فشل القلب :( Flashcards
بسم الله الرحمن الرحيم الرحمن وبه نستعين
اللهم إنا نعوذ بك من الهم والحزن والعجز و الكسل والجبن و البخل وغلبة الدين وقهر الرجال
According to onset (Course):
Acute heart failure (AHF) & chronic heart failure (CHF
According to level of COP:
Low & High (due to anemia or thyrotoxicosis) Heart failure
According to site affected:
left or right heart failure
Diastolic Heart failure: Left ventricles is not able to fill blood during diastole → ↓ amount of blood pumped out than normal
Treatment:
-ve inotropic drugs (β blockers, calcium channel blockers e.g. Verapamil),
Diuretics (in volume overload) &
ACEI (to prevent remodeling)
Systolic Heart failure:
is the failure of the heart to pump an adequate blood supply for the metabolic needs of the body if
there is an adequate venous return
Clinical S/S of low COP failure (systolic HF)
- ↓ Ejection fraction (↓SV/ ↑EDV).
- Congestive s/s ذ(due to ↑ preload): Leg edema, Congested tender liver, Dyspnea, cough,…
- Low COP s/s (due to ↑ afterload): Fatigue (↓ exercise tolerance), cold extremities, cyanosis,.
Sodium-glucose co-transporter 2 (SGLT2) inhibitors:
Dapagliflozin
Nitrates ?
Venodilators :decrasing VR imrpoving pulmnary congestion and congestivs symptomas
as leg edema and cough and dyspnea
Hydralazine ?
Atretiodilator decreasing the Resistance of afterload and increasing COP
decreasing the Low cop sympstoms as fatigue and cold extremities
Mixed dilators?
ACcute heart failure : Na nitroprusside
Chrnoic heart failure : ARBS ARNI ACEI
Mecahnism of action of ACEI ?
Incerasing Braykinin and NO and PGs so VD of blood vessels
Decrasing Ang2 formation and so :
1- VD of blood vessels due to blcok vc activity on V1
2-Prevention of cardiac remodeling
3-Decreasing NE release decreasing BP wihtlut refleax Tachycardia
4-Decreasing Aldosterone inducing getting rid of H2o and Na
Indications of ACEI ?
Hypertension
Heartfailire
MI : Acute with BB and fibrimolytic and aspirin prevention of Arrhythmia 2ry to hypokalemia and inducing sympathtic activity
Post MI : Decreasing Aldosternoe induced Remodeling preventing Heart failure
Nephropathy: diabetic or non diabetic:
Adverse effects of ACEI ?
Most seroius: angiodema
serious:
Contraidicated in renal hypoperfusion :
bilateral renal artery stenosis used in unilateral
extensive dose of loop diuretics
Bonemarrow derpession
Fetotoxic 2,3 trimester teratogenic 1trimester
most common : increasing cough and dyspnea due to bradykinin
less common : Hypotenison with 1st dose
Hyperkalamia BB and K sparings
hypersensitivity
git upest
Most seroius: OF ACEI?
Angioedema
All ACEI are prodrugs (need liver activation) except
Captopril & Lisinopril.
All prodrugs are long acting.
Captopril: Short acting مهمه →
taken 3 times daily
Lisinopril: Renal elimination
(Given in Liver dysfunction)
Fosinopril:
Dual elimination
has greater effect on Heart ACE suitable in both renal &
hepatic Dysfunction
Enalaprilat: active metabolite of enalapril:
used IV in
emergency
2Angiotensin receptor blocker (ARBS) SartanS
- Block AT1 receptors which mediate most of
pathological CVS effects of Ang II - Spare AT2 receptors → VD & antiproliferative effect
Indications of ARBS?
As ACEI IN COUGH
Hypertension
Heartfailire
MI : Acute with BB and fibrimolytic and aspirin prevention of Arrhythmia 2ry to hypokalemia and inducing sympathtic activity
Post MI : Decreasing Aldosternoe induced Remodeling preventing Heart failure
Nephropathy: diabetic or non diabetic:
Adverse effects of ARBS?
نفس االعراض الجانبيه ماعدا الكحه
Most seroius: angiodema
Contraidicated in renal hypoperfusion :
Bilateral renal artery stenosis used in unilateral
extensive dose of loop diuretics
Bonemarrow derpession
Fetotoxic 2,3 trimester teratogenic 1trimester
most common : increasing cough and dyspnea due to bradykinin
less common : Hypotenison with 1st dose
Hyperkalamia BB and K sparings
hypersensitivity
git upest
Advantages of ACEI and ARBS?
