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first year revision > cardiovascular > Flashcards

cardiovascular Flashcards

1
Q

define AF

A

irregular atrial contraction caused by chaotic impulses

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2
Q

causes of AF

A

hypertension,
ischaemic heart disease, MI,
cardiomyopathy
rheumatic heart disease

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3
Q

clinical signs in atrial fibrillation

A

left atrial thrombus
apical+radial pulse defect
palpitation

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4
Q

2 main types of atrial fibrillation treatment

A

rate control: first line. control fast ventricular rate

rhythm control: acute onset, restore sinus rhythm

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5
Q

examples of rate control drugs

A 
beta blockers (metoprolol, bisoprolol)
rate limiting calcium channel blockers (verapamil, diltizem)
digoxin: bed bound patients
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6
Q

when is rhythm control used for Atrial fibrillation?

A

new- onset
HF exacerbated by AF
atrial flutter
identifiable reversible cause

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7
Q

2 types of rhythm control methods

A
  1. pharmacological: amiodarone, flecainide, beta blockers

2. electrical: DC cardioversion

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8
Q

treatment for AF onset of 48hours +

A

increase thromboembolism risk, need minimum of 3 weeks of anticoagulant to reduce risk before cardioversion

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9
Q

treatment for AF onset less than 48hours

A

low risk of thromboembolism, immediate electrical or pharmo cardioversion

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10
Q

when and why is anticoagulant given for AF

A

CHA2DS2-VASc score 2 or more
AF leads to stasis of blood in left atrial appendage forming thrombus
clot could move to cerebral, limb, abdominal causing stroke/ ischemia

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11
Q

how is AF confirmed

A

ecg: absent p wave, fibrillation baseline

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12
Q

mechanism of aspirin

A

antiplatelet: Irreversible inhibition of cyclooxygenase and thromboxane A2

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13
Q

unstable vs stable angina

A

unstable pain at rest, relieved by GTN

stable pain while running or excercise

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14
Q

heparin/ LWMH mechanism

A

anticoagulant: increase the action of anti-thrombin III to inhibit factor Xa

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15
Q

mecahnsim of clopidogrel

A

antiplatelet: Inhibition of the adenosine diphosphate (ADP) receptor.

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16
Q

anticoagulant vs anti platelet

A

Anticoagulants slow down your body’s process of making clots.
Antiplatelets, prevent blood cells called platelets from clumping together to form a clot, ie, after heart attack or stroke or prevention

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17
Q

immediate/ initial management for all ACS patient

A 
MOAN
morphine
oxygen (94)
nitrates (GTN)
aspirin + ticagrelor/clopidogrel
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18
Q

site and artery for V1-V4

A

anterior

LAD

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19
Q

site and artery for I, aVL V3-V6

A

anterolateral

circumflex, LAD

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20
Q

site and artery for I, aVL, V5-V6

A

Lateral

circumflex

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21
Q

STEMI management

A

PCI (w/ anitplatelet)
Thrombolysis

ACEi (prevent cardiac remodelling)
BB (reduce mortality)

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22
Q

2 main treatments for NSTEMI and UA

A

dual antiplatelet
antithrombotic: fondaparinux (2.5mg)
BB

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23
Q

post MI management

A

dual antiplatlet therapy (asparin + clopidogrel) for 1 year
High dose atorvastatin for high cholesterol
No alcohol

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24
Q

ACS diagnostic

A

ECG

raised troponin T & I (STEMI & NSTEMI, myocardial necrosis)

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25
Q

examples of tachycardia

A

Atrial fibrillation, atrial flutter, SVT (AVNRT, AVRT)

Ventricular Tachycardia

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26
Q

causes for tachycardia vs bradycardia

A

increase vs decrease automaticity
tachy: triggered activity & reentrant circuit
Brady: conduction block

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27
Q

causes of increased automaticity

A

increase sympathetic trunk tone

increase metabolic activity

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28
Q

examples of increased sympathetic tone

A

hypovolemia
hypoxia
sympathomimetic drugs
pain/ anxiety

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29
Q

examples of increase metabolic activity

A

fever

hyperthyroidism

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30
Q

causes of hypoxia

A

decrease in RBC
lung disease
PE

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31
Q

slow/ block AV conduction drugs

A

bb, ccb, digoxin

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32
Q

causes of decreased automaticity

A 
increase parasympathetic/vagal tone
slow AV conduction drugs 
decrease metabolic activity
hyperkalemia
Cushing triad
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33
Q

examples of decreased metabolic activity

A

hypothermic

hypothyroidism

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34
Q

what is the cushing’s triad

A

bradycardia
irregular respiration
hidden pulse pressure

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35
Q

2 types of triggered activity/ after depolarization (main cause of ventricular tachycardia)

