CV complications Flashcards
MAP =
= CO x SVR
= (SV x HR) x SVR
where SVR is systemic vascular resistance
CO in terms of VO2 (minimum oxygen consumption), CaO2 (arterial oxygen content), and CvO2 (mixed venous oxygen content)
What is the interpretation of this equation?
CO = VO2/(CaO2 - CvO2)
=> cardiac output is influenced by the oxygen demand of the tissues, and how much oxygen i bring to the tissues, and how much oxygen leaves the tissues
> the requirements of the tissues are met by the oxygen that is left there
> > when you run, the heart it is told by the tissues, “we need more oxygen”, and this is done by increasing HR or SV (CO = HR x SV)
possible CV complications
- Rate and Rhythm
* Rate
* Regular or irregular - Arterial blood pressure
- Circulating volume
normal HR vs tachycardia for dog
normal: 60-140
tachycardia: >180
normal HR vs tachycardia for cat
normal: 100-160
tachycardia: >240
normal HR vs tachycardia for horse
normal: 28-40
tachycardia: >60
normal HR vs tachycardia for foal
normal: 60-90
tachycardia: >110
normal HR vs tachycardia for cow
normal: 50-80
tachycardia: >100
what do we want to see on a normal electrocardiogram?
Make sure rhythm is sinus
* Only possible if ECG monitoring
* All waves should be present
- A “P” wave for every “QRS”
- A “QRS” for every “P” wave
pathophysiology of a normal to slow HR
Adequate diastolic filling- stroke volume
Too slow- negative effect on MAP, CO
pathophysiology of a fast HR
> Inadequate diastolic filling- stroke volume
Too fast- negative effect on MAP, CO
Myocardial hypoxia
what four factors contribute to stroke volume?
-preload
-afterload
-contractility
-rhythm
influence of high vascular resistance on cardiac output
high resistance may drop cardiac output
=> CO = MAP/SVR
animal species have different normal blood pressures. If pressures tend to be high, cardiac output tends to be….
low
-and vice versa; low pressures correspond to high cardiac outputs
CO relationship to MAP and SVR
CO = MAP / SVR
when might we see bradycardia with hypotension? what can trigger it? what drugs might cause this?
Increased parasympathetic activity
* Increased Vagal tone
Can be triggered by
* Oculocardiac reflex (trigeminovagal)
* Atrioventricular blocks and/or impaired SA to AV node conduction
– Heart disease (e.g.,Sick sinus syndrome)
- Drug induced
– Opioids (morphine, butorphanol, hydromorphone, fentanyl)
hypothermia and electrolyte abnormalities, specifically hyperkalemia, can cause what cardiac issues
bradycardia with hypotension or normal MAP
> if hyperkalemia caused by eg. urethral obstruction, may not see bradycardia due to counteracting effects of pain
when might we see bradycardia with hypertension? what is the root cause of this? what drugs can cause this?
§ Increased parasympathetic activity
- Drug induced
> Alpha 2-agonists (xylazine, romifidine, detomidine, dexmedetomidine)- due to hypertension that increases vagal tone - Baroreflex response to hypertension
> Vasoconstrictors that increase MAP
– Phenylephrine, Norepinephrine
– Increased intracranial pressure
» Cushing’s response or ischemic response to an increase in intracranial pressure (ICP)
HYPERTENSION FIRST and then BRADYCARDIA
when do we treat bradycardia?
§ Treat if marked bradycardia
§ Treat if hypotension or low cardiac output is associated with it
§ Treat if rhythm is markedly irregular and/or arrhytmias are also present
dont treat if hypertension => might exacerbate and decrease further the cardiac output
how can we treat bradycardia with hypotension, or no change in MAP?
depends on the reason for it, but in general, anticholiergics are effective
-for sick sinus syndrome, also can install pacemaker. anticholinergic may not be effective here.
- generally, treat underlying cause too if possible
how can we treat bradycardia with hypertension?
depends on the reason:
-if due to a2-agonist, anticholinergic may further decrease cardiac output
>can use reversal (atipamezole), and lidocaine also works
-if due to increased ICP, can use osmotic (mannitol or hypertonic saline)
what can cause tachycardia?