PRMAM
Preload and afterload relieving symptoms
Renoprotective especially in DM
Mixed VD withous reflex tachycardia or Na and H2O reterntion
Aldosterone prevention from remdeling and fibrosis and Hypolaemia induced arrhythmia
Mortality decrease especially with BB or Diuretics
ACEI and ARBS? are
Renoprotective
Hypolaemia induced arrhythmia and ACEI AND ARBS?
Aldosterone prevention from remdeling and fibrosis and Hypolaemia induced arrhythmia
Advantages ARBs Over ACEI ?
Increasing NO and BK increasing Cough
Antagonize at AT1 Ang II form ACE And non ACE FROM Hormonal escape Phenomenon
AT2 Activation VD -antiProliferative
disadvantages:lack of vasodilator effect of BK (PG & NO)
Sacubitril -valsartan combination called? is used in place ?
(Angiotensin Receptor Neprilysin Inhibitor= ARNI)
of ACEIs or
ARBS in patient with LVEF < 40%
Neprilysin inhibitors: Sacubitril
Mechanism of action:
• Inhibits endopeptidase Neprilysin → ↓ breakdown Natriuretic Peptides (NPs) & angiotensin II
• ↑ NP → direct vasodilation, ↑ GFR → ↓release of renin from the kidney, Loss of H20 and sodium in urine (Natriuretic)
Hydralazin mechanism of action and indicztions ?
It open K channels casuing hyperplarization preventing Ca entery into vessel wall acquering its VD effect
- Heart failure with Nitrates but ACEI are better
- HTN IV with Eclampsia
-HTN IV with Eclampsia
hYDRALAZINE
hYDRALAZINE TOLEARNCE DUE TO ?
By time , it stimulates Sympathatic and Renin Angiotensin system
casuing reflex tachycardia salt and water retention increasing BP !!
Na nitroprusside ?Mechanisms and Indications ?
NO donor casuing increased cAMP preventing Ca entery to the blood vessel wall casuing VD
Potent very Rapid and Short IV
Hypertensice emergencies
Severe acute heart failure
Adverse effects of Na nitroprusside?
Hypotension and (Myocardial Ischemia due to reflex tachy cardia ) Cyanide toxicity due to liver dysfuction Thiocyanat toxicity due to renal dysfunction
Thiocyanat toxicity due to
renal dysfunction
Precautions with Na nitroprusside Precautions: • ???= (Avoid drop < 95/70 mmHg) • Solution should be ? • Avoid prolonged use
Slowly IV with BP monitoring
freshly prepared & protected from light by opaque foil
especially in hepatic & renal dysfunction to avoid toxicity
Diuretics in systolic heart failure?
Decreasing blood voulme and vr and pulmnary congestion and edema and the orthopnea and ncturnal dyspnea
Loop of choice !
Thiazid in loop refreact.
Sppironolocatones + loop _ ACEI
Adnvatages of Spironolactone?
Aldosterone anagonist:L
decreasing mortality by 30 %
1-Prevent water and Na retention decreasing blood voulme
2-Prevent Hypokalemia induced arrhythmia
3-Prevent aldosternoe mediated cardiac Remodeling
f
SPRINOLOACTONE USED CASUTILUSLY WITH ? WHY?
ACEI OR IN RENAL IMPAIRMENT
TO AVOID RISK OF HYPERKALEMIA
Mortality rate by heart failure is decreasd by?
عن ابن ادريس الشافعي
ما شبعت منذ ست عشرة سنة إلا شبعة اطرحتها لان الشبع يثقل البدن
ويغشي القلب ويزيل الفطنة و يجلب النوم ويضعف صاحبه عن العبادة
ACEI
ARBS
BB
Spironolactone
BB IN HEAR FAILURE
MBC
Metoprolol
Bisoprolol
Carvediolol
low dose gradually increased to avoid woresining in cardiac function
Multiple actions neurohormonal antagonist
Carvedilol:
• ↑ ejection fraction → improve symptoms
• ↓ Disease progression
• Reduce hospitalization & mortality rate
Drawbacks of chronic sympahtic stimulation on Heart?
Tachycardia and increasd O2 demeand
Renin angiotenisn system activation and Remodeling and Hypertrophy dilatation
Production of Cardic cytokines and Intelukeins induce hypertrophy apotoisis fibrosis
ACEI
ARNI
BB
MRA
HFrEF
bb avoided in ?
Hypotension
pulmonary congestion
AV Block
has delayed onset of action
decreasing mortaility rate
Attention: The advantages of the following in HF: 1. ACEIs OR ARNI 2. β blockers 3. Spironolactone (MRA) 4. SGLT2 inhibitor (
Advantages of BB?
Antagonist of sympathatic aactivity and RAS
decreasing HR giving time for diastolic coronary filling
decreasing afterload and so decreasing O2 demean
Cardioprotection Block catecholamines and Ang2 induced arrhymia myocardial damage and apotpiss
Improve LV dysfunctions decreasing reinien and RAS
Upregulation of B1 Receptros improving contractility
How BB decreases the O2 demand of Heart?
