CHF Flashcards
CHF mechanism (circle), 5 points
decr. contractility –> decr CO –> compensatory neurohormonal activation (SNS, RAAS)) –> incr. SVR –> incr. Afterload ///// –> further cycle to decr. contractility
Left sided, what congestion?
pulmonary
Right sided, what congestion?
systemic venous
left sided, presentation?
Cardiomegaly –> displaced point of maximum impulse, S3 sound
Pulmonary edema –> dyspnea, orthopnea, PND – paroxysmal nocturnal dyspnea, crackles
PULM. EDEMA NEBUTINA!!!!! JEIGU LETAI PROGRESUOJA HF, TAI GALI NEBUT, NES DRENUOJASI PER LIMFINE SISTEMA (buco case in UW)
right sided, presentation?
hepatomegaly, splenomegaly, ascites, edema
what is HRpEF?
Symptoms/signs + EF => 50 proc.
what is HRmrEF?
Symptoms/signs + EF 41-49 proc.
what is HRrEF?
Symptoms/signs + EF=< 40 proc.
how is defined systolic dysfunction in early stage of HF?
echo shows EF < 50 proc. in the absence of HF symptoms.
how is defined diastolic dysfunction in early stage of HF?
Echo shows a preserved EF (>50%) without chamber dilation.
HFpEF develops due to diastolic dysfunction, which frequently occurs in the setting of prolonged systemic hypertension (ie, increased afterload).
why HF at the beginning is asymptomatic?
Compensatory eccentric hypertrophy in response to LV volume overload.
Neurohormonal mechanisms help maintain CO and organ perfusion in the setting of declining cardiac function. Mechanisms: 1. Sympathetic NS activation,
2. RAAS
Mechanism of decompensation UW.
2 groups that leads to LV volume overload?
LV systolic dysfunction (ischemia, cardiomyopathy)
Valvular dysfunction (ie. AoR or MR)
In what valve pathology may occur Left ventricle overload?
Ao regurgitation, Mitral regurgitation
Mechanism of decompensation UW.
We have LV volume overload. what happens next and what effect on CO?
LV volume overload -> LV streches –> inc. SV via Frank-Starling
////////THIS INITIALLY MAINTAINS CO
Mechanism of decompensation UW.
LV overload -> streches –> whats next permanent outcome?
chronic volume overload –> eccentric hyperthrophy
Mechanism of decompensation UW.
LV hronic volume overload –> eccentric hyperthrophy –> what further process and effect on CO?
Increased SV ir maintained at expense of INCREASED WALL STRESS
///////THIS PRESERVES CO
Mechanism of decompensation UW.
volume->hypertrophy -> incr. wall stress –> whats next and what result?
Overwhelming wall stress –> LV enlargement and contractile dysfunction ——–> DECOMPENSATED HF
in eccentric - what hypertrophy?
sarcomeres added in series. Seen in volume overload – dilated cardiomyopathy, ischemic heart disease, aortic or mitral regurgitation.
in concentric - what hypertrophy?
sarcomeres added in parallel. Seen in pressure overload – chronic hypertension, aortic stenosis. Also seen in acromegaly.
what belongs to neurohormonal stimulation? 3
SNS, RAAS, antidiuretic hormone
what 3 components increase hemodynamic stress?
Incr. HR and contractility
vasoconstriction
incr. Extravascular volume
what neuroh. maintains Incr. HR and contractility?
SNS
what neuroh. cause vasoconstriction?
SNS and RAAS
what neuroh. cause incr. extracellular volume?
RAAS and ADH
viscious decompensated cycle.
turim HF = volume overload, reduced CO, myocardial stretch
what happens due to this? mainly systemic flow and pressure
decreased renal perfusion (leads to renin secretion) , decreased baroreceptor stretch —–> vasoconstriction (NoA from SNS and ATII from RAAS) and salt+water retention (aldosterone) –> Increased preload and afterload —————> further promotes features mentioned in the question.
This pathway: RAAS and SNS (NoA) –> exacerbate HF
viscious decompensated cycle.
turim HF = volume overload, reduced CO, myocardial stretch
ANP and BNP pathway?
incr. ANP and BNP –> vasodilation and salt + water excretion –> decr. afterload and preload.
