study d4 Flashcards
heart failure
what is it, signs, treatment
- heart unable to pump sufficiently to maintain blood flow to supply body’s O2 requirement
- in systolic heart failure, this is due to decreased effectiveness of ventricles (pump)
- causes: cardiomyopathies, myocardial infarction, hypertension, valvular diseases
signs:
* decreased force of contraction (heart)
* decreased tissue perfusion
* oedema (pulmonary or peripheral)
* diaphoresis
Treatment
* aims to reduce symptoms –> workload on failing heart, preload, reduce afterload
adverse effects
* symptoms of inadequate output = fatigue, poor perfusion
* symptems of excessive congestion = œdema, dyspnea
compensation for hf
reduced contractility → reduced cardiac output → (+ compensation)
1. Dilatation of the heart due to volume overload
2. Activation of sympathetic nervous system to increase contractility, heart rate and blood pressure
3. Activation of renin-angiotensin-aldosterone system
4. Water retention and increased circulating volume
↑ heart rate (tachycardia)
↑ venous return / preload (dilatation)
↑ peripheral resistance / afterload
SGLT-2 inhibitors
- e.g. - “gliflozins” → dapagliflozin, empaglifozin, canaglifozin
- inhibit Na+/glucose reabsorption in proximal tubule of the kidney
- diuretic effect through increased loss of Na+ and glucose
this leads to reductions in circulation volume and reduced preload
adverse effects :
* fungal infections, polyuria, hypotension, euglyemic diabetic, ketoacidosis
Cardiac glycosides
physiological effects, and adverse effects
Cardiac Glycosides
(example: DIGOXIN)
Mechanism of action:
* block Na+-K+ ATPase;
* note: there is a competition between digoxin and extracellular K+, therefore low extracellular K+ can increase effect of these drug
* results in increased intracellular Ca2+ levels
narrow therapeutic index
* dangerous if patients are hypokalemic
* low extracellular K+ increases effect of cardiac glycosides
Physiological Effects:
Mechanical:
↑ force of contraction
(positive inotropic effect)
Electrical:
↓ heart rate /
↓ atrioventricular conduction
Adverse effects
Nausea, vomiting
arrhythmias (late afterdepolarizations)
treatment of overdose:
administration of neutralizing anti-digoxin
antibody fragments (Digibind)
beta adrenergic agonist
what’s the danger
Beta adrenergic agonists
examples: dopamine, dobutamine
mechanism of action:
* increase force of contraction and heart rate
* dobutamine stimulates beta1-adrenergic receptors
danger: can result in arrhythmias
limited used due to adverse effects and short half-life
phosphodiesterase inhibitors
name them, effects
phosphodiesterase:
milrinone, inamrinone
- inhibiting enzyme responsible for the degradation of cAMP and cGMP –> cAMP levels are increased
- effect: increase the force of contraction of the heart and increase relaxation of vascular smooth muscles
their use is limited by the numerous adverse effects (linked to the non specificity of the inhibition)
Anxiolytics
Benzodiazepines –> clinical uses, adverse effects
- benzodiazepines enhance the effect of GABA
ex. lorazepam (Ativan), clonazepam, diazepam
Adverse effects:
* drowsiness, ataxia (lack voluntary coordination of muscle movement)
* dangerous when combined with alcohol
* can cause anterograde amnesia
* risk of moderate dependence* and abuse*; tolerance (14d +)
prolonged use may lead to withdrawal syndrome
= insomnia, anxiety, tremors, …
Clinical Uses:
* sedation (before surgery), reduce anxiety ,
muscle relaxation
Antidote: flumazenil
* benzodiazepine receptor antagonist
* can trigger seizures (rebound effect)
Rohypnol and GHB
anxiolytic
Flunitrazepam (Rohypnol)
* approved for use in Europe/South America
* 10X more potent* than diazepam
GHB = gamma hydroxybutyrate
* found in the brain
* acts on GABA receptors
* often contain toxic residues leftover from their chemical synthesis
when combined with alcohol, these drugs can cause: fainting, anterograde amnesia, respiratory depression, bradycardia, hypotension
Non benzodiazepines
z
(zopiclone, zolpidem)
* anxiolytic drugs that not share the same chemical structure as benzodiazepines but that act on the same GABAA receptor
* used for the treatment of insomnia
* can induce sleep without decreasing stages of restorative sleep
* fewer adverse effects affecting coordination/memory
* generally, shorter duration and onset of action than benzodiazepines
buspirone
decreases the release of serotonin
(5-HT)
* less sedative
* fewer interactions with alcohol
* less abuse than benzodiazepines
* does not act very quickly
side effects: dizziness, lightheadedness
adrenergic
alpha and beta
Adrenergic:
Alpha-2 agonist (clonidine)
may reduce physical symptoms but not particularly effective at reducing anxiety on the emotional level
Beta adrenergic Antagonists (propranolol)
often used for the treatment of social phobia, performance anxiety and anxiety related to the memory of stressful event