- ↓ Heart Rate → ↑ diastolic time →↑ coronary filling
2. ↓ After load (↓Blood Pressure)
BB AS CARDIOPROTECTOR
Block catecholamines and Ang2 induced arrhymia myocardial damage and apotpiss
bb Improve LV dysfunctions
bb Improve LV dysfunctions
decreasing reinien and RAS
BB improving contractility
Upregulation of B1 Receptross ( in long standing HF)
Direct effect OF Dioxin ?
(+VE inotropic effect)
Inhibits membrane bound Na+/K+ ATPase pump →
↑intracellular Na+ →
Ө outflux of cytosolic Ca++ →
↑ activity of excitable tissues in cardiac, smooth muscles & neurons [ ↑ intracellular Na+ & Ca++]
Indirect effect of digoxin
- ↑ vagal tone on heart (Central stimulation of vagal nucleus)
- ↓ Sympathetic activity in patients with heart failure
secondary to improvement of COP
how digoxin is + INOTROPE?
Incrasing cytosolic Ca and moving troponinc c incrasing contractility
Decreasing Venous pressure and EDV due to better cardiac emptying
decreasing sypmathtaic activity and Preload and afterload symptomps through?
a1 : vasuclar tone decrasing cardiac load
b1 : decrasing Hr and renin and aldosternoe and na retenroion decreasing edema
Diuresis increasing COP ,RBF, Aldosterne antagonism
how digoxin is + INOTROPE?
Incrasing cytosolic Ca and moving troponinc c incrasing contractility
Decreasing Venous pressure and EDV due to better cardiac emptying
decreasing sypmathtaic activity and Preload and afterload symptomps through?
a1 : vasuclar tone decrasing cardiac load
b1 : decrasing Hr and renin and aldosternoe and na retenroion decreasing edema
Diuresis increasing COP ,RBF, Aldosterne antagonism
Decreasing Venous pressure and EDV by digoxin how?
due to better cardiac emptying
Digoxin
decreasing sypmathtaic activity and Preload and afterload symptomps through?
decreasing sypmathtaic activity and Preload and afterload symptomps through?
a1 : vasuclar tone decrasing cardiac load
b1 : decrasing Hr and renin and aldosternoe and na retenroion decreasing edema
digoxin and diuresis?
Diuresis increasing COP ,RBF, Aldosterne antagonism
Electrical effect: arrhythmogenic of digoxin ?
↑ Intracellular Na + & Ca++
→Shift membrane potential toward firing level at the end of Action potential (AP) → Delayed after depolarization (DAD) → Ventricular premature beats, tachycardia, or Fibrillation
Open K+ channels → rapidly end AP → ↓ atrial APD → converts Atrial flutter to Atrial fibrillation (AF) & paroxysmal to permanent AF
CNS stimulation by digoxin
- Vagal center (Nucleus) (therapeutic doses)
- CTZ (supra-therapeutic dose): early s/s of toxicity
- Visual & cortical → visual disturbances, hallucination (toxic doses)
Direct vasoconstriction
↑ Ca++ in vessel wall. This effect is antagonized by digitalis
induced ↓ in sympathetic activity
Vagal stimulation by diogoxin ?
SAN decresing HR For optimum digitalization
Atria decreasing APD casuing Af to AF
DECREASING AVN Conduction
Digoxin and decrasing AVN ?
By vagal stimulation:
فيونكة يحمي البطين من النبضات الزيادة في الأذين
Overdoes > heart block bradycardia give atropine
Termination of PSVT By - re-entry phenomenon
Contraindication of Digoxin >?
SH ARVA Sick sinus syndrome Partial Heart block HOCM Acute MI Rhematic carditis Ventricular Tachycardia AF+ WPW
most solid indication OF Digoxin?
AF+Heart failure
↓ AVN conduction (↑EFR) →
control ventricular rate in AF
counteract its atropine like action of proacinamide?
Digoxin
Indications of Digoxin?
PSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVT
Systolic heart failure
AF + Heart failure
Chronic AF without Heart failure
PSVT!!!!
PSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVT
DIGOXIN IN Chronic AF without Heart failure
WITH
VERAPAMIL and BB TO CONTROL VENTRICULAR RATE
BEFORE PROCAINCMID TO CONTROL its atropine like action
WHY BS antibiotics problem with digoxin
Absorption: 2/3 oral dose is absorbed. Rest is inactivated by bacterial flora (BS antibiotics kill bacteria flora
that inactivate digoxin→ ↑ amount absorption)
Hemodilasys not effective in Digoxin toxicity????
