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Pharmacology > Cardiac failure > Flashcards

Cardiac failure Flashcards

Signs and symptoms Preload , afterload, contractility Drugs in management of chronic heart failure Diuretics ACE inhibitors Beta blockers

1
Q

Symptoms of heart failure

A

Orthopnoea
Exertional dyspnoea
Fatigue
PND

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2
Q

Signs of heart failure

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

Name 10 factors in the pathophysiology of heart failure

A 
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
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4
Q

Preload and role in HF

A

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

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5
Q

Afterload definition

3 types

A

The load against which the heart contracts

Systemic resistance
Blood vessel resistance
Volume of blood ejected

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6
Q

Mechanism of system activated for inotropic support and contractility

A

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

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7
Q

Drugs that reduce mortality

A

ACE I/ARB
Beta blockers
Aldosterone
Hydralazine and nitrates

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8
Q

Drugs reducing hospitalization

A

Digoxin

Ivabradine

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9
Q

Drugs reducing symptoms

A

Diuretics

IV iron

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10
Q

AF management

A

Cardioversion
Ablation
Pulmonary vein isolation

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11
Q

Thiazide diuretics MOA

A

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

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12
Q

Adverse drug reactions of hydrochlorothiazide

A

Hypokalemia and hypomagnesaemia
Hypovolaemia
Orthostatic hypotension
Increased risk of diabetes

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13
Q

Spironolactone MOA

A

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

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14
Q

Spironolactone adaverse reactions

A

Hyperkalaemia

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

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15
Q

Furosemide MOA

A

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

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16
Q

Furosemide adverse reactions

A 
Urate retention leads to gout
Hypokalemia hypomagnesemia, hyponatremia, hypocalcaemia
Decreased glucose tolerance 
Allergic tubulointerstitial nephritis
Myalgia
Ototoxic in high IV doses
Hypochloraemic alkalosis
17
Q

Low ceiling diuretics

A

Higher doses not recommended because of biochemical repercussions

18
Q

High ceiling diuretics

A

Less incidence of adverse affects with administration of higher doses

19
Q

Importance if preload reduction in heart failure

A

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

20
Q

RAAS

A

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.

21
Q

Action of angiotensin II on kidney

A

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.

22
Q

Role of aldosterone secretion by angiotensin II

A

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

23
Q

Angiotensin effects on brain

A

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.

24
Q

How do ACE inhibitors decrease mortality

A

prevention of progressive LV remodeling,

prevention ofsudden deathand arrhythmogenicity

structural stability of the atherosclerotic process

25
Q

Ace inhibitor contraindications

A

Renal artery stenosis
Pregnancy
previous angioedema

26
Q

Why ACE I and spironolactone should be used cautiously together

A

Can cause hyperkalaemia

27
Q

Clinical features of ACE inhibitors induced angioedema

A

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.

28
Q

ACE inhibitor induced angioedema management

A

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

29
Q

Role of ARBs in heart failure

A

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.

30
Q

How do beta blockers improve heart failure

A

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

31
Q

Beta blockers used in heart failure. Why?

A

Carvedilol
Metoprolol
Bisoprolol

All reduce mortality

32
Q

Which heart failure patients are treated with beta blockers?

A

LV systolic dysfunction

33
Q

Contraindications to beta blocker therapy

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

Pharmacology (13 decks)

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