This pathway: natriuretic. counteracts heart failure (eventually overwhelmed)
main function of ANP and BNP?
stimulate vasodilation and salt and water excretion, counteracting the effects of the SNS and RAAS
what is the main aim of medical therapy of HF?
Primarily targeted toward the inhibition of detrimental neurohormonal pathways involving the SNS and RAAS. However, an additional strategy involves augmenting beneficial counter-regulatory mechanisms, such as those involving natriuretic peptides.
what right atrial pressure in early HF?
normal/decreased
what right atrial pressure in late HF?
elevated
UW table. Acute decompensated HF
what are pulmonary symptoms? 5
Acute dyspnea, orthopnea , paroxysmal nocturnal dyspnea, tachypnea, accessory muscle use
UW table. Acute decompensated HF
Vascular symtoms? 3
Hypertension common; hypotension suggests severe disease
Tachycardia
UW table. Acute decompensated HF
pulmonary auscultation?
Diffuse crackles with possible wheezes (cardiac asthma)
UW table. Acute decompensated HF
heart auscultation? venos?
Possible S3, jugular venous distention, peripheral edema
UW table. Acute decompensated HF
Treatment. Normal or elevated BP with normal end organ perfusion? 3
- Supplemental oxygen
- Intravenous loop diuretic (eg, furosemide) Treatment
- Consider intravenous vasodilator (eg, nitroglycerin)
UW table. Acute decompensated HF
Treatment. Hypotension or signs of shock?
- Supplemental oxygen
- Intravenous loop diuretic (eg, furosemide) as appropriate
- Intravenous vasopressor (eg, norepinephrine)/inotropes
why may be hypertension in HF?
Chronic hypertension is a common cause of heart failure due to concentric left ventricular hypertrophy and resulting diastolic dysfunction.
how decompensated HF cause MR?
Increased LVEDV causes impaired valve closure due to dilation of mitral valve annulus and lateral papillary muscle displacement with restricted movement of the chordae tendineae.
The mitral regurgitation resolves with reduction in LVEDV, resulting in disappearance of the accociated murmur.
Decompensated HF is a common cause of …….?
SECONDARY (functional) mitral regurgitation.
WHAT is very important feature to evaluate in patients with HF (in any pathway)?
HYPOPERFUSION - present or not?
ESC. Decompensated HF
No hypoperfusion –> give i/v diuretics –> yra atsakas -> optimizuoti medical therapy
Ka daryt jeigu nera atsako?
Increase diuretic dose and/or combine second diuretic.
ESC. Decompensated HF
You give increased diuretic doses and/or combined second diuretic.
what need to evaluate for further decisions?
Drug resistance/end renal failure present or not
If not -> optimizuoti medical therapy
If YES –> consider RENAL REPLACEMENT therapy
ESC. Decompensated HF
You see there is hypoperfusion –> ka daryti?
loop diuretics and consider inotropes
ESC. Decompensated HF
Hypoperfusion –> got diuretic+inotropes. What evaluate then?
Hypoperfusion and congestion relief?
if Yes - medical therapy
in NO –> CONSIDER VASOPRESORS
ESC. Decompensated HF
Hypoperfusion and no relief -> gave NoA –> whats next to evaluate?
Persistent hypoperfusion, organ damage?
No - medical therapy
yes - mechanical circulatory support AND/OR renal replacement therapy
ECS. Pulmonary edema symptoms?
Symptoms: dyspnea with orthopnea, respiratory failure (hypoxemia-hypercapnia), tachypnea, >25 breaths/min, and increased work of breathing.
ECS. Pulmonary edema 3 components of treatment?
oxygen, iv diuretic
if BP >= 110 mmHg - consider vasodilators
if BP < 110 –> inotropes or vasoconstrictors
ECS. Pulmonary edema
if hypoperfusion is present? treatment
give i/v diuretics +/- inotropes or vasopresors
ECS. Pulmonary edema
if hypoperfusion is NOT present? treatment
give i/v diuretics
ECS. Pulmonary edema
aim of treatment?
CONGESTION RELIEF.
ESC. Right ventricular failure
Optimize fluid status –> evaluate whether marked congestion or not.
what to do in both cases?
No congestion –> consider careful fluid administration
Yes congestion –> Loop diuretics
ESC. Right ventricular failure
congestion –> gave diuretics –> what evaluate and do then?
evaluate whether present peripheral hypoperfusion/persistent hypotension?
