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Fall 2020 Advanced Patho > HTN/Cardiovascular Patho Pt 2 > Flashcards

HTN/Cardiovascular Patho Pt 2 Flashcards

1
Q

Hypertension

=

When ___ or more Diastolic BP measurements are greater than __mmHg or

____ or more Systolic BP measurements are _____ (on separate visits)

A

A consistent elevation of systemic arterial blood pressure

2 or more DBP >90

3 or more SBP 140

No precise value for BP considered safe or pathological - Dependent on gender, size, etc

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2
Q

Classification of BP for Adults

  • Optimal
  • Prehypertension
  • Hypertension
    • Stage 1 (mild)
    • Stage 2 (moderate) aka severe, malignant HTN
A
  • <120, <80
  • 120-139, 80-89
    • 140-159, 90-99
    • _>_160, _>_100
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3
Q

Types of Hypertension

(2)

A

Primary Hypertension (95% of all HTN) - Essential or Idiopathic HTN (main problem, is the primary disease in question)

Secondary Hypertension (secondary complication to some other primary disease)

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4
Q

Secondary Hypertension Common Causes

  1. Renal Origin (2)
  2. Endocrine Origin (3)
  3. Hemodynamic/Cardiovascular (3)
  4. Neurologic (2)
A
  1. Chronic Renal Disease, Renal Artery Stenosis
  2. Adrenalcortical Hyperfunction, Hyperthyroid, Pregnancy induced
  3. Hypervolemia, Rigidity of the Aorta, Coarctation of the Aorta
  4. Increased ICP, Sleep Apnea
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5
Q

Secondary HTN Causes (Notes)

  • Renal artery stenosis: _____ blood flow to kidneys -> renal _____ assumes BP is ___ since renal BP is low -> kidneys produce _____ amount of renin, ang II, aldosterone -> elevates BP
  • Hyperfunction of adrenocorticotropic hormones: (2)
  • Hypervolemia, rigidity/coarctation of aorta: affects function of _____ that are responsible for regulating BP
A
  • Decreased -> baroreceptors assumes low BP -> excessive renin
  • aldosterone/glucocorticoids
  • baroreceptor function
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6
Q

Risk Factors with Primary HTN

  1. _____ History
  2. ___ age
  3. Gender: males ___, women ___
  4. Race:
  5. High dietary _____ intake
  6. D____
  7. S____
  8. O_____
  9. Heavy _____ consumption
  10. Low dietary/____deficiences (3)
  11. St____
A
  1. Family
  2. Old
  3. males <55, women>74
  4. African American
  5. sodium
  6. Diabetes
  7. Smoking
  8. Obesity
  9. Alcohol
  10. Mineral deficiences (K, Mg, Ca)
  11. Stress
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7
Q

Primary HTN (Notes)

  • (1): Form of HTN very typical of old age that stems from widespread atherosclerosis causing a hardening of arteries (systolic elevated but diastolic not as elevated or normal)

Although we consider primary HTN as idiopathic bc no verifiable causes there are risk factors

  • Females: have protective reproductive ____ (estrogen/progesterone)
    • Post menopause, womens risk tends to _____ with men
  • AA: high risk mediated by?
  • Sodium: high dietary sodium v common in what foods?
  • Diabetic: chronic _____
  • Smoking: ______ damage
  • Low Ca, K, Mg: effects what?
A
  • Isolated Systolic HTN ​
    • hormones, equalize after menopause
    • Sodium sensitivity/Renin
    • higher shelf-life, canned foods
    • hyperglycemia
    • epithelial
    • effects excitability of smooth muscle in vasculature
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8
Q

Blood Pressure = CO x TPR

A whole host of factors contribute to a rise and fall of TPR and CO and can cause persistent, elevated BP

  • CO effected by (2) Factors
  • TPR effected by (3) Factors
A
  • Blood Volume, Cardiac Factors
  • Humoral Factors, Neural Factors, Local Factors
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9
Q

Hypothetical Scheme for the Pathogenesis of Essential Hypertension

______ Influence + ______ Factors

(3)

A

Genetic Influence + Environmental Factors

  • Defects in Renal Sodium Homeostasis
  • Functional Vasoconstriction
  • Defects in Vascular Smooth Muscle Growth
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10
Q

Patho of Essential Hypertension

A
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11
Q

Genetic Predispositions to HTN (Notes)

  1. _____ handling, kidneys have a harder time _____ it than others
  2. Individuals who have vasculature that response more ____ to circulating ______
  3. Defective smooth ____ growth (when individuals are prone to _____ of vascular smooth muscle -> _____ lumens -> HTN)

Note: Genetic vulnerability does not _____ appearance of HTN, interaction with _____ promotes it more

