Week 7 Flashcards

Question

What are the two types of heart failures and what kind of dysfunction are they each associated with?

Answer 1

* Reduced Ejection Fraction Heart Failure - associated with systolic dysfunction * Preserved Ejection Fraction Heart Failure - associated with diastolic dysfunction

Answer 2

Impaired contractility and increased afterload

Answer 3

* **Coronary artery disease** – lack of perfusion does not get blood to myocardial cells → myocardial cells cannot contract fully * Myocardial infarction, transient myocardial ischemia * **Chronic volume overload** – chronic dilation of the ventricles causes remodeling of the ventricle walls to be more fibrotic * Mitral/aortic regurgitation * **Dilated cardiomyopathies** – fibrosis and myocyte atrophy cause impaired contraction (myocytes grow in series instead of in parallel – decreased ability to cross-link)

Answer 4

* Increased Afterload * Hypertension – Ventricle contracting against increased pressure → less volume leaves ventricle * Aortic stenosis – Ventricle contracting against increased pressure → less volume leaves ventricle

Answer 5

Impaired early diastolic relaxation and Increased stiffness of the ventricular wall

Answer 6

* Impaired early diastolic relaxation – external force limits ventricular filling * Cardiac tamponade

Answer 7

* LVH, fibrosis, restrictive cardiomyopathy

Answer 8

* Frank-Starling Mechanism * Acute: increase in preload causes an increase in stretching (cross-linking) of cardiac muscle * Chronic: increase in preload causes dilation (remodeling of myocardium)

Answer 9

* Adrenergic system * Acute: drop in CO → drop in BP (BP = CO x TPR) → decrease in baroreceptor firing → increase in sympathetic activity * Chronic: down regulation of beta receptors, increased catecholamine releases causes increase intracellular Ca2+ → activation of apoptosis pathway

Answer 10

* Acute: decreased CO → decreased GFR → renin, angiotensin II, aldosterone release → increase in vasoconstriction and volume retention → increases preload * Chronic: excessive stimulation of RAAS receptors causes hypertrophy and fibrosis

Answer 11

* Antidiuretic Hormone (ADH – vasopressin) * Acute: released from posterior pituitary gland in response of low BP → increase in water retention → increase in preload * Chronic: excessive stimulation causes hypertrophy and fibrosis

Answer 12

* Natriuretic Peptides * Atrial natriuretic peptide (ANP) – released in response to atrial distension * B-type natriuretic peptide (BNP) – released when ventricular myocardium is subjected to hemodynamic stress * Correlated with severity of HF * Result in excretion of Na+ and water, vasodilation, inhibition of renin secretion, and antagonize effects of ATII and vasopressin * Not fully sufficient to counteract the other hormones

Answer 13

* Development of ventricular hypertrophy * Acute: increased mass of muscle fibers helps maintain contractile force and counteracts the elevated ventricular wall stress * Chronic: unfortunately, increased stiffness of the hypertrophied wall causes higher-than-normal diastolic ventricular pressures, which are transmitted to the LA and pulmonary vasculature

Answer 14

Precipitating Factors * Increased metabolic demands – supply does not meet demand * Fever, infection, anemia, tachycardia, hyperthyroidism, pregnancy * Increased preload – increases pulmonary capillary pressure à pulmonary edema/congestion → decreased gas exchange * Sodium diet, renal failure, excessive fluid * Increased afterload – decreased forward CO * Hypertension, PE * Impaired contractility – decreased forward CO * Negative inotropes, CAD, alcohol * Sudden inappropriate HR – decreased CO or decreased diastolic filling * Bradycardia, tachycardia

Answer 15

* I: No limitation of physical activity * II: Slight limitation of activity. Dyspnea and fatigue with moderate exertion (walking upstairs quickly) * III: Marked limitation of activity. Dyspnea with minimal exertion (walking upstairs slowly) * IV: Severe limitation of activity. Symptoms are present even at rest.

Answer 16

* Prevalence: 5.1 million with 500,000 new cases annually * Increase over the next few years as elderly population increases * “Old person’s disease” – ages 70-89 * Males have a higher mortality rate * HFrEFF barely has an increased mortality

Answer 17

* Symptoms * Peripheral edema * RUQ discomfort (due to hepatic enlargement)

Answer 18

* Physical findings * Elevated JVP * RV Heave * Right sided S3

Answer 19

* Symptoms * Dyspnea * Orthopnea * PND * Fatigue

Answer 20

* Physical Findings * Diaphoresis * Tachycardia * Pulmonary rales, wheezes * Loud P2 * S3 (in systolic dysfunction HF) * S4 (in diastolic dysfunction HF) * LV heave

