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CVS Pharma papre 1 > فشل القلب :( > Flashcards

فشل القلب :( Flashcards

1
Q

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):

A

Acute heart failure (AHF) & chronic heart failure (CHF

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2
Q

According to level of COP:

A

Low & High (due to anemia or thyrotoxicosis) Heart failure

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3
Q

According to site affected:

A

left or right heart failure

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4
Q

Diastolic Heart failure: Left ventricles is not able to fill blood during diastole → ↓ amount of blood pumped out than normal
Treatment:

A

-ve inotropic drugs (β blockers, calcium channel blockers e.g. Verapamil),

Diuretics (in volume overload) &

ACEI (to prevent remodeling)

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5
Q

Systolic Heart failure:

A

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

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6
Q

Clinical S/S of low COP failure (systolic HF)

A
  • ↓ 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,.
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7
Q

Sodium-glucose co-transporter 2 (SGLT2) inhibitors:

A

Dapagliflozin

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8
Q

Nitrates ?

A

Venodilators :decrasing VR imrpoving pulmnary congestion and congestivs symptomas
as leg edema and cough and dyspnea

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9
Q

Hydralazine ?

A

Atretiodilator decreasing the Resistance of afterload and increasing COP
decreasing the Low cop sympstoms as fatigue and cold extremities

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10
Q

Mixed dilators?

A

ACcute heart failure : Na nitroprusside

Chrnoic heart failure : ARBS ARNI ACEI

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11
Q

Mecahnism of action of ACEI ?

A

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

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12
Q

Indications of ACEI ?

A

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:

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13
Q

Adverse effects of ACEI ?

A

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

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14
Q

Most seroius: OF ACEI?

A

Angioedema

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15
Q

All ACEI are prodrugs (need liver activation) except

A

Captopril & Lisinopril.

All prodrugs are long acting.

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16
Q

Captopril: Short acting مهمه →

A

taken 3 times daily

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17
Q

Lisinopril: Renal elimination

A

(Given in Liver dysfunction)

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18
Q

Fosinopril:

A

Dual elimination
has greater effect on Heart ACE suitable in both renal &
hepatic Dysfunction

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19
Q

Enalaprilat: active metabolite of enalapril:

A

used IV in

emergency

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20
Q

2Angiotensin receptor blocker (ARBS) SartanS

A
  1. Block AT1 receptors which mediate most of
    pathological CVS effects of Ang II
  2. Spare AT2 receptors → VD & antiproliferative effect
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21
Q

Indications of ARBS?

A

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:

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22
Q

Adverse effects of ARBS?

A

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

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23
Q

Advantages of ACEI and ARBS?

A

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

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24
Q

ACEI and ARBS? are

A

Renoprotective

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25
Q

Hypolaemia induced arrhythmia and ACEI AND ARBS?

A

Aldosterone prevention from remdeling and fibrosis and Hypolaemia induced arrhythmia

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26
Q

Advantages ARBs Over ACEI ?

A

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)

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27
Q

Sacubitril -valsartan combination called? is used in place ?

A

(Angiotensin Receptor Neprilysin Inhibitor= ARNI)
of ACEIs or
ARBS in patient with LVEF < 40%

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28
Q

Neprilysin inhibitors: Sacubitril

A

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)

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29
Q

Hydralazin mechanism of action and indicztions ?

A

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
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30
Q

-HTN IV with Eclampsia

A

hYDRALAZINE

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31
Q

hYDRALAZINE TOLEARNCE DUE TO ?

A

By time , it stimulates Sympathatic and Renin Angiotensin system
casuing reflex tachycardia salt and water retention increasing BP !!

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32
Q

Na nitroprusside ?Mechanisms and Indications ?

A

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

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33
Q

Adverse effects of Na nitroprusside?

A 
Hypotension and (Myocardial Ischemia due to reflex tachy cardia )
Cyanide toxicity due to liver dysfuction
Thiocyanat toxicity due to renal dysfunction
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34
Q

Thiocyanat toxicity due to

A

renal dysfunction

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35
Q 
Precautions with Na nitroprusside
Precautions:
• ???= (Avoid drop < 95/70 mmHg)
• Solution should be ?
• Avoid prolonged use
A

Slowly IV with BP monitoring
freshly prepared & protected from light by opaque foil
especially in hepatic & renal dysfunction to avoid toxicity

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36
Q

Diuretics in systolic heart failure?

