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VTS(ECC) Preparation > Cardiovascular system & cardiac emergencies > Flashcards

Cardiovascular system & cardiac emergencies Flashcards

1
Q

What do clinical signs of pericardial effusion normally reflect?

A

Poor cardiac output and systemic venous congestion

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2
Q

What are some echocardiographic findings of pericardial effusion?

A

right atrial collapse, mass lesions, poor left ventricular filling, effusion, abnormal cardiac wall motion

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3
Q

What is immediately indicated for cardiac tamponade?

A

Pericardiocentesis

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4
Q

What are the clinical signs or symptoms of pericardial effusion?

A

Exercise intolerance, dyspnoea, tachypnoea, ascites, collapse/syncope, +- cough, GI signs, pulsus paradoxus, weak femoral pulses, muffled heart sounds

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5
Q

What are some nursing interventions for pericardial effusion?

A

ECG & Resp monitoring, IVFT, oxygen therapy (where indicated), monitor jugular distension, BP and pulse monitoring, patient comfort

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6
Q

What are some radiographic findings of pericardial effusion?

A

Globoid cardiac shadow ‘ basketball heart’, cardiomegaly, pleural effusion, hepatomegaly, caudal vena cava distension, pulmonary oedema, tracheal deviation, metastatic lung lesions

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7
Q

What is a pericardial effusion?

A

Fluid accumulation within the pericardium which leads to cardiac dysfunction that is most commonly neoplastic or idiopathic in origin.

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8
Q

What is cardiac tamponade?

A

Cardiac tamponade is when there is increased intrapericardial pressure that exceeds normal diastolic pressure leading to reduced ventricular filling and therefore reduced cardiac output.

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9
Q

What are the signs of cardiac tamponade?

A

Tachypnoea, dyspnoea, reduced arterial BP, weak femoral pulses, tachycardia, jugular distension

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10
Q

What is pulsus paradoxus?

A

abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration (>10mmHg).

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11
Q

What is the normal amount of pericardial fluid?

A

0.25ml/kg of body weight

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12
Q

What are the 2 most common neoplasms causing pericardial effusions and what are their characteristics?

A

Haemangiosarcoma: most common, haemorrhagic effusion (HCT >7%, TP >30%), most arise in RA or auricle or heart base.
Chemodectoma: heart base mass, arise from chemoreceptor of the aorta.

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13
Q

When would you most likely encounter a transudative pericardial effusion? What are some characteristics?

A

Congestive heart failure, hypoalbuminaemia, congenital pericardial malformations, toxaemias.
clear, low cell count <1000ug/L (<8000 when modified), SG <1.012, protein <2.5g/dL

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14
Q

When would you most likely encounter a exudative pericardial effusion? What are some characteristics?

A

extension of pleural or mediastinal infection, bite wounds, plant awn migration, some bacteria i.e. aspergillosis, actinomycosis, coccidiodomycosis, leptospirosis, idiopathic pericardial effusion
cloudy or opaque, high nucleated cell count (>3000/ul), protein >3g/dl, SG >1.015

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15
Q

What dictates the rate of cardiac tamponade?

A

Rate of pericardial fluid accumulation and distensibility of the pericardial sac.
Rapid + small vol = intrapericardial pressure increase rapidly due to pericardial tissue stretching slowly
Slow + large vol = implies gradual filling and ability to maintain lower intracardial pressure for longer as the pericardium has time to stretch

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16
Q

What is meant by the term cardiomyopathy’?

A

Heart muscle disease that is associated with cardiac dysfunction.

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17
Q

What are the four basic types of cardiomyopathies?

A
  1. Dilated cardiomyopathy 2. Restrictive cardiomyopathy 3. Hypertrophic cardiomyopathy 4. Arrhythmogenic right ventricular cardiomyopathy (ARVC)
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18
Q

What is the etiopathogenesis of HCM?

A

ventricular hypertrophy in the absence of haemodynamic and metabolic cause.
- nondilated ventricle
- maine coon and ragdoll cats at most risk

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19
Q

What is the etiopathogenesis of RCM?

A

impaired ventricular filling in the absence of ventricular wall thickening (hypertrophy) or pericardial disease. Applied when there is atrial enlargement with normal or near normal ventricle.
- unknown cause but myocardial functional deficits (i.e. fibrosis) impair relaxation and result in diastolic dysfunction
- sequelae of endomyocardial inflamamtion

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20
Q

What occurs as a result of impaired myocardial relaxation and diminished chamber compliance in feline cardiomyopathies?

A

Altered presure-volume relationship where diastolic pressure is high and ventricular volume in normal or small. This results in atrial enlargment and venous congestion
- low stroke volume
- lower cardiac output

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21
Q

What causes impaired myocardial relaxation in HCM?

A

Intrinsic functional deficits in cardiomyocytes and ischaemia related to hypertrophy, as well as abnormalities in intramural coronary arteries.

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22
Q

What explains poor chamber compliance in feline cardiomyopathies?

