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Z MD1 Cardiac physiology > The heart - things that can go wrong (cardiac failure, hypertrophy, MI, angina) > Flashcards

The heart - things that can go wrong (cardiac failure, hypertrophy, MI, angina) Flashcards

1
Q

what is the mechanism behind the treatment of cardiac failure?

A

remove the fluid - decreasing preload Vasodilation - decreasing afterload

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1
Q

what does myocardial failure cause (vital signs)

A

low BP low CO high PAWP High PVR (compensation)

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2
Q

what is the body’s compensation to cardiac failure

A

retains fluid to increase cardiac output However this may cause an increased LVEDP over 20-30 mmHg leading to pulmonary congestion and leg oedema

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2
Q

aortic stenosis murmur is which type of murmur

A

crescendo-decrescendo ejection systolic

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2
Q

what sign do you see on an ECG during an MI

A

ST elevation (and sometimes depression)

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4
Q

Treatment of LVH

A

underlying condition: valves etc Hypertension weight oss

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5
Q

cardiac hypertrophy definition

A

increase in LV mass relative to body size

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6
Q

Why does cardiac failure occur

A
  • loss of myocardial muscle (IHD, cardiomyopathy) - pressure overload (aortic stenosis, hypertension –> leads to ventricular hypertrophy) - volume overload (valve regurgitation, shunts)
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7
Q

Two uses of measuring end diastolic pressure?

A
  1. a measure of the filling of the ventricles 2. a measure of the venous pressure driving fluid out of the capillaries
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8
Q

how can we measure RIGHT Ventricular EDP?

A
  1. catheter inserted via a vein across the tricuspid valve 2. JVP (at the end of diastole VP=RAP=RAV
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8
Q

increased RVEDP causes what

A

systemic oedema

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8
Q

How do you get right heart failure

A

global heart disease specific right heart disease left heart failure

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8
Q

What does dehydration cause (vital signs)

A

low BP low CO Low PAWP Normal PVR

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9
Q

how does eccentric hypertrophy compensate for volume load?

A

heart size is bigger (increased LVEDV) so maintains SV and EF

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10
Q

consequences of LV remodeling?

A

increase heart failure mortality

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10
Q

3 types of re-entry tachycardias

A

atrial flutter - re-entry circuit in RA A-V nodal re-entry tachycardia - re-entry circuit in AV node Ventricular tachycardia - re-entry circuit in ventricle around a scar

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11
Q

why does cardiac hypertrophy/remodeling occur

A

myocardial infarction cardiac damage eg mycarditis volume overload pressure overload obesity, diabetes, renal failure (systemic diseases) infiltration Genetric

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11
Q

concentric hypertrophy

A

increased LV mass and relative wall thickness

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11
Q

what is the maximum LVEDP before pulmonary congestion occurs

A

20-30 mmHg

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12
Q

Diastolic dysfunction can lead to what?

A

pulmonary congestion

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13
Q

where is oedema seen the most

A

ankles, legs, sacrum, scrotum

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14
Q

which artery supplies the inferior side of the heart

A

right coronary artery

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16
Q

normal growth of the heart in embryo and in childhood

A

embryo - cell proliferation = hyperplasia childhood = cell hypertrophy

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17
Q

how does AF lead to pulmonary congestion

A

fast rate decreases LV filling time causing increased LA pressure –> pulmonary congestion

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19
Q

in what condition will pulmonary artery wedge pressure not measure the LVEDP accurately

A

mitral stenosis (there will be a pressure gradient between LA and LV)

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20
Q

How does concentric hypertrophy compensate for pressure load?