A
  1. Sodium, excreting
  2. rapidly to vasoconstrictors
  3. muscle overgrowth -> narrows lumens -> HTN

Genetic does not guarantee, environment promotes it more

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12
Q

Genetic Predispositions to HTN (Notes)

  • _______/back and forth of Vascular wall _____ and Vascular _____
    • ​As wall thickens -> greater vascular _____ to constrictors which will then cause smooth muscle to _____ by thickening more -> higher genetic _______
  • Sodium group
    • ​Inadequacy of excretion -> net sodium and water _____ -> elevated _____/ECF -> increased ___ -> since BP = __x___ -> BP increases
    • In addition, when plasma increases -> _____ receptors stimulated to release (1) that causes _______ -> increases ____ -> increased BP (interacts wtih wall thickness again)
A
  • Potentiation, thickening, reactivity
    • ​reactivitiy, adapt, vulnerability
  • Sodium Group
    • ​retention -> plasma -> CO -> COxTPR = BP
    • stretch, atrial natriuretic peptide, vasoconstriction -> TPR -> increased BP
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13
Q

Other Patterns of Altered Blood Pressure

(3)

How to diagnose?

A

White Coat Hypertension

Reverse White Coat Hypertension or “Masked Hypertension”

Alterations in Circadian Patterns of BP (“non-dipping” or a lack of night time drop in BP)

24 hr Ambulatory BP monitoring (takes BP Q20min)

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14
Q

White Coat Hypertension

=

False ______

A

Phenomenon where individuals who go into clinical settings (going to doctors), their BP elevates bc anxiety, goes back to normal when they leave

False Positive

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15
Q

Masked Hypertension

=

False ______

A

Reverse White Coat HTN, those that go through most of their days in HTN, but when in clinical settings it doesn’t measure in the HTN range (ie those with busy/hectic lives, in doctor’s office away from stressors, time to relax in waiting room)

False Negatives

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16
Q

Non-Dipping

=

  • Graph of Normal Circadian Pattern
    • ____ SBP on average is lower than _____ SBP: due to _____ release patterns (higher during _____ hours, peaks when you wake), cortisol contributes directly to elevation of BP bc increases _____ of vasculature
A

Pathological issue that leads to loss of night time dipping, v dangerous -> even someone with normal healthy BP who just has this condition -> increased risk for CV complications

  • Sleeping SBP < Waking SBP, cortisol, waking, constriction
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17
Q

BP Treatment Algorithm (Notes)

  • First Option =
    • (3)
  • In general, start with ____ med (diuretic, ARB, BB, CCB) if not working ____ dosing or _____ -keep playing with it till it works
  • Barriers to Tx
    • Most people aren’t given the ____ to be able to first manage with lifestyle modifications
    • NOTORIOUSLY LOW _____ _______ why?
A
  • Lifestyle Modifiications
    • Exercise
    • Low fat, low sodium, mediterranean diet
    • Control Stress
  • one med, increase or combine
  • tools
  • MEDICATION ADHERENCE - bc only sx in advanced disease “silent killer” -> soo when asymptomatic ppl are taking meds with SE and don’t like it
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18
Q

BP Treatment Algorithm

  • Lifestyle Modifications
    1. Not at goal pressure < ___/___ or < ___/___ for pts with (2)
  • Initial drug choices without compelling indications
    1. Stage 1 HTN (SBP 140-159 or DBP 90-99) =
    2. Stage 2 HTN (SBP > 160 or DBP > 100) =
  • Initial drug choices with compelling indications: ____ antihypertensive drugs as needed (diuretics, ACEI, ARB, BB, CCB)
  • If Not at goal BP =
A
  1. <140/90, <130/80 w DM, CKD
  2. Thiazide diuretic for most, may consider ACEI, ARB, BB, CCB or combination
  3. Two drug combo (usually thiazide + ACEI, ARB, BB, CCB)
  • Other
  • Optimize dosage or add additional until goal is achieved. Consider consultation w hypertension specialist.
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19
Q

Other Strategies for BP Control

(3)

A

Home BP Monitoring

Paced Respiration

Screening for anxiety, panic, or other similar disorders

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20
Q

Alternative BP Strategies (Notes)

  • Home BP Monitoring: results in _____ mechanism, unclear could be _____, unconscious/conscious small modifications
  • Pace Respiration: guided reduction of ___ from 12-16 -> __-__, __-__ min per day (min ____ min per week) = effectiveness of ____ (one theory is that it enhances _____ reflex)
  • Panic/Anxiety Disorder: subcategory of _____ HTN
A
  • biofeedback, empowerment
  • RR 6-10, 5-10 min/day, 40min/wk, meds, baroreceptor
  • Secondary
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21
Q