A

Hypertrophy and fibrosis which stiffen the ventricle

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23
Q

Describe systolic anterior motion of the mitral valve.

A

Abnormal drag forces cause systolic movement of the mitral valve leaflets towards the septum. This causes a dynamic left ventricular outflow tract obstruction leading to mitral valve regurgitation. This decreases the preload and also afterload, increasing contractility. Still unsure of prognostic indicator in HCM but poorer prognosis observed. It is most commonly associated with causing cardiac murmurs in cats.

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24
Q

What is the most common site of thrombus formation in feline heart disease?

A

Left atrium

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25
Q

How does FATE occur?

A

Partial or full dislodgement of a thrombus (likely from the LA) forms an embolism typically in the aortic trifurcation - or terminal point of the abdominal aorta.

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26
Q

What is the assumed risk factors and causes of FATE?

A
  • feline cardiomyopathies
  • blood stasis associated with LA enlargement
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27
Q

How does the clinical syndrome of FATE result??

A

Not solely by the arterial occlusion caused by the thrombus but also by the release of vasoactive mediators by the thrombus (serotonin, prostaglandins) which decrease blood flow via collateral circulation. This contributes to the development of ischaemia.

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28
Q

What are some signs and symptoms of feline cardiomyopathy?

A
  • tachypnoea
  • dyspnoea
  • signs of CHF
  • presence of a heart murmur (SAM)
  • cyanosis
  • signs of thromboembolism (cold HL, weak/absent femoral pulse, hypothermia, painful HL, HL ataxia)
  • inappetence
  • bradycardia
  • crackles on lung auscultation
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29
Q

What are some echocardiographic findings of feline HCM?

A
  • ventricular hypertrophy without chamber dilation
  • Left atrial enlargement due to diastolic dysfunction
  • Mitral valve regurgitation (due to LA enlargement and +- SAM)
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30
Q

How do we treat FATE?

A
  • narcotic analgesia i.e. fentanyl CRI
  • antithrombotics i.e. LMWH, dalteparin, clopidogrel
  • oxygen therapy where indicated
  • warming to at least 37.2r (shown to improve short term survival to 50%)
  • treatment of CHF
  • treatment of underlying heart disease
  • reduce stree
  • potentially low dose aspirin
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31
Q

What should be routinely monitored in FATE patients?

A
  • HR
  • BP
  • rectal temperature
  • pain
  • oxygenation
  • RR + RE
  • pulse quality (particularly femoral pulse)
  • peripheral temperature and pad colour
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32
Q

How do we treat feline heart failure?

A
  • oxygen therapy
  • anxiolysis
  • diuretic therapy
  • nitrate therapy
  • potentially b-blockers
  • ACE inhibitors
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33
Q

What should be routinely monitored in feline heart failure patients?

A
  • HR
  • RR + RE
  • Body weight
  • Urination
  • BP
  • Body temperature
  • Water intake
  • PCV/TP
  • Kidney function
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34
Q

What is dilated cardiomyopathy? What are some risk factors of DCM?

A

Chamber dilation and impaired systolic - and often diastolic - dysfunction of one or both ventricles. It is an adult onset disease and some breed predisposition has been identified in: doberman, boxers, cocker spaniels, great danes and wolf hounds. It has also been associated with taurine deficiency in cats.

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35
Q

What are some physical exam findings in patients with DCM?

A
  • systolic apical murmur 1-3/6
  • chaotic heart rhythm (Afib, VPC)
  • Signs of L or R heart failure
  • cardiogenic shock
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36
Q

What are thoracic radiographic findings in patients with DCM?

A
  • cardiomegaly
  • signs of CHF
  • hepatomegaly
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37
Q

What are some echocardiographic findings in patients with DCM?

A
  • mitral and/or tricuspid valve insufficiency
  • ventricular and atrial dilation
  • reduced systolic and potentially diastolic function
  • increased E-point septal separation
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38
Q

How is DCM treated long term?

A
  • Diuretics (furosemide 1-4mg/kg PO q8-12; spironolactone 1-2mg/kg PO q12; hydrochlorothiazide 1mg/kg PO q24)
  • ACE inhibitors (enalipril 0.5mg/kg PO q12-24; benazipril 0.25-0.5mg/kg PO q12-24; lisinopril 0.5mg/kg PO q24)
  • Digoxin 0.003mg/kg PO q12
  • Pimobendan 0.25-0.3mg/kg PO q12
  • diet (low sodium, high protein)
  • supplements (taurine 500mg PO q12, Omega-3, L-carnitine)
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39
Q

What is arrhythmogenic right ventricular cardiomyopathy (ARVC)? What breed is is commonly identified in and how is it identified?

A

ARVC is a myocardial disease that is characterised by fatty or fibrofatty infiltration of the RV due to a genetic mutation that codes striatin. It causes the myocardium to break down over time and results in lethal tachydysrhythmias. It is often referred to as ‘boxer cardiomyopathy’ due to high prevalence in boxers. It is identified via Holter study (VPC >100 in 24h, R-on-T and fast rate tachydysrhythmia).

