Cardiology Flashcards
(142 cards)
1
Q
What are the types of cardiac muscle
A
- All striated
- Atrial and ventricular (like sekeltal mucles with proloned contraction)
- specialised exictatory and conductive fibres (automaticity with few contractile fibrils)
2
Q
What allows the cardiac mucle to function as a syncytium
A
Intercalated disks with gap junctions to allow rapid ion diffusion
3
Q
What happens in Phase 0 of the cardiac AP
A
Depolarisation
- fast sodium channels open
4
Q
What happens in Phase 1 of the cardiac AP
A
Initial repolarisation
- Fast sodium channels close
- potassium starts to leave
5
Q
What happens in Phase 2 of the cardiac AP
A
Plateau
- Calcium channels open
- fast potassium channels close
6
Q
What happens in Phase 3 of the cardiac AP
A
Rapid repolarisation
- calcium channels close
- slow potassium channels open
7
Q
What happens in Phase 4 of the cardiac AP
A
Resting membrane potential
- maintained -80 to 90mV
8
Q
What is excitation contraction coupling
A
Mechanism where the AP causes myofibrils to contract
- similar to skeletal muscle where AP causes calcium influx
- difference is the process of calcium mediated calcium release allowing more calcium influx from ECF becuase SR is not as well developed
9
Q
Briefly outline the path of electrical transmission in the cardiac cycle
A
- AP generation in SAN
- travels through atria to AVN
- Delay for atrial contraction
- Travels down bundles to purkinje fibres then ventricles
10
Q
What does the P wave on the ECG represent in the cardiac cycle
A
- atrial depolarisation
- it is followed by atrial contraction
11
Q
What does the QRS wave on the ECG represent in the cardiac cycle
A
- ventricular depolarisation
- it is followed by ventricular contraction
12
Q
What does the T wave on the ECG represent in the cardiac cycle
A
- ventricular repolarisation
- comes just beofre the end of ventricular contraction and causes muscle relaxation
13
Q
How much blood does atrial contraction contribute to ventricular filling
A
20%
80% flows in passively
14
Q
What is ventricular isovolumetric contraction
A
- contraction but no emptying
- pressure build up to open semilunar valves
15
Q
What is the ventricular ejection period
A
- LV pressure >80mmHh and RV pressure >8mmHg the semilunar valves open
- 60% ventricular blood ejected
16
Q
What is ventricular isovolumetric relaxation
A
- rapid relaxation at the end of systole
- muscle relaxes but volume unchanged
- artery back pressure closes semilunar valves
17
Q
What is end diastolic volume
A
The amount of blood in the ventricle at the end of diastole
18
Q
What is stroke volume
A
The amount of blood ejected by the ventricles during systole
19
Q
What is end systolic volume
A
- the blood remaining in the ventricle after systole
20
Q
What is the ejection fraction
A
Fraction of end diastolic volume that is ejected (approx 60%)
21
Q
What is the first heart sound (S1)
A
AV valve closure
22
Q
What is the second heart sound (S2)
- name some causes of a split S2
A
Semilunar (aortic/pulmonic) valve closure
- Split S2 - pulmonic valve closes after aortic valve - Healthy large breed dog, heartworm, pulmonic stenosis, primary pulmonary hypertenison
23
Q
What is the third heart sound (S3)
- name some examples
A
Rapid ventricular filling
- DCM, PDA, mitral insufficiency, anaemia in cats
24
Q
What is the fourth heart sound (S4)
A
Blood flow into the ventricles in atrial contraction
- just before S1
- due to increased ventricular stiffness
25
On the volume pressure diagram of the cardiac cycle what does each phase represent (volume x axis, pressure y)
1- filling
2 - isovolumetric contraction
3 - ejection
4 - isovolumetric relaxation
EW = net external work
width = stroke volume
26
What is preload
degree of tension on muscle when it begins to contract
= end diastolic pressure
27
What is afterload
Load against which muscle exerts contractile force
= pressure in aorta leaving ventricle
28
What is the Frank starling mechanism
The more the heart is stretched during filling --> the greater the force of contraction --> and the greater the quantity of blood pumped into aorta
29
* Effect of sympathetic activation on the heart
* Where is sympatethetic activation happening
* Explain process
- Increase heart rate and contractility
- All heart but mainly ventricles
NE --> stimuates B1 receptors --> increased Na and Ca permeability (influx) --> more positive RMP and greater contractility
30
* Effect of parasympathetic activation on the heart
* Where is parasympatethetic activation happening
* Explain process
- vagal stimuation slows heart rate + slightly decreases contractility
- SAN and AVN
ACH --> increases K+ permeability (efflux) --> increased hyperpolarisation --> harder to generate AP
31
What mechanisms allow automaticity of the nodal fibres
* Funny sodium channels allow Na+ influx between heartbeats - causing slow increase in RMP
* When -40mv reached L type calcium channels activated and cause AP
32
What is the RMP of nodal fibres
and ventricular fibres
* -55 to 60mV
* -90mV
33
What is the diagnostic approach to ECG
* Calculate the heart rate - fast or slow?