Left Ventricular Hypertrophy (LVH)

Hypertensive Heart Disease

  • Hypertension leads to LVH as a result of increased ______ imposed on the heart
  • Wall Tension = LV __ X LV ___ / LV ___
  • LVH leads to smaller (1) and increased (1)
  • LVH increases risk of (4)
A
  • workload
  • LV SP x LV Radius/ LV Wall Thickness
  • Smaller Radius, Increased End diastolic filling pressure
  • Ventricular Arrhythmias, Sudden Cardiac Death, Death from MI, Chronic Heart Failure
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22
Q

LVH Notes

  • LVH is an adaptation to a chronically elevated cardiac (1)
    • Preload:
    • Aterload:
  • HTN increases ventricular afterload -> heart has to generate more ____ -> heart adapts by _____ of ventricular muscle
A
  • afterload (Diastolic BP)
    • Volume of ventricular filling (more filling, heart has to work harder to cause ejection)
    • Any pressure that opposes ventricular ejection (usually aortic diastolic pressure)
  • force -> hypertrophy
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23
Q

LVH Notes

  • (1): The force needed to generate a particular ventricular pressure at a particular ventricular radius
  • LVH: _____ change that _____ wall thickness and _____ radius -> pathologic effects of reduced __ and __
  • AKA Structural Heart Disease
    • Is an ____ adaptation to HTN
    • Can measure using ___
    • Increases risk for ventricular arrhythmias how? cardiac arrest, death from MI how?
    • Increases progression to (1)
  • Doesn’t take long for someone to develop LVH from elevated BP, but good thing is its _____ (quickley resolves once BP is under control)
A
  • Wall Tension
  • Pathological, increases thickness, decrases radius -> SV and CO
    • early
    • US
    • Structure of heart changes path of action potential, hypertrophy not proportional and leaves ventricle vulnerable to ischemia/hypoxic injury
    • CHF
  • reversible
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24
Q

Ischemic Heart Disease

LVH is type of Ischemic Heart Disease = imbalance of heart muscle (2)

Overall (1) of the heart determines (1)

  • Supply (3)
  • Demand (3)
A

imbalance of O2 demand and O2 supply

workload determines O2 demand

  • Coronary Vessel Patency
  • Ventricular Wall Compression
  • Diastolic filling time (HR)
  • Myocardial Contractility
  • Heart Rate
  • Wall stress (preload, afterload)
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25
Q

Coronary Circulation

Coronary arteries - branch off ______

Coronary veins - drain into ____ _____

A

Aorta

Vena Cava

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26
Q

Coronary Circulation (Notes)

Coronary Vessels Patency: heart can only extract __ from blood in _____ circulation

  • During systole arteries are _______
  • 2 main that branch off from aorta
    1. _____
    2. _____
      1. ​_____
      2. _____
A

O2, Coronary

  • Compressed (clamped off)
    1. Right coronary artery (RCA)
    2. Left coronary artery (LCA)
      1. ​Left Anterior Descending (LAD)
      2. Left Circumflex Branch: loops around to back of heart
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27
Q

Areas of Perfusion of Coronary Arteries

  • Perfuses left lateral, posterior surface
  • Perfuses much of inferior wall, loops around and perfuses much of posterior surface
  • Perfuses much of anterior surface and most important part of heart: ventricular septum bc where bundles of His are located
A
  • Left Circumflex Descending (LCD)
  • Right Coronary Artery (RCA)
  • Left Anterior Descending (LAD)
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28
Q

Coronary Artery Disease (Ischemic Heart Disease)

Ischemic Heart disease is an _____ between myocardial (1) and (1)

  • Myocardial O2 demand determined by (4)
  • Myocardial O2 supply determined by (3)
A

Imabance of O2 demand and O2 supply

  • Demand
    • Heart Rate
    • Contractility
    • Overall workload (preload/afterload)
    • Wall tension
      • ​Tension proportional to = LV systolic pressure X LV radius / LV wall thickness
  • Supply
    • Diastolic Perfusion Pressure
    • Coronary Vascular Resistance (F = *O2 Carrying Capacity
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29
Q

Blood Flow Reduced During Systole

  • Blood flow in LCA plummates to ____ during ______
  • Doesn’t fully recover until?
A
  • zero during SYSTOLE
  • beginning of diastole bc perfuses itself mainly in diastole
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30
Q

Coronary Vascular Resistance

  • Extrinsic and Intrinsic Mechanisms
    • Extrinsic:
    • Intrinsic:
A
  • Parasymphatic and sympathetic inervation
  • Influence of local metabolites on endotheial releasing factors
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31
Q

Coronary Vascular Resistance (Notes)

