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HF Flashcards

1
Q

What is heart failure

A

Cardiac output and blood pressure in adequate inorder to achieve metabolic demands and satisfactory tissue perfusion despite normal venous pressure ,resulting inadequate delivery of oxygen to the tissues

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2
Q

Diagnosis of heart failure

A

1) Symptoms and signs of heart failure
2) Eco cardiographic evidence of the cardiac disfunction

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3
Q

Three types of cardiac failure

A

LVF
RVF
CCF

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4
Q

Types of high output cardiac failure

A

Anaemia
thyrotoxicosis

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5
Q

Causes for systolic heart failure

A

decrease contractility
MI(IHD)
Myocarditis
DCM (DM. Alcohol)

Increase preload volume overload
MR
AR

Hyperdinamic circulation
Aneamia
Thyrotoxicosis

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6
Q

Causes for diastolic heart failure

A

decrease preload
MI
restrictive cardio myopathy
constructive pericarditis
MS/ TS
A Fib

Increase afterload
LVH deu to hypertension
Aortic stenosis
HOCM
coactation of aorta

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7
Q

Courses for acute heart failure

A

MI
Rheumatic fever
IE w/ valve damage
Arrythmia
Myocarditis
Pulmonary embolism

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8
Q

Causes for chronic heart failure

A

Aneamia
Cardiomayopathy
HTN
IHD
Chronic Valvular Heart diseased

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9
Q

What are the 3 compensatory mechanism caused by heart failure

A

1) activation of sympathetic nervous system

2) activation of rening angiotenzine system

3)Myocardial hypertrophy

(These mechanisms results in sodium and water retention, increase cardiac contractivity ,heart rate etc. so that patient will remain asymptomatic)

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10
Q

What is myocardial remodeling

A

After many months of these compensatory mechanism a series of adaptive changes in the myocardium happen.
Hypertrophy, loss of myosites and interstitial fibrosis

So the heart is unable to work as a pump and develop symptoms and signs of heart failure

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11
Q

What are the three ways that hard failure appears

A

1) reduction cardiac output :forward failure

2) increase Venus system pressure : backward failure

3) changes in the heart

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12
Q

What are the main 8 causes for left heart failure

A

IHD
HTN
Valvular heart diseases(MS,AS,MR,AR)
CARDIOMYOPATHY
Myocarditis
RF
Congenital heart diseases (vsd)
IE

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13
Q

What are the main three things happen in impaired lift ventricular function

A

Decrease CO
Pulmonary oedema
Cardiomegaly

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14
Q

Main symptoms of left heart failure

A

Breathlessness
Orthopnea
PND
Cough. (dry and productive pink frothy sputum)

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15
Q

Signs of lvf

A

Sob
Cyanisis
Tachycardia
Hypotension
Displace apex
Gallop rhythm
Bilateral fine endinspiratory crepitations

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16
Q

DD s for acute breathlessness

A

Non cardiac pulmonary oedema
ARDS
RF
Fluid overload

Bronchopneumonia

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17
Q

How congestive cardiac failure occur. (2)

A

1) left heart failure courses right heart failure by pulmonary hypertension

2) conditions which affect both ventricle at same time

Anaemia
Thyrotoxicosis
Cardio myopathy
Myocarditis

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18
Q

Evidence of right heart failure

A

Pedal oedema
RHC pain
Raised JVP
Hepatomegaly
Ascites
Anorexia (GIT Venus congestion)

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19
Q

DDs for CCF

A

Nephrotic syndrome
Cirrhosis
CRF
Cor pulmonale

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20
Q

Causes for right ventricular failure

A

PHT
Cor pulmonale

PE
Pulmonary stenosis
RV infarction

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21
Q

principles of left ventricular failure management

A

1) make the patient stable and treat pulmonary edema
2) confirm diagnosis and look for underline cause
3) long term treatment

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22
Q

Plan of left ventricular failure management (four steps)

A

1] basic measures
Initial treatment IV frusamide,
morphin , O2
Arrange investigations

Treat the cause (MI : streptokinase)

2] if no improvement ABG
If low BP- INOTROPES
other DDs

3] mechanical ventilation

4] follow up

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23
Q

Why investigations needed

A

Confirm diagnosis
Exclude differential diagnosis
Asses the severity of disease
Find the underlying cause