Answer 21

AT RISK * Stage A: High risk for developing HF * Stage B: asymptomatic LV dysfunction HF * Stage C: past or current symptoms of HF * Stage D: End-stage HF

Answer 22

* Stage A: High risk for developing HF * **Treatment:** * **Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)**

Answer 23

* Treatment used for A: * Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol) PLUS * **Treatment for B:** * **ACEI (indicated in PMHx of MI or decreased EF)** * **Beta-blockers (indicated in recent MI)** * **ICD** * **Digoxin: reduces progression of HF**

Answer 24

Treatment used for A: * Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol) PLUS Treatment for B: * ACEI (indicated in PMHx of MI or decreased EF) * Beta-blockers (indicated in recent MI) * ICD * Digoxin: reduces progression of HF PLUS * **Treatment for C** * **Hydralazine-Isosorbide Dinitrate Combo (balanced vasodilator)** * **Biventricular Pacing/Cardiac Revascularization Therapy (CRT): device placed that stimulates ventricular contraction at same time** * **Indicated in QRS ≥ 120ms and LVEF ≤ 35%** * **Neprilysin inhibitor**

Answer 25

Treatment used for A: * Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol) PLUS Treatment for B: * ACEI (indicated in PMHx of MI or decreased EF) * Beta-blockers (indicated in recent MI) * ICD * Digoxin: reduces progression of HF PLUS Treatment for C * Hydralazine-Isosorbide Dinitrate Combo (balanced vasodilator) * Biventricular Pacing/Cardiac Revascularization Therapy (CRT): device placed that stimulates ventricular contraction at same time * Indicated in QRS ≥ 120ms and LVEF ≤ 35% * Neprilysin inhibitor PLUS * **Treatment/Care for stage D:** * **Surgical therapy: cardiac transplantation, valve repair/replacement** * **Drugs** * **Palliative care**

Answer 26

* What effect do they have? * Balanced vasodilators (dilate arteries and veins both) * What is the rationale of that effect? * Reduces BP * Decreases preload and afterload → reduces myocardial oxygen demand * Limits remodeling (aldosterone) * What are side effects? * Monitor potassium, especially if combining! * CANNOT COMBINE ACEI AND ARBs

Answer 27

MOA: * Hydralazine: vasodilates arteries * Isosorbide: vasodilates veins Rationale * Reduces BP * Decreases preload and afterload → reduces myocardial oxygen demand * Limits remodeling (aldosterone)

Answer 28

MOA: * Balanced vasodilators (arteries and veins) Rationale: * Reduces BP * Decreases preload and afterload → reduces myocardial oxygen demand * Limits remodeling (aldosterone)

Answer 29

MOA * Acute: decreases contractility and HR * Chronic: increases contractility (due to up-regulation of beta receptors) Rationale * In HF, beta receptors are down-regulated due to chronic compensatory sympathetic stimulation * Beta blockers can up-regulate beta receptors à resulting in increased contractility

Answer 30

*_**\*\*PNEUMONIC ALERT BIATCHES: Furosemide (FURY has no wrath aka potent)\*\***_* MOA: * Inhibits sodium reabsorption at the Loop of Henle blocking Na/K/Cl Rationale * Reduces BP – works well in renal failure * More potent, helps with edema Side Effect * Dehydrating * Hypokalemia * Hyperuricemia * Ototoxicity

Answer 31

MOA: * Blocks Na/K ATPase → resulting in greater driving force for Na/Ca exchanger → increased intracellular Ca * Positive Inotrope * Hypokalemia – increases effectiveness (risk Digoxin toxicity) * Hyperkalemia decreases effectiveness Rationale * Increase in contractility → Increase SV and CO → leads to increased reflex vagal tone → reduce O2 demand Side Effects * Chromatopsia * Drug Interaction: * Diuretics * P-glycoprotein inhibitors * Quinidine, Verapamil * Tx toxicity: w/ potassium or Digibind

Answer 32

MOA * Beta-1 agonist Rationale * Increases SV by increasing contractility Side Effects * Tachycardia, arrhythmias, angina, myocardial ischemia

Answer 33

Dobutamine and dopamine are similar in MOA, Rationale, and Side Effects MOA * Low dose: stimulate dopamine receptors to vasodilate (Ehhh) * Intermediate dose: stimulate beta-1 receptors (GOOD) * High dose: stimulate alpha-1 receptors (BAD) Rationale * Increases SV due to increased contractility Side Effects * Tachycardia, arrhythmias, angina, myocardial ischemia

Answer 34

MOA * Increase cAMP by phosphodiesterase-3 → activation of Ca channels → positive inotrope Rationale: * Vasodilation → decrease BP, preload, afterload Side Effects * Teratogenicity, hypotension, hyperkalemia

