Cardiac failure Flashcards
Signs and symptoms Preload , afterload, contractility Drugs in management of chronic heart failure Diuretics ACE inhibitors Beta blockers
Symptoms of heart failure
Orthopnoea
Exertional dyspnoea
Fatigue
PND
Signs of heart failure
Raised JVP cardiomegaly Pleural effusion 3rd and 4th heart sounds Bibasal crackles Peripheral oedema Tender hepatomegaly Ascites Tachycardia
Name 10 factors in the pathophysiology of heart failure
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
Preload and role in HF
The amount of of blood left in ventricle after systole. This should stretch myocardium leading to increased contraction. This function is depressed in HF
Afterload definition
3 types
The load against which the heart contracts
Systemic resistance
Blood vessel resistance
Volume of blood ejected
Mechanism of system activated for inotropic support and contractility
The baroreceptors of SNS activated in HF and helps maintain cardiac output
Drugs that reduce mortality
ACE I/ARB
Beta blockers
Aldosterone
Hydralazine and nitrates
Drugs reducing hospitalization
Digoxin
Ivabradine
Drugs reducing symptoms
Diuretics
IV iron
AF management
Cardioversion
Ablation
Pulmonary vein isolation
Thiazide diuretics MOA
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
Adverse drug reactions of hydrochlorothiazide
Hypokalemia and hypomagnesaemia
Hypovolaemia
Orthostatic hypotension
Increased risk of diabetes
Spironolactone MOA
Competes with aldosterone in collecting ducts leading to reduced Na absorption
In heart failure significantly reduces fibrotic effect of aldosterone on heart
Spironolactone adaverse reactions
Hyperkalaemia
Estrogen like adverse reactions e.g. gynecomastia ED., menstrual abnormalities
Furosemide MOA
Stimulates NaCl excretion by blocking sodium potassium 2 chloride in thick ascending limb
Furosemide adverse reactions
Urate retention leads to gout Hypokalemia hypomagnesemia, hyponatremia, hypocalcaemia Decreased glucose tolerance Allergic tubulointerstitial nephritis Myalgia Ototoxic in high IV doses Hypochloraemic alkalosis
Low ceiling diuretics
Higher doses not recommended because of biochemical repercussions
High ceiling diuretics
Less incidence of adverse affects with administration of higher doses
Importance if preload reduction in heart failure
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
RAAS
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.
Action of angiotensin II on kidney
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.
Role of aldosterone secretion by angiotensin II
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
Angiotensin effects on brain
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.
How do ACE inhibitors decrease mortality
prevention of progressive LV remodeling,
prevention ofsudden deathand arrhythmogenicity
structural stability of the atherosclerotic process
Ace inhibitor contraindications
Renal artery stenosis
Pregnancy
previous angioedema
Why ACE I and spironolactone should be used cautiously together
Can cause hyperkalaemia
Clinical features of ACE inhibitors induced angioedema
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.
ACE inhibitor induced angioedema management
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
Role of ARBs in heart failure
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.
How do beta blockers improve heart failure
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
Beta blockers used in heart failure. Why?
Carvedilol
Metoprolol
Bisoprolol
All reduce mortality
Which heart failure patients are treated with beta blockers?
LV systolic dysfunction
Contraindications to beta blocker therapy
Asthmatics if not cardio selective Cocaine induced coronary vasospasm Long QT syndrome Bradycardia Hypotension Patients with Raynauds phenomenon