A

early(EAD): phase 3 of electrical potential

late (LAD): phase 4 of electrical potential

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36
Q

causes of early after depolarization EAD

A

decrease in K+, Ca+, magnesium

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37
Q

causes of late after depolarization LAD

A

tachycardias

overload of intracellular calcium

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38
Q

EAD vs LAD physiology

A

trigger occurs on polarization of myocardial cells
EAD: early trigger of during depolarization, increase QT interval
DAD: late trigger after depolarization is complete

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39
Q

physiology of AVRT(atrioventricular reentry tachycardia)/ Wolff Parkinson white

A

contain bundle of Kent: bi direction accessory pathway

normal: AV node-> bundle of his & Purkinje fibres-> ventricule depolarize
abnormal: AV node-> bundle of Kent-> comes back down= re-entery circuit

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40
Q

physiology of AVNRT

A

reentry due to 2 SA->AV node pathways
path 1: slow w/ short refractory
path 2: fast w/ long refractory
2 electrical signal travel and refract at different speed causing electrical conduction to travel back from AV-> SV node = problematic

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41
Q

causes of conduction block

A 
RCA occlusion causing inferior MI 
fibrosis of AV node 
hyperkalemia 
drugs (BB, CCB, digoxin)
amyloidosis & sarcoidosis
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42
Q

tachycardia treatment: regular rhythm+ narrow QRS

A
  1. vagal manoeuvre

2. adenosine

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43
Q

ventricular tachycardia ecg

A

wide QRS + regular rhythm/ broad complex tachycardia

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44
Q

ventricular tachycardia treatments

A
  1. amiodarone+ procanimide

2. DC shock cardioversion (do this first if they have symptoms of shock, chest pain, HF)

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45
Q

ventricular fibrillation ECG

A

wide QRS with irregular rhythm

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46
Q

ventricular fibrillation treatment

A

VERY dangerous

CPR+defibrillation and repeat

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47
Q

Common death cause in first hour inferior wall MI

A

Arrhythmia: ventricular fibrillation

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48
Q

presentations of aortic stenosis

A

ejection systolic murmur radiates to carotid

soft/ absent S2, narrow pulse pressure

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49
Q

presentation of pulmonary stenosis

A

ejection systolic, crescendo descendo

ventricular thrill/ heave

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50
Q

presentation of mitral regurgitaion

A

pansystolic murmur radiates to axilla

soft s 1 with s 3

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51
Q

what is ventricular septal defect

A

congenital opening causing blood flowing from left to right ventricle
pansystolic murmur
may occur post MI

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52
Q

where is VSD heard

A

louder at the left sternal edge

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53
Q

infective endocarditis symptoms

A

fever, splinter, haemorrhages, splenomegaly

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54
Q

pathophysiology of infective endocarditis

A

innerlining/ endothelial/ valve infection

infection of platelet fibrin complex by posited bacteria-> vegetation-> break off and migrate to other parts of body

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55
Q

what is vegetation during infection

A

vegetation: collection of fibrin, platelets, WBC, RBC debris and bacteria

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56
Q

mutation change in Down’s syndrome

A

trisomy 21: three copies of 21st chromosomes

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57
Q

cardiac defect asso w/ Down syndrome

A

atrioventricular septal defect

other: VSD, tetralogy of fallot, patent ductus arteriosus

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58
Q

clinical signs of tricuspid regurgitation

A

prominent, pulsatile, large CV wave in JVP

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59
Q

clinical signs of tricuspid stenosis

A

af, hepatomegaly, peripheral oedema

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60
Q

what is a early diastolic murmur heard loudest on lower left sternal edge

A

aortic regurgitation with high risk of aortic dissection

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61
Q

murmur asso w/ Marfan’s syndrome

A

aortic regurgitation

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62
Q

2 murmurs during hypertrophic cardiomyopathy

A

ejection systolic: left ventricular outflow obstruction

mid late systolic: systolic anterior motion of mitral valve

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63
Q

causes of aortic stenosis

A

calcification
congenital bicuspid valve
rheumatic heart disease

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64
Q

causes of pulmonary stenosis

A

Noonan syndrome
tetralogy of fallot
congenital rubella syndrome

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65
Q

pathology of hypertrophic cardiomyopathy

A

mutation of B-myosin heavy chain or myosin binding protein C

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66
Q

murmur best heard on expiration leaning forward and lying on left side

A

aortic regurgitation and mitral stenosis

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67
Q

causes of hypertrophic cardiomyopathy

A

pulmonary/ aortic stenosis-> ventricle pump harder-> ventricular hypertrophy
mitral/ tricuspid stenosis-> aorta pump harder-> atrial hypertrophy

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68
Q

causes of dilated cardio myopathy

A

pulmonary/ aortic regurg-> blood flow back and stretch-> ventricular dilatation
mitral/ tricuspid regurg-> blood flow back and stretch-> atrial dilatation