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40
Q

What medications are selected to treat ARVC

A

Sotalol, mexilitine, lidocaine. L-carnitine may also be considered.

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41
Q

What are some symptoms of ARVC?

A
  • collapse
  • syncope
  • AFib
  • VPC
  • Sudden death
  • LHS heart failure
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42
Q

What is cardiogenic shock?

A

Cardiogenic shock is cardiac dysfunction which results in inadequate cellular energy production, despite adequate intravascular volume.

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43
Q

List the clinical signs of cardiogenic shock.

A
  • global hypoperfusion
  • Unresponsiveness/disorientation/depression
  • tachycardia or bradycardia (with or without arrhythmia)
  • cool extremeties
  • pallor and prolonged CRT
  • Metabolic acidosis with or without compensatory respiratory alkalosis
  • GI signs
  • Azotaemia
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44
Q

What is the goal of treating cardiogenic shock?

A

Restoration of cardiac output to normalise tissue perfusion and cellular metabolism.

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45
Q

What are some examples of systolic failure that may result in cardiogenic shock?

A

DCM, Sepsis, endomyocarditis, mechanical failure (rare) and myocardial infarction.

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46
Q

What are some examples of diastolic failure that may result in cardiogenic shock?

A

Cardiac tamponade, HCM, tachydysrhythmia, hypovolaemia.

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47
Q

What is the basic definition of heart failure?

A

Pathophysiologic state where the heart is unable to pump sufficient blood to meet the metabolic demands of the tissue while maintaining normal arterial and venous pressures.

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48
Q

What is the basic definition of systolic heart failure?

A

A defect in the contractile or pumping function of the heart.

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49
Q

What is the basic definition of diastolic heart failure?

A

A defect in the relaxation or filling function of the heart.

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50
Q

What is the basic definition of congestive heart failure?

A

A clinical syndrome that results from abnormal cardiac function causing accumulation and retention of fluid leading to signs of oedema and congestion.

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51
Q

What is the basic definition of forward heart failure?

A

Decrease in cardiac output that results in inadequate delivery of blood to the arterial system resulting in organ hypoperfusion. Congestion of organs and tissues occurs due to reduced renal perfusion, and the accumulation of plasma fluid and ECF. I.e. DCM.

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52
Q

What is the basic definition of backward heart failure?

A

Increased pressure within the pulmonary vasculature and LA due to elevated filling pressures. This causes elevated capillary hydrostatic pressures and transudation of fluid into the interstitium leading to pulmonary oedema. I.e. MVD.

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53
Q

What is the basic definition of circulatory failure?

A

When there is inadequate delivery of oxygenated blood to meet the metabolic demands of body tissue.

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54
Q

What is meant by the term myocardial infarction?

A

Myocardial damage due to a lack of oxygenated blood supply to the heart leading to myocardial tissue death likely from malignant dysrhythmia or CHF. Can also result from hypercoagulable or hypofibrinolytic states.

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55
Q

What is meant by the term traumatic myocarditis?

A

myocardial injury associated with malignant arrhythmias as a result of blunt force thoracic trauma.

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56
Q

What is believed to cause myocardial contusion?

A

compressive and contusive forces of the thoracic cage, and rapid acceleration/deceleration of the thoracic cavity.

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57
Q

What is suspected to cause dysrhythmias in myocardial contusion?

A

the ratio of refractory period and action potential duration, and elevation of resting membrane potential in damaged myocaridal cells.

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58
Q

What is the most common dysrhythmia seen in traumatic myocarditis? What are some other possible dysrhythmias?

A

1 VPC and ST segment elevation

Other: Afib, sinus arrest, 2-3 AVB

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59
Q

How is traumatic myocarditis diagnosed?

A

Based primarily on high index of suspicion:
1. F# of extremeties, spine or pelvis
2. External evidence of thoracic trauma
3. Rad evidence of contusions, pneumothorax, haemothorax, diapragmatic rupture. rib F#
4. Neurological injury
* Histopath gold standard but only achievable through biopsy

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60
Q

What is the treatment goal of traumatic myocarditis?

A

Not to completely resolve cardiac dysrhythmias but to obtain HR <140bpm and re-establish adequate tissue perfusion.
- antiarrhythmic therapy i.e. lidocaine, procainamide, cautious use of b-blockers

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61
Q

What may cause a bradydysrhythmia?

A
  • alterations of autonomic tone
  • electrolyte disturbances
  • drug exposure
  • trauma
  • hypoxia
  • inflammation/infiltration of myocardium
  • degenerative disease of the conduction system
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62
Q

Draw ‘sinus arrhythmia’. What is a sinus arrhythmia? What are the characteristics? When is it treated?