  • During Exercise, HR goes up, diastole time shortens -> less time to be perfused; Compensation of this =
  • Not so healthy heart (Atherosclerosis) = Endothelial _____ so can’t release what?
A
  • Ability of vessels endothelium to dilate (remember NO causes vasodilation) - happens normally in a healthy heart
  • dysfunction -> can’t release Nitric Oxide and vasodilate when demand increased -> ischemia -> angina (nitrogylcerin replaces function of NO)
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32
Q

Local Metabolic Changes

O2, CO2, Acidity, Adenosine

  • What causes Vasoconstriction?
    • What is released?
  • What causes Vasodilation?
    • What is released?
A
  • Increased O2, Decreased CO2, Acidity, Adenosine
    • Endothelin
  • Decreased O2, Increased CO2, Acidity, Adenosine
    • Nitric Oxide (EDRF) Endothelial Relaxing Factor
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33
Q

Coronary Heart Disease Types

  1. Chronic Ischemic Heart Disease
    • ​​_____ Angina
    • ____ Angina
    • _____ Myocardial Ischemia
  2. Acute Coronary Syndrome​​​
    1. _____ Elevation
    2. ​_____ Elevation
    • _____ Angina
    • Both can lead to?
A
  1. Chronic Ischemica Heart Disease
    • ​​Stable
    • Variant
    • Silent
  2. Acute Coronary Syndrome
    1. ​ST-segment (STEMI)
    2. Non-ST segment (NSTEMI)
    • Unstable
    • Acute MI
34
Q

Coronary Heart Disease Types (Notes)

  • Chronic Ischemic Heart Disease: has to do with _____ to increase oxygen ____ as oxygen ____ increase (so ischemia is _____ driven) -> _____ angina
  • Acute Coronary Syndrome: abrupt change in blood _____ (usually asctd with _____ of atherosclerotic plaque) completely ____ vessel and causes death of tissue/___, if NOT occlusive -> _____ angina
A
  • inability, supply, demand (demand driven) -> stable
  • supply, rupture, OCCLUDES -> MI, NOT OCCLUSIVE -> unstable angina
35
Q

Atheroslcerotic Plaques

  • What type of plaque causes stable angina?
    • ​That progresses to (1) disease, _____ loss or dysfunction
  • What type of plaque causes acute coronary syndromes?
    • ​Plaque rupture + non-occlusive clot =
    • Plaque rupture + larger occlusive clot =
A
  • Stable fixed
    • ​Chronic ischemic heart disease, Endothelial loss/dysfunction
  • Unstable
    • ​Abrupt ischemia (unstable angina)
    • Acute MI - ST elevation
36
Q

Chronic Stable Ischemic Heart Disease

  • Occult coronary disease is so prevalent among _____ countries that it is the ____ rather than the exception
  • Most individuals with non-obstructive coronary disease are completely ______
  • ______ is also very often asymptomatic but can also manifest as ischemic cardiac pain in the form of _____

Three Basic categories of Cardiac Ischemic Pain

  1. A diffuse _____ component
  2. A better defined ______ component conforming to a distribution of ______
  3. An interpretive component modulated by ______ factors
A
  • industrialized, norm
  • asymptomatic
  • Ischemia, angina
  1. visceral
  2. somatic, dermatomes
  3. psychological
37
Q

Cardiac Ischemic Pain (Notes)

Varies greatly depending on ______

  1. Diffuse Visceral Component: ischemia that stimulates (1) nerves in the heart -> awareness of signal is complicated (1)
  2. Somatic Component conforming to a distribution of dermatomes: AKA _____ Pain
  3. Interpretive component by pschological factors: We modulate our experience by?
A

GENDER

  1. Afferent autonomic nerves -> ambiguous feeling of feeling not well, abdominal unease
  2. Referred Pain
  3. How much we expect it to hurt/fear (anticipatory feeling) - is not all in your head, there are descending inputs to this experience of pain that makes it worse

pic of referred pain

38
Q

Chronic Stable Angina

Most patients with stable angina describe (2) rather than (1)

  • Sometimes described (4) sensation
  • Some discomfort located outside the chest (5)
  • Some people experience ____, profound f____, w____, or s_____

Usually ischemic episodes are ____ (__-__ min) and are brought on by (1) or (1)

  • _____ can be very _____ and can be lowered by exposure (3)

20% of patients experience “____ ___” angina

A

retro-sternal chest discomfort or distress rather than pain

  • heaviness, burning, tightness, choking
  • arms, shoulders, back, jaw, epigastrium
  • dyspnea, fatigue, weakness, syncope

brief (3-5min), physical activity or emotional stress

  • Threshold predictable (ie. after 10 steps), cold weather, smoking, ingesting a meal

