise in preload is a compensatory response that activates the Frank-Starling mechanism to help maintain stroke volume despite the loss of inotropy.
--> If preload did not rise, the decline in stroke volume would be even greater for a given loss of inotropy.
***With systolic dysfunction, there is also an increase in blood volume that contributes to increased ventricular filling and end-diastolic volume and pressure.***
136
T or F: in acute sysHF there is no change in EDPVR
T:
because the ventricle do not undergo remodeling (anatomic dilation), which would increases the ventricular compliance (and bring the curve down)
BUT GOES DOWN ON THE ESPVR
137
Why does loss of inotropy lead to lowered stroke volume?
A loss of inotropy results in a decrease in the shortening velocity of cardiac fibers. Because there is only a finite period of time available for ejection, reduced ejection velocity results in less blood ejected per stroke. The residual volume of blood within the ventricle is increased (increased end-systolic volume) because less blood is ejected.
138
What can results if left ventricle are involved in sysHF?
If the left ventricle is involved, then left atrial and pulmonary venous pressures also rise. This can lead to pulmonary congestion and edema.
139
What can results if right ventricle are involved in sysHF?
If the right ventricle is in systolic failure, the increase in end-diastolic pressure will be reflected back into the right atrium and systemic venous vasculature. This can lead to peripheral edema and ascites.
140
Why is there less ventricular filling in diasHF?
A reduction in ventricular compliance, as occurs in ventricular hypertrophy, increases the slope of the ventricular end-diastolic pressure-volume relationship (EDPVR) and results in less ventricular filling.
141
What is an important and deleterious consequence of diastolic dysfunction?
An important and deleterious consequence of diastolic dysfunction is the rise in end-diastolic pressure.
--> If the left ventricle is involved, then left atrial and pulmonary venous pressures will also rise. This can lead to pulmonary congestion and edema.
--> If the right ventricle is in diastolic failure, the increase in end-diastolic pressure will be reflected back into the right atrium and systemic venous vessels. This can lead to peripheral edema and ascites.
142
What can cause ventricular hypertrophy?
- chronically increased volume load (preload) or increased pressure load (afterload)
- disease of the heart (valve disease, cardiomyopathies), genetic abnormalities (e.g., hypertrophic cardiomyopathy), and as a consequence of coronary artery disease
143
What may cause chronic pressure overload?
chronic hypertension or aortic valve stenosis
144
What kind of remodelling does the ventricle undergo under chronic pressure overload?
concentric hypertrophy:
radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres
145
Why is concentric hypertropy compensatory in diastolic heart failure?
This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress.
146
What is the issue with concentric hypertrophy in diasHF?
This type of ventricle becomes "stiff" (i.e., compliance is reduced), which can impair filling and lead to diastolic dysfunction.
147
What kind of remodelling does the ventricle undergo under both chronic pressure and volume overload?
eccentric hypertrophy:
The chamber radius is increased and the wall thickness is increased moderately. Chamber dilation occurs as new sarcomeres are added in-series to existing sarcomeres.Mechanically, dilation increases the ventricular compliance.
***The dilated ventricle has elevated wall stress and oxygen demand, and lower mechanical efficiency. So reduced EF***
148
What can cause chronic ventricular dilation?
1) chronic volume overload stimulated by elevated ventricular end-diastolic pressures (e.g., as occurs in aortic and mitral regurgitation; systolic dysfunction)
2) hypervolemic states triggered by ventricular failure or renal failure
3) intrinsic disease such as idiopathic dilated cardiomyopathy or known causes of dilated cardiomyopathy (e.g., alcohol-induced; viral)
149
What are the effects of natruretic peptides?
Natriuresis
Diuresis
Improve glomerular filtration rate & filtration fraction
Inhibit renin release
↓ circulating angiotensin II
↓ circulating aldosterone
Systemic vasodilation
Arterial hypotension
Reduced venous pressure
Reduced pulmonary capillary wedge pressure
--> Taken together, these actions of NPs decrease blood volume, arterial pressure, central venous pressure, pulmonary capillary wedge pressure, and cardiac output.
150
What factors can contribute to edema?
Increased capillary hydrostatic pressure (as occurs when venous pressures become elevated by gravitational forces, in heart failure or with venous obstruction)
Decreased plasma oncotic pressure (as occurs with hypoproteinemia during malnutrition)
Increased capillary permeability caused by proinflammatory mediators (e.g., histamine, bradykinin) or by damage to the structural integrity of capillaries so that they become more "leaky" (as occurs in tissue trauma, burns, and severe inflammation)
Lymphatic obstruction (as occurs in filariasis or with tissue injury)
151
T or F: increasing cardiac output decreases venous pressure
T
