heart failure

Question 1

definition of heart failure according to AHA?

Answer 1

HF is a complex clinical syndrome with symptoms and signs that result from any structural or functional impairment of ventricular filling or ejection of blood

Question 2

introduction of hf
and when it reffers to CHF

Answer 2

Heart failure is inability of the heart to pump enough blood to meet the blood flow and metabolic demands of the body
It results from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

When the condition is accompanied with S & S of congestion it is referred to as CHF

Question 3

what are Four major determinants contribute to left ventricular (LV) workload?

Answer 3

Preload: forces acting on the venous side of circulation that affect myocardial wall tension
Afterload: tension in the ventricular wall as contraction (systole) occurs
Contractility: the myocardium’s intrinsic ability to develop force and shorten its fibers independent of preload and afterload
Heart rate (HR)

Question 4

what is Stroke volume (SV) and normal level?

Answer 4

is the volume of blood ejected by the heart with each systolic contraction
(normal, 4–7 L/minute)

Question 5

Cardiac output (CO)

Answer 5

is the amount of blood pumped in 1 minute (CO = SV × HR).

Question 6

Left ventricular ejection fraction (LVEF)
and normal level

Answer 6

is the percentage of LV end-diastolic volume expelled during each systolic contraction (normal, 60%–70%).

Question 7

Systolic dysfunction

Answer 7

also known as low ejection fraction HF, is when the LVEF is <40%.

Question 8

Compensatory Mechanisms in CHF

Answer 8

Hemodynamic Responses:
* Increased contractility
* Increased HR
* Vasoconstriction: leading to cardiac remodelling
Neural Responses: Symapthetic ANS
Renal Responses: RAAS
Hormonal Responses: Aldosterone
Cardiac Remodeling

Question 9

Cardiac remodeling and its 3 types

Answer 9

Progression of HF results in a process referred to as cardiac remodeling

1. Restrictive cardiomyopathy: the left ventricular walls may be normal, hypertrophic, or slightly dilated
2. Dilated cardiomyopathy: results in thinning of the left ventricular walls and a decrease in systolic function
3. Hypertrophic cardiomyopathy: there is a marked thickening of the left ventricular walls leading to diastolic or systolic failure

Question 10

types of heart failure

Answer 10

1. Low output, systolic dysfunction(dilated cardiomyopathy)
2. Diastolic dysfunction
3. High-output failure
   (uncommon)

Question 11

Systolic Dysfunction due to

Answer 11

decreased contractility
* Dilated cardiomyopathies (dilated left ventricle)
* Reduction in muscle mass (e.g. myocardial infarction)
↑Afterload
* pressure overload: HTN, aortic stenosis

• EF less than 40

less blood pump out of the ventricle in each beat causing accumulation of blood in ventricles

Question 12

diastolic dysfuntion

Answer 12

Restriction in Ventricular Filling
Thickened left Ventricle (hypertrophic cardiomyopathy
Stiff left ventricle (restrictive cardiomyopathy)
impaired left ventricular filling
pressure and/or volume overload)
Pericardial disease (e.g. pericarditis, pericardial tamponade)

Question 13

Drugs That May Precipitate or Exacerbate HF

Answer 13

Agents Causing –ve Inotropic Effect
Antiarrhythmics(disopyramide, flecainide))
betablocker
non dihydropyridine ccb
Itraconazole
Terbinafine
Cardiotoxic Agents
Doxorubicin
Daunorubicin
Cyclophosphamide
Cocaine & Amphetamines (Long-term use)

Agents Causing Na+ and Water Retention
* nsaid, cox II inhibtor, salisylate
* androgen, estrogen, glucocorticoid
* Na+-containing drugs (e.g. carbenicillin disodium)
Thiazolidinediones
Licorice

Na and water retetion: Slangent
Cardiac: deadly drug after coctail (ddac)

Question 14

Congestion in HF

Answer 14

Left-Sided Heart Failure:
Results from LV dysfunction – Blood backs up into Left atrium – Pulmonary congestion and edema

Right-Sided Failure:
Results from diseased right ventricle - Blood backs up into right atrium and venous circulation – Peripheral oedema & Ascites

Question 15

Diagnostic Tests:

Answer 15

Clinical history
Physical Exam
ECG
Initial lab investigations (e.g. SrCr, CBC)
Chest X-ray
Transthoracic Echocardiography
Radionuclide Angiography
Coronary Angiography
Cardiac MRI
Assessment of Functional Capacity: e.g. NYHA

Question 16

Classification / Staging of HF

Answer 16

Stage A: At-Risk for Heart Failure

Stage B: Pre-Heart Failure

Stage C: Symptomatic Heart Failure

Stage D: Advanced Heart Failure

Question 17

Stage A: Heart Failure

Answer 17

• Patients at risk for HF but without current or previous symptoms or signs of HF.
• No structural or functional heart disease or abnormal biomarkers.
• This stage includes individuals with conditions like hypertension, diabetes, obesity, or a family history of cardiomyopathy.

Question 18

Stage B: Heart Failure

Answer 18

patients without current or previous symptoms/signs of HF but with evidence of 1 of the following:
Structural heart disease
Evidence of increased filling pressures
Risk factors and increased natriuretic peptide levels or persistently elevated cardiac troponin in the absence of competing diagnoses

Question 19

Stage C: Heart Failure

Answer 19

Patients with current or previous symptoms/signs of HF.

Question 20

Stage D: Heart Failure

Answer 20

Patients with current or previous symptoms/signs of HF and:
Marked HF symptoms that interfere with daily life.
Recurrent hospitalizations despite attempts to optimize guideline-directed medical therapy (GDMT).