Warm up: chest pain at onset of physical exercise but once warmed up that angina goes away (a form of stable chronic angina)

39
Q

Areas most commonly associated with Referred Pain

Darker areas =

Only __% of Women present with chest pain, more often ____, ___ pain, etc

A

More severe

30% women present with chest pain, more often indigestion, back pain

40
Q

Some Major Causes of Anginal Chest Pain

Coronary Artery Disease (2)

Other Cardiac Disorders (4)

A
  • Fixed Obstructive coronary disease (most common)
  • Coronary disease with dynamic flow (ie unstable angina)
  • Aortic Stenosis: narrowing of aortic valve, greatly increases afterload, leads to LVH
  • Hypertrophic Cardiomyopathy: congenital
  • Hypertensive Heart Disease and LVH: asctd w HTN
  • Mitral Valve Prolapse
41
Q

Angina Classification

Ischemic heart disease is, in the majority of cases, a consequence of _____ of the ___ _____ and develops when BF is _______

The major EFFECTS of ischemic heat disease include ____ _____ (chest pain)

  1. Chronic Stable Angina

  • ​Activity evoking, Limits to normal activity
    1. ​Class I
    2. Class II
    3. Class III
    4. Class IV

  1. _____ Angina AKA?
  2. _____ ______
A

Atherosclerosis, Coronary Arteries, inadequate BF

Angina Pectoralis

  1. Chronic Stable Angina
    1. ​Prolonged Exertion, None
    2. Walking > 2 blocks, Slight
    3. Walking < 2 blocks, Marked
    4. Minimal or rest, Severe
  2. Unstable Angina (Acute coronary syndrome)
  3. Myocardial Infarction
42
Q

Ischemic Heart Disease and the ECG

There are predicable changes in the ECG that often happen with imbalances of myocardial O2 supply and demand

  • ST segment depression =
  • ST segment elevation =
A
  • most commonly associated with “demand ischemia” (upon exertion, ie exercise testing)
  • most commonly associated with “supply ischemia” (upon occlusion
43
Q

ST Depression

Problem with ______

  • Most commonly associated with?
  • Exercise stress test helps to identify ______ the presence of?
A

DEMAND

  • demand ischemia
  • noninvasively, coronary artery disease/other cardiac syndrome thats causing ischemia
44
Q

ST Elevation

Problem with ______

  • Most commonly associated with ____ of myocardial tissue: caused by ______ problem, a _____ NOT by change in demand
A

SUPPLY

  • death, supply, blockage
45
Q

Acute Coronary Syndrome

Acute Coronary Syndrome describes a spectrum of clinical symptoms ranging from ______ to ____ to ____

The major pathophysiological mechanism for ACS is ____ or fissure of a plaque with a superimposed _____

____ ____ is a syndrome ______ between chronic stable angina and MI

  • A clinical diagnosis based on a history of chest pain and _____ of MI by ___ and _____ testing for myocardial necrosis
  • The chest pain will be (1) or (1)
  • May also represent ______ symptoms of _____ stable angina
A

Unstable Angina, NSTEMI, STEMI

rupture, thrombus

Unstable Angina, intermediate

  • exclusion by ECG, biomarkers
  • prolonged at rest or new onset
  • accelerating, previously stable angina
46
Q

Acute Coronary Syndrome

  • ECG -> (2)
  • Cardiac Markers
    • Negative -> (1)
    • Positive -> (1)
A
  • ST elevation, No ST elevation
  • Cardiac Markers
    • Unstable Angina
    • MI (STEMI or NSTEMI)
47
Q

Classification of Unstable Angina

  • What Severity Class I-III?
    • Angina at rest within 48 hours (angina at rest, acute)
    • New onset of severe angina, no pain at rest
    • Angina at rest within past month but not within preceding 48 hours (angina at rest, subacute)
  • Can also group patients on
    • Presence of ____-cardiac condition, ____ MI, ____ for stable angina, presence of transient ___ changes during chest pain
A
  • Severity Class
    • Class III
    • Class I
    • Class II
  • Group patients
    • extra cardiac condition, previous, treatment, ST
48
Q

Myocardial Infarction

Myocardial Infarction is a term used when there is evidence of myocardial _____ consistent with ischemia

The classic symptoms of MI

  • intense, oppressive, durable, excrutiating chest ______ with an impending sense of ____ and radiation of pain to ___
  • chest h____ or b_____, radiation to (5)

Also common is ____ skin, signficant ______ (may indicate extensive MI), and elevated ___

Other symptoms may be related to an intense ____ response: like (3)