* Is the QRS wide or narrow (>70ms = wide)
* Is the RR interval regular or irregular
* Is there a P for every QRS
* Is there a QRS for every P and are they related
* Is the rhythm sustained or paroxysmal
34
If there are no P waves what could the rhythm be?
- A fib - tachycardic, irregular, F waves, supraventricular
- Atrial standstill - bradycardic, regular
- sinus node arrest (periods without p)
35
What are the two types of atrial stanstill and what are the common causes
- Persistent - atrial cardiomyopathy (English springer)
- Transient - hyperkalemia (dog addisons, cat obstruction)
36
If you have bradycardia and p waves that are not related to the QRS
AV block
- First degree - prolonges PR interval
- Second degree: type 1 - PR prolongation then block
- Second degree: type 2 - fixed no of non-conducted p waves before QRS
- Third degree: Complete dissociation
37
What test can you use to determine if AV block is pathologic or physiologic
atropine (abolish high vagal tone)
38
At 25mm/second one big box is how many seconds
0.2s
39
At 50mm/second one big box is how many seconds
0.1s
40
What is the pen x 10 rule
* One bic pen = 30 boxes
* count QRS complexes in 30 boxes
* for 25mm/s x 10
* for 50mm/s x 20
41
In eindhovens triangle of mean electrical axis what is:
- Lead 1
- Lead 2
- Lead 3
Which lead follows the normal electrical impulse direction
- 1 (one L) - towards left arm
- 2 (two L) - towards left leg
- 3 (3 L) - left arm to left leg
Lead 2 follows normal impulse from SAN to LV
42
Bundle branch block has what characteristics
- Underlying sinus rhtyhm
- p for every QRS
- wide QRS complexes
- consistent PR interval
- RBBB has deep S waves in lead 2
43
Atrial fibrilation is commonly caused by what structural change
Atrial enlargement
44
Dobermanns with DCM have which mutation
PDK4 and Titin
45
Boxers with ARVC have which mutation
Striatin
46
Cats with HCM have which mutation
Myosin binding protein C
47
* What is a class 1 anti-arrhythmic
- What phase does it effect
- Name an example
- What is its use
- Contraindications
- Na+ channel blocker
- Phase 0 - slows depolarisation
- Lidocaine, mexillitine
- used form VT
- not effective for SVT
- contraindicated for AV block
- Mexilletine - GI distress
- Lidocaine avoid in cats - sensitive to CNS effects
48
* What is a class 2 anti-arrhythmic
- What phase does it effect
- Name an example
- What is its use
- Contraindications
- Beta blockers
- Phase 4 - slows depolarisation
- Atenolol, propanolol
- Used for SVT and VT
- contraindicated for AV block
- Propanolol - not in asthma
- Atenolol - caution with renal insufficiency
49
* What is a class 3 anti-arrhythmic
- What phase does it effect
- Name an example
- What is its use
- Adverse effect
- K+ channel blocker
- Phase 3 - prolongs repolarisation
- VT and SVT
- Sotalol and amiodarone
- Amiodarone can cause hepatotoxicity, pulmonary fibriosis and blood dyscrasias
50
* What is a class 4 anti-arrhythmic
- What phase does it effect
- Name an example
- What is its use
- What can it not be used for
- Contraindications
- Ca channel blocker
- Phase 2 - slows nodal depolarisation
- diltiazem, verapamil
- SVT or a fib
- ineffective for VT
51
Left bundle branch block will cause a MEA deviation in which direction?
