Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 |