A

thicker wall reduces or normalises wall stress (La Place’s law) –> maintains systolic function, cardiac output and LVEDP

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21
Q

common causes for concentric and eccentric hypertrophy

A

concentric - often due to pressure overload eccentric - often due to volume overload

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22
Q

what is the order of the great vessels in the aortic arch going away from the heart

A

brachiocephalic, left carotid, left subclavian

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23
Q

LV hypertrophy decompensation

A

LV dilation –> increased LVEDV –> LVESV –> decreased EF. Reduced systolic function and CO –> increased LVEDP –> eventual cardiac failure

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23
Q

through early intervention you can reduce infarct size.. this reduces what…

A
  • early mortality and morbidity (in hospital) - late mortality and morbidity (1 year +)
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24
Q

inappropriate adaptations of cardiac failure

A

Na and water retention to increase blood volume K+ loss –> hypokalaemic vasoconstriction (due to low CO) Renin-angiotension-aldosterone system –> increased BP Sympathetic nervous system - increased HR and contractility

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24
Q

which leads are maximal for atrial depolarisation

A

leads II (positive deflection) and V1 (usually negative)

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25
Q

which leads are the inferior leads

A

II, III and aVF

26
Q

what is the order of the structures at the right inguinal crease

A

femoral nerve, femoral artery, femoral vein

28
Q

consequences of LVH - increases risk for

A

IHD Cardiac failure AF Stroke Diastolic dysfunction

29
Q

how can we measure LEFT ventricular EDP?

A
  1. catheter inserted via an artery across the aortic valve 2. measure pulmonary artery wedge pressure (at the end of diastole PAWP = VP = AP
29
Q

investigations of a murmur include

A

transthoracic echocardiogram transoesophageal echo

30
Q

treatment of cardiac failure

A

diuretics (frusemide) aldosterone antagonists (spirolactone) ACE inhibitors angiotensin receptor antagonists digoxin - positive inotropic effect (short term) beta blockers - protect heart from toxic effect of NA

30
Q

what are the cardiac markers we look for in an MI

A

creatine kinase - not specific for cardiac muscle troponin I - specific for cardiac muscle (not positive until 3-6 hours from onset)

31
Q

what does septic shock cause (vital signs)

A

low BP high CO Normal PAWP Low PVR

33
Q

clinical features of right heart failure

A

oedema

34
Q

normal heart size depends on

A

body size/BSA family history/genetics athletic conditioning BP Angiotensin II, Catecholamines

34
Q

what causes atrial fibrillation

A

rotors in the left atrium around the pulmonary veins which drive the rapid rhythm were the atria has multiple circuits going on

35
Q

differential diagnosis for chest pain

A
  • acute MI - unstable angina - dissecting aortic aneurysm - pneumonia - oesophagitis - muscle spasm
37
Q

how does left heart failure lead to right heart failure

A

pulmonary venous hypertension –> pulmonary congestion –> chronic hypoxia –> pulmonary vasoconstriction –> pulmonary arterial hypertension –> right heart failure

38
Q

how do we reduce infarct size

A

by increasing myocardial oxygen supply - reperfusion of infarct zone by opening artery by thrombolysis with streptokinase/alteplase, or by percutaneous coronary intervention (balloon +/- stent)

39
Q

how does calcium increase contractility

A
  • increases the number of cross bridges - increases the sensitivity to calcium of troponin
40
Q

Definition of Cardiac failure

A

cardic output less than what the body needs

42
Q

Identification of LVH

A

Clinical - forceful apex beat, S4, S3 ECG - tall voltages, T wave inversion CXR - large heart (eccentric) or normal size (concentric) Echo MRI/CT

42
Q

what properties do you see if a patient is having unstable angina

A
  • ruptured plaque - arterial thrombus - narrowed/transient occlusion of artery or occlusion of artery with collateral blood supply - abnormal ECG NO MUSCLE NECROSIS OR POSITIVE CARDIAC ENZYMES
43
Q

what is the endocrine control for cell hypertrophy of the heart during childhood?