A

necrosis

  • chest pressure, impending doom, radiation to left arm
  • heaviness, burning, radiation to jaw, neck, shoulder, back, both arms

pale, tachycardia, elevated BP

fear: nausea, vomiting, dyspnea

Elevated BP from stress response OR drop in BP bc of drop in CO (no matter how much stress hormone) - might hear crackles from backup of blood into lungs

Differential: Aortic dissection presents similarly

49
Q

Myocardial Infarction

Myocardial infarction is a term used when there is evidence of myocardial Necrosis consistent with ischemia

Some signs include:

  • Detection of _____ (especially ____)
  • ____ Changes (3)

MIs can be classified in many ways including by

  • _____ (microscopic, moderate, large…10%, 10-30%, >30% of LV myocardium respectively)
  • ____ changes
  • By _____ (anterior, posterior, inferior, lateral, etc)
A

signs

  • Biomarkers (Troponin)
  • ECG (ST elevation, exaggerated Q wave, T wave inversion)

classified

  • Size
  • EKG
  • Location
50
Q

Cardiac Enzyme Changes with MI

(3)

Which ones are not specific to cardiac - just shows any muscle injury?

Which one is cardiac specific, so we see a much greater, more rapid elevation?

A

Troponin

Creatine Kinase

Lactate Dehydrogenase

Lactate and Creatinine

Troponin

51
Q

Q wave

What happens to the Q wave?

Q wave abnormalities is usually goes with what type of MI?

A

Too large of a Q wave

STEMI

52
Q

T Wave Inversion

Is a sign of what?

A

Tends to be signs of a recent or active MI (a very early change in ECG)

53
Q

Location of Obstruction and Major Subgroups of MI

A
54
Q

Location of Obstruction and Major Subgroups of MI

  • Right Coronary Artery (RCA) Obstruction
    • ​If proximal RCA is occluded:
    • If distal RCA is occluded
  • Left Anterior Descending (LAD) Obstruction
    • ​Proximal LAD occluded:
    • Mid LAD
    • Distal LAD (___ common)
  • Left Circumflex Artery Obstruction
    • ​LCA occluded:
A
  • RCA
    • ​Moderate to large inferior (posterior, lateral, right ventricular)
    • Small inferior
  • LAD
    • ​”widow maker”: high mortality, occlusion is located proximal to the first septal perforator, compromised perfusion to purkinje conduction tissue**
    • Mid LAD
    • Distal LAD: less common
  • LCA
    • ​Moderate to Largery Anterior and Posterior left infarctions

RCA obstruction: how proximal, close to the aorta is it? - the more proximal, the larger area of infarction bc artery descends

Mid and distal LAD better mortality but less common

55
Q

Time is Muscle (Notes)

  • Cardiac muscle DOES NOT _______
  • What is the picture showing?
  • Post MI: body goes through cardiac ______ (significant _____ and dead area is replaced by _____ tissue)
    • Important to avoid (1)
    • Cardiac remodeling is a form of _____ heart disease, why?
  • Treatment?
A
  • regenerate
  • postmortem LAD dead tissue
  • remodeling (inflammation -> fibrous scar tissue)
    • Anti-inflammatory analgesics: interferes with healing process and most catastrophically can cause ventricular rupture
    • Structural: bc fibrous/scar tissue does not expand, contract, or conduct action potential -> increased risk of arrhythmias, sudden cardiac death, death from subsequent MIs, progression to CHF
  • Cardiac cath through femoral artery
56
Q

Heart Failure (Acute v. Chronic)

Heart Failure: When the heart cannot generate enough ___ to match ____ needs

Acute Heart Failure (or Acute Decompensation)

  1. ____ Myocardial Infarction
  2. _____ Cardiac _____
    • Due to cardiac arrhythmia or other manifestation of impaired ____ system
    • Myocardial _____
  3. Acute _____ of ____ Heart Failure
    • Generally either from severe acute (1) or (1)
A

CO, metabolic

  1. Fatal
  2. Sudden Cardiac Death
    • conduction
    • remodeling from healing from MI or LVH
  3. Decompensation of Chronic Heart Failure
    • severe acute pulmonary edema or cardiorenal syndrome (poor response to diuretics) - usually happens with acute volume overload -> fluid backup to lungs
57
Q

Chronic Heart Failure

Causes (4) General Categories

A

Abnormal Cardiac Muscle Function

Abnormal Left Ventricular Volume

Abnormal Left Ventricular Pressure

Abnormal Left Ventricular Filling

58
Q

Chronic Heart Failure Causes

Abnormal Cardiac Muscle Function (2)

Abnormal Left Ventricular Volume (2)-(3)

