Question |
Answer |
The circulatory system |
deoxygenated blood to the heart via veins >IVC to right side/atrium to the rt ventricle> pushes blood to pulmonary artery> lungs> saturated w/O2 red to the heart via 4n P. veins on the left side/atrium> l. ventricle pushes to aorta> arteries> organs |
We care about which chamber the most? |
the ventricles |
If there’s a problem in the left ventricles, what would be affected? |
backup> effects the lungs |
Back up means what? |
hydrostatic pressure (ie; can push water into the alveoli instead of air) |
Manifestations of left sided heart failure is? |
1) dyspnea> manifestations exaggerated with exertion> worst when you lie flat, 2) orthopnea, 3) paroxysmal nocturnal dyspnea, 4) cough, 5) PE> all from pulmonary congestion |
Manifestations of right sided heart failure |
systemic venous congestion> venous neck distention, liver, splenomegaly, portal htn, lower limb edema, ascites |
If you have both left and right sided issues= |
CHF |
CHF is dx how? |
only by the s/s? pulmonary (1) dyspnea> 2) orthopnea, 3) paroxysmal nocturnal dyspnea, 4) cough, 5) PE)> or venous systemic congestion (venous neck distention, liver, splenomegaly, portal htn, lower limb edema, ascites) |
Heart is graded based on? |
cardiac output |
Heart failure is |
low CO |
Cardiac output (CO) is ? |
CO= SV (70) X HR (70) = 4900 or 5L> the volume of blood pumped by each ventricle per minute (CO= left ventricle) |
Heart failure is when the CO is < than ______L? |
4 |
3 determinants of stroke volume (SV)> |
|
Stroke volume (SV) is? |
Volume of blood pumped per beat (70) |
Preload |
whatever volume/ pressure amt ventricle filled before contraction> the more preload, the more the CO |
Afterload |
vascular resistance felt by left ventricle d/t high arteriole pressure = high afterload |
Systole and diastole |
contraction/ejects and relaxation/fills |
Heart failure with systolic dysfunction |
when the heart fails to contract |
Heart failure with diastolic dysfunction |
when the heart fails to do its diastolic fx |
The higher the preload, the ______ the stroke volume and the ______ CO |
better, the higher |
The higher the afterload, the_______ the SV, the _________ CO |
lower, the lower |
Cardiac contractility |
increase it by whipping the heart with the SNS ^ contractility and HR |
The more you fill the heart, the more it contracts >when stretched, it performs better, why? |
Heart muscles are filled with 2 fibers myosin and actin> overlap and form cross-bridges when they contract> if too much overlap when the heart is empty, there’ll be minimal cross-bridges, but as it fills it’s optimal. |
EDV end diastolic volume/ preload |
ventricle fills during diastole (135) = maximum amt |
Frank starling curve/ preload |
as more blood is returned to the heart and the EDV ^, the heart automatically pumps out a correspondingly ^ SV. |
What will increase CO? |
Higher preload, lower afterload, higher contractility, higher heart rate |
Stroke volume (SV) |
amount of blood ejected per beat |
End diastolic volume (EDV) |
amount of blood that accumulates in the ventricles before contraction |
Do your ventricles empty out completely? |
NO, out of 135, maybe about 70, what remains in the heart is 65. The 65 is the ESV- end systolic volume |
Stroke volume |
SV= EDV-ESV? the whole (diastole filling) minus what’s left in the ventricle after contraction= what’s ejected |
End systolic volume |
65ml |
Ejection fraction |
50-60% Refers to the percentage of blood that’s pumped out of a filled ventricle with each heartbeat. EF = SV / EDV % [70/135 = 52%] |
Ejection fraction is a measurement of what? |
EF is a volume measurement, that reflects ventricular systolic function (low EF = systolic dysfx |
Does low EF mean HF? |
Low EF = heart failure (systolic dysfunction) |
Diastolic dysfunction effect EF? |
NO, it’s normal |
Normal EF does NOT exclude heart failure because |
heart failure can occur if you have systolic dsfx or diastolic |
Compensatory Song |
fill me more (no blood), feed me more (SNS), and I’m going to give you more |
Fill me more |
kidneys> renin angiotensin system fill the heart with more blood so that the organs are supplied |
Feed me more |
SNS causes the heart to contract for better cardiac output |
Who is sad with the compensatory system? |
the heart because it’s sick and compensation makes it worse |
Heart failure is the end result of 2 important conditions |
HTN and ischemic heart disease |
Heart failure is not a disease |
it’s a condition which complicates chronic diseases |
When you fill the LV with 135ml (EDV)/preload, and eject 70 (SV) = |