A

GF/IGF and thyroxine

45
Q

where is the catheter positioned to measure pulmonary artery wedge pressure

A

Go in through the IVC, through RA and RV into the pulmonary artery. Balloon inflated - measures pulmonary artery pressure

46
Q

which leads are the lateral leads

A

I, aVL and V6

47
Q

Athletes heart may show

A

findings may overlap HCM - eccentric hypertrophy with normal cardiac function

48
Q

which drugs would slow the ventricular rate inAF

A

digoxin beta blocker calcium channel blocker amiodarone adenosine

49
Q

what can unstable angina be (in clinical terms)

A

either: - recent onset chest pain - recent increase in chest pain - no muscle necrosis

51
Q

eccentric hypertrophy

A

increased LV mass but normal relative wall thickness

52
Q

cardiac remodeling definition

A

increased relative wall thickness WITHOUT increase in LV mass

53
Q

increased LVEDP causes what

A

pulmonary oedema

54
Q

re-perfusion of the infarct area is only effective within …

A

6hours

56
Q

why do you have to be careful when giving treatment for cardiac failure

A

may reduce the CO too low and and reduce BP

57
Q

why are people with diastolic dysfunction dependent on the atria working well?

A

they need the little extra squeeze of blood from the atria into the ventricles

59
Q

How does LV remodeling occur post MI

A

increased LV volume and more spherical shape leads to myocyte hypertrophy and apoptosis and interstitial fibrosis

60
Q

what properties do you see if a patient is having an MI?

A
  • ruptured plaque - arterial thrombus - occluded artery - muscle necrosis - abnormal ECG - positive cardiac enzymes
62
Q

2 mechanisms of tachycardia

A

automatic focus (due to a single cell firing very fast) re-entry (signal may get diverted up the wrong way - around in circles)

63
Q

which vessel is used during cardiac catherisation

A

femoral artery +/- vein

65
Q

what is the problem in diastolic heart failure

A

filling of the ventricle Due to reduced LV compliance –> causing increased LVEDP required to fill the LV –> therefore causing increased pulmonary venous pressure

66
Q

why is long term sympathetic nervous stimulation bad for cardiac failure

A

causes vasoconstriction, ventricular arrhythmias, direct toxic effect

67
Q

mitral regurgitation is which type of murmur?

A

pan-systolic murmur

68
Q

what causes oedema?

A
  • increases in systemic venous pressure (causes fluid to leak out) - decreased osmotic pressure (plasma proteinloss: renal or liver failure) - blocked lymphatics (cancer) - increased capillary permeability (infection)
69
Q

what can ST depression be due to?

A
  • MI - myocardial ischaemia - changes in electrolytes - drugs - RVH -LVH - conduction abnormalities
71
Q

how is LV remodeling prevented/reduced? Which drugs?

A

Angiotensin blocking beta-adrenergic blocking

72
Q

how can diastolic dysfunction lead to pulmonary congestion?

A

thick muscle (stiff) –> means you need increased LVEDP to achieve same preload. Therefore increased LA and Pulmonary vein pressure = causing pulmonary congestion

73
Q

clinical features of left heart failure

A

SOB Fatigue tachycardia lung creps””

74
Q

which artery supplies the anterior side of the heart

A

Left anterior descending artery

75
Q

causes of RV hypertrophy

A

congenital (TGA) PH Right heart valve regurgitation

76
Q

which leads are the anterior leads

A

V1-V5

78
Q

Hypertrophic cardiomyopathy Pathology and consequences

A

increased LV wall thickness (especially of septum) cellular hypertrophy and myocyte disarray Causes LV outflow tract obstruction, diastolic dysfunction and ventricular arrhythmias

79
Q

what structure determines the pulse rate in AF?

A

AV node

80
Q

which artery supplies the lateral side of the heart

A

circumflex artery (branch of L coronary artery)

81
Q

what are some of the complications resulting from an MI?

A
  • VF - Sudden death - heart failure (due to decreased contractility) - cardiogenic shock (due to not enough blood perfusing vital organs due to heart failure) - death

Z MD1 Cardiac physiology (13 decks)

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