A
  • Myocardial Infarction
  • Cardiomyopathies
  • Valve insufficiency
  • Blood volume expansion associated with high output states
    • Chronic anemia
    • Infusion of a large volume of IV fluids in a short period of time
    • Pregnancy
59
Q

Chronic Heart Failure Causes

Abnormal Left Ventricular Pressure (3)

Abnormal Left Ventricular Filling (3)

A
  • Hypertension
  • COPD
  • Aortic or pulmonic valve stenosis
  • Mitral valve stenosis
  • Tricuspid valve stenosis
  • AFib
60
Q

Right Sided Heart Failure

Congestion of _____ Tissues

(3)

A

Peripheral Tissues

  1. Dependent edema and ascites
  2. GI tract congestion (anorexia, GI distress, weight loss)
  3. Liver congestion (signs related to impaired liver function)
61
Q

Left Sided Heart Failure

  1. (1): ____ intolerance and signs of decreased tissue _____
  2. (1)
    • ​​Impaired ____ exchange -> ____ and signs of _____
    • Pulmonary ____
      • ______
      • Cough with ____ sputum
      • Paroxysmal _____ dyspnea
A
  1. Decreased Cardiac Output: activity, perfusion
  2. Pulmonary Congestion
    1. ​gas -> cyanosis, decreased tissue perfusion
    2. Edema
      • Orthopnea
      • Cough w Frothy sputum
      • Nocturnal
62
Q

Right Sided HF Notes

Can start on either side or other but will lead to failure of other side

  • tends to hapen when the right side is forced to ____ hard (pulmonary __) at all bc it is normally not designed to generate high _____, is initially a ___ ___ system that generates just enough pressure to pump blood to pulmonary circulation
    • Ex) ____: deoxygenation of blood in pulmonary circulation causes unique pulmonary vessels to _____ -> raises the pulmonary _____ -> increases right side ____ -> increased pressure right side of heart has to work against
    • Leads to decreased __ on ___ side
A
  • work (HTN), pressure, low pressure system normally
    • COPD, vasoconstrict, pressure, afterload
    • decreased CO on left side
63
Q

Left Sided HF Notes

  • might fail ____ due to elevated ____ pressure, left sided cardiac ___ not strong enough
    • Effects: ____ CO, ____ congestion (imparied gas exchange), ____ intolerance
    • Leads to increased pressure in _____ circulation and ___ sided failure
A
  • first, arterial, muscle
    • decreased CO, pulmonary congestion, activity intolerance
    • pulmonary, right
64
Q

Chronic Heart Failure

Makes up majority of HF cases

Progresses slowly but contains two important components that represent two phases (brings about all the clinical manifestations)

  1. Structural _____ of cardiac tissue as a result of cardiac tissue damage or death - causes a reduction in cardiac _____
  2. Multiple _____ events in response to decreased cardiac function makes up majority of _____ issues of CHF
A
  1. remodeling -> reduced function
  2. compensatory events -> pathological issues
65
Q

Vicious Cycle of HF (Notes)

  • Usually starts with (1)
    • Body Compensates by: increased (4)
    • Vicious Cycle: all of above increases _____ of the heart and if this heart is post MI, is going to lead to more ____ and more damage -> further decline in __ -> which responds with more _____ (body’s response is what causes a downward ____)
  • Therefore, most treatments are designed to do what?
A
  • decreased CO
    • increases HR, SV (contractility), BP, blood volume
    • workload, ischemia, further decline in CO -> more compnesation, spiral
  • Limit body’s adaptation to decreased CO in order to preserve heart function
66
Q

The pathophysiology of heart failure involves changes in

(2)

A

Cardiac Function

Neurohormonal Responses

67
Q

Patho of HF

Cardiac Function

  • (1): Relacement of healthy cardiac tissue with in-elastic fibrous tissue that has decreased contractile function and an altered inotropic function
  • (1)
A
  • Cardiac Remodeling
  • Decreased CO
68
Q

Patho of HF

Neurohormonal Responses (to decreased CO and SV)

  • Activation of _____ nerves
  • Activation of ____ system
  • Increased release of (2)

The net effect of these neurohormonal responses is to

  • Produces (1) (to help maintain arterial pressure)
  • Produces (1) (increased venous pressure)
  • Increases blood ______
A
  • sympathetic
  • RAAS
  • ADH and Atrial natriuretic peptide (increases responsiveness of vascular smooth muscle)
  • Arterial vasoconstriction
  • Venous constriction
  • volume
69
Q

Patho of Chronic HF Chart

  • Increased _____ Stimulation
    • Effects
      • Increased ___ and _____ -> increased O2 demand
      • Increased __ -> increases afterload
  • Increased _____ System (dt decreased blood flow to kidneys)
    • Effects
      • Increased _______ which also causes constriction
      • Increased ______ (sodium and water retention) to increase blood volume and more blood to heart -> increases _____
A
  • Sympathetic
    • HR, Contractility
    • BP
  • RAAS
    • Ang II
    • Aldosterone -> preload
70
Q

Alterations in the Frank Starling Mechanism with CHF

The greater the LV end diastolic pressure what happens to CO?