Distribution: 2/3 oral dose is unbound to plasma protein → ↑Vd → (Hemodialysis is not effective in toxicity)
Elimnation of Digoxin explain
Elimination: 2/3 dose excreted unchanged in urine. Rest excreted hepatically in bile. Has long t1/2 (36 hours) • Has low therapeutic index: Therapeutic plasma level (0.5 to 1.5 ng/ml) close to toxic level (> 2 ng/ml)
Dosing of digoxin
- Therapy with digoxin is commonly initiated and maintained at a dose of 0.25 mg daily
- Lowe doses (0.125 mg) should be used in patients > 70 year or in renal impairment
- Dose adjustment in renal impairment is important
Adverse effects of Digoxin ?
Cardiac arrhytgmia
CNS Halluscinations
Git
Gyncomastia
cardiac arrhtymia and Digoxin?
Suprevent. and Vent, tachycardia premature beats fibrillations due Ca overload
Siuns brady cardia and Heart block due to Vagal Stimulation
CNS adverse effects?
Confusion
Hallucination
green yellow vision
Erthrromycin and dgioxin ?
Kill git flora that take 1/3 digoxin increasing its absoprtion
Antiarrthymic drung and pharmacko kinetic interaction with digoxin
Procainamice and Amiodarnoe and Verapapil
decereeasing its excretion
decrasing binding with plasma proteins digitalis toxciity so they are contraiindicated there
instead we use Lidocaine Better in ? ventricular arrhythmia
Digitalis induced tachyarryhtmia?>
Diuretics decreasing k mg increasing ca
CORTICOSTERIOIDS Decreasing K
Hypercalcemia
sympathomimetics
Digitalis induced Bradyarrhytmia?
BB and CCB Decreasing AVN conduction and
May cause HB
ECG changes in Digoxin?
Prolonged PR interval due Vagal stimulation and Reduction of AVN conduction
Shortened QRS ,QT interval due to Shorteining of APD And reploarization
Depressed ST sement
Flat or inverted T wave
Treatment of digoxin toxicity?
PLAD SND
Stop digoxin and K losing diuretics
Potassium cholride KCL if K < 3,5 mEq /L NEVER IN Hyperkalemia or Heart Block
Lidocaine phenytoin ventricular arrhytmia
Atropine to overcome bradycardia and Heart block (Cardiac pacing)
Digi-Band Fab : antibodies against digoxin excreting it in urine
Dopamine ?
D1 In low dose increasing RBF
B1 in intermdeiate dose +inotropic INCREASIGN COP
a1 in high dose VC INCREASING BP
Arrhygmogenic
Acute heart failure
chronic refractory heart failure
Cardiogenic shock in hypotension and renal impairment
Dobutamine
B1 ONLY + INOTROPIC LESS INCREASE IN HR
LESS ARHTHMOGENIC
AS dopamine but in normotensives + preserved renal functions
Phosphodiesterase II inhibitors?
Increasing cAMP AND CARDIAC Contractility
Arterilodilator and Venulodilator decreasing Preload And AfterLoad
Adverse effects of PDI2?
Thrombocytopenia
Arrhythmia
Git upset
Tolvaptan ?
V2 antagonist
induce excretion of Elctrolyte free water to correct diltuonal hyponatremia induced by ADH
In systolic Heart Failure Especially with Resistance to loops
Nesritide
IVI ? Then?
Recombinant type of B-naturetic peptide
Vasodilation of Arterioles and venules decreasing Loads
In decompensated Heart Failure
Adverese effect : Hypotension
Acute decompensated heart failure therapy ?
O2 supplementation
(Loop diuretic) in acute pulmonary edema
(Vasodialtors) decreasing Loads:
1-Nitroglyciern no hypotension
2-Nitroprusside Severe Hypertension
(Morphine) with AMI
+Inotropics
Venous Thromboembolism prophylaxis
sodium-glucose co-transporter 2 (SGLT2) inhibitors: e.g. dapagliflozin
o Oral antidiabetic drug used in heart failure with or without DM
o Added to ACEIs or ARNI, β blocker, MRA combination in HFrEF → ↓ worsening of s/s and ↓mortality rate
Heart failure associated with AF: Add:
β blocker, digoxin & direct oral anticoagulant (e.g. Rivaroxaban)
Ivabradine (see angina) is used if heart rate >
70 b/min (if response to β blocker is poor)
• Digoxin: used if the patient still symptomatic in essential therapy or
if heart failure is associated with atrial fibrillation
Treatment of co-morbidities e.g is essential
. Hypertension,
ISHDs
& DM
• N-3 polyunsaturated fatty acids can
reduce mortality in heart failure
الحمدلله الذي أنزل علي عبده الكتاب ولم يجعل له عوجا
إنه من يتق ويصبر فإن الله لا يضيع أجر المحسنين