§ CNS stimulation
* Increased sympathetic activity
»
* Hypercapnia
* Drug induced
– Ketamine
– Sympathomimetics (dobutamine, dopamine, ephedrine, epinephrine)
– Anticholinergics (glycopyrrolate, atropine)
* Superficial anesthetic plane and pain
* Shock/hypotension
– Sympathetic response
* Phaeochromocytoma
* Hyperthyroidism
* Heart disease
how can we cure increased sympathetic activity due to hypercapnia?
- Adjust ventilation: RR x VT, flows, soda lime freshness
how can we treat drug induced increases in sympathetic activity? what drugs could cause this?
could be due to ketamine, sympathomimetics, or anticholinergics
* Wait and/or stop administration
how can we treat tachycardia due to superficial anesthetic plane and pain?
- Analgesia, adjust depth
how can we treat tachycardia due to shock or hypotension?
- Treat underlying cause- fluids
how can we treat tachycardia due to phaeochromocytoma?
- Beta-blocker
how can we treat tachycardia due to hyperthyroidism?
regulate thyroid function
how can we treat tachycardia due to heart disease?
- Improve cardiac output- inotropes, control volume
what is commonly associated with AV blocks
-bradycardia
§ Conduction from atria to ventricles is impaired
* Slow conduction (1st degree AV-block); not a great worry
* P waves not followed by QRS complex (2nd and 3rd degree)
what can cause AV blocks?
§ Drug induced
* Alpha2-agonists
* Underdosed anticholinergic drugs
> Elicit increased parasympathetic tone (transient effect)
§ Organic disease
how can we treat AV blocks?
depends on cause:
* Reversal of alpha2-agonist
* Anticholinergics
* Isoproterenol
* 2nd type II and 3rd degree can only be treated with artificial pacemaker
*can also give lidocaine
how can we treat atrial fibrilation in small animals? how does it arise?
§ Small animals: Can occur suddenly in dogs of large breeds.
§ Not always treated if the patient is able to maintain normal hemodynamic function
§ Diltiazem, Atenolol
how can we treat atrial fibrilation in a horse?
§ Quinidine
§ Transvascular electrical conversion
what is a ventricular premature contraction? what do we see on an electrocardiogram?
§ Ectopic focus in ventricle originates the ventricular depolarization
§ Not associated with atrial activity
* No P wave
* Premature
* Bizarre QRS
why are ventricular premature contractions a problem?
§ Premature nature prevents adequate diastolic filling
* Pulse deficit
causes of ventricular premature contractions?
- Heart disease- Hypertrophic-, Dilated cardiomyopathy
- Myocardial hypoxia
- Myocardial depressant factors (GDV, splenic tumors)
- Arrhythmogenic drugs (thiopental, B1-agonists- sympathomimetics)
- Irritation of ventricles (cardiac catheterization)
how to treat ventricular premature contractions?
- lidocaine. the rest is supportive
* Prevents ectopic activity by blocking sodium channels during action potential
-oxygenation, control underlying cause, improve contractility
– VPCs may not be eliminated despite efforts
* Attempt to maintain MAP and CO within acceptable values
what is ventricular tachycardia? what happens if it is not treated? how do we treat?
§ More than 3 VPCs in sequence
§ Can become ventricular fibrillation if untreated
§ Tachycardia is part of this arrhythmia
* Some VT with slower rates (HR <100) in dogs do not result in extreme adverse hemodynamic function
§ Same etiology and treatment as for VPCs
* More aggressive
a low blood pressure may mean what about perfusion?
- A low blood pressure may mean inadequate perfusion
When is hypotension a concern? why?
- Deep plane of anesthesia
- Dehydrated patient
- Shock
- Associated with arrhythmias
- Weak pulses
- Abnormal blood gases
§ If any of these are present, then:
* Hypotension is associated with decrease blood flow to vital organs
how do we treat hypotension, generally?
§ Correct volume
* Fluids
§ Enhance contractility
* Sympathomimetics (inotropes)
* Decrease anesthetic depth
§ Vasodilatory shock
* Increase vascular resistance
§ Control arrhythmias
§ If associated with bradycardia
* Anticholinergics
§ If associated with tachycardia
* Analgesia, anesthetic plane, B1-blocker
what must we assess for hypotension treatment? (3)
-anaesthetic depth
-volemia
-contractility