A
  • usually secondary to systemic disease that causes increased vagal tone. The resolution of the disease process results in increased heart rate and resolution.
  • P wave associated with QRS complex
  • may have wandering pacemaker if marked vagotonia the cause
  • usually narrow QRS complexes
  • if reduced consciousness, hypertension and abnormal breathing concerns of increased ICP (cushing’s reflex)
  • if severe bradycardia having systemic effects treat with anticholinergic i.e. atropine, glycopyrrolate
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63
Q

Draw ‘sinus arrest’. What is sinus arrest? What are the characteristics? When is it treated?

A

prolonged pause with no atrial activation or p wave

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64
Q

What is a sinus block?

A

Failure of an impulse to leave the sinus node

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65
Q

What causes syncope in bradydysrrhythmia?

A

Sinus arrest over 6-8sec causing significantly reduced cardiac output

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66
Q

What is sick sinus syndrome (SSS)?

A

Periods of normal sinus rhythm or sinus bradycardia interspersed by periods of long sinus arrest (10-12sec). It occurs when junctional and ventricular pacemakers fail to initiate escape beats.

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67
Q

Describe bradycardia-tachycardia syndrome

A

Variant of SSS where the heart fluctuates between a tachycardic and bradycardic state.

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68
Q

Draw 1AVB. What are the characteristics? What is likely to cause it?

A

atrial impulses are conducted to the ventricles but the P-R interval in prolonged (>130ms Dogs; >90ms Cats).
- increased vagal tone
- drug induced (Ca blockers, digoxin, b blockers)
- AV node fibrosis

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69
Q

Draw TYPE I 2AVB. What are the characteristics?

A

Some p waves not associated with a QRS that may or may not compromise a patient’s haemodynamic state. Type I the P-R Interval increases and ends in heart block.
- Usually benign

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70
Q

Draw TYPE 2 2AVB. What are the characteristics?

A

Unexpected occurrence of blocked p wave. P-R interval constant before the block. QRS +- wide
- Usually worsens
- Atropine 0.04mg/kg IV

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71
Q

Draw 3AVB. What are the characteristics? What is likely to cause it?

A

Absence of conducting p waves to ventricles. Independant atrial and ventricular activities. There is a resulting significant decrease in cardiac output.
- 20-60bpm Dogs; 60-120bpm Cats
- myocardial fibrosis, inflammation, infiltration, drug toxicity (Ca blockers, digoxin, b blocker), age-related fibrodegenrative disease
- In cats most likely associated with structural heart disease.

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72
Q

Draw atrial standstill. What are the characteristics? What is likely to cause it?

A

No atrial activity where there is lack of p waves with a regular ventricular/AV nodal escape rhythm.
- Hyperkalemia common cause (temporary): narrowing T wave, low heart rate <100bpm, diminished p wave amplitude and widening QRS. K+ >5.5-6mmol/L
- persistent atrial standstill rare

73
Q

What are some of the common treatments of bradyarrhythmias?

A
  • parasymoatholytics i.e. atropine, glycopyrrolate (vagally mediated arrhythmias and SSS)
  • sympathathomimetic inotropes: b-adrenergic activity to increase heart rate i.e. dopamine and dobutamine
  • pacemaker therapy i.e. transcutaneous, transvenous
74
Q

What are supraventricular tachyarrhythmias (SVT’s)?

A

Tachyarrhythmia’s originating above the ventricles i.e. atria and atrioventricular junction

75
Q

What two classes of SVT’s are there?

A
  1. Atrial tachyarrhythmia
  2. AV nodal-dependent tachyarrhythmia
76
Q

What is VHS? What score generally indicates a patient has cardiomegaly?

A

Verterbral heart scale. It is used to gage if a patient has cardiomegaly and potentially heart disease. A general score >12-13 (short axis + long axis) indicates cardiomegaly and is suggestive of heart disease.

77
Q

How do you calculate MAP

A

[2x sys + diastolic]/3

78
Q

What is preload?

A

measure of how much the ventricle is stretched at the end of diastole and the volume of blood in the left ventricle just before it contracts.

79
Q

How do we measure preload?

A
  • CVP
  • left ventricular end-diastolic diameter
  • pulmonary capillary wedge pressure
80
Q

What causes low preload?

A

Congestion of the systemic vessels leading to systemic retention of blood and therefore less blood in the ventricles.

81
Q

What causes increased preload?

A

Constriction of systemic vessels and reduced cardiac output leads to more blood being returned to the ventricles.
Poor contractility of the ventricle resulting in overfilling of the ventricles.
Leads to congestive heart failure.

82
Q

What is afterload?

A

The force against which the heart ejects.

83
Q

What happens if afterload is increased?

A

It is harder for blood to leave the heart resulting in lower stroke volume and therefore reduced cardiac output. Systemic vascular resistance is sometimes used to evaluate afterload.

84
Q

How does the body respond to hypotension?

A

The body vasoconstricts to improve BP but this can also increase afterload and therefore reduce CO.

85
Q

What is contractility?

A

The pumping action of the heart and the contracting properties of the myocytes.

