Cardiovascular Syste Advanced Patho

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