| 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 |
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