86
Q

What might cause increases in contractility?

A

When calcium in heart muscle cells is increased by chemicals produced in the body or drugs. I.e. positive inotropes, increased preload, increased sympathetic tone

87
Q

What is heart failure?

A

The inability of the heart to supply adequate blood flow to meet the metabolic demands of the body or can only supply adequate blood flow with excessive increases in ventricular filling pressures.

88
Q

What is low-output or forward failure?

A

The heart is unable to pump enough blood to the tissues. This causes a decreased amount of delivered oxygen to the tissues.

89
Q

What is congestive or backward failure?

A

Increases in pulmonary or systemic venous pressures causes fluid to leak from capillary beds and accumulate in tissues (oedema) or body cavities (effusion).

90
Q

What are some general causes of LHS HF?

A
  • PDA
  • Mitral valve degeneration or regurgitation
  • DCM
  • Infective endocarditis
  • SubA stenosis
91
Q

What are some general causes of RHS HF?

A
  • Tricuspid valve degeneration or regurgitation
  • DCM
  • Pulmonic stenosis
  • Heartworm disease
  • Pericardial disease
92
Q

What are some general causes of HF in cats?

A
  • HCM
  • RCM
  • DCM
  • Cardiomyopathy associated with hyperthyroidism
93
Q

What are the most common client complaints for heart disease/failure?

A
  • weakness
  • collapse/syncope
  • exercise intolerance
  • tachypnoea and/or dyspniea
  • Cough
  • Abdominal distension (ascites)
  • Open-mouth breathing (cats)
94
Q

What are common physical findings in patients with heart disease and heart failure?

A
  • systolic murmurs >3
  • precordial thrills (murmur >5)
  • gallop sounds
  • irregular pulses
  • arrhythmias
  • respiratory changes i.e. tachypnoea, dyspnoea
  • cyanosis
  • low blood pressure
  • jugular venous distention
  • weakness
  • hepatomegaly
  • abdominal distension
95
Q

What are some echocardiographic findings in patients with LHS HF?

A
  • Left atrial enlargement
  • cardiomegaly
  • large pulmonary veins
  • arrhythmia
96
Q

What are some diagnostic findings of patients with RHS HF?

A
  • enlarged vena cava
  • right heart enlargement
  • globoid heart suggesting pericardial effusion
  • tortuous and dilated pulmonary arteries (heartworm)
  • arrhythmia
97
Q

What are the goals of emergent heart failure treatment?

A
  • reduce oxygen consumption
  • improve the oxygen content of the blood
  • reduce the regurgitant fraction and afterload
  • minimise stress
  • reduce venous pressure
  • improve contractility and cardiac output
  • decrease work of breathing
98
Q

How is emergent CHF treated?

A
  • furosemide/loop diuretics
  • oxygen therapy
  • sedation (butorphanil, acp, oxymorphone)
  • venodilators (nitroglycerin)
  • arterial dilators (hydralazine, amlodipine)
  • Positive inotropes (pimobendane, dopamine, dobutatmine)
99
Q

What portion of an ECG tracing represents atrial contraction and depolarization of the sinus node?
a. QRS complex
b. ST segment
c. P wave
d. QT interval

A

c.

100
Q

Which of the following drugs can be administered to reduce afterload in patients suffering from heart failure?
a. Butorphanol
b. Furosemide
c. Nitroprusside
d. Lidocaine

A

c.

101
Q

Electrical alternans can be described as:
a. increased T wave amplitude
b. beat-to-beat variation on QRS amplitude
c. absent ST segment
d. occasional dropped P waves

A

b.

102
Q

The purpose of the renin-angiotensin-aldosterone system is to:
a. increase water retention and increase blood pressure
b. reduce cardiac workload
c. promote vasodilation
d. promote sodium excretion

A

a.

103
Q

Taurine deficiency can cause which cardiac disease in cats that are not fed a commercial diet?
a. Dilated cardiomyopathy
b. Chronic valvular heart disease
c. Caval syndrome
d. Hypertrophic cardiomyopathy

A

a.

104
Q

Electrical alternans is pathognomonic for which cardiac emergency?
a. Pericardial effusion
b. Congestive heart failure
c. Systemic thromboembolism
d. Myocardial infarction

A

a.

105
Q

A complete but transient conduction interruption from atria to ventricles where every QRS has a P wave but not every P wave has a QRS is:
a. first-degree AV block
b. second-degree AV block
c. third-degree AV block
d. This doesn’t describe AV block

A

b.

106
Q

Which type of analgesia would be best for a cat with systemic thromboembolism?
a. Kappa agonist
b. Mixed agonist/antagonist
c. Partial mu agonist
d. Pure mu agonist

A

d.

107
Q

Blood pressure is a product of which components?
a. SVR × HR
b. CO × SV
c. CO × SVR
d. SV × SVR

A

c.