Left
52
Left apical holosystolic murmur
Mirtal insufficency
53
Right apical holosystolic murmur
tricuspid insufficiency
54
Left basilar holosystolic crescendo-decrescendo murmur
Aortic stenosis
Pulmonic stenosis
ASD
55
Right cranial thoracic holosystolic murmur
VSD
56
Early diastolic decrescendo murmur
Aortic insufficiency (endocarditis)
57
Continuous left basilar machinery murmur
PDA
58
Normal pulse pressure
40mmHg (120mmHg systolic and 80mmHg diastolic)
59
What congenital heart disease is associated with bounding pulses
PDA
60
What congenital heart disease is associated with narrow pulse pressure
Sub aortic stenosis associated with pulsus parvus et tardus - narrow pulse pressure
61
Pulse deficits are due to which type of arrhythmia
premature ventricular beats
62
What is pulsus paradoxus and when is it seen
pulse strength falls during inspiration when cardiac tamponade present
63
What is syncope
* collapse that involves transient loss of consciousness due to insufficient blood flow to the brain
* short duration and followed by rapid recovery to normal.
64
Common causes of cardiogenic syncope
- Sustained bradyarrhythmias (high grade AV block + ventricular stanstill)
- Sustained tachyarrhythmias that have marked effect on SV - eg VT
65
What is neurocardiogenic syncope (vasovagal syncope)
- hyopotentsion caused by bradyarrhythmia + inapproprate reflex vasodiation
- Sudden increases in vagal tone
66
Which breed are predisposed to vasovagal syncope when excited
Boxers
67
High left ventricular pressures can stimulate a neurocardiogenic reflex (and syncope) called what?
Bezold-Jarisch reflex
68
Normal mean arterial pressures
Systemic 90-100mmHg
Pulmonary 20mmHg
69
What are the 4 main mechanisms of heart failure
- imapired cardiac filling (pericardial disease, HCM)
- Increased resistance to ejection (afterload) - (pulmonic and aortic stenosis, HOCM, PHT)
- Impaired ejection or volume overload (DCM, L-R shunts, anaemia)
- Arrhythmias (sustanied tachyarrhythias or chronic bradyarrhythmias)
70
Progression of heart disease to failure occurs due to which maladaptive mechanisms
- SNS activation (increased contractility and preload, activation of RAAS)
- RAAS activation (vasoconstriction and water retention, mediated inflammaion and fibrosis)
71
What are the types of atrial naturietic peptide and where are they found
- what triggers their release
- What is their action
- whats is their use
- ANP - atria
- BNP - atria
- CNP - vascular endothelim
- triggered by stretch
- Opposite effect to RAAS
- NT-PRO ANP and NT-proBNP markers of heart disease
72
ADH has which receptors, where and for what function
V1A (vasculature and heart) - vasoconstricion and inotropy
V2 (Kidney) - water regulation via aquaporin
V2 (baroreceptors) - augment baroreceptor reflexes to lower HR and maintain BP
73
Which two hormones can cause local vasculature constriction/dilation
Endothelin - constriction
Nitric oxide - dilation
74
What changes are associated with cardiac remodelling
- mycoyte hypertrophy
- fibrosis and collagen deposition
- calcium cycling abnormlities
- oxidative damage
75
What is the definition of heart failure
inability to sustain sufficient cardiac output to provide metabolic requirements at normal cardiac filling pressures
76
What is forward failure and what are the signs
- inadequate cardiac output with normal pressures
- manifestations of hypotension
77
What is backward failure and what are the signs
- excessive filling pressures with normal cardiac output
- pulmonary oedema, pleural effusion or ascites
78
Abnormalities in preload can be managed by what drug type
drugs that reduce circulating volume - diuretics and vasodilators
- loop diuretics most potent
- venodilator nitroglycerin
79
Abnormalities in afterload can be managed by what drug type
Vasodilators to reduce systemic vascular or pulmonary vascular resistance
- ACEI (benazepril), Amlodipine
- sildenafil
80
Abnormalities in myocardial contractility can be managed by what drug type
positive inotropes
- Dobutamine, pimobendan, digoxin
