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Pharm Test 4 > CV complications > Flashcards

CV complications Flashcards

1
Q

MAP =

A

= CO x SVR
= (SV x HR) x SVR

where SVR is systemic vascular resistance

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2
Q

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?

A

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)

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3
Q

possible CV complications

A
  1. Rate and Rhythm
    * Rate
    * Regular or irregular
  2. Arterial blood pressure
  3. Circulating volume
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4
Q

normal HR vs tachycardia for dog

A

normal: 60-140
tachycardia: >180

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5
Q

normal HR vs tachycardia for cat

A

normal: 100-160
tachycardia: >240

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6
Q

normal HR vs tachycardia for horse

A

normal: 28-40
tachycardia: >60

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7
Q

normal HR vs tachycardia for foal

A

normal: 60-90
tachycardia: >110

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8
Q

normal HR vs tachycardia for cow

A

normal: 50-80
tachycardia: >100

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9
Q

what do we want to see on a normal electrocardiogram?

A

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

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10
Q

pathophysiology of a normal to slow HR

A

Adequate diastolic filling- stroke volume
Too slow- negative effect on MAP, CO

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11
Q

pathophysiology of a fast HR

A

> Inadequate diastolic filling- stroke volume
Too fast- negative effect on MAP, CO
Myocardial hypoxia

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12
Q

what four factors contribute to stroke volume?

A

-preload
-afterload
-contractility
-rhythm

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13
Q

influence of high vascular resistance on cardiac output

A

high resistance may drop cardiac output

=> CO = MAP/SVR

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14
Q

animal species have different normal blood pressures. If pressures tend to be high, cardiac output tends to be….

A

low
-and vice versa; low pressures correspond to high cardiac outputs

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15
Q

CO relationship to MAP and SVR

A

CO = MAP / SVR

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16
Q

when might we see bradycardia with hypotension? what can trigger it? what drugs might cause this?

A

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)
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17
Q

hypothermia and electrolyte abnormalities, specifically hyperkalemia, can cause what cardiac issues

A

bradycardia with hypotension or normal MAP

> if hyperkalemia caused by eg. urethral obstruction, may not see bradycardia due to counteracting effects of pain

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18
Q

when might we see bradycardia with hypertension? what is the root cause of this? what drugs can cause this?

A

§ 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

19
Q

when do we treat bradycardia?

A

§ 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

20
Q

how can we treat bradycardia with hypotension, or no change in MAP?

A

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

21
Q

how can we treat bradycardia with hypertension?

A

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)

22
Q

what can cause tachycardia?

A

§ 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

23
Q

how can we cure increased sympathetic activity due to hypercapnia?

A
  • Adjust ventilation: RR x VT, flows, soda lime freshness
24
Q

how can we treat drug induced increases in sympathetic activity? what drugs could cause this?

A

could be due to ketamine, sympathomimetics, or anticholinergics
* Wait and/or stop administration

25
Q

how can we treat tachycardia due to superficial anesthetic plane and pain?

A
  • Analgesia, adjust depth
26
Q

how can we treat tachycardia due to shock or hypotension?

A
  • Treat underlying cause- fluids
27
Q

how can we treat tachycardia due to phaeochromocytoma?

A
  • Beta-blocker
28
Q

how can we treat tachycardia due to hyperthyroidism?

A

regulate thyroid function

29
Q

how can we treat tachycardia due to heart disease?

A
  • Improve cardiac output- inotropes, control volume
30
Q

what is commonly associated with AV blocks

A

-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)

31
Q

what can cause AV blocks?

A

§ Drug induced
* Alpha2-agonists
* Underdosed anticholinergic drugs
> Elicit increased parasympathetic tone (transient effect)

§ Organic disease

32
Q

how can we treat AV blocks?

A

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

33
Q

how can we treat atrial fibrilation in small animals? how does it arise?

A

§ 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

34
Q

how can we treat atrial fibrilation in a horse?

A

§ Quinidine
§ Transvascular electrical conversion

35
Q

what is a ventricular premature contraction? what do we see on an electrocardiogram?

A

§ Ectopic focus in ventricle originates the ventricular depolarization
§ Not associated with atrial activity
* No P wave
* Premature
* Bizarre QRS

36
Q

why are ventricular premature contractions a problem?

A

§ Premature nature prevents adequate diastolic filling
* Pulse deficit

37
Q

causes of ventricular premature contractions?

A
  • Heart disease- Hypertrophic-, Dilated cardiomyopathy
  • Myocardial hypoxia
  • Myocardial depressant factors (GDV, splenic tumors)
  • Arrhythmogenic drugs (thiopental, B1-agonists- sympathomimetics)
  • Irritation of ventricles (cardiac catheterization)
38
Q

how to treat ventricular premature contractions?

A
  1. 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

39
Q

what is ventricular tachycardia? what happens if it is not treated? how do we treat?

A

§ 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

40
Q

a low blood pressure may mean what about perfusion?

A
  • A low blood pressure may mean inadequate perfusion
41
Q

When is hypotension a concern? why?

A
  • 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

42
Q

how do we treat hypotension, generally?

A

§ 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

43
Q

what must we assess for hypotension treatment? (3)

A

-anaesthetic depth
-volemia
-contractility

Pharm Test 4 (10 decks)

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