A

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

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37
Q

Adnvatages of Spironolactone?

A

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

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38
Q

SPRINOLOACTONE USED CASUTILUSLY WITH ? WHY?

A

ACEI OR IN RENAL IMPAIRMENT

TO AVOID RISK OF HYPERKALEMIA

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39
Q

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

A

ACEI
ARBS
BB
Spironolactone

40
Q

BB IN HEAR FAILURE

A

MBC
Metoprolol
Bisoprolol
Carvediolol

low dose gradually increased to avoid woresining in cardiac function

41
Q

Multiple actions neurohormonal antagonist

A

Carvedilol:
• ↑ ejection fraction → improve symptoms
• ↓ Disease progression
• Reduce hospitalization & mortality rate

42
Q

Drawbacks of chronic sympahtic stimulation on Heart?

A

Tachycardia and increasd O2 demeand
Renin angiotenisn system activation and Remodeling and Hypertrophy dilatation
Production of Cardic cytokines and Intelukeins induce hypertrophy apotoisis fibrosis

43
Q

ACEI
ARNI
BB
MRA

A

HFrEF

44
Q

bb avoided in ?

A

Hypotension
pulmonary congestion
AV Block
has delayed onset of action

45
Q

decreasing mortaility rate

A 
Attention:
The advantages of the following in HF:
1. ACEIs OR ARNI 
2. β blockers
3. Spironolactone (MRA)
4. SGLT2 inhibitor (
46
Q

Advantages of BB?

A

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

47
Q

How BB decreases the O2 demand of Heart?

A
  1. ↓ Heart Rate → ↑ diastolic time →↑ coronary filling

2. ↓ After load (↓Blood Pressure)

48
Q

BB AS CARDIOPROTECTOR

A

Block catecholamines and Ang2 induced arrhymia myocardial damage and apotpiss

49
Q

bb Improve LV dysfunctions

A
50
Q

bb Improve LV dysfunctions

A

decreasing reinien and RAS

51
Q

BB improving contractility

A

Upregulation of B1 Receptross ( in long standing HF)

52
Q

Direct effect OF Dioxin ?

A

(+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++]

53
Q

Indirect effect of digoxin

A
  1. ↑ vagal tone on heart (Central stimulation of vagal nucleus)
  2. ↓ Sympathetic activity in patients with heart failure
    secondary to improvement of COP
54
Q

how digoxin is + INOTROPE?

A

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

54
Q

how digoxin is + INOTROPE?

A

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

55
Q

Decreasing Venous pressure and EDV by digoxin how?

A

due to better cardiac emptying

56
Q

Digoxin

decreasing sypmathtaic activity and Preload and afterload symptomps through?

A

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

57
Q

digoxin and diuresis?

A

Diuresis increasing COP ,RBF, Aldosterne antagonism

58
Q

Electrical effect: arrhythmogenic of digoxin ?

A

↑ 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
59
Q

CNS stimulation by digoxin

A
  • Vagal center (Nucleus) (therapeutic doses)
  • CTZ (supra-therapeutic dose): early s/s of toxicity
  • Visual & cortical → visual disturbances, hallucination (toxic doses)
60
Q

Direct vasoconstriction

A

↑ Ca++ in vessel wall. This effect is antagonized by digitalis
induced ↓ in sympathetic activity

61
Q

Vagal stimulation by diogoxin ?

A

SAN decresing HR For optimum digitalization
Atria decreasing APD casuing Af to AF
DECREASING AVN Conduction

62
Q

Digoxin and decrasing AVN ?

A

By vagal stimulation:
فيونكة يحمي البطين من النبضات الزيادة في الأذين
Overdoes > heart block bradycardia give atropine
Termination of PSVT By - re-entry phenomenon

63
Q

Contraindication of Digoxin >?

A 
SH ARVA 
Sick sinus syndrome
Partial Heart block
HOCM
Acute MI
Rhematic carditis
Ventricular Tachycardia
AF+ WPW
64
Q

most solid indication OF Digoxin?