108
Q

Which of the following is not a factor of stroke volume?
a. Heart rate
b. Cardiac preload
c. Cardiac contractility
d. Cardiac afterload

A

a.

109
Q

What is systemic hypertension?

A

A sustained pathological increase in systemic arterial BP

110
Q

What are the reference ranges for normotensive, prehypertensive, hypertensive and severe hypertensive?

A

N: <140
Pre: 140-159
H: 160-179
Sev: >180

111
Q

What is blood pressure and what determines it?

A

Blood pressure is the outward force exerted on the intravascular blood column against the blood vessel wall
BP = CO X SVR

112
Q

What are some neurological target organ damage’s associated with systemic hypertension?

A
  • hypertensive encephalopathy
  • cerebral infarction
113
Q

What are some ocular target organ damage’s associated with systemic hypertension?

A
  • retinal detachment
  • retinal oedema
  • retinal haemorrhage
  • vitreal haemorrhage
  • secondary glaucoma
114
Q

What are some cardiovascular target organ damage’s associated with systemic hypertension?

A
  • hypertensive cardiomyopathy
  • aortic dissection (rare) (cats)
115
Q

What are some renal target organ damage’s associated with systemic hypertension?

A
  • Rapid glomerulosclerosis and fibrosis leading to proteinuria
116
Q

What are the common conditions associated with systemic hypertension

A
  • fear, stress, anxiety
  • CKD or AKD
  • hyperthyroidism
  • cushing’s disease
  • DM
  • corticoid steriod therapies
  • polycythemia
  • pheochromocytoma
  • primary hyperaldosteronism
117
Q

What are some clinical signs of systemic hypertension?

A
  • Altered mentation
  • Ataxia
  • Seizures
  • Epistaxis
  • Headache
  • Sudden onset blindness
  • vision impairment
118
Q

The two valves commonly affected by infective endocarditis are?

A
  • mitral valve
  • aortic valves
119
Q

What are the 4 sequelae of IE?

A
  • thromboembolism
  • CHF
  • severe arrhythmias
  • immune mediated disease i.e polyarthritis, glomerulonephritis
120
Q

What is the common treatment for IE?

A

1-2 weeks of aggressive, broad-spectrum, IV antibiotic therapy, followed up by 6-8 weeks of oral antibiotics.

Other therapies include CHF treatments, arrhythmia treatment.

121
Q

What is the basic pathophysiology of IE?

A

After endothelial injury there is bacterial adherence to the disrupted cardiac valve (mechanical or inflammatory lesion). The exposure of extracellular proteins, thromboplastin and tissue factor cause activation of coagulation resulting in the formation of a ‘coagulum’ of fibrinogen, fibrin, PLT proteins that avidly bind to bacteria. There is then adhesion and incorporation of microbials into the endothelium (MSCRAMMS) which induce PLT aggregation and proinflammatory response. These MSCRAMMS release enzymes that form a vegetative lesion on usually the mitral or aortic valves and proliferate often leading to cordae tenidae rupture, severe mitral regurge and congestive heart failure.

122
Q

Why do AB’s struggle to penetrate lesions in IE?

A

Fibrinous vegetative lesions that have little access to phagocytes

123
Q

What are the most common bacteria in IE?

A
  • staphylococcus spp
  • streptococcus spp
  • E. coli
  • Bartonella
124
Q

How is IE diagnosed?

A

ECHO - visualisation of lesion and valvular insufficiency

125
Q

What are some clinical abnormalities seen in IE?

A
  • Heart murmur
  • Bounding femoral pulse
  • Fever
  • Arrhythmias
  • CHF
  • Leukocytosis (mature neutrophilia and monocytosis)
  • mild to severe thrombocytopaenia
  • Anaemia
  • Hypercoaguloble state
  • low albumin
  • increased liver enzymes
  • pre renal or renal azotaemia
  • increased UPC
126
Q

How do ACE inhibitors treat hypertension? What are some examples and indications for their use?

A

Competitively inhibit ATI conversion to ATII where ATII is a potent vasoconstrictor. Thus, blocking this conversion results in vasodilation and a reduction in preload and afterload. Benazipril, enalipril, ramipril and lisinopril are examples and are indicated in..
- mitral valve insufficieny
- CHF due to DCM
- glomerular hypertension

127
Q

What are the side effects of ACE inhibitors

A
  • weakness
  • lethargy
  • azotaemia
  • hyperkalaemia
128
Q

How do angiotensin II receptor blockers (ARBs) treat hypertension? What are some examples and indications for their use?

A

Displace ATII to cause a dose dependent drop in peripheral resistance without effecting HR + CO. Losartan, telmisartan are examples and are indicated for use for hypertension during heart disease.

129
Q

How do adrenergic receptor antagonists treat hypertension? What are some examples and indications for their use?

A

Block the binding of norepinephrine to the smooth muscle receptors causing vasodilation and reduction in blood pressure. Prazosin is a selective adrenergic receptor agonist used to reduce peripheral resistance.

