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141 Cards in this Set

  • Front
  • Back
what do you see on chest xray in heart failure?
peribronchial cuffing = fluid in hilar area
curly bee lines = due to fluid in interstitium -> engorged lymphatics
upper lobe diversion -
what do you see on a chest xray if they have mitral valve problem?
enlarged LA -> lose the normal curve / dip
which coronary artery supplies the anterior wall of LV?
LAD
Which coronary artery supplies lateral wall of LV?
circumflex
which coronary artery supplies the posterior wall of the LV?
right coronary
Which coronary artery supplies the SAN and AVN?
right coronary
What is the intrinsic rate of teh SAN?
80 /min
What's the normal delay between SAN firing and LV contraction?
150ms
What happens if heart stops for 10 seconds? what is this called?
we lose consciousness
called stokes-adams attack
how long does it take with no blood supply to the brain to get permanent brain damage?
10 minutes
What is the 'run off' phase in the cardiac cycle?
the aortic valve is closed -> blood runs off from the distended aorta
When do we have blood flow to the heart?
during diastole
What is the time period of one big box in ECG?
0.2 seconds
How long should the PR segment be?
120-200ms
How long should the QRS be?
80-120ms (ie less than 3 small boxes)
Which leads in the ECG look at the IV septum
V3 and V4
Which leads look at the inferior surface of teh heart?
II, III and avF
which leads look at lateral surface of the heart?
aVL and I
Also, V6
What's the normal ECG axis?
-30->90
What is first degree heart block? What do we see on ECG?
Every wave that starts in SAN will eventually get to the ventricles, but there's a delay along the way
-> on ECG, PR is greater than 200ms (1 big square)
There will always be P wave before QRS
What is second degree heart block?
The excitation doesn't always spread through the AVN or bundle of His
What is Mobitz Type I (aka wenkebach) heart block?
It's the first type of 2nd degree block
We get progressive lengthening of PR then failure of conduction then PR starts short and we go through whole cycle again
What is mobitz type II heart blokc?
It's the second type of 2nd degree heart block
The PR segment doesn't length. But we occasionally don't have conduction through AVN/bundle of his -> P wave won't be followed by QRS
Can be in ratios eg 2:1 or 3:1
What is third degree heart block? what do you see on ECG?
There's normal atrial contraction, but it's not conducted into the ventricles -> QRS complexes are independent of P waves
On ECG, see both P waves and QRS's. Sometimes they might overlap etc.
QRS's are abnormally shaped and longer than normal
What's the difference between atrial fibrillation and atrial flutter on an ECG?
Fibrillation -> chaotic baseline
Flutter -> sawtooth baseline (very characteristic appearance)
What happens in bundle branch blocks on ECG?
Get widened QRS complex
What do we see in ECG of RBBB?
MARROW
Look at V1 - see RSR' (looks like an M)
W in V6
The QRS complexes will be widened
What do we see in ECG of LBBB?
Harder to identify than RBBB. Every QRS will be longer than 120ms
WILLIAM - look in V6 for M
How do we determine if a Q wave is 'pathological' on ECG?
Height: greater than 25% of total QRS
Width: greater than one small box
Do you get pathological Q wave with non-STEMI?
No. need infarcted tissue
Is cardiac muscle striated?
Yes
Are there mitochondria in ventricular cells?
Yes. They make up 30% of cell surface area
Why is the force produced p/ area in ventricular cells not maximal?
Because of the high density of mitochondria (make up 30% of cell surface area)
What is the important molecule in the gap junctions between ventricular cells?
Connexin 43 -> ions can pass rapidly
How long does an AP in skeletal muscle last?
In cardiac muscle?
Skeletal -> 2ms --> can get tetanus
Cardiac -> 300ms -> can't get tetanus (contraction lasts about 300ms too)
Which ions are responsible for the initial depolarisation in cardiac muscle cells? Then which ones are responsible for the long plateau phase?
Sodium comes in rapidly initially - kicks off the depolarisaiton
Then Ca2+ responsible for the long plateau phase
At the end of contraction of heart muscle, how do we get rid of the Ca2+?