A

AF+Heart failure
↓ AVN conduction (↑EFR) →
control ventricular rate in AF 

65
Q

counteract its atropine like action of proacinamide?

A

Digoxin

66
Q

Indications of Digoxin?

A

PSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVT

Systolic heart failure
AF + Heart failure
Chronic AF without Heart failure
PSVT!!!!

PSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVTPSVT

67
Q

DIGOXIN IN Chronic AF without Heart failure

WITH

A

VERAPAMIL and BB TO CONTROL VENTRICULAR RATE

BEFORE PROCAINCMID TO CONTROL its atropine like action

68
Q

WHY BS antibiotics problem with digoxin

A

Absorption: 2/3 oral dose is absorbed. Rest is inactivated by bacterial flora (BS antibiotics kill bacteria flora
that inactivate digoxin→ ↑ amount absorption)

69
Q

Hemodilasys not effective in Digoxin toxicity????

A

Distribution: 2/3 oral dose is unbound to plasma protein → ↑Vd → (Hemodialysis is not effective in toxicity)

70
Q

Elimnation of Digoxin explain

A

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)

71
Q

Dosing of digoxin

A
  • 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
72
Q

Adverse effects of Digoxin ?

A

Cardiac arrhytgmia
CNS Halluscinations
Git
Gyncomastia

73
Q

cardiac arrhtymia and Digoxin?

A

Suprevent. and Vent, tachycardia premature beats fibrillations due Ca overload

Siuns brady cardia and Heart block due to Vagal Stimulation

74
Q

CNS adverse effects?

A

Confusion
Hallucination
green yellow vision

75
Q

Erthrromycin and dgioxin ?

A

Kill git flora that take 1/3 digoxin increasing its absoprtion

76
Q

Antiarrthymic drung and pharmacko kinetic interaction with digoxin

A

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

77
Q

Digitalis induced tachyarryhtmia?>

A

Diuretics decreasing k mg increasing ca
CORTICOSTERIOIDS Decreasing K
Hypercalcemia
sympathomimetics

78
Q

Digitalis induced Bradyarrhytmia?

A

BB and CCB Decreasing AVN conduction and

May cause HB

79
Q

ECG changes in Digoxin?

A

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

80
Q

Treatment of digoxin toxicity?

A

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

81
Q

Dopamine ?

A

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

82
Q

Dobutamine

A

B1 ONLY + INOTROPIC LESS INCREASE IN HR
LESS ARHTHMOGENIC

AS dopamine but in normotensives + preserved renal functions

83
Q

Phosphodiesterase II inhibitors?

A

Increasing cAMP AND CARDIAC Contractility

Arterilodilator and Venulodilator decreasing Preload And AfterLoad

84
Q

Adverse effects of PDI2?

A

Thrombocytopenia
Arrhythmia
Git upset

85
Q

Tolvaptan ?

A

V2 antagonist
induce excretion of Elctrolyte free water to correct diltuonal hyponatremia induced by ADH
In systolic Heart Failure Especially with Resistance to loops

86
Q

Nesritide

A

IVI ? Then?

Recombinant type of B-naturetic peptide
Vasodilation of Arterioles and venules decreasing Loads
In decompensated Heart Failure
Adverese effect : Hypotension

87
Q

Acute decompensated heart failure therapy ?

A

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

88
Q

sodium-glucose co-transporter 2 (SGLT2) inhibitors: e.g. dapagliflozin

A

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

89
Q

Heart failure associated with AF: Add:

A

β blocker, digoxin & direct oral anticoagulant (e.g. Rivaroxaban)

90
Q

Ivabradine (see angina) is used if heart rate >

A

70 b/min (if response to β blocker is poor)

91
Q

• Digoxin: used if the patient still symptomatic in essential therapy or

A

if heart failure is associated with atrial fibrillation

92
Q

Treatment of co-morbidities e.g is essential

A

. Hypertension,
ISHDs
& DM

93
Q

• N-3 polyunsaturated fatty acids can

A

reduce mortality in heart failure

94
Q

الحمدلله الذي أنزل علي عبده الكتاب ولم يجعل له عوجا

إنه من يتق ويصبر فإن الله لا يضيع أجر المحسنين

A

CVS Pharma papre 1 (4 decks)

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