normal heart, CO 70sv x 70 hr=4900 (5L) |
When you have an A+ heart, with EDV 135, and SV 90= |
CO= 90 (SV) x 70 (HR) = 6300 |
Failing heart, with EDV 135ml, and sv 40= |
CO= 40sv x hr70= 3600= heart failure |
Compensatory mechanisms try to increase CO by increasing the preload, but this occurs at the expense of increased filling pressures |
congestion-caused by angiotensin II and aldosterone |
Compensatory mechanisms try to increase CO by ^ SNS |
chronic SNS is bad- this occurs at the expense of increased cardiac work load- worsening of cardiac condition& remodeling |
Compensatory kidney/RAAS system |
^preload, good for the body, bad for the heart> congestion, ^work, remodeling d/t angiotensin and aldosterone |
Compensatory SNS |
^contractility, ^HR, ^afterload, good for the body (^co/BP), bad for heart> remodeling, ^workload |
Endothelin release by vascular endothelium |
another mechanism to help increase BP by the blood vessels |
The ONLY compensatory mechanism with a purely beneficial effect from a CARDIAC perspective |
diuresis through BNP/ANP= vcongestion/workload¬> Natriuretic Peptides like Lasix> lose Na+ and water |
The ONLY lab test with diagnostic and prognostic values in CHF |
BNP- when negative, it excludes–> in proportion with severity- normal level is 100 |
Compensatory mechanisms of HF |
Frank-Starling Mechanism, SNS, Renin-angiotensin-aldosterone system, Natriuretic peptides (ANP, BNP), Endothelins, Myocardial hypertrophy and remodeling |
SNS |
sense BP with baroreceptors in neck arteries |
HF starts with a cardiac insult and then the SNS rx |
baroreceptor detectors>SNS >^ ? cardiac rate/contractility/CO>? ^vasoconstriction> |
HF starts with a cardiac insult and then the kidneys rx |
“OMG we’re bleeding to death”> renin> angiotensin I> converted to angiotensin II by ACE> vasoconstricts, ^aldosterone (Na+/water), ^ADH/vasopressin |
2 major risk factors of heart disease |
ischemic heart disease and htn |
How to dx HF? |
by hx |
2 categories of heart failure |
systolic and diastolic |
Systolic |
heart failure with systolic dysfunction> EF goes v |
Diastolic |
heart failure with diastolic dysfunction> EF is normal/preserved |
How do you categorize HF > |
echocardiogram |
Low ejection fraction HF is called |
systolic> HFRF heart failure reduced fraction when EF <40%- both have low CO |
Preserved ejection fraction name |
HFPF heart failure preserved fraction> diastolic- normal- EF > 50%-both have low CO |
Need to know difference between HFRF and HFPF because |
tx is different |
An ischemic heart is |
a dilated heart> systolic |
HTN heart dz causes |
diastolic, hypertrophied heart |
Normal myocyte stressed out increases in |
size/hypertrophy? in length and diameter proportionately? symmetric hypertrophy |
Ischemic Heart disease |
myocyte increases in length more than width> dilated ventricle> Eccentric hypertrophy> lowered EF |
Hypertensive Heart disease> |
myocyte increases in width more than length> concentric hypertrophy> hypertrophied/thick/stiff> preserved ejection fraction |
Ischemic heart disease |
number 1 killer every year, except 1918 >flu |
What supplies the heart with O2? |
Coronary arteries, and less blood = ischemia |
Flow of blood in arteries |
the most important determinant is the diameter |
Smaller diameter will equal? |
resistance |
If ? of the coronary artery is obstructed, what will the flow and resistance be? |
resistance is 2x2x2x2=16 (inverse to 4th power of radius) and the flow is ? x ? x ? x ? x ? = 1/16 directly proportional to 4th power |
If you have 2/3 obstruction of an artery, what is the flow and resistance? |
Flow is 1/3 x 1/3 x 1/3 x 1/3= 1/81 and resistance = 81 |
Cardiac surgeons will not do surgery unless obstruction is > ___%? |
70 |
When the diameter goes down, the resistance goes ________ and the flow goes _______- |
up, down |
When the diameter goes up, the resistance goes ______and the flow goes __________ |
down, up |
In ischemic heart disease |
it’s all about the coronaries becoming narrowed |
Arterial side |
higher pressure, lower volume (? 1/6 of blood volume) |
Venous side |
lower pressure, higher volume (? 2/3 of blood volume) |
Endocardium is the |
inner lining of the heart, which the coronary artery feeds, but receives the least amount of blood because it’s the furthest away> 1st part that dies with obstruction |
Sub endocardial infarction |
1st part of the heart that dies w/obstruction, does not result in ST elevation, does not show as ST elevation- nonSTEMI, troponin goes ^, obstruction furthest from coronary |
When obstruction is local, what happens to the heart? |