- The Ca2+ that came from the outside is pumped out through the NaCa exchanger (3Na in down conc gradient, 1 Ca out)
- The Ca2+ from SR is pumped back into it by the Ca2+ ATPase on SR membrane
T/F: in the heart, we can increase force of contraction by recruiting more muscle cells?
FALSE This is what happens in skeletal muscle, but every cell is involved in every contraction of the heart ie can't change the number of cells involved
How do we increase the force of heart contraction?
Increased Ca2+ release from SR
What receptor on the heart binds adrenaline?
beta receptors
What is the effect of adrenaline on the heart?
Acts on Ca2+ chs on SR membrane -> increased release of Ca2+ -> increased force of contraction
Also acts on the Ca2+ ATPase pump on the SR (via phopholamban) -> increased rate of reuptake to allow for faster HR
How does adrenaline help to increase the HR?
It acts on Ca2+ ATPase on the SR membrane -> increased rate reuptake of Ca2+-> shortened relaxation time -> faster HR
What is phopholamban
it regulates the Ca2+ ATPase pump on SR membrane of cardiac cells
Why can HR only speed up to 180bpm?
About that, there's inadequate time for filling
How many ATP units per glucose do you get with oxidative glycolysis?
38
How many ATP units p/gluc do you get with anaerobic glycolysis?
2
What sort of glycolysis does the heart muscle use? What does this require?
Aerobic -> need:
- large blood supply
- lots of mitos
- small diameter so O2 can diffuse into cell
How do cardiac glycosides work?
block NaK ATPase pump -> increased Na+ inside
THis then stuffs up the NaCa2+ exchanger -> decreased pumping of Ca2+ out of the cell -> increased conc Ca2+ and hence increased force of contraction
Where do sympathetic nerve fibres originate in spinal cord?
Thoracolumbar region
Where in spinal cord do parasympathetic nerve fibres originate?
Cranial and sacral regions
Where exactly in the spinal cord do the symp NS neurons originate?
In the intermediolateral (IML) cell column
What does vagus stimulation of SAN do?
What NT and what receptor?
Slows HR
NT = ACh
receptor = muscarinic
What does symp NS stimulation of SAN do?
What NT and what receptor?
Increased HR
NT = noradrenaline
receptor = beta 1
Which BV has more symp innervation: arteries or arterioles?
ARTERIOLES
Are symp nerves vasoconstrictors or vasodilators?
constrictors
What percentage of the total TPR is due to arteriolar contribution?
80%
What does neuropeptide Y do?
It increases the action of NA on smooth muscle and decreases its release
This is designed to conserve NA during intense and prolonged activity
During heart failure, does distribution of CO change
Yes
What happens to kidney blood flow during heart failure
the decreased CO is redistributed -> flow to kidneys is decreased significantly -> renal problems
What happens to a person's pressure volume loop in dilated cardiomyopathy?
It's shifted to the right significantly
What is the preload?
Ventricular wall tension at the end of diastole
What is afterload?
The ventricular wall stress that develops during systolic contraction
ie the pressure that ventricle is acting against to eject its contents
What happens if you increase preload in healthy heart?
Increase SV (frank starling)
What happens in you increase preload in someone with a diseased heart?
The contractility is somewhat impaired -> won't have the normal F-S relationship
SV will increase a bit but not as much as it would in healthy heart
What happens if you increase afterload in healthy heart?
Increased SV
What happens if you increase afterload in a diseased heart?
Won't be able to increase SV as much as a healthy heart due to decreased contractility -> won't maintain SV in the face of changing afterload
What sort of remodelling do we get in pressure overload? How are the myofibrils added in relation to those already there?
Pressure overload -> want to increase force of contraction
-> we add the myofibrils in PARALLEL with old ones
-> we get concentric hypertrophy
What sort of remodelling do we get in volume overload? How are the myofibrils added in relation to those already there?
Myofibrils are added in series -> get bigger chamber
= ECCENTRIC hypertrophy
Do we get diastolic or systolic dysfunction with concentric hypertrophy?
Diastolic - the chamber is smaller -> can't fill as well
Do we get diastolic or systolic dysfunction with eccentric hypertrophy?
