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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
in what condition will pulmonary artery wedge pressure not measure the LVEDP accurately
mitral stenosis (there will be a pressure gradient between LA and LV)
20
How does concentric hypertrophy compensate for pressure load?
thicker wall reduces or normalises wall stress (La Place's law) --\> maintains systolic function, cardiac output and LVEDP
21
common causes for concentric and eccentric hypertrophy
concentric - often due to pressure overload eccentric - often due to volume overload
22
what is the order of the great vessels in the aortic arch going away from the heart
brachiocephalic, left carotid, left subclavian
23
LV hypertrophy decompensation
LV dilation --\> increased LVEDV --\> LVESV --\> decreased EF. Reduced systolic function and CO --\> increased LVEDP --\> eventual cardiac failure
23
through early intervention you can reduce infarct size.. this reduces what...
- early mortality and morbidity (in hospital) - late mortality and morbidity (1 year +)
24
inappropriate adaptations of cardiac failure
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
24
which leads are maximal for atrial depolarisation
leads II (positive deflection) and V1 (usually negative)
25
which leads are the inferior leads
II, III and aVF
26
what is the order of the structures at the right inguinal crease
femoral nerve, femoral artery, femoral vein
28
consequences of LVH - increases risk for
IHD Cardiac failure AF Stroke Diastolic dysfunction
29
how can we measure LEFT ventricular EDP?
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
investigations of a murmur include
transthoracic echocardiogram transoesophageal echo
30
treatment of cardiac failure
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
what are the cardiac markers we look for in an MI
creatine kinase - not specific for cardiac muscle troponin I - specific for cardiac muscle (not positive until 3-6 hours from onset)
31
what does septic shock cause (vital signs)
low BP high CO Normal PAWP Low PVR
33
clinical features of right heart failure
oedema
34
normal heart size depends on
body size/BSA family history/genetics athletic conditioning BP Angiotensin II, Catecholamines
34
what causes atrial fibrillation
rotors in the left atrium around the pulmonary veins which drive the rapid rhythm were the atria has multiple circuits going on
35
differential diagnosis for chest pain
- acute MI - unstable angina - dissecting aortic aneurysm - pneumonia - oesophagitis - muscle spasm
37
how does left heart failure lead to right heart failure
pulmonary venous hypertension --\> pulmonary congestion --\> chronic hypoxia --\> pulmonary vasoconstriction --\> pulmonary arterial hypertension --\> right heart failure
38
how do we reduce infarct size
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
how does calcium increase contractility
- increases the number of cross bridges - increases the sensitivity to calcium of troponin
40
Definition of Cardiac failure
cardic output less than what the body needs
42
Identification of LVH
Clinical - forceful apex beat, S4, S3 ECG - tall voltages, T wave inversion CXR - large heart (eccentric) or normal size (concentric) Echo MRI/CT
42
what properties do you see if a patient is having unstable angina
- 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
what is the endocrine control for cell hypertrophy of the heart during childhood?
GF/IGF and thyroxine
45
where is the catheter positioned to measure pulmonary artery wedge pressure
Go in through the IVC, through RA and RV into the pulmonary artery. Balloon inflated - measures pulmonary artery pressure
46
which leads are the lateral leads
I, aVL and V6
47
Athletes heart may show
findings may overlap HCM - eccentric hypertrophy with normal cardiac function
48
which drugs would slow the ventricular rate inAF
digoxin beta blocker calcium channel blocker amiodarone adenosine
49
what can unstable angina be (in clinical terms)
either: - recent onset chest pain - recent increase in chest pain - no muscle necrosis
51
eccentric hypertrophy
increased LV mass but normal relative wall thickness
52
cardiac remodeling definition
increased relative wall thickness WITHOUT increase in LV mass
53
increased LVEDP causes what
pulmonary oedema
54
re-perfusion of the infarct area is only effective within ...
6hours
56
why do you have to be careful when giving treatment for cardiac failure
may reduce the CO too low and and reduce BP
57
why are people with diastolic dysfunction dependent on the atria working well?
they need the little extra squeeze of blood from the atria into the ventricles
59
How does LV remodeling occur post MI
increased LV volume and more spherical shape leads to myocyte hypertrophy and apoptosis and interstitial fibrosis
60
what properties do you see if a patient is having an MI?
- ruptured plaque - arterial thrombus - occluded artery - muscle necrosis - abnormal ECG - positive cardiac enzymes
62
2 mechanisms of tachycardia
automatic focus (due to a single cell firing very fast) re-entry (signal may get diverted up the wrong way - around in circles)
63
which vessel is used during cardiac catherisation
femoral artery +/- vein
65
what is the problem in diastolic heart failure
filling of the ventricle Due to reduced LV compliance --\> causing increased LVEDP required to fill the LV --\> therefore causing increased pulmonary venous pressure
66
why is long term sympathetic nervous stimulation bad for cardiac failure
causes vasoconstriction, ventricular arrhythmias, direct toxic effect
67
mitral regurgitation is which type of murmur?
pan-systolic murmur
68
what causes oedema?
- 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
what can ST depression be due to?
- MI - myocardial ischaemia - changes in electrolytes - drugs - RVH -LVH - conduction abnormalities
71
how is LV remodeling prevented/reduced? Which drugs?
Angiotensin blocking beta-adrenergic blocking
72
how can diastolic dysfunction lead to pulmonary congestion?
thick muscle (stiff) --\> means you need increased LVEDP to achieve same preload. Therefore increased LA and Pulmonary vein pressure = causing pulmonary congestion
73
clinical features of left heart failure
SOB Fatigue tachycardia lung creps""
74
which artery supplies the anterior side of the heart
Left anterior descending artery
75
causes of RV hypertrophy
congenital (TGA) PH Right heart valve regurgitation
76
which leads are the anterior leads
V1-V5
78
Hypertrophic cardiomyopathy Pathology and consequences
increased LV wall thickness (especially of septum) cellular hypertrophy and myocyte disarray Causes LV outflow tract obstruction, diastolic dysfunction and ventricular arrhythmias
79
what structure determines the pulse rate in AF?
AV node
80
which artery supplies the lateral side of the heart
circumflex artery (branch of L coronary artery)
81
what are some of the complications resulting from an MI?
- 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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