a transmural infarction= STEMI, ST elevation- the whole thickness of ms dies. |
Left main coronary artery supplies the |
left ventricle> circumflex > left anterior descending> septum |
Right main coronary artery supplies the |
right ventricle |
Why is important to know the arteries? |
EKG will show where the blockage and death of cells is occurring> then angiography |
Mortality in females in post-menopausal females is ____ |
higher than males |
The worst risk factor for ischemic heart disease is__________and the most common is _______? |
diabetes, HTN |
Peripheral arterial dz (PAD) |
hurts when walking, and heart should be checked out also |
Family hx |
the death has to be premature- person has to be YOUNG- for males <55yo and females <65yo |
The pathogenesis of CAD is |
atherosclerosis- the formation of fibro-fatty lesions in the intimal lining of large and medium-sized arteries |
Atherosclerosis |
endothelial cell injury: LDL, smoking, hypertension |
LDL |
becomes oxidized, traumatic to lining? damage> injury/inflammation> macrophages get stuck there> formation of foam cells> unstable and stable plaque |
Stable plaques |
Have thick fibrous caps, partially block arteries, Do not tend to form clots or emboli, Implicated in chronic stable angina |
Unstable plaque |
Have thin fibrous caps, acute coronary syndromes, can rupture, thrombus can form, may completely block the artery, may break free= embolus, unstable angina and myocardial infarction |
Stable angina |
chest pain on exertion> never to the ER |
Unstable angina |
can to you to ER and sometimes grave? acute coronary syndromes, 1) unstable angina, 2) non STEMI, 3) STEMI because the plaque ruptured? unstable/thin cap |
The 2 types of plaque can… |
be there in the same pt |
Chronic stable angina |
predictable pattern of exertional chest pain- relieved by rest |
Stable angina |
permanent narrowing, fixed lesion |
Demand-related ischemia |
when you get angina/pain upon exertion because the heart is demanding more blood |
demand-related ischemia |
Fixed Pattern, NO change w/respiration (pleuritic), NO change with body position, NO tenderness, Dull pain (compressing, squeezing, crushing), 15-30 minutes, Radiates to the jaw or left arm |
Supply related ischemia |
less blood flow pain, unstable plaque, pain even at rest, prolonged pain not relieved by rest or meds, new onset pain |
Can we get ischemia/infarction with no chest pain? |
yes> diabetic pts, women (SOB), elderly (SOB) |
New pain at rest |
not chronic stable angina> acute coronary syndrome> ER |
New pain, rest pain, prolonged pain, worst pain |
> listen to story> ER |
How to dx chronic stable angina |
hx, exertional pain, EKG, stress EKG, ECHO (dobutamine), angiography, nuclear scanning |
After an abnormal stress test, what’s the next step? |
angiography will localize the lesion |
Can we have ischemic heart dz w/no obstruction, atherosclerosis, plaque, etc.? |
Yes> spasm >variant angina, or vasospastic> r/t calcium> young age (20s) > EKG changes during attack only |
Tx for demand related ischemia |
beta blockers and calcium channel blockers |
Supply related ischemia |
unstable plaque? pain is d/t less supply of blood to the heart d/t plaque becoming loose? s/s? new, worse, prolonged, rest pain- also at exertion. |
Supply related ischemia |
significant obstruction> sub endocardium effected> ST segment does not show, troponin will be ^ |
Transmural infarction |
when 100% of the heart dies |
If pt has chest pains, what do you do? |
EKG> if not elevated, do enzymes (nonSTEMI) |
If EKG shows ST elevations, what do you do? |
send to the cath lab, no need for enzymes |
EKG is doing what? |
taking pictures of the DIRECTION of the electricity in the heart. Leads are cameras. When electricity moving towards electrode, + EKG ^ST. When moving away, ST segment depressed. |
Dead tissues have electricity? |
NO, and viable surrounding tissue will move towards dead tissue, away from camera/leads= depressed=nonSTEMI |
When thickness of myocardium has died, which way will electricity move? |
towards the leads and cameras? ST elevation? transmural infarction |
Unstable angina |
hx dx |
Non STEMI |
enzyme dx |
STEMI |
ST elevation/EKG, enzyme |
Serum biomarkers |
troponin and CKMB both do not show up in the 1st 4 hrs so > myoglobin |
If pt developed a 2nd heart attack, which biomarker will help? |
CKMB |
MONA |
morphine, oxygen (if pt hypoxic), nitrates and ASA? only aspirin will decrease mortality by 25-40% (plt aggregation) |
Angioplasty or thrombolytic, which is superior? |
Angio> if unavailable, do the TPA |