130
Q

How do B-blockers treat hypertension? What are some examples and indications for their use?

A

Competitively inhibit b-adrenergic receptors and counter catecholamines leading to a reduction in sympathetic effects causing a reduction in blood pressure. The also block renin release to reduce HR, contractility and SVR. Examples are propanalol, atenolol and they are used in HCM, Vtach, and SVT’s

131
Q

What are some side effects of B-blockers?

A

bronchospasm in asthmatic cats
hyperkalaemia
bradycardia
insulin resistance
depression

132
Q

How do aldosterone blockers treat hypertension? What are some examples and indications for their use?

A

Decrease Na reabsorption and increase water, salt and K excretion and decrease BP through RAAS. An example of this is spironalactone which is also a weak diuretic.

133
Q

How do calcium channel blockers treat hypertension? What are some examples and indications for their use?

A

Block the influx of Ca into smooth muscle cells and therefore decrease SVR. There is a drop in voltage spike and nodal firing which result in a lowered HR and BP. These are used in hypertensive crisis and an example is amlodipine

134
Q

What are the side effects of Calcium channel blockers?

A
  • weakness
  • tachycardia
  • constipation
  • vomiting
135
Q

How do arterial dilators treat hypertension? What are some examples and indications for their use?

A

Decrease resistance and improve relaxation of smooth muscles including the heart. Examples are hydralazine and sodium nitroprusside. Indicated in hypertensive crisis and heart failure

136
Q

How are hypertensive emergencies addressed?

A

Hypertensive emergencies are clinical signs associated with a elevation in Bp (usually over 180-200mmHg). Initial goal is to reduce MAP <25% within first hour and reduce BP to 160/100 within the next 6-12 hours.

137
Q

Too rapid reduction in blood pressure in a hypertensive emergency may cause ischaemia to which areas of the body?

A
  • coronary
  • cerebral
  • renal
138
Q

What is the drug of choice in hypertensive emergencies?

A

sodium nitroprusside or hydralazine

  • enalipril (#2)
139
Q

What are the goals of diuretics?

A
  • enhance the secretion of water, solutes and toxins from
  • promote urine flow
  • decrease urine concentration of solutes and toxins
140
Q

What emergencies are diuretics used in?

A
  • oliguric renal failure
  • CHF
  • Ascites in liver failure
  • decompensated CKD
  • fluid/electrolyte disorders
141
Q

What type of diuretics provide the best diuresis and why? What is the name of the most commonly used one?

A

Loop diuretics as there is minimal reabsorption occurring and there is a large amount of filtrate at this nephron site.

Furosemide

142
Q

In CHF what is the main goal of therapy and which diuretic strategy is used?

A

Reduce pulmonary oedema and +- pleural effusion and decrease preload as well as the extracellular fluid volume. Loop diuretics such as furosemide are used. Sometimes spironalactone is used in conjunction with furosemide.

143
Q

In hypertension what is the main goal of therapy and which diuretic strategy is used?

A

Reduce preload and intravascular volume. Thiazides and furosemide are used.

144
Q

What are class I anti-arrhythmic and how do they work? What drugs fall into this category?

A

Sodium channel blockers: inhibit fast sodium channels to increase the effective refractory period to reduce both HR and BP

Lidocaine, procainamide, quinidine, mexilitine, flecanide

145
Q

What are class II anti-arrhythmic and how do they work? What drugs fall into this category?

A

B blockers: block b receptors at the SA and AV node to reduce sympathetic stimulation which reduces overfiring of the effected node and thus slows nodal conduction resulting in reduced HR and SVT or VT activity.

Atenolol, propanolol, esmolol, metoprolol

146
Q

What are class III anti-arrhythmic and how do they work? What drugs fall into this category?

A

Potassium channel blocker: increase the effective refractory period by increasing the Q-T interval by blocking repolarisation via potassium channels.

Amiodarone, sotalol

147
Q

What are class IV anti-arrhythmic and how do they work? What drugs fall into this category?

A

Calcium channel blockers: Blocks release of calcium into myocytes to reduce automaticity of contractions and reduce rate of depolarization, and prolongs the effective refractory period.

Amlodipine, diltiazem, hydralazine

148
Q

What are pulmonary artery catheters used for? What can they measure?

A
  • CO
  • SVR
  • SvO2
  • PCWP
  • RV end diastolic volume
  • selecctive angiography
149
Q

How are PAC’s placed?

A

Placed through the right side of the heart and right ventricular outflow and into the pulmonary artery

150
Q

How does a PAC measure CO?

A

1.5ml/kg NaCl or 5% dextrose of a known temperature injected into proximal port and detected by thermistor.

CO = Change in blood temp/Time

151
Q

When are PAC used?

A
  • to monitor haemodynamic instability during and after cardiac surgery
  • guide vasopressor and inotropic treatment in cardiogenic shock
  • allow us to have real time SvO2 to optimise O2 delivery
152
Q

What are some complications of PACs?