Not present –> it considered as relief of symptoms –> follow up
Yes -> give vasopresors and/or inotropes
ESC. Right ventricular failure
symptoms not relieved after hypoperfusion treatment with vasopresors?
right ventricular assist device AND/OR renal replacement therapy OR consider palliative cate
ESC. Right ventricular failure
first line treatment for venous congestion?
diuretics
ESC. Right ventricular failure
when indicated vasopressors/inotropes?
Noradrenaline and/or inotropes are indicated for low cardiac output and haemodynamic instability.
Since inotropic agents may aggravate arterial hypotension, they may be combined with norepinephrine if needed
UW table. HF with preserved EF > 50 proc.
what dysfunction?
Diastolic
UW table. HF with preserved EF > 50 proc.
heart causes? 3
HTN with concentric LVH,
restrictive cardiomyopathy, hyperthrophic cardiomyopathy
UW table. HF with preserved EF > 50 proc.
Valvular causes? 2
Aortic stenosis/regurgitation
mitral stenosis/regurgitation
UW table. HF with preserved EF > 50 proc
Pericardial causes?
constrictive pericarditis,
cardiac tamponade
UW table. HF with preserved EF > 50 proc
systemic causes (high output failure)?
thyrotoxicosis, severe anemia, large AV fistula
UW table. HF with preserved EF > 50 proc.
Management. 4 points
Control blood pressure and HR
Address concurrent conditions: AF and myocardial ischemia
Treat volume overload with diuretics
Exercise training/cardiac rehabilitation
Poor prognostic factors in systolic HF.
Higher NYHA functional class
…….
Presence of S3 gallop
Elevated jugular venous pressure
Low blood pressure(< 100/60 mm Hg)
Moderate to severe mitral regurgitation
Low maximal oxygen consumption (peak VO2)
Resting tachycardia
Poor prognostic factors in systolic HF. CLINICAL
…..
Resting tachycardia
Presence of S3 gallop
Elevated jugular venous pressure
Low blood pressure(< 100/60 mm Hg)
Moderate to severe mitral regurgitation
Low maximal oxygen consumption (peak VO2)
Higher NYHA functional class
Poor prognostic factors in systolic HF.
Higher NYHA functional class
Resting tachycardia
…….
Elevated jugular venous pressure
Low blood pressure(< 100/60 mm Hg)
Moderate to severe mitral regurgitation
Low maximal oxygen consumption (peak VO2)
S3 gallop
Poor prognostic factors in systolic HF.
Higher NYHA functional class
Resting tachycardia
Presence of S3 gallop
……
Low blood pressure(< 100/60 mm Hg)
Moderate to severe mitral regurgitation
Low maximal oxygen consumption (peak VO2)
elevated jugular pressure
Poor prognostic factors in systolic HF.
Higher NYHA functional class
Resting tachycardia
Presence of S3 gallop
Elevated jugular venous pressure
………
Moderate to severe mitral regurgitation
Low maximal oxygen consumption (peak VO2)
Low blood pressure(< 100/60 mm Hg)
Poor prognostic factors in systolic HF.
Higher NYHA functional class
Resting tachycardia
Presence of S3 gallop
Elevated jugular venous pressure
Low blood pressure(< 100/60 mm Hg)
………….
Low maximal oxygen consumption (peak VO2)
Moderate to severe mitral regurgitation
Poor prognostic factors in systolic HF.
Higher NYHA functional class
Resting tachycardia
Presence of S3 gallop
Elevated jugular venous pressure
Low blood pressure(< 100/60 mm Hg)
Moderate to severe mitral regurgitation
………………
Low maximal oxygen consumption (peak VO2)
Poor prognostic factors in systolic HF. LABORATORY?
Hyponatremia!!!!!!!
Elevated pro-BNP levels
Renal insufficiency
Poor prognostic factors in systolic HF.
What about hyponatremia?
Parallels the severity of HF and is independent predictor of adverse clinical outcomes. It is caused by renin, NoA and antidiuretic hormone. Treatment involves fluid restriction, ACEI and loop diuretics.
Poor prognostic factors in systolic HF. ECG?
