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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
CXR changes
Cardiomegali Prominent upper lob veins Alveolar Shadowing Kerley line Bat wing appearance Interstitial edema
26
Echo changes
Evidence of left ventricular dysfunction(ejection faction less than 45 %) Underline causes (valvula abnormalities)
27
BNP and HF
Elevated in heart failure sensitive Marker for heartfailure
28
What are the other investigations (except CXR Echo ECG)
Fbc Fbs Lipid profile Urine full report Blood urea and serum electrolyte Serum TSH Blood culture Trop ABG
29
How to manage acute pulmonary edema
Sit upright High oxygen IV cannula Frusamide Morphin Cardiac monitoring Pulse oximetry Other investigations
30
Step 2 Management
ABG IV inotropes {dobutamin, dopamine,NA} Consider other diagnosis
31
Step 3 HF management
Mechanical ventilation Intra ventricular devices
32
Step 4. (patient improved)
Oral drugs (frusamide,ACEi Follow up
33
**Non pharmacological** management of chronic congestive cardiac failure
Diet (salt restriction, fluid restriction) Avoid alcohol Stop smoking Rest and mobilization Maintain ideal body weight Education about illness , drugs
34
Main **drug management** of congestive cardiac failure
1. Diuretics (Frusamide,Thiazide, Spiranolacton) 2. Others ACEI BB DIGOXIN vasodilator ( nitrate hydralazine) Inotropes
35
ACEI eg:
Captopril Enalapril
36
What is the first line therapy to all patients with **ejection fraction less than 40%**
ARB (Losartan)
37
BB for HF eg:
Carbadilol Bisoprolol
38
Action of Digoxin
Increase contractility Reduce heart rate Dose adjust according to the weight and renal function
39
INOTROPES in HF
Dobutamin Dopamin
40
What are the complications that made from heart diseases cause heart failure
*Increase workload on heart* *Insufficiency of myocardium* *Both*
41
What are the pathological changes superimposed in CCF
1 Myocyte apoptosis 2 Cytoskeleton alteration 3 Extra cellular material deposition
42
Difference between physiological and pathological hypertrophy of the heart.
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
Features of hypertrophic myocyte
Increase protein synthesis Additional sarcomeres Increase mitochondria Enlarge nuclei Induction fetal genes Abnormal proteins Fibrosis
44
How Dyspnea occur in left ventricular failure
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
Morphology of heart in left heart failure
Usually heart is hypertrophy with or without dilation Can have LA dilation and thrombie formation Myocyte hypertrophyte and interstitial fibrosis
46
Pure right heart failure causes
Following chronic lung diseases Tricuspid or pulmonary valve diseases Myocardial diseases affect right side
47
Morphology of right heart failure
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
effects and **pathological changes** that occur in following organ due to heart failure? **Liver, lung, brain kidney**?
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
2 main targets of using drugs in heart failure
Improve mobidity. Symptomatic Improve mortality. Suvival
50
What is improve mobidity in heart failure
Improve forward failure( fatigue. Exertinal Dyspnea) Improve backward failure(P oedema,gen. Oedema)
51
**improve mortality** survival Benefit drugs
ACEI ARB BB Spiranolacton Nitrate+Hydralazine
52
**Improve mobidity** symptomatic benefit
Loop diuretics Digoxin Nitrates
53
A,B,D,D,S
ACEI/ARB BB DIGOXIN DIURETICS SPIRANOLACTON
54
ACEI. ARB. actions
**Reduce** Vesoconstriction Aldosterone production Activation of SNS
55
BB MOA. (metaprolol,carvadilol,bisoprolol)
Blanting of activated sympathy nervous system Reduce risk of sudden death via arithmetic effect
56
BB clinical uses
**Chronic stable HF** **Asymptomatic HF** NOT FOR UNSTABLE HF
57
What need to monitor when giving BB
Low BP Bradycardia Cardiac decompensation
58
Loop diuretics MOA
It reduces pre load by **increase water loss and venodilation**
59
Adverse effects of loop diuretics
Hypokalemia hyponatremia Hypotension Hyperuricemia and gout Rashes and photosensitivity Transient deafness and tinnitus Temporary increase serum TAG and cholesterol
60
Digoxin indications
**Only in symptomatic chronic heart failure** Supraventricular tachyarrhythmia
61
What are the **direct and indirect** mechanism of **Digoxin**
**indirect** Vagal activity Slow SA to AV **Direct** Inhibit Na K ATPase Incrase intra cellular Ca Increase contractility and excitability
62
Problems of Digoxin
Anorexia vomiting nausea Ventricular tachyarrhythmia Colour vision affect Gynecomastia
63
Digoxin containdications
Complete HB 2nd degree AV block WPW Ventricular tachyarrhythmia LV outflow tract obstruction
64
Uses of Spiranolacton
Symptomatic chronic HF Add on theropy persistent symptoms in diuretics ACEI and BB Cirrhosis
65
Adverse effects of Spiranolacton
Hyperkalemia Gynecomastia Hyponatremia
66
Contraindications fro Spiranolacton
Hyperkalemia Hyponatremia Renal failure
67
Nitrats MOA
Venodilation causes reduce pre load
68
When use Nitrate + Hydralazine
In chronic HF - symptomatic and survival benifits
69
Hydralazine MOA
Arterial dilator **Disadvantage** Reflex sympathetic activation Stimulate renin release

CVS (8 decks)

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