Question 21

Non-pharmacological Treatment

Answer 21

Dietary modifications e.g. Sodium and fluid restriction
Risk factor reduction e.g. smoking & alcohol cessation
Immunizations: influenza and pneumococcal vaccines (to reduce risk of serious respiratory infections)
Moderate physical activity

Daily weighing is recommended & any increase in weight or decline in exercise tolerance might indicate exacerbation
increase in weight 1-2 kg –> pheripheral edma loop dirutic pnr for 2-3 days twice

Question 21

Goals in Pharmacotherapy of HF

Answer 21

slowing disease progression, and improving survival in chronic HF act by targeting neuro-hormonal blockade.

These include: ACE inhibitors, ARBs, β-blockers, and aldosterone antagonists

Question 22

Management of HF Stage A patients:

Answer 22

Goals for Stage A
minimize the impact of diseases that can injure the heart.
Key Lifestyle Modifications:
regular physical activity, maintaining normal weight, healthy dietary, and avoiding smoking

Medications:
Antihypertensive and lipid-lowering therapies: to decrease the risk for stroke, MI, and HF.
ACE inhibitors should be considered in high-risk vascular disease patients.

Question 23

Management of HF Stage B patients

Answer 23

Goals for Stage B HF Patients:
prevent or slow the Syndrome of Clinical HF
Interfere with neurohormonal pathways
Key Medications:
ACE inhibitors (ACEi): In patients with LVEF ≤ 40%,
Statins: In patients with a history of (MI) or (ACS)
Beta-blockers: history of ACS and LVEF ≤ 40%, beta-blockers can be added to ACEi therapy

Question 24

hormone that increased in HF

Answer 24

Norepinephrine, Ag2 & aldosterone levels

Question 25

Management of HF Stage C patients
goals and treament?

Answer 25

goals:
alleviating fluid retention, Minimize disability, Slow disease progression, Reduce hospitalizations and mortality

treatment:
Diuretics: for patient with fluid retention, improving symptoms, relive congestion and preventing worsening HF.
Thiazides: Added to loop diuretics only if not responding to moderate/high doses, to minimize electrolyte abnormalities.

Neurohormonal antagonists:to minimize the effects of the RAAS and SNS.
ARNi is ARB + Neprilysin inhibitors (Valsartan + Sacubitril) reduced the cardiovascular death or HF hospitalization by 20% but avoid concurent with ace or after 36 hrs of ace dose or in case of angioedema.
**ACE inhibitors (or ARBs),
β-blockers, and aldosterone antagonists **
Digoxinmay be added to improve symptoms.
hydralazine and isosorbide dinitrate in black patients.

avoiding excessive sodium intake is reasonable to reduce congestive symptoms
In some cases, these include the combination of ACE inhibitors and ARBs, although the evidence for this option is limited.

Question 26

Management of HF Patients with advanced stage D disease:

Answer 26

goal: improve quality of life.
Treatment:
mechanical support,
transplantation,
continuous use of I.V. vasoactive therapies

In addition to maintaining an optimal regimen of chronic oral medications.

Question 27

Diuretics for HF

Answer 27

Indicated for rapid symptomatic relief of congestion or cardiac distension
Guidelines recommend diuretics, both acutely and chronically, but ONLY if clinical volume overload is evident.

Question 28

ACEI in HF

Answer 28

drug of choice in HF even in low lf failure
initaited low does and increased to high dose
ace + BB typically used
ace + aldoestron = dont use together

side effects
if angioedma its CL and stop using if occur
cough continue using

captopril is DOC in emergency
Have both preload- and afterload-reducing properties and consequent volume reducing potential.

Question 29

Benefits of ACE inhibitors & ARBs in CHF

Answer 29

Improvement in: LV size and function, Clinical symptoms & QoL
Increase exercise tolerance
Decrease disease progression
Reduce rate of: Hospitalization & Mortality

also effective in preventing HF development in high-risk patients e.g. post – MI when used early.

Question 30

Beta-Adrenergic blocking agents in HF

Answer 30

bb + ace first line
bisoprolol, metoprolol or carvedilol
initiated at low doses, with gradual increase as tolerated.
Symptoms can worsen with β-blockers, and it may take weeks or months before patients notice improvement.

It may take 2 to 3 months of therapy to see a beneficial response with some agents e.g. metoprolol

Abrupt withdrawal of beta-blockers therapy can lead to clinical deterioration and should be avoided

Question 31

Aldosterone antagonists in HF

Answer 31

are mid dirutic
Recommended when EF < 35%
Spironolactone most common 25-20 mg
Hyperkalemia risk in elderly and kidney disese or use with ace

Question 32

hydralazine and nitrate in HF

Answer 32

hydralazine = dialted artery = decrease afterload
nirate = dialted venus = decease preload

complementary action when used together and effective in pulmonary edma

used in patient non responsive to bb and ace

Question 33

Digoxin in HF

Answer 33

have negative introtropic effect, which increase contrctility,
use 0.125-0.20 mg daily with therapeutic level 1ng/ml
Digoxin has many D/D interactions e.g. Amiodarone, Atorvastatin, CCBs.
Ocular manifestations of digoxin toxicity include xanthopsia, or seeing yellow.

Question 34

Digoxin toxicity and management

Answer 34

toxicity:
* hypokalemia
* hyper ca+ and hyper mg+
* renal failure
* drug that cause digoxin tox: quidine, verapmil, loop dirutic

managment:
discountine therpy
serum k+ level if less give k+ supps
if arrythemia and severe toxicity give antidote digoxin specific AB ( digibind)