QRS > 120 msec
LBBB pattern
Poor prognostic factors in systolic HF. CARDIO ECHO?
……
Concomitant diastolic dysfunction
Reduced right ventricular function
Pulmonary hypertension
Severe LV dysfunction
Poor prognostic factors in systolic HF. CARDIO ECHO?
Severe LV dysfunction
………
Reduced right ventricular function
Pulmonary hypertension
Concomitant diastolic dysfunction
Poor prognostic factors in systolic HF. CARDIO ECHO?
Severe LV dysfunction
Concomitant diastolic dysfunction
……
Pulmonary hypertension
Reduced right ventricular function
Poor prognostic factors in systolic HF. CARDIO ECHO?
Severe LV dysfunction
Concomitant diastolic dysfunction
Reduced right ventricular function
…..
Pulmonary hypertension
Poor prognostic factors in systolic HF. ASSOCIATED CONDITIONS?
Anemia
Atrial fibrillation
Diabetes mellitus
cardiomyocytes functions? 3
Contractile
Electrical conduction
Endocrine capability to regulate blood volume
ANP and BNP. under what mechanism they are released?
Volume overload (hypervolemia) leads to stretching and increased wall stress of the myocardial ventricular walls –> in response, the ventricular myocardium releases BNP;
similarly, the atrial myocardium releases ANP in response to atrial stretching.
ANP and BNP.
What is their mechanism of action once they are released?
Once secreted, ANP and BNP bind to natriuretic peptide receptors to activate guanylate cyclase and form cyclic GMP, which stimulates 1. Diuresis and 2. Peripheral vasodilation to help alleviate volume overload.
ANP and BNP.
Effect on vessels?
vasodilation, incr. capillary permeability
Arteriolar and venular vasodilation –> decrease preload (incr. venous compliance) and afterload (Decr. peripheral resistance) –> reduce strain on the myocardium and cardiac work.
Also increased capillary permeability, leading to fluid extravasation into the interstitium and a decrease in circulating blood volume.
ANP and BNP. effect on kidney?
Incr. GFR, diuresis, renin inhibition
The afferent arterioles are dilated and the efferent arterioles are constricted, raising the GFR and increasing urinary excretion of sodium and water.
Renin secretion from the juxtaglomerular cells is inhibited, counteracting RAAS activity. = facilitated diuresis.
ANP and BNP. effect on adrenal glands?
Decr. aldosterone
Secretion of aldosterone from the zona glomerulosa cells is inhibited, further counteracting RAAS activity and bolstering the increase in sodium and water excretion. = facilitated diuresis.
ANP and BNP.
Natiuretic peptides induce vasodilation and diuresis by antagonizing the actions of RAAS.
.
ANP and BNP.
The effect on vessels would be counteracted by what?
angiotensin II-induced vasoconstriction
BUT angiotensin II activity is blocked by combining the neprilysin inhibitor with an angiotensin II-receptor blocker.
ANP and BNP.
what shows opposite effect?
RENIN from RAAS (stimulates vasoconstriction and fluid retention)
what increases resp. rate in pulmonary pathologies?
Alveolar juxtacapillary receptors increase respiratory rate in response to pathologic alveolar processes (eg, pulmonary edema, pneumonia). Those receptors become stimulated when engorged by blood or when pulmonary edema occurs as in CHF, microembolism in lungs. Those receptors are situated in the alveoli near the pulmonary capillaries.
BNP during MI?
BNP levels often increase during myocardial infarction.
what is neprilysin?
It is metalloprotease, which brokes down and deactives BNP and ANP.
AND
inactives ATII
what is neprilysin inhibitor?
sacubitril
when we use neprilysin inhibitor, be have active ATII –> vasoconstriction. how to manage?
neprilysin inhibitors are combined with an angiotensin II-receptor blocker (eg, sacubitril-valsartan) to mitigate these negative effects
Neprilysin inhibition combined with angiotensin II receptor blockade improves CO in HF via a reduction in the cardiac work required to attain a certain stroke volume;
however, cardiac contractility is not significantly affected.
.
ECS. General HF diagnostics algorithm.
Risk factors + symptoms+ Abnormal ECG
THEN BNP:
- normal –> HF unlikely
- Increased –> Do cardioEho
abnormal findings on caridoecho –> define HF type according to EF percentage. ———-> treatment.