Answer 35

* Hypertriglyceridemia * Elevated fasting TGs without a clear secondary cause \>150 * Average to below average LDLc

Answer 36

* Diet – weight loss and caloric restriction

Answer 37

* Eliminate secondary causes: hypothyroidism, DM, drugs, EtOH excess, renal disease, estrogens, obesity

Answer 38

* Medical therapy (indicated in TG levels \> 500mg/dL) * Fibrates – PPAR alpha agonist (nuclear transcription factor) * Niacin * Fish Oil

Answer 39

* Niacin * Increases HDL

Answer 40

Fish oil * reduces TG

Answer 41

* Fibrates – PPAR alpha agonist (nuclear transcription factor) * MOA: decreased TG and cholesterol synthesis and increases LPL activity (cleaves TGs from lipoproteins) leading to increased LDL * Must include statin therapy due to increased LDL levels * Examples: fenofibrate, gemfibrozil

Answer 42

* P_AO₂ = P_IO₂ – (P_ACO₂ / R) = F_IO₂ (P_atm – 47) – (P_ACO₂ / R) * R reflects the ratio of O₂ consumption for every molecule of CO₂generated * The greater the value, the more CO₂ is generated (i.e. fever, sepsis, more anaerobic respiration) * Typically 0.8

Answer 43

* A-a gradient = P_AO₂ – P_aO₂ * The normal pressure gradient across the alveolar space is 5 mmHg * If the pressure gradient is large, that means the O₂ in the alveolus is not able to get across the barrier to saturate the blood (aka a diffusion impairment)

Answer 44

* Acidemia – low blood pH (not used clinically) * Alkalemia – high blood pH (not used clinically) * **Acidosis** – increased acid content, but the pH may or may not be low due to buffering, compensation, or competing acid-base disorders * **Alkalosis** – decreased acid content, but the pH may or may not be high due to buffering, compensation, or competing acid-base disorders

Answer 45

* Buffers * Weakly dissociated acid or bases that are capable of minimzing pH swings by mass effect on equilibrium * Most common buffer is the bicarbonate-carbonic acid buffer * H₂CO₃ ⇔ H⁺ + HCO₃^- * Other buffers used: albumin, intracellular blood proteins, hemoglobin, bone (holds large reservoir of HCO₃^-)

Answer 46

* CO₂ + H₂O ⇔ H₂CO₃ ⇔ H⁺ + HCO₃^- * CO₂ is blown off by the lungs * HCO₃^- is excreted by the kidneys * Lungs: hyperventilate in response to metabolic acidosis * Kidneys: increase bicarb reabsorption or elimination in response to respiratory acidosis or alkalosis

Answer 47

* **Respiratory alkalosis**: lungs are hyperventilating → decrease in CO₂ → increase in pH → kidneys respond by excreting bicarb to make blood more acidic * **Respiratory acidosis**: lungs are hypoventilating → increase in CO₂ → decrease in pH → kidneys respond by reabsorbing bicarb to make blood more basic

Answer 48

* **Metabolic acidosis**: kidneys are excreting too much bicarb → decrease in pH → lungs respond by blowing off CO₂ to make blood more basic * **Metabolic alkalosis**: kidneys are reabsorbing too much bicarb → increase in pH → lungs respond by hypoventilating to keep CO₂ to make blood more acidic

Answer 49

* pH ~ [HCO₃^-] / P_aCO₂

Answer 50

* If there are two competing acid-base disorders, the pH may remain within normal limits (i.e. respiratory acidosis and metabolic alkalosis)

Answer 51

**Respiratory acidosis**: HCO₃^- increases with an increase in pCO₂ **Respiratory alkalosis:** HCO₃^- drops for an increase in pCO₂

Answer 52

* Steps to approaching acid-base status * Identify the predominant acid-base abnormality * Using the table with the pH, bicarb, and pCO₂ for all conditions (memorized) * Calculate the expected degree of compensation to see if a single acid-base abnormality exists (NB. compensation takes time!) * the changes in HCO₃^- for every pCO₂ will be given on test * Make the diagnosis * Etiologies

Answer 53

* Respiratory alkalosis (hyperventilation) * Anxiety or pain * CNS disease * Sepsis (increase in bacteria generating lactic acid from anaerobic respiration) * Hypoxia, V/Q mismatch, severe anemia (low O₂ getting delivered to periphery so you breathe more)

Answer 54

* Respiratory acidosis (hypoventilation) * Disorders of gas exchange (inability to blow off CO₂) * COPD, asthma, pneumonia, pulmonary edema, foreign body aspiration, laryngospasm, chest wall trauma, tension pneumothorax * Respiratory center abnormalities * CNS lesions, sedatives