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69
Q

infective endocarditis murmurs

A

aortic/ mitral regurgitation

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70
Q

symptoms of murmur

A

SAD
syncope
angina
dyspnea

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71
Q

complication of mitral regurgitation

A

HF and pulmonary oedema

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72
Q

aortic regurgitation clinical signs

A

Displaced apex (chronic)
Soft S1
HF
Corrigan’s pulse/collapsing pulse

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73
Q

clinical signs of mitral stenosis

A

mallar flush

tapping apex

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74
Q

murmur during pericarditist

A

triphasic systolic and diastolic rub

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75
Q

general causes for AV block

A

increased vagal tone
normal variant
drugs
mitral valve surgery

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76
Q

define 1st degree AV block

A

delayed in conduction through av node

ecg pr interval 200ms+

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77
Q

causes of 1st degree AV block

A

coronary artery disease
hypokalemia
hypomagensium

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78
Q

treatment of 1st degree AV block

A

no treatments unless symptomatic

pacemakers considere due to risk of AF

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79
Q

define 2nd degree AV block (Mobitz I)

A

non constant, progressively longer PR due to fatigue of AV cells
ie, every 4 P, 3 QRS

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80
Q

causes of Mobitz I

A

myocardial infarction

hyperkalemia

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81
Q

treatments of Mobitz I

A

may cause bradycardia + hypotension

atropine if needed

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82
Q

define 2nd degree AV block (Mobitz II)

A

constant pr interval with intermittent non conducted P wave

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83
Q

causes of Mobitz II

A

structural heart disease

myocardial ischemia/ firbosis

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84
Q

symptoms of Mobitz II and complete heart block

A

syncope, fatigue, chest pain, death

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85
Q

treatment for Mobitz II

A

pacemaker

DON’T use atropine may lead to complete block

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86
Q

define 3rd degree/ complete heart block

A

no association between atria and ventricles/ P and QRS

junctional ventricular escapee rhythm

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87
Q

causes of 3rd degree/ complete heart block

A

inferior myocardial infarction
av blocking agents
degeneration of conduction system

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88
Q

treatment for 3rd degree/ complete heart block

A

transcutaneous/ transvenous pacemaker

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89
Q

why is mobitz 2 more dangerous than mobitiz 1

A

risk of becoming haemodynamic unstable
severe bradycardia
progression to 3rd degree heart block
syncope, sudden cardiac death

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90
Q

Define stroke volume

A

Amount of blood pumped out of the heart from each contraction

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91
Q

Define cardiac output

A

The amount of blood pumped out of the heart in one minute

CO=HR x SV

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92
Q

Preload vs after load

A

Preload: stretching of cardiomyocytes at the end of diastole
After load: pressure ventricles need to exert against to eject blood out during systole

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93
Q

Inotropy, what cause positive inotropic effect

A

Myocardial contractility/ force of muscular contraction

stimulation of beta 1 adrenergic receptor leads to positive inotropic effect

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94
Q

How is preload increased

A

Increase venous pressure-> increased venous return-> increase end diastolic volume-> increase cardiomyocyte stretch/ preload

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95
Q

What is the frank starling law

A

Increased preload/ Cardiac muscle stretch = increase force of contraction/ stroke volume

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96
Q

How does afterload and Inotropy (contractility) affect stroke volume

A

Decreased after load with increased Inotropy= increased SV

Increase after load with decreased Inotropy = decreased SV

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97
Q

3 determinants of Stroke volume

A

Preload
Myocardial contractility
After load

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98
Q

What are the 2 determinants of Mean arterial Pressure (MAP)

A
  1. Cardiac output

2. Systemic vascular resistant

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99
Q

MAP formula

A

diastolic pressure + 1/3 (systolic pressure- diastolic pressure)

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100
Q

Define systemic vascular resistance

A

Resistance to blood flow offered by all systemic vasculature excluding pulmonary vasculature
Determined by vasodilation and vasoconstriction

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101
Q

2 factors that influence preload

A
  1. Venous return

2. Filling time: longer = more blood in ventricles

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102
Q

2 factors that influence after load

A
  1. Vascular resistance: increased pressure from vasoconstriction= harder for heart to pump against= decrease SV
  2. Valvular disease: stenosis valves
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103
Q

3 factors that Effect of Inotropy/ contractility

A
  1. Muscular function: hypertrophy
  2. Autonomic nervous system
    parasympathetic vs sympathetic (beta 1 adrenergic)
  3. drugs
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104
Q

Compensatory mechanisms for decreased cardiac output

A

baroreceptor

RAAS

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105
Q

what is compensatory mechanism for?

A

When decreased in cardiac output is detected

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106
Q

How does increase preload as a compensatory mechanism effect the heart and body during heart failure

A

Increase EDV, compensate for reduced ejection fraction to maintain CO
Large increase: pulmonary oedema, ascites, peripheral oedema

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107
Q

How may increase heart rate as a compensatory mechanism effect the heart and body during heart failure

A

Sinus tachycardia

CO= SV x HR

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108
Q

describe function of chemoreceptors during decreased tissue perfusion

A

poor tissue perfusion= increased lactic acid.=decreased pH / increase artery PCO2
activates chemoreceptors=^ resp rate, leads to more CO2 being ‘blown off’ =resp compensation in metabolic acidosis.