A

As end diastolic pressure goes up, CO goes down

71
Q

Stages of Heart Failure

  • At ____ for Heart Failure
    • STAGE A =
    • STAGE B =
  • ____ Heart Failure
    • STAGE C =
    • STAGE D =
A
  • Risk for HF
    • High risk for developing HF
    • Asymptomatic LV dysfunction
  • Has HF
    • Past or Current Symptoms of HF
    • End stage HF
72
Q

Stage A HF

=

  • E.g Patients with
    • H_____
    • Ath_____ disease
    • D____
    • _____ syndrome
    • OR patients using ____ with HF or CM
  • Therapy Goals
    • Treat ____
    • Encourage _____ cessation
    • Treat ____ dissorders
    • Encourage regular _____
    • Discourage ____ intake, illicit ___ use
    • Control ____ syndrome
  • Drugs ___ or ____ in appropriate patients (see text) for vascular disease or diabetes
A
  • high risk but without structural heart disease or sx of HF
  • Patients with
    • HTN
    • Atherosclerosis
    • Diabetes
    • Metabolic
    • cardiotoxins
  • Therapy Goals
    • HTN
    • smoking
    • lipid
    • exercise
    • alcohol, drug
    • metabolic
  • ACEI or ARBS
73
Q

Stage B HF

=

  • E.g Patients with
    • previous __
    • LV _____ including LVH and low EF
    • Asymptomatic ____ disease
  • Therapy Goals
    • All measures under stage A
    • Drugs (2)
    • Devices in Selected Patients (1)
A

Structural heart disease w/o heart disease or sx of HF

  • E.g patients with
    • MI
    • remodeling
    • asx valvular disease
  • Therapy Goals
    • ACEI or ARB or BB in appropriate patients
    • Implantable defibrillators
74
Q

Stage C HF

=

  • E.g Patients with
    • Known _____ heart disease AND ___ or fatigue, reduced ____ tolerance
  • Therapy Goals
    • All measures under stages A and B
    • Dietary ___- restriction, drugs for routine use
    • _____ for fluid retention
    • A___
    • B___
  • Drugs in Selected Patients
    • Aldosterone ____
    • A _ _ _
    • D_____
    • Hy____/ni_____
  • Devices in Selected Patients
    • Biventricular ______
    • Implantable ______
A

Structural Heart disase WITH prior or current symptoms of HF

  • E.g patients with
    • Known structural heart disease AND SOB, reduced exercise tolerance
  • Therapy goals
    • salt restriction
    • Diuretics
    • ACEI
    • BB
  • Drugs
    • antagonists
    • ARBS
    • Digitalis
    • Hydralizine/nitrates
  • Devices
    • Pacing
    • Defibrillators
75
Q

Stage D HF

=

  • Eg. Patients who have marked ____ at ____ despite maximal medical _____ (e.g those who are currently ____ or cannot be safely discharged from hospital without specialized interventions)
  • Therapy Goals
    • Appropriate measures under stages A, B, C
    • Decision re appropriate lvl of care
  • Options
    • Compassionate (1) care/h____
    • Extraordinary measures such as?
A

Refractory HF requiring specialized interventions

  • symptoms, rest, therapy, hospitalized
  • Options
    • end of life care/hospice
    • heart transplant, chronic inotropes, permanent mechanical support, experimental surgery or drugs
76
Q

Medications (Notes)

(6)

Again, all meds are designed to minimize what?

A

Body’s natural response to drop in CO

ACE Inhibitors

Angiotensin Receptor Blockers

Aldosterone Antagonists

Beta Blockers

Digoxin

Diuretics

77
Q

ACE Inhibitors

=

A

Reduces production of Angiotensin II -> will reduce vasoconstriction and volume overload

78
Q

Angiotensin Receptor Blockers

=

Aldosterone Antagonists

=

A

Similar to ACEI but blocks the receptors to angiotensin

Specifically aimed at limiting sodium and water retention

79
Q

Beta Blockers

=

Digoxin

=

A

Decreases HR -> reduces O2 demand on heart -> preserves heart function

Increases contractility of heart (given much later stages of HF (elderly))-> trying to maintain minimal heart function (is the outlier of these drugs)

80
Q

Diuretics

=

+/- Sodium Restricted Diets

A

Limits Fluid Retention

Fall 2020 Advanced Patho (15 decks)

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