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24
Q

ECG changes consider in heart failure

A

Ischemia
LVH
Rhythm

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25
Q

CXR changes

A

Cardiomegali
Prominent upper lob veins
Alveolar Shadowing
Kerley line
Bat wing appearance
Interstitial edema

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26
Q

Echo changes

A

Evidence of left ventricular dysfunction(ejection faction less than 45 %)

Underline causes (valvula abnormalities)

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27
Q

BNP and HF

A

Elevated in heart failure

sensitive Marker for heartfailure

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28
Q

What are the other investigations (except CXR Echo ECG)

A

Fbc
Fbs
Lipid profile
Urine full report
Blood urea and serum electrolyte
Serum TSH
Blood culture
Trop
ABG

29
Q

How to manage acute pulmonary edema

A

Sit upright
High oxygen
IV cannula
Frusamide
Morphin
Cardiac monitoring
Pulse oximetry

Other investigations

30
Q

Step 2 Management

A

ABG
IV inotropes {dobutamin, dopamine,NA}

Consider other diagnosis

31
Q

Step 3 HF management

A

Mechanical ventilation

Intra ventricular devices

32
Q

Step 4. (patient improved)

A

Oral drugs (frusamide,ACEi

Follow up

33
Q

Non pharmacological management of chronic congestive cardiac failure

A

Diet (salt restriction, fluid restriction)

Avoid alcohol

Stop smoking

Rest and mobilization

Maintain ideal body weight

Education about illness , drugs

34
Q

Main drug management of congestive cardiac failure

A
  1. Diuretics
    (Frusamide,Thiazide, Spiranolacton)
  2. OthersACEI
    BB
    DIGOXIN
    vasodilator ( nitrate hydralazine)
    Inotropes
35
Q

ACEI eg:

A

Captopril
Enalapril

36
Q

What is the first line therapy to all patients with ejection fraction less than 40%

A

ARB
(Losartan)

37
Q

BB for HF eg:

A

Carbadilol
Bisoprolol

38
Q

Action of Digoxin

A

Increase contractility
Reduce heart rate

Dose adjust according to the weight and renal function

39
Q

INOTROPES in HF

A

Dobutamin
Dopamin

40
Q

What are the complications that made from heart diseases cause heart failure

A

Increase workload on heart
Insufficiency of myocardium
Both

41
Q

What are the pathological changes superimposed in CCF

A

1 Myocyte apoptosis
2 Cytoskeleton alteration
3 Extra cellular material deposition

42
Q

Difference between physiological and pathological hypertrophy of the heart.

A

According to the web search results, physiological and pathological hypertrophy of the heart are two different types of cardiac enlargement that occur in response to different stimuli and have different outcomes¹².

Physiological hypertrophy is a normal and adaptive process that occurs during development, pregnancy, or exercise. It is characterized by normal organization of cardiac structure and function, increased contractility, and enhanced angiogenesis¹²³. Physiological hypertrophy is regulated by beneficial signalling pathways, such as insulin, IGF1, PI3K, AKT1, and mTOR².

Pathological hypertrophy is an abnormal and maladaptive process that occurs in settings of disease, such as hypertension, myocardial infarction, or cardiomyopathy. It is characterized by altered organization of cardiac structure and function, decreased contractility, fibrosis, inflammation, and oxidative stress¹²³. Pathological hypertrophy is regulated by detrimental signalling pathways, such as angiotensin II, endothelin-1, GPCR, calcineurin-NFAT, and MAPK².

Physiological hypertrophy is generally reversible and protective, whereas pathological hypertrophy is often irreversible and progressive, leading to heart failure and increased mortality¹²³. Therefore, understanding the mechanisms of physiological and pathological hypertrophy might help to develop novel therapeutic strategies for preventing or reversing cardiac dysfunction².