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109
Q

What is the function of BNP

A

Protein released by cardiomyocytes during excessive stretching
Good negative predictive Used to measure likelihood of HF (excludes HF if normal amount)

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110
Q

Causes of acute HF

A

Acute myocardial dysfunction
Acute valvular disease
Pericardial tamponade

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111
Q

Causes of chronic HF

A

Cardiomyopathy
Ischaemic heart disease
Aortic stenosis
AF

112
Q

Define systolic HF

A

ejection fraction below 40% :
decreased stroke volume,
increased preload + decreased contractility
eccentric remodelling

113
Q

Define diastolic HF

A

decreased stroke volume and total volume= ejection fraction remained.
Impaired ventricular filling/ preload
usually due to ventricular hypertrophy
concentric remodeling

114
Q

Define cardiac remodeling

A

Changes in cardiac size, shape, function in response to cardiac injury or increased load

115
Q

Define congestive cardiac failure

A

Combination of left and right failure

116
Q

What leads to left sided HF

A

systolic: ischemic heart disease, hypertension, dilated cardiomyopathy
diastolic: hypertension, hypertrophy, aortic stenosis, hypertrophic + restrictive cardiomyopathy

117
Q

how does RAAS mechanism activation work?

A

reduced CO-> activate RAAS-> increase venous pressure/vasoconstriction, water and sodium reabsorption-> increased preload-> increase contraction strength

118
Q

what are heart failure cells

A

so much fluid in capillaries-> rupture leaking blood to alveoli-> alveolar macrophages eat up RBC (hemosiderin laden macrophages)

119
Q

how does left HF cause pulmonary oedema

A

decreased CO-> back up in left atrium-> pulmonary circulation-> increase pressure in pulmonary capillaries-> pulmonary odema-> decrease gas exchange-> dyspnea

120
Q

how is systemic circulation effected during right HF

A

blood backs up in the body for right HF

JVP distention, splenomegaly, hepatomegaly, ascites, pitting edema

121
Q

What leads to right sided HF

A

caused by left HF: Pulmonary hypertension
Pulmonary/ tricuspid valve disease
cor pulmonale
ventricular septal defect (blood flow from left to right )

122
Q

Cause of cor pulmonale

A

Alteration of right ventricular structure/ dysfunction due to pulmonary hypertension
COPD, PE, interstitial lung disease

123
Q

What is high output HF

A

CO> 8L/min

Heart can’t meet increased demand for perfusion despite normal cardiac function

124
Q

Causes of high output HF

A 
Increase metabolic demand (hyperthyroidism)
Reduced vascular resistance (thiamine deficiency, sepsis)
Significant shunting (large arteriovenosu fistula)
125
Q

Diagnostic of HF

A

TTE when BNP is raised, murmur present, abnormal ecg

Cardiac MRI if TTE is non-diagnostic

126
Q

What does TTE measure for in HF and how is it classified

A

Ejection fraction
HF with reduced ejection fraction: <40%
HF with minimally reduced ejection fraction: 40%-49%
HF with preserved ejection fraction: 50% or more

127
Q

What does echocardiogram looks for

A

Evidence of previous MI
ventricular/ valve hypertrophy
Conduction abnormalities/ AF

128
Q

What does CXR look for

A 
Cardio megaly
alveolar shadowing oedema 
Kerley B lines (fluid in lobules)
Pleural effuction 
Upper lobe diversion
129
Q

Management for HF with preserved ejection fraction

A

Loop diuretic: furosemide 20 mg OD

130
Q

Treatment for HF due to left ventricular systolic dysfunction

A
  1. ACEi (rampiril1.25mg) + beta blocker (bisoprolol 1.25 mg)
    loop diuretic (fureosemide 20mg)
  2. Spironolactone
  3. digoxin
131
Q

Mechanism of spironolactone

A

antagonist of mineralcortisone receptor of aldosterone dependent Na/ K+ exchange site at distal convoluted renal tubule
(hypertension and HF)

132
Q

Symptoms of congestive heart failure

A

Orthopnoea, paroxysmal nocturnal dysponoea, ankle swelling

133
Q

Treatment for acute pulmonary oedema secondary to acute left ventricular dysfunction

A 
FOND
Furosemide
Oxygen 
Nitrates 
Diamorphine IV
134
Q

Symptoms of hypertension

A

Palpitations
Angina
Headaches
Blurred vision

135
Q

What are the four grades of Keith wage et barker system for hypertension

A

1: generalized arteriolar narrowing
2: focal narrowing and arteriovenous nipping
3: retinal haemorrhages, cotton wool spots
4: papilloedema

136
Q

Diagnostic of stage 1 & 2 hypertension

A

If clinical BP is 140/90 mmHg->Ambulatory BP measurements, 2 measurements an hour during waking hours and confirm with average value

