فشل القلب :( Flashcards

Question

Hypolaemia induced arrhythmia and ACEI AND ARBS?

Answer 1

Aldosterone prevention from remdeling and fibrosis and Hypolaemia induced arrhythmia

Answer 2

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)

Answer 3

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

Answer 4

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)

Answer 5

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

Answer 6

hYDRALAZINE

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

renal dysfunction

Answer 11

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

Answer 12

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

Answer 13

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

Answer 14

ACEI OR IN RENAL IMPAIRMENT | TO AVOID RISK OF HYPERKALEMIA

Answer 15

ACEI ARBS BB Spironolactone

Answer 16

MBC Metoprolol Bisoprolol Carvediolol low dose gradually increased to avoid woresining in cardiac function

Answer 17

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

Answer 18

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

Answer 19

Hypotension pulmonary congestion AV Block has delayed onset of action

Answer 20

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

Answer 21

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

Answer 22

1. ↓ Heart Rate → ↑ diastolic time →↑ coronary filling | 2. ↓ After load (↓Blood Pressure)

Answer 23

Block catecholamines and Ang2 induced arrhymia myocardial damage and apotpiss

Answer 24

decreasing reinien and RAS

Answer 25

Upregulation of B1 Receptross ( in long standing HF)

Answer 26

(+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++]

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

due to better cardiac emptying

Answer 31

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

Answer 32

Diuresis increasing COP ,RBF, Aldosterne antagonism

Answer 33

↑ 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 ```

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

VERAPAMIL and BB TO CONTROL VENTRICULAR RATE | BEFORE PROCAINCMID TO CONTROL its atropine like action

Answer 42

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

Answer 43

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

Answer 44

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)

Answer 45

* 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

Answer 46

Cardiac arrhytgmia CNS Halluscinations Git Gyncomastia

Answer 47

Suprevent. and Vent, tachycardia premature beats fibrillations due Ca overload Siuns brady cardia and Heart block due to Vagal Stimulation

Answer 48

Confusion Hallucination green yellow vision

Answer 49

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

Answer 50

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

Answer 51

Diuretics decreasing k mg increasing ca CORTICOSTERIOIDS Decreasing K Hypercalcemia sympathomimetics

Answer 52

BB and CCB Decreasing AVN conduction and | May cause HB

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

B1 ONLY + INOTROPIC LESS INCREASE IN HR LESS ARHTHMOGENIC AS dopamine but in normotensives + preserved renal functions

Answer 57

Increasing cAMP AND CARDIAC Contractility | Arterilodilator and Venulodilator decreasing Preload And AfterLoad

Answer 58

Thrombocytopenia Arrhythmia Git upset

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

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

Answer 65

if heart failure is associated with atrial fibrillation

Answer 66

. Hypertension, ISHDs & DM

Answer 67

reduce mortality in heart failure