Systolic - the walls are thinner -> can't generate as great a force
What % of all HFs are due to diastolic dysfunction?
30%
What happens to EF in diastolic HF?
It is normal or increased (contraction isn't affected) ie we say EF > 55%
What happens to EF in systolic HF?
It's decreased (<55%)
Where is ACE found?
In the lungs
What does ACE do?
Converts angioI to angioII
And breaks down bradykinin
Where are A type natriuretic peptides produced?
in the atria
Where are Btype natriuretic peptides produced?
In the ventricles
Where are C type natriuretic peptides produced?
in the vascular endothelium
what is the effect of natriuretic peptides?
they're beneficial in HF (opposite to renin-angio system)
increased Na+ and H20 excretion
vasodilation
inhibition of renin and antagonism of angio II
what symptoms do you get in heart failure?
Those related to reduced CO: fatigue, effort intolerance, renal and hepatic problems, cognitive impairment, sleep disturbance
Those related to congestive problems: peripheral oedema, dyspnoea, orthopnoea + PND
What's the treatment protocol for acute heart failure?
Lasix
Morphine (respiratory depression)
Nitrates (vasodilators -> decreased VR and decreased afterload)
Oxygen
Position upright to decrease pulmonary congestion / Positive pressure to help with breathing
What are the three groups of diuretics?
Loop diuretics
Thiazide diuretics
K+ sparing diuretics
What furusemide and how does it work?
Loop diuretic
It inhibits the NaK2Cl symptort in the ascending loop of Henle
-> decreased NaCl reabsorption -> decreased BV -> decreased preload and reduced oedema (peripheral and pulmonary)
What happens to K+ levels with furusemide use?
We have high conc of Na+ in the collecting tubule - some of this gets exchanged for K+ -> decreased K+ in body
ie HYPOKALAEMIA
What does angioII do?
- increased symp NS activity -> vasoconstriction
- thirst -> increased BV
- increased reabsorption Na and H20 at kidneys
- Acts on adrenal cortex -> aldosterone release
- Pituitary gland -> ADH release
- Breaks down bradykinin
What do ACE Is do?
Drop angioII levels-> decreased BP and decreased BV
Also increased bradykinin = a vasodilator -> further drops the BP
What are the side-effects of ACE Is?
- hypotension (we sometimes use them for hypertension treatment, but if your BP was normal to start with, could dangerously drop BP)
- renal problems
- Hyperkalaemia (because of dropped aldosterone levels)
- Dry cough (bradykinin)
- Fetal injury
When are ACE Is contra-indicated?
- pregnancy
- renal disease
- hyperkalaemia
- hypotension
- angioedema
Which is more effective: ACE Is or ARBs?
They have same efficacy!
When would you use ARBs?
If they weren't tolerating ACEIs (dry cough eg)
How do ARBs work?
They block the AT1 receptor = responsible for angioII's BP effects
What is the difference between ACE Is and ARBs in terms of their impact on angio II?
- ACE I stops production of most of angio II though some is made independent of ACE
- ARBs completely block all angio II from doing it's job ie more complete blockade
What is the difference between ACE Is and ARBs in terms of their impact on vasodilation
ACEIs - get the contribution of bradykinin as well as angioII inhibtion
ARBs - even though they more compleletly block angioII's actions, because they don't have an impact on bradykinin, they have pretty much same overall effect
What advs do ARBs have over ACEIs?
- Don't get the dry cough
- Angio II is still able to act on the AT2 receptors - this may have some beneficial CV effects
What are the effects of catecholamines on the heart?
they bind to beta 1 receptors and:
- increase HR
- increase contractility
- increase speed of AV node conduction
What do beta blockers do?
They decrease HR, decrease contractility and decrease speed of conduction through the AV node
Do beta blockers have greater effect on cardiac function at rest or during exercise?
During exercise because this is when the symp NS is activated and would normally be amping up cardiac function
Are beta blockers all the same?
no. very heterogenous group of drugs
What is metoprolol?
Beta blocker
Is there survival benefit with beta blockers in heart failure?
Yes
What are the side effects of beta blockers?