137
Q

Confirm Hypertension diagnosis other than ABPM

A

home BP monitoring:
evening & night for 4-7 days
Seated, taken twice each time 1 min apart
Average without day 1

138
Q

Stage 1 hypertension measurement

A

ABPM: 135/85 or more

Clinic BP 140/90 or more

139
Q

Stage 2 hypertension measurement

A

ABPM: 150/95 or more
Clinical: 160/100 or more

140
Q

Stage 3 hypertension measurement

A

Clinic BP: 180/120 or more

141
Q

Define malignant hypertension

A

BP> 190/120 with signs of papilloedema/ retinal haemorrhage

142
Q

treatments of hypertension for diabetic + younger than 55

A

ACEi
ARB
BB

143
Q

treatments of African + older than 55

A

CCB

Diuretic

144
Q

Treatments for malignant hypertension

A

IV nitroprusside, labetalol, glyceryl trinitrate

Phentolamine

145
Q

What are the 2 mechanism allowing exchange between capillaries and extracellular fluids

A
  1. Diffusion: net movement of solutes (O2, CO2) down their respective concentration gradients due to random motion of individual molecules
  2. Bulk flow: movement of water and solutes together due to pressure gradient
146
Q

What are the 2 pressure gradients in bulk flow

A
  1. Hydrostatic pressure push fluid out of blood capillaries (arteriolar to venous 37-17)
  2. Oncotic pressure push fluid into blood capillaries (25 through out )

Net outward pressure on fluid at arterioles side, net inward pressure at venous side

147
Q

Function of alpha 1 adrenergic recpetor

A

Located in vascular smooth muscle, induce vasoconstriction

148
Q

What are the 2 barorecptor that maintain blood pressure

A

Carotid sinus baroreceptor - glossopharngyngeal nerve

Aortic arch baroreceptors - vagus nerve

149
Q

Phase 0 of cardiac action potential

A

Rapid depolarization
Rapid sodium influx
-96mv to +52 mV

150
Q

Phase 1 of cardiac action potential

A

Early repolarization

Efflux of potassium

151
Q

Phase 2 of cardiac action potential

A

Plateau

Slow influx of calcium

152
Q

Phase 3 of cardiac action potential

A

Final repolarization

Efflux of potassium

153
Q

Phase 4 of cardiac action potential

A

Restoration of ionic concentration
Na+ / K+ ATPase
Slow entry of Na+ to decrease potential difference until threshold is reached

154
Q

Inotropic vs chronotorpic vs dromotropic vs lusitropic

A

inotropic (contractility), chronotropic (heart rate), dromotropic (rate of conduction through AV node) and lusitropic (relaxation of myocardium during diastole) effects

155
Q

Class I antiarrhythmitics

A

Inhibit fast sodium channels, phase 0
Quinidine, flecainide, procainimide
Many side effects, Nausea vomiting, negative Inotropic effect

156
Q

Class II antiarrthythmics

A

Beta blockers
Negative inotropic and chronotorpic
Phase 4/ refractory period
SE: bronchocontriction (dont use for asthmatics), bradycardia, heart block

157
Q

Mode of action of beta blockers

A

Competitive antagonist of catecholamines, bind to beta receptors without activating them

158
Q

Class iii antiarrhythmics

A

Block potassium channels K+
Phase 3
amiodarone

159
Q

Class iiii antiarrhythmics

A

Non-dihydropryidine CCB, block conduction at AV node
Verapamil, diltizem
Phase 2

160
Q

Non-dihydropyridines vs dihydropyridines

A

Antiarrhythmics: verapamil, diltizem

Anti-hypertensive: nifedipine, amlodipine

161
Q

Mode of action for digoxin

A

Cardiac glycosides, increase intracellular Na+, Ca2+, contractility through inhibiting Na+/ATPase pump on

162
Q

Mode of action for adenosine

A

Acts on SA node to reduce heart rate and AV node to slow conduction

163
Q

Mode of action for atropine

A

M2 antagonist blocks acetylcholine effect, inhibits vagal activity to increase heart rate

164
Q

three types of infective endocarditis

A

native valves
prosthetic valve
IV drug

165
Q

organisms that cause native valve endocarditis

A

streptococcal: alpha-haemolytic, strep. bovis

enterococci

166
Q

organism causing prosthetic valve endocarditis

A

early: coagulase negative staphylococcus (more common)
late: streptococcus

167
Q

iv drug and dental related infective endocarditis organisms

A

staphylococcus aureus

streptococci viridans

168
Q

complications of infective endocarditis bacterial vegetation

A

break off-> embolic event-> formation of abscesses

activation of immune system->clustering of immune complexes in the vegetation-> immune mediated vasculitis

169
Q

IE diagnostic

A

3 sets of blood culture

TTE/ TOE

170
Q

dukes major criteria for IE

A
  1. microbiological criteria: microorganism found in 2 blood cultures
  2. evidence of endocardial involvement: vegetation/ abscess evidence on echo
171
Q