81
Abnormalities in cardiac filling can be managed by what drug type
Positive lusciotropes
- luscitrope - diltiazem
82
Abnormalities in heart rate can be managed by what drug type
Anti-arrhythmics or pacemakers
83
Furosemide
- use
- mechanism
- adverse effects
- Loop diuretic
- Block Na/K/Cl co-transporter in loop of Henle
- rare ototoxicity and AKI
84
Spironolactone
- use
- mechanism
- adverse effects
- potassium sparing diuretic
- Inhibits aldosterone receptors in collecting duct and DCT
- facial dermatitis in cats
85
Torsemide
- use
- mechanism
- Loop diuretic
- Block Na/K/Cl co-transporter in loop of Henle
- used when refractory to furosemide
86
Hydrochlorothiazide
- use
- mechanism
- drug interraction
- Thiazide diuretic
- Blocks Na/Cl symporter in distal tubule
- also results in K, Mg loss into urine
- decreases calcium loss in urine
- don't combine with loop diuretic
87
Benazepril
- use
- mechanism
- adverse effects
- ACE inhibitor
- prevents ATII production and decreases aldosterone
- Vasodilation (preferrential of efferent arteriole) and inhibition of fluid retention
- Azotemia, GI signs, hyperkalemia
88
Amlodipine
- use
- mechanism
- unusual adverse effects
- Calcium channel blocker (L type)
- peripheral arteriolar vasodilator
- gingival hyperplasia and peripheral oedema dog
89
Sildenafil
- use
- mechanism
* Phosphodiesterase 5 inhibitor (PDE5)
* vasodilator of pulmonary vasculature
90
Diltiazem
- use
- mechanism
* Lusciotrope, antiarrhythmic
* calcium channel blocker
91
Dobutamine
- use
- mechanism
- adverse effects
* Positive inotrope
* Beta -1 adrenergic agonist
* Some weak B2 and A1 effects
* tachycardia, premature complexes, seizures
92
Dopamine
- use
- mechanism
- adverse effects
* Positive inotrope
* Acts on alpha and B1 and B2 receptors
* nausea, vomiting, ectopic beats
93
Pimobendan
- use
- mechanism
- adverse effects
* positive inotrope and vasodilator
* calcium sensitisation and phosphodiesterase 3 inhibitor (PDE3)
* GI disease, hypotension
94
Sick sinus syndrome
- conduction changes
- clinical signs
- predisposed breeds
- treatment
- failure of impulse formation from the SAN
- Weakenss, lethargy, collapse or syncope
- WHWT, cockers, mini schnauzer
- Pacemaker or symathomimetics (theophylline, terbutaline)
95
Jugular pulsation is seen with which cardiac disease
Any disease with tricuspid regurgitation
- PHT, tricuspid valve dysplasia, pulmonic stenosis
96
PDA
- abnormality
- clinical findings
- Breed predisposition
- patent ductus arteriosus allowing blood flow from aorta to pulmonary artery
- Typically L-R shunting but can reverse if severe PHT occurs
- Erythrocytosis, machinery continuous left thoracic murmur and hyperdynami pulses, if shunt reverses may have differential cyanosis (HL cyanotic)
- most common congenital heart disease in dogs, second most common in cats
97
Atrial septal defects
- abnormality and pathology
- breed predispositions
- murmur
* ASD leads to R heart failure withut evidence PHT
* ASD cats - Persian and chatreux
* ASD dogs - boxer and doberman
* ASD left basilar murmur (due to flow across PV as a result of L-R shunting)
98
Ventricular septal defects
- abnormality and pathology
- breed predispositions
- murmur
* VSD leads to pulmonary overcirculation and L heart failure
* VSD dogs - Keeshond, ESS, English bulldog
* VSD most common congenital abnormality in cats
* VSD - right holosytolic harsh murmur
99
Pulmonic stenosis
- abnormaliy and pathology
- murmur type
- pulmonary artery leaflets thickened
- R CHF
- left basilar crescendo-decrescendo murmur
100
Aortic stenosis
- abnormality and pathology
- murmur type
- breed predisposition
* valvular or sub valvular thickineing/stenosis
* LCHF and ventricular arrhythmia
* Valvular AS - Bull terrier
101
Tetralogy of fallot
- pathology
- breed predisposition
* RV outflow tract obstruction due to infandibular obstruction, RV hypertrophy, VSD, rightward positioned aorta (+/- pulmonic valve hypoplasia)
* English bulldog, Keeshond
102
MMVD
- pathology