A
  • embolis or thrombis
  • PA rupture
  • infection
  • arrhythmias
  • carotid artery puncture
  • haemothroax
  • pneumothorax
  • tricuspid valve damage
  • tamponade
153
Q

What is temporary cardiac pacing used for?

A

correct profund bradycardia that is medically refractory and is resulting in a patient being haemodynamically unstable

154
Q

What is transcutaneous TCP?

A

Electrode patches placed on the patient surface over the heart and secured with elastoplast.

155
Q

What is transoesophageal TCP?

A

Catheter placed into the oesophagus just dorsal to the heart.

156
Q

What is transvenous TCP?

A

Sheath introduced catheter in either the saphenous or jugular vein and advanced into the RV.

157
Q

What are the indications of TCP?

A
  • Support HR + BP until permanent pacemaker placed
  • Support HR + BP in dogs with silent sinus nodal dysfunction that have profound, refractory bradycardia under anaesthesia
  • Haemodynamically unstable patients that must be stablised before permanent pacemaker is placed
  • Cardiac arrest or reversible bradycardia due to drug OD that doesn’t require permanent pacing
158
Q

Draw the tree of life

A

(image)

159
Q

Mitral murmurs

A

Heard over the mitral valve (Left side of the heart)

160
Q

Tricuspid murmurs

A

Heard over the tricuspid valve (Right side of the heart)

161
Q

Pulmonic murmurs

A

Best heard at the 3rd intercostal space ventral to the shoulder

162
Q

Aortic murmurs

A

Loudest at 4th intercostal space slightly below the point of the shoulder

163
Q

Local determinants of SVR

A

CO2
NO
Prostaglandins
Histamine

164
Q

Systemic determinants of SVR

A

Vasopressin
Angiotensin II
SNS

165
Q

Causes of hypotension

A

Reduced preload i.e. haemorrhage, dehydration, fluid losses
Reduced cardiac function i.e. cardiomyopathies, SIRS, electrolyte disturbances, hypoxia
Reduced SVR i.e. SIRS, electrolyte imbalances, drugs, toxins, vasoactive mediators

166
Q

Baroreceptor reflex (hypotension)

A

Drop in BP > baroreceptor stretching > decreased stimulus to vasomotor centre in medulla > increased SNS > increased SVR, HR, contractility & CO

  • baroreceptor reflex moment-to-moment BP regulator
167
Q

Chemoreceptor reflex (hypotension)

A

Drop in tissue O2 tension or increased CO2 or decreased pH > excitement of vasomotor centre > SNS > promotion of fluid from ISS to IVS > maintenance of preload, blood volume & MAP.

168
Q

Normal BP in dogs (S&H pg 49)

A

SAP: 110-190
DAP: 55-110
MAP: 80-130

169
Q

Normal BP in cats (S&H pg 49)

A

SAP: 120-170
DAP: 70-120
MAP: 60-130

170
Q

Treatment options for hypotension

A

Fluid resuscitation
Positive inotropes
Vasopressors
Blood products

171
Q

Treatment of hypertensive crisis

A

Reduce ABP by 25% in first hour and then aim for 160/100-110mmHg over the following 2-6 hours

172
Q

Calcium function

A

Maintenance of vascular tone
Impulse formation and conduction
Excitation-contraction coupling

173
Q

Types of calcium channels and which one is most sensitive to b-blockers

A

Long lasting = L type ** most sensitive to b-blockers
Neuronal = N rtpe
Transient = T type

174
Q

How do calcium channel blockers work

A

Block transmembrane flow of Ca through voltage-gated L-type channels to decrease intercellular Ca concentration and each class have different binding sites but primarily work on pacemaker cells, cardiac myocytes and vascular smooth muscle. Thus rate of depolarisation through pacemaker cells is reduced dropping HR (negative chronotropy), reducing the release of Ca from the SR and decreased force of contraction.

175
Q

Normal b-adrenergy

A

B1: heart, kidneys and adipose tissue
- stimulate increased heart rate, increased contractility and increased AV velocity
B2: bronchial and vascular smooth muscle
- produce relaxation

176
Q

B-blockade

A

Reduces catecholamine and b-adrenergic activity by reducing transmembrane Ca flow and down regulation of cAMP synthesis
- lowered AV contractility, lowered HR, slows excitation through AV node
- B2 blockade = bronchodilation, decreased insulin release, renin release

177
Q

Ca blocker overdose

A

Extension of therapeutic effects (negative inotropy and chronotropy)
Decreased CO, BP, perfusion & cardiovascular shock
Mild hyperkalaemia (b blockers)
NCPO (b blockers)
Dyspnoea due to bronchospasm
Seizures

178
Q

Treatment of Ca and b blocker overdose

A

Decontamination (Messi, gastric lavage and AC)
Support respiratory and cardiovascular function (ventilation, vasopressin’s, CaGlu, parasympatholytics, glucagon)
ECT
ILE

VTS(ECC) Preparation (21 decks)

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