43
Q

Features of hypertrophic myocyte

A

Increase protein synthesis
Additional sarcomeres
Increase mitochondria
Enlarge nuclei
Induction fetal genes
Abnormal proteins
Fibrosis

44
Q

How Dyspnea occur in left ventricular failure

A

When left ventricular failure occurs it increases the end systolic volume

causes left ventricular dilation

then mitral valve ring stretched

causes Mitral regurgitation

then pulmonary congestion and edema occurs

Dyspnea and cough

45
Q

Morphology of heart in left heart failure

A

Usually heart is hypertrophy with or without dilation

Can have LA dilation and thrombie formation

Myocyte hypertrophyte and interstitial fibrosis

46
Q

Pure right heart failure causes

A

Following chronic lung diseases

Tricuspid or pulmonary valve diseases

Myocardial diseases affect right side

47
Q

Morphology of right heart failure

A

Hypertrophy and dilation of right ventricle and atrium

Engorgement of systemic and Portal circulation

Congestive hepatomegaly
Congestive splenomegaly
Congestion of bowel
Effusions
Dependent edema

48
Q

effects and pathological changes that occur in following organ due to heart failure? Liver, lung, brain kidney?

A

Heart failure can cause a variety of changes in the body. The liver can become congested and enlarged, leading to abdominal swelling and pain². The lungs can become congested with fluid, leading to shortness of breath and coughing¹. The brain can be affected by heart failure in several ways, including reduced blood flow and oxygen delivery, which can lead to confusion, memory loss, and difficulty concentrating¹. Kidney function can also be affected by heart failure. In some cases, the kidneys may not receive enough blood flow and oxygen, which can lead to kidney damage³.

49
Q

2 main targets of using drugs in heart failure

A

Improve mobidity. Symptomatic

Improve mortality. Suvival

50
Q

What is improve mobidity in heart failure

A

Improve forward failure( fatigue. Exertinal Dyspnea)

Improve backward failure(P oedema,gen. Oedema)

51
Q

improve mortality survival Benefit drugs

A

ACEI
ARB
BB
Spiranolacton
Nitrate+Hydralazine

52
Q

Improve mobidity symptomatic benefit

A

Loop diuretics
Digoxin
Nitrates

53
Q

A,B,D,D,S

A

ACEI/ARB
BB
DIGOXIN
DIURETICS
SPIRANOLACTON

54
Q

ACEI. ARB. actions

A

Reduce

Vesoconstriction
Aldosterone production
Activation of SNS

55
Q

BB MOA. (metaprolol,carvadilol,bisoprolol)

A

Blanting of activated sympathy nervous system

Reduce risk of sudden death via arithmetic effect

56
Q

BB clinical uses

A

Chronic stable HF
Asymptomatic HF

NOT FOR UNSTABLE HF

57
Q

What need to monitor when giving BB

A

Low BP
Bradycardia
Cardiac decompensation

58
Q

Loop diuretics MOA

A

It reduces pre load by increase water loss and venodilation

59
Q

Adverse effects of loop diuretics

A

Hypokalemia hyponatremia
Hypotension
Hyperuricemia and gout
Rashes and photosensitivity
Transient deafness and tinnitus
Temporary increase serum TAG and cholesterol

60
Q

Digoxin indications

A

Only in symptomatic chronic heart failure

Supraventricular tachyarrhythmia

61
Q

What are the direct and indirect mechanism of Digoxin

A

indirect
Vagal activity
Slow SA to AV

Direct
Inhibit Na K ATPase
Incrase intra cellular Ca
Increase contractility and excitability

62
Q

Problems of Digoxin

A

Anorexia vomiting nausea

Ventricular tachyarrhythmia

Colour vision affect

Gynecomastia

63
Q

Digoxin containdications

A

Complete HB
2nd degree AV block
WPW
Ventricular tachyarrhythmia
LV outflow tract obstruction

64
Q

Uses of Spiranolacton

A

Symptomatic chronic HF

Add on theropy persistent symptoms in diuretics ACEI and BB

Cirrhosis

65
Q

Adverse effects of Spiranolacton

A

Hyperkalemia
Gynecomastia
Hyponatremia

66
Q

Contraindications fro Spiranolacton

A

Hyperkalemia
Hyponatremia
Renal failure

67
Q

Nitrats MOA

A

Venodilation causes reduce pre load

68
Q

When use Nitrate + Hydralazine

A

In chronic HF - symptomatic and survival benifits

69
Q

Hydralazine MOA

A

Arterial dilator

Disadvantage
Reflex sympathetic activation
Stimulate renin release

CVS (8 decks)

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