- what breeds are predisposed
* Myxomatous mitral valve disease
* Adult onset progressive degeneration of the mitral valve causing mitral regurgitation and left sided heart disease
* CKCS, Dachshund, Yorkie, mini poodle
103
What percentage of CKCS over the age of 7y and 10y are affected by MMVD
50% and 100%
104
MMVD ACVIM stages
A: at risk but no structural abnormalities
B1: structural abnormalites, no CHF, MR not severe enough to need treatment
B2: structural abnormalites, no CHF, MR severe enough to need treatment
C: CHF
D: refractory CHF
105
What are the EPIC trial inclusion criteria for initiating medical treatment in MMVD
Murmur ≥3/6, La/Ao in diastole in R short axis view ≥1.6, LVIDDN ≥1.7 or VHS >10.5
106
What is the systolic pulmonary artery pressure in order to diagnose pulmonary hypertension
- >25mmHg
107
Infective endocarditis
- valves typically affected
- typical bacteria
- Proportion of dogs with arrhythmia
- Proportion of dogs with negative blood culture
- prognosis
- mitral and/or aortic
- Acute: gram negative, Chronic - gram positive
- Arrhythmia in 50-75% typically VPC or VT
- Negative blood culture in 60-70%
- Overall guarded but better with isolated mitral valve disease, gram +ve bacteria on infections from integuement.
108
DCM
- pathology
- causes
- breed predispositions
- diagnosis
- LV systolic dysfunction and eccentric hypertrophy
- Idiopathic/genetic or acquired (doxorubicin, taurine deficiency or legume rich diet)
- Large breeds (doberma, great diane, irish wolfhound etc)
- Genetic mutation in dobermans PDK4 and titin
- taurine deficient DCM in cockers
- normal echo does not exclude, no of PVC/24hrs (>300) NTproBNP 90% spec and 70% sens for preclinical DCM
109
ARVC
- pathology
- clincial signs
- breed predisposition and mutation
- diagnosis
- arrhythmogenic right ventricular cardiomyopathy
- replacement of RV myocardium with fatty or fibrous tissue
- venbtricular arrhythmia and sudden death
- Boxers - mutation in striatin, and english bulldog
- >100 PVC/24hrs suggestive for boxer, echo often normal
110
HCM
- pathology
- genetic mutations identified
- phenotypes
- murmur prevalance
- treatment
- hypertrophic cardiomyopathy
- increased LV wall thickeness with non-dilate LV chamber
- mutations in myosin binding protein C (MYBPC£) identified in maine coon and ragdolls
- multiple phenotypes: HCM, RCM, DCM, ARVC and NSCM
- murmur in 78-92% cats with HCM (left apical parasternal systolic)
- Clopidogrel in ACVIM B2
111
ATE
- risk factors
- prognosis
- complications
- treatment
- LAE with smoke
- better prognosis: normothermic, one limb affected and partial motor function
- reperfusion injury and hyperkalemia
- tPA, LMWH
112
Chemodectoma
- tumor type
- location
- breed predisposition
- neuroendocrine tumour
- heart base
- May cause pericardial effusion
- Middle aged to older english bulldogs, boxers and boston terriers
113
Cardiac haemangiosarcoma
- location
- breed predisposition
- metastasis
- treatment
- right atrium, commonly causes pericardial effusion
- GSD, Poodle, Golden Retriever, English Setter, and Scottish Terrier
- metastasis very common, most commonly to lungs
- pericardectomy and chemo (doxorubicin protocols better MST)
114
What is tamponade
- what is the effect of tamponade
- What blood pressure would be consistent
- impairment of ventricular filling due to a space-occupying effect within the pericardial space, most often from pericardial effusion
- reduces CO and SV
- concern if BP <90mmHg
115
What is pulsus paradoxus and when it seen
- greater than 10mmHg fluctuation in systolic arterial pressure during breathing
- seen with pericardial effusions
116
Which breed are over-represented for pericardial effusion
Golden retreiver, other middle-large breed dogs
117
Where should pericardiocentesis be performed
- right thorax, cardiac notch decreases potential for lung injury
- just cranial to the rib, 4th or 5th intercostal space
118
When measuring blood pressure using an oscillometric technique the point at which maximum amplitude fluctuations occur within the cuff is
