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Cardio > Exam Review Week 2 > Flashcards

Exam Review Week 2 Flashcards

1
Q

What is normal BP?

A

systolic: under 120; diastolic: under 80

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2
Q

What is prehypertension?

A

systolic: 120-139; diastolic: 80-89

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3
Q

What is Stage 1 hypertension?

A

systolic: 140-159; diastolic: 90-99

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4
Q

What is Stage 2 hypertension?

A

systolic: 160+; diastolic: 100+

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5
Q

What is the % of patients with hypertension? Pre-hypertension?

A

30% prehypertension, 30% hypertension

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6
Q

What can hypertension lead to?

A

increased afterload, leading to heart failure, MI and myocardial ischemia; arterial damage and atherosclerosis, leading to aortic aneurysm and dissection, stroke, retinopathy, and nephrosclerosis and renal failure

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7
Q

How do you calculate BP?

A

BP = CO x TPR

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8
Q

What factors regulate CO?

A

filling pressure, heart rate, force of contraction

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9
Q

How does sodium retention affect CO?

A

retaining sodium means retaining fluid - volume goes u,p, causing filling pressure to go up and CO to increase

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10
Q

How does the sympathetic system affect CO?

A

increases HR, increases force of contraction

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11
Q

How does the parasympathetic system affect CO?

A

decreases HR

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12
Q

What increases vasoconstriction?

A

norepinephrine, angiotensin; these both increase vascular resistance

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13
Q

What decreases vasoconstriction?

A

nitric oxide - this decreases vascular resistance

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14
Q

What are the 2 major systems that regulate blood pressure?

A
  1. autonomic nervous system; 2. Renin-Angiotensin-Aldosterone System
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15
Q

How does the autonomic nervous system affect blood pressure?

A

Regulated through the brain, sympathetic nerves, and adrenal glands; Increases cardiac output and peripheral resistance; Increases renin release from the kidneys; Feedback loop by baroreceptors

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16
Q

How does the Renin-Angiotensin-Aldosterone System affect blood pressure?

A

Regulated through the kidney, blood stream, and adrenal glands; Increases sodium (and water) retention and peripheral resistance (increases BP); Feedback loop in kidney

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17
Q

How do the carotid and aortic arch baroreceptors work?

A

responsive to stretch - BP goes up, vessel stretches, baroreceptors notice (activation increases); if BP goes down, then there is less activation up the nerves
pretty easy to palpate
can be manipulated by MD b/c it’s a mechanical receptor

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18
Q

What is the reflex to acute bleeding?

A

Response of the baroreceptor reflex to acute hemorrhage. The reflex is initiated by a decrease in mean arterial pressure (Pa). The compensatory responses attempt to increase Pa back to normal. These responses include decreased stretch on baroreceptors, decreased firing rate of carotid sinus, decreased parasympathetic activity to the heart (and increased HR), and increased sympathetic activity to the heart and blood vessels.

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19
Q

How does standing affect BP?

A

Standing leads to pooling of blood in veins, decrease in arterial pressure, baroreceptor reflex, increase in sympathetic outflow, and therefore increase in arterial pressure toward normal

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20
Q

What are the steps of the Renin-Angiotensin-Aldosterone System?

A

Prorenin is in the Juxtaglomerular cells, renin is formed, released into plasma, Angiotensinogen, Angiotensin I, and then Angiotensin-converting Enzyme (from lungs, kidney) causes production of Angiotensin II

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21
Q

What is Angiotensin II?

A

Stimulates the synthesis/secretion of aldosterone in the adrenal cortex, and Aldosterone acts on renal distal tubule and collecting duct – increases Na+ reabsorption (increases ECF volume and blood volume, increases CO); leads to vasoconstriction in arterioles (increases TPR); directly stimulates Na+ - H+ exchange in renal proximal tubule and increases reabsorption of Na+ and HCO3- (increases CO); Increases thirst and water intake; stimulates antidiuretic hormone (increases water reabsorption in collecting ducts - increases CO; vasoconstriction – increases TPR)

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22
Q

What stimulates renin secretion?

A

Renin secretion is stimulated by decreased renal perfusion (sensed by mechanoreceptors), decreased Na+, also sympathetic activation

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23
Q

What is the difference in timing between the major systems that regulate pressure?

A

autonomic nervous system reacts in seconds to minutes, while renin-angiotensin-aldosterone system takes hours to days (even weeks!)

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24
Q

What other mechanisms (beside the major systems) can regulate BP?

A
  1. Chemoreceptors in Carotid and Aortic Bodies
  2. Central chemoreceptors
  3. Antidiuretic hormone
  4. Cardiopulmonary (Low-Pressure) Baroreceptors
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25
Q

How do chemoreceptors in aortic carotid bodies affect BP?

A

Affects sympathetic vasoconstrictor centers; Sensitive to decreases in PO2 and increases in CO2; Also, sensitive to decreases in pH (particularly when PO2 is decreased)

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26
Q

What do central chemoreceptors do to affect BP?

A

Medullary chemoreceptors are sensitive to changes in PCO2 or pH (less sensitive to changes in PO2); they affect changes in outflow of the medullary vascular centers; Ischemic brain causes PCO2 increases and pH decreases which causes sympathetic outflow increase leading to arteriolar vasoconstriction, which increases TPR

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27
Q

What is antidiuretic hormone?

A 
Stimulated by angiotensin II; Also increased by increases in serum osmolarity; produced by posterior lobe of the pituitary gland; in V1 receptors (vascular smooth muscle)
cause vasoconstriction (increased TPR); in V2 receptors (renal collecting ducts) cause increased water reabsorption
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28
Q

What are the cardiopulmonary baroreceptors?

A

found in veins, atria, and pulmonary artery; Increase in blood volume leads to increase in venous and atrial pressure and baroreceptor activation; increases atrial natriuretic peptide (ANP) secretion by atria - Relaxation of vascular smooth muscle causes vasodilation and decreased TPR. Also, vasodilation in the kidney leads to increased Na+ and water excretion; Decreases antidiuretic hormone

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29
Q

How do cardiopulmonary baroreceptors increase HR?

A

Information from atrial receptors travel in vagus nerve to the nucleus tractus solitarius (just like with high pressure baroreceptors); the response, however is different (the medullary cardiovascular center activation leads to heart rate increase – Bainbridge reflex); increases CO, increasing renal perfusion and