5 of the dukes minor criteria for IE

A 
predisposing heart condition/ IVDU
fever
vascular phenomenon
immunological phenomenon
microbiological evidence
172
Q

staph aureus treatment

A

flucloxacillin 12g/day

vancomyocin for penicillin allergy

173
Q

oral streptococci/ streptococcus bovis treatment

A

4 weeks:
penicillin/ amoxicillin/ ceftriaxone
vancomycin for penicillin allergy

2 weeks:
add gentamicin

174
Q

empirical Treatment for IE (highly suspected but organism not known yet)

A

native: vancomycin and gentamicin

prosthetic valve: vancomycin, gentamicin, rifampin

175
Q

define cardiac tamponade

A

accumulation of pericardial fluid in the pericardial space between parietal and visceral pericardium

176
Q

what is the beck’s triad

A

classical feature of cardiac tamponade

hypotension, raised JVP, muffled heart sounds

177
Q

causes of cardiac tamponade

A

pericarditis
tuberculosis
injury, stabbing

178
Q

cardio tamponade diagnostic

A

ECHO

see pericardial effusion and haemodynamic impact on the heart

179
Q

cardiac tamponade treatment

A

needle pericardiocentesis

180
Q

what are the 3 wave and 2 descents of JVP

A

3 wave
A,C,V

2 descent
X, Y

181
Q

what is the A wave in JVP, when is it large or absent?

A

atrial contraction

large: tricuspid & pulmonary stenosis, pulmonary hypertension
absent: atrial fibrillation

182
Q

define cannon ‘a’ wave

A

atrial contraction against closed tricuspid valve

ie, complete heart block, ventricular tachycardia

183
Q

what does C wave of JVP represent

A

closure of tricuspid valve

not normally visible

184
Q

what does V wave of JVP represent, when is it large?

A

passive filling of blood into atrium against closed tricuspid valve
large: tricuspid regurgitation

185
Q

what does x and y descent represent

A

x: fall in atrial pressure during ventricular systole
y: opening of tricuspid valve

186
Q

cyanotic heart disease

A

tetralogy of fallot
transposition of great arteries
tricuspid atresia

187
Q

when does tetralogy of fallot appear

A

1-2 months

188
Q

four characteristics of tetralogy of fallot

A

ventricular septal defect
right ventricular hypertrophy
pulmonary stenosis
overriding aorta

189
Q

x ray finding of TOF

A

boot shaped heart

190
Q

ecg of left ventricular hypertrophy

A

increased QRS amplitude

191
Q

treatment of TOF

A

surgical repair in two parts

beta blockers for cyanotic episodes

192
Q

causes of ventricular septal defect

A

chromosomal disorders (down, Edwards, patau syndromes)
congenital infections
post MI

193
Q

VSD symptoms

A

failure to thrive
HF symptoms (hepatomegaly, tachypnoea, tachycardia, pallor)
pan systolic murmur

194
Q

complications of VSD

A

aortic regurgitaiton
infective endocarditis
eisenmenger’s complex
right HF

195
Q

what is esienmenger’s complex

A

high right ventricular pressure from hypertrophy exceed left pressure-> reversal of blood flow
heart-lung transplant

196
Q

AVNRT ecg

A

no p wave, fast rate, regular rhythm

197
Q

treatments of AVNRT/ paroxysmal supraventricular tachycardia

A

carotid sinus massage and adenosine administed

198
Q

murmur likely heard in rheumatic heart disease

A

opening snap on S2 followed by rumbling mid-diastolic murmur

199
Q

causes of pericarditis

A

viral/ bacterial infection
respiratory infection
tuberculosis
post MI: Dressler’s syndrome

200
Q

presentation of pericarditis

A

pleuritic Chest Pain aggrevated by breathing deeply and improved by leaning forward, mild fever and nausea

201
Q

ecg of pericarditis

A

global saddle-shaped ST elevation with PR depression

202
Q

treatment of pericarditis

A

NSAID/ analgesia

aspirin, ibuprofen

203
Q

main cause of death during 4-7 days post MI

A

myocardial wall rupture

papillary muscle rupture

204
Q

ecg for hyperkalemia

A

peaked T wave
prolonged PR
p wave flatted
widen QRS

think of it as: when is potassium present the most in an action potential? phase 3 and 1, 3= t wave, 1-QRS, too much potassium exaggerates those phases making it longer and more prominent

205
Q

ecg for hypokaelmia

A

U wave
ST depression
absent T wave

206
Q

ecg: p wave

A

P-waves: atrial depolarisation

207
Q

ecg: QRS

A

QRS complexes (<120 ms): ventricular depolarisation.

208
Q

ecg: t waves

A

T-waves: ventricular repolarisation.

