Cardiac failure

Question 1

Symptoms of heart failure

Answer 1

Orthopnoea
Exertional dyspnoea
Fatigue
PND

Question 2

Signs of heart failure

Answer 2

Raised JVP
cardiomegaly
Pleural effusion
3rd and 4th heart sounds 
Bibasal crackles
Peripheral oedema
Tender hepatomegaly
Ascites
Tachycardia

Question 3

Name 10 factors in the pathophysiology of heart failure

Answer 3

Preload 
Outflow resistance 
Contractility 
Neurohormonal and sympathetic activation (salt and water)
Myocardial remodeling
Change in myocardial gene expression 
Endothelial function in HF
ADH
Abnormal Ca homeostasis 
Apoptosis 
Natriuretic peptide

Question 4

Preload and role in HF

Answer 4

The amount of of blood left in ventricle after systole. This should stretch myocardium leading to increased contraction. This function is depressed in HF

Question 5

Afterload definition

3 types

Answer 5

The load against which the heart contracts

Systemic resistance
Blood vessel resistance
Volume of blood ejected

Question 6

Mechanism of system activated for inotropic support and contractility

Answer 6

The baroreceptors of SNS activated in HF and helps maintain cardiac output

Question 7

Drugs that reduce mortality

Answer 7

ACE I/ARB
Beta blockers
Aldosterone
Hydralazine and nitrates

Question 8

Drugs reducing hospitalization

Answer 8

Digoxin

Ivabradine

Question 9

Drugs reducing symptoms

Answer 9

Diuretics

IV iron

Question 10

AF management

Answer 10

Cardioversion
Ablation
Pulmonary vein isolation

Question 11

Thiazide diuretics MOA

Answer 11

Acts by blocking Na channel on DCT. Competes for chloride site and leads to sodium and chloride excretion. This reduces plasma volume and increases renin activity, aldosterone secretion and leads to urinary potassium loss

Question 12

Adverse drug reactions of hydrochlorothiazide

Answer 12

Hypokalemia and hypomagnesaemia
Hypovolaemia
Orthostatic hypotension
Increased risk of diabetes

Question 13

Spironolactone MOA

Answer 13

Competes with aldosterone in collecting ducts leading to reduced Na absorption
In heart failure significantly reduces fibrotic effect of aldosterone on heart

Question 14

Spironolactone adaverse reactions

Answer 14

Hyperkalaemia

Estrogen like adverse reactions e.g. gynecomastia ED., menstrual abnormalities

Question 15

Furosemide MOA

Answer 15

Stimulates NaCl excretion by blocking sodium potassium 2 chloride in thick ascending limb

Question 16

Furosemide adverse reactions

Answer 16

Urate retention leads to gout
Hypokalemia hypomagnesemia, hyponatremia, hypocalcaemia
Decreased glucose tolerance 
Allergic tubulointerstitial nephritis
Myalgia
Ototoxic in high IV doses
Hypochloraemic alkalosis

Question 17

Low ceiling diuretics

Answer 17

Higher doses not recommended because of biochemical repercussions

Question 18

High ceiling diuretics

Answer 18

Less incidence of adverse affects with administration of higher doses

Question 19

Importance if preload reduction in heart failure

Answer 19

Improves symptoms by hemodynamic stabilization . Done by relieving LAP and countering excessive EDV to limit ventricular wall stress and functional mitral incompetence thereby improving forward blood flow

Question 20

RAAS

Answer 20

Activation of the JG cells occurs in response to decreased blood pressure, beta-activation, or activation by macula densa cells in response to a decreased sodium load in the distal convoluted tubule

Ronin is released and cleaves Angioatensinogen to AgI.

After angiotensin I is converted to angiotensin II by ACE, it has effects on the kidney, adrenal cortex, arterioles, and brain by binding to angiotensin II type I (AT) and type II (AT) receptors.

Question 21

Action of angiotensin II on kidney

Answer 21

In the proximal convoluted tubule of the kidney, angiotensin II acts to increase Na-H exchange, increasing sodium reabsorption. Increased levels of Na in the body acts to increase the osmolarity of the blood, leading to a shift of fluid into the blood volume and extracellular space (ECF). This increases the arterial pressure of the patient.

Question 22

Role of aldosterone secretion by angiotensin II

Answer 22

Angiotensin II also acts on the adrenal cortex, specifically the zona glomerulosa. Here, it stimulates the release of aldosterone. Aldosterone is a steroid hormone that causes an increase in sodium reabsorption and potassium excretion at the distal tubule and collecting duct of the nephron. Aldosterone works by stimulating the insertion of luminal Na channels and basolateral Na-K ATPase proteins. The net effect is an increased level of sodium reabsorption

Question 23

Angiotensin effects on brain

Answer 23

First, it binds to the hypothalamus, stimulating thirst and increased water intake.

Second, it stimulates the release of antidiuretic hormone (ADH) by the posterior pituitary. ADH, or vasopressin, acts to increase water reabsorption in the kidney by inserting aquaporin channels at the collecting duct.

Finally, angiotensin II decreases the sensitivity of the baroreceptor reflex. This diminishes baroreceptor response to an increase in blood pressure, which would be counterproductive to the goal of the RAAS.

Question 24

How do ACE inhibitors decrease mortality

Answer 24

prevention of progressive LV remodeling,

prevention ofsudden deathand arrhythmogenicity

structural stability of the atherosclerotic process

Question 25

Ace inhibitor contraindications

Answer 25

Renal artery stenosis Pregnancy previous angioedema

Question 26

Why ACE I and spironolactone should be used cautiously together

Answer 26

Can cause hyperkalaemia

Question 27

Clinical features of ACE inhibitors induced angioedema

Answer 27

swelling of the lips, tongue, throat or face. Another (less common) presentation is abdominal pain and diarrhoea due to swelling of the gut. This problem does not cause hives or itching.

Question 28

ACE inhibitor induced angioedema management

Answer 28

Discontinue meds If a patient presents with minimal swelling, supportive care and airway monitoring are recommended. However, if a case includes respiratory distress, stridor, drooling, or edema of the tongue or floor of the mouth, intubation and mechanical ventilation may be required for airway protection These target the inflammatory response and bronchoconstriction but do not interfere with the bradykinin pathway. These agents include epinephrine, antihistamines, and corticosteroids Fresh frozen plasma acts anecdotally against bradykinin C1-INH, ecallantide, and icatibant. C1-INH and ecallantide are primarily used to treat HAE as they inhibit conversion of precursors to bradykinin

Question 29

Role of ARBs in heart failure

Answer 29

ARBs may be better tolerated since they do not interfere with the degradation of bradykinin that is responsible for cough and possibly other side effects of ACE inhibitors.

Question 30

How do beta blockers improve heart failure

Answer 30

inhibition of the chronotropic and inotropic effects of the beta1‐receptors E and NE, a possible effect on regression in myocardial mass, and a possible normalisation in ventricular shape. Beta‐blockers are thought to reverse cardiac remodelling 

Question 31

Beta blockers used in heart failure. Why?

Answer 31

Carvedilol Metoprolol Bisoprolol All reduce mortality

Question 32

Which heart failure patients are treated with beta blockers?

Answer 32

LV systolic dysfunction

Question 33

Contraindications to beta blocker therapy

Answer 33

``` Asthmatics if not cardio selective Cocaine induced coronary vasospasm Long QT syndrome Bradycardia Hypotension Patients with Raynauds phenomenon ```