- can act a bit on bronchial smooth muscle -> exacerbate asthma/COPD
- can also cause some arterial vasospasm -> worsen raynaud's and/or PVD
- slowing of AVN conduction could cause complete conduction block
Which groups of people do we not give beta blockers to / do we have to be really careful with?
moderate to severe asthma / COPD
if they're bradycardic (less than 50) or hypotensive
What is hydralazine?
Arterial vasodilator -> decreased afterload and hence increased SV
What do nitrates do?
Venous venodilation -> decreased preload
What do the inotropes do?
Increase Ca2+ conc in the cardiac cells -> increased foce of contraction
What does dobutamine do?
It stimulates beta Rs on the heart -> increased force of contraction
What is the effect of digoxin?
Increased contractility (due to increased conc Ca2+)
Prolonged refractory period in the AVN (good if you have supraventricular arrhythmias)
What are the side effects of digoxin?
- Life threatening arrhythmias
- Nausea, vomiting
Confusion
What is ouabain?
SHort acting digitalis drug (like digoxin)
Does digoxin have a small or large toxic-therapeutic ratio?
Small -> high potential for toxicity
What is nesiritide?
B type natriuretic peptide homolog -> vasodilation, increased Na+ and H20 excretion and it blocks renin-angio-adlo system
Approx how many cells in the body?
10^14
Approx how many capillaries in the body? how many cells does each cap supply?
10^10
each cap supplies approx 10^4 cells
What is the relationship between flow through a tube and radius?
Flow rate is proportional to radius^4
Is the heart affected by postural changes?
no
WHat are the normal pressures in the right and left atria?
Right - 3-5mmHg
left - 5-10mmHg
What pressure do the ventricles start at at the beginning of diastole?
1-3mmHg
What is the max pressure reached in the right ventricle during systole?
20-25mmHg
What is the max pressure reached in the LEFT ventricle during systole?
110-130mmHg
What is the pulmonary arterial pressure normally?
25/12
What is the aortic pressure normally?
120/80
Are there sarcomeres in cardiac muscle?
Yes
hence it's striated
What is low output heart failure?
when the heart isn't pumping out enough blood to reach the normal metabolic needs of the body
What is high output heart failure
When the body is for some reason demanding a higher CO
eg Beri beri, thyrotoxicosis, pregnancy, anaemia
This is more rare than low output HF
What are some common precipitating causes of heart failure?
fever
anaemia
systemic infection
arrhythmia
What is cardiomyopathy?
Its an intrinsic dysfunction of teh contractile function of the myocardium
What things are common underlying causes of heart failure
coronary artery disease
valve disease
cardiomyopathy
restrictive cardiomyopathy
What are the three types of cardiomyopathy?
- dilated CM
- hypertrophy CM
- restrictive CM
What causes dilated cardiomyopathy?
excess EtOH consumption
Viral myocarditis
Peripartum state
Why does excessive EtOH consumption cause dilated cardiomyopathy?
It inhibits mitochondrial oxidative phosphorylation and FA oxidation
What is the most common cardiac abnormality found in young athletes who die suddenly?
hypertrophic cardiomyopathy
What causes restrictive cardiomyopathy?
Fibrosis or scarring of the heart. Or infiltration of the myocardium by abnormal substance
In australia, what is the most common cause of restrictive cardiomyopathy?
Amyloidosis (most common in women)
What is adriamycin?
anti-cancer drug that can cause cardiomyopathy
according to the NY heart association's scaling of HF symptoms, what is class 1?
class 1 -> no symptoms even during exercise
according to the NY heart association's scaling of HF symptoms, what is class 2?
class 2 -> mild symptoms during medium exercise (eg stairs, big hill)
What is class 3 in the NY heart association's scaling of HF symptoms?
Class 3 -> you have severely decreased capacity during even slight exercise. The only time you're fine is at rest
What is class 4 in the NY heart association's scaling of HF symptoms?
Class 4 -> symptomatic at rest
What are the physical signs of heart failure?
- peripheral oedema
- elevated JVP
- displaced apex beat
What proportion of patients presenting to their GP drink in a harmful or hazardous way?
1/6
What did william harvey discover?
That blood flows in a continuous circle around the body
he also denied the presence of pores in the IV septum