209
Q

ecg: U waves

A

U-waves: sometimes seen, origin disputed. May be pathological if follows abnormal T-wave

210
Q

treatments for stable angina

A
  1. BB + GTN
  2. long acting nitrate (ie, isosobride)
  3. non urgent/ out patient angiogram
211
Q

what is the erb’s point for?

A

third intercostal space

S3 and S4

212
Q

another type of irregular irregular rhythm

A

ventricular ectopics

213
Q

how is amiodarone administered

A

use central line or large bore peripheral cannula in large vein

214
Q

grades of murmur

A

1: Difficult to hear
2: Quiet
3: Easy to hear
4: Easy to hear with a palpable thrill
5: Can hear with stethoscope barely touching chest
6: Can hear with stethoscope off the chest

215
Q

what is 2: 1 heart block

A

P waves remain normal
QRS complex occurs after alternative P wave (after every second P wave)
150 bpm for ventricular rate
ie, atrial flutter

216
Q

where does RCA supply

A

Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area

217
Q

where does left circumflex supply

A

Left atrium

Posterior aspect of left ventricle

218
Q

where does LCA supply

A

Anterior aspect of left ventricle

Anterior aspect of septum

219
Q

normal QRS time

A

<0.12s

220
Q

treatments for hypertension

A

55+, non-black patient A or B OR 55- or black then C.

221
Q

what are FBC, U+E, LFT important for in regards to cardiovascular

A

FBC (anaemia)
U+E (prior to ACEi and other meds)
LFTs (prior to statins)

222
Q

medication for angina

A

GTN spray
Aspirin (e.g. 75mg once daily)/clopidogrel is an alternative
Atorvastatin 80mg once daily
Calcium channel blocker (e.g. amlodipine 5-10mg once daily) or;
Beta blocker (e.g. bisoprolol 5mg once daily)

223
Q

normal cardio thoracic ratio

A

<0.5 or <1:2

224
Q

complications of prothetic valves

A

Thrombus formation
Infective endocarditis
Haemolysis causing anaemia

A click replaces S1 for metallic mitral valve
A click replaces S2 for metallic aortic valve

225
Q

medication for chronic HF

A

ACEi, BB

loop diuretics

226
Q

What lung disease does left HF correlate to?

A

Pulmonary oedema

227
Q

typical presentation of Wolff Parkinson white

A

syncope+ palpation
slurred upstroke/ wide QRS and short PR
delta wave in V1

228
Q

risk of post MI

A 
dressler's: pericarditis (autoimmune phenomenon/leukocytosis)
papillary rupture (CHF, mitral regurgitation symptoms)
229
Q

side effect amiodarone

A

dizziness
visual disturbance
unco-ordination

230
Q

function of CCB

A

angina, hypertension, negative inotropic effect

stop for HF

231
Q

which congenital defect is Turner and Marfan’s syndrome asso w/

A

turner: coarctation of aorta (part of aorta is more narrow)

marfan’s: aortic dissection

232
Q

hyperkalemia treatment

A

calcium glutinate

233
Q

what is the function of baroreceptors

A

when decreased blood pressure/ cardiac output is detected: they increase sympathetic & decrease paraysympathtic stimulation

achieve: increase BP, HR, vasocontriction, adrenaline and noradrenaline is released from medulla

234
Q

where are baroreceptors located

A

aortic arch and carotid sinus

act on the medulla

235
Q

what does increase in blood pressure to do sympathetic discharge

A

baroreceptor activity will also increase -> decrease sympathetic discharge:
ventricular muscle causing decrease contractility /fall in stroke volume
venous system causing increased compliance

236
Q

what does increase in blood pressure do to parasympathetic discharge

A

baroreceptor activity will also increased which send signal to increased parasympathetic discharge to the SA node so decrease firing/ HR can be achieved

237
Q

ECG changes during hypocalcemia

A

prolong QT

238
Q

mode of action/ purpose of thiazide diuretic

A

inhibit sodium reabsorption by blocking Na+ CI symptorer at distal convoluted tubule (step 3 hypertension treatment)

239
Q

mode of action: DOAC (ie, rivaroxaban)

A

direct inhibition of clotting factor Xa

240
Q

LVEF formula

A

(SV/EDV) x 100%

241
Q

mode of action: loop diuretic (ie, furosemide)

A

inhibit Na-K- Cl cotransporter in thick ascending loop of Henle

242
Q

five steps of atherosclerosis

A
  1. endothelial dysfunction + proinflammatory changes
  2. fatty infiltration by LDL and oxidize
  3. macrophage phagocytose LDL then turn into foam cells
  4. foam cells release growth cytokines encouraging SMC proliferation and migration from tunica media inward to intima
243
Q

progression of atherosclerosis from SMC proliferation to thrombus formation

A
  1. SMC proliferation synthesize collagen-> hardening of atherosclerotic plaque
  2. at the same time, foam cells die lipid content release (plaque rupture)
  3. thrombosis from rupture causes blood coagulation forming thrombus (dangerous, stops blood flow)
244
Q

mode of action: atorvastatin

A

HMG-CoA reductase inhibitor dug reducing plasma cholesterol lvl
HMGCoA: in mevalonate pathway occurs in liver hepatocytes