mean arterial pressure
119
Central venous pressure
* A normal CVP range is 0-5 cm H2O
* pressure in RA
120
Intrinsic rate of the canine sino-atrial node
150-180 bpm
121
On pulsed-wave Doppler recording of the mitral inflow what do the A wave and E wave represent
A wave = atrial contraction
E wave = rapid ventricular filling
122
What are the most common causes of systemic hypertension in:
- Dogs
- Cats
- Dogs: CKD (especially glomerular), HAC and BM
- Cats: CKD, idiopathy, HyperT4
123
What are the manifestiations of target organ damage in systemic hypertension
- Ocular (retinal detachment, haemorrhage, multifocal oedema) - most common
- Renal (hypertenisve nephrosclerosis causing glomerulonephritis and proteinuria)
- Cardiac (cardiac hypertrophy and duastolic dysfunction)
- Neurological (hyeprtensive encephalopathy, ischemic myelopathy seen in cats)
- Vascular (vasculopathy- uncommon)
124
What are the IRIS stages of hypertension
* Normotensive: <140 mm Hg: minimal TOD risk
* Prehypertensive: 140-159 mm Hg: low TOD risk
* Hypertensive: 160-179 mm Hg: moderate TOD risk
* Severely hypertensive: >180 mm Hg: high TOD risk
125
Systemic hypertension treatment
- cats
- dogs
- Cats: amlodipine (60-100% cats respond), telmisartan, ACEI in combination
- Dogs: ACEI, amlodipine or telmisartan
126
What is Virchow's triad
Virchow’s triad suggests thrombus formation is promoted by:
- stasis of blood flow,
- hypercoagulability
- endothelial dysfunction
127
ATE
- clinical signs
- most common location
- pain, pallor, pulselessness, paresis or paralysis and poikilothermia
- Distal aortic trifurcation
- 75% cats gas bilateral pelvic limb involvement
128
Omega -3 FA supplementation
- source
- benefits
* Fish oil
* decreases cytokine and inflammatory mediator production
* studues documented improvement in MMVD LA diameter with omega-3FA supplemetation
129
What is the equation for blood flow through a vessel
Ohm’s Law (F = (ΔP)/R)
F = blood flow, ΔP = pressure difference between P1 and P2 (P1-P2), R = resistance
CO= arterial pressure/total peripheral resistance
130
What is Reynolds number and what does it measure
- tendency for tubulence
- Re = (v∗d∗p)/n
- (v = velocity, d = diameter, p = density, n=viscosity)
- if>2000 turbulent flow defintely occurs
131
How do you measure peripheral vascular resistance
calculated indirectly from measurements of blood flow and pressure difference
PVR = ΔP/F
132
what is conductance and what is the equation
* conductance is the measure of flow through a vessel for a given pressure difference
* conductance = 1/resistance
* conductance ∞ Diameter^4
133
What is Poiseuille's law
* integrates the velocities of flowing blood in vessel (slowest near the wall to fastest on the inside)
* helps demonstrate the importance of arteriolar constriction and dilation determining blood flow
F =(πΔPr^4)/8nl
(F = rate of blood flow, ΔP = pressure difference, r = radius, n = viscosity, l = length of vessel)
134
What is the law of Laplace
Law of Laplace T= ΔP x (r/h)
T = wall tension, "ΔP=transmural pressure gradient, r=radius, h=wall thickness"
135
How is vascular distensibilty measured
vascular distensibility = (Increase in volume)/(Increase in pressure x original volume)
136
How is vascular compliance measured
Vascular compliance = (Increase in volume)/(Increase in pressure)
137
How is pulse pressure calculated
Pulse pressure = stroke volume/arterial compliance
Difference between systolic and diastolic blood pressure
138
Net filtration pressure in capillaries is determined by what
capillary hydrostatic pressure, interstitial hydrostatic pressure, capillary collois osmotic pressure and interstitial osmotic pressure
139
What are three humoral vasoconstrictors
- Norepinephrine and epinephrine
- Angiotensin II
- ADH
140
What are two humoral vascodilators
- Bradykinins
- Histamine
141
Which ions will contribute to vasodilation
- increased K+, increased H+, Increased CO2
142
which ion will contribute to vasoconstriction
* increased calcium