245
Q

pathophysiological mechanism for leg oedema during RIGHT HF

A

increased venuole hydrostatic pressure because blood backs up into venous system as they can’t get in

246
Q

mode of action: GTN

A

relax smooth muscles via activating guanylate cyclase

247
Q

treatment for leg claudication

A
  1. exercise program

2. angioplasty

248
Q

side effect of amlodipine (ccb)

A

ankles swelling

headache

249
Q

pulmonary oedema from left HF but not congestive HF symptoms

A

SOB when lying down
needs pillow at night to breathe
no limb swelling

250
Q

oncogene tested during biopsy for breast cancer

A

HER2

251
Q

route parasympathetic stimulation causing negative chronotropic effect

A

from release of Acetylcholine onto M2 receptors in SA node, acts to reduce slope fo pacemaker potential

(parasympathetic only acts on SA node)

252
Q

route of sympathetic stimulation causing positive chronotropic effect

A

mediated by noradrenaline onto B1 receptors, increase slope of pacemaker potential, rate of conduction through AV node, rate of myocardial relaxation

(sympathetic acts on SA, AV, ventricle)

253
Q

how is force generated in the heart

A

calcium and ATP dependant cross bridge cycles, making plateau phase important bc it allow calcium induced calcium release allowing enough calcium to be present.

254
Q

define blood pressure

A

outward hydrostatic pressure exerted against the vessels by blood
product of CO and SVR
90-105mmHg

255
Q

causes of arterioles smooth muscle constriction

A

serotonin

thomboxane A2

256
Q

causes of arterioles smooth muscle dilation

A

acidosis, hypoxia, hypercapnia

fever, inflammation, nitric oxide

257
Q

sympathetic effect of arteriole smooth muscle

A

Alpha: skin, gut, kidneys-> contraction and reduce flow
Beta: cardiac and skeletal muscle-> dilatation and increase flow

258
Q

how does angiotensinogen become angiotensin 2

A

Renin catalyzes conversion angiotensinogen into angiotensin I. angiotensin-converting enzyme (ACE) converts angiotensin I into an angiotensin II

259
Q

describe renin

A

hormone related from granular cells in juxtamedullary apparatus of kidney in response to reduced BP, low sodium , sympathetic stimulation

260
Q

effects of angiotensin 2

A

stimulates thirst
vasoconstriction
aldosterone release

261
Q

describe aldosterone

A

hormone that increase sodium reabsorption in the kidney which results in increased fluid reabsorption, blood volume, and BP

262
Q

treatment for stable angina

A

stop smoking
aspirin+ statin (modify risk)
GTN (symptomatic relief)

263
Q

layers of the heart inner to outer

A 
endocardium 
myocardium 
visceral layer of serous pericardium (epicardium)
pericardial space
parietal layer of serous pericardium 
fibrous pericardium
264
Q

define TIA (transient ischaemic attack)

A

brief disruption of blood supply to the brain caused by embolism, thrombus that will resolve, if not and worsen-> ischaemic stroke

265
Q

what are the 2 types of stroke

A

ischaemic

haemorrhages

266
Q

describe ischaemic stroke

A

occlusion of blood vessels that supply brain parenchyma leading to infection (necrosis secondary to ischaemia)

267
Q

procedure after stroke is detected, diagnostic and treatments

A

send to stroke unit
CT head
thrombolysis if needed

268
Q

describe haemorrhages stroke

A

bleeding w/ in brain parenchyma, ventricular system, subarachnoid space

269
Q

causes of ischemic stroke

A
  1. thrombosis (local blockage due to atherosclerosis from hypertension/ smoking)
  2. emboli (propagation of blood clot that leads to acute obstruction and ischeamia from AFib, carotid artery disease)
270
Q

cause of haemorrhages stroke

A

hypertension
brain tumour
trauma

271
Q

define sepsis

A

dysregulated host response to infection leading to life-threatening organ dysfunction-> may lead to septic shock

272
Q

what is sepsis 6 / bufalo

A 
blood cultures 
urine output 
fluids 
antibiotics 
lactate 
oxygen
273
Q

define shock

A

circulatory failure resulting in inadequate tissue perfusion and insufficient delivery of oxygen.

274
Q

four types of shock

A

hypovolemic
distributive (septic, anaphylactic, neurogenic)
cardiogenic
obstructive

275
Q

define hypovolemic shock

A

occurs secondary to a reduction in intravascular volume.

decrease blood pressure, poor tissue perfusion (^ lactic acid)

276
Q

define distributive shock

A

peripheral vasodilatation leading to abnormal volume distribution and inadequate perfusion.

277
Q

symptoms of shock

A

hypotension, decrease oxygen, low cardiac output

fast resp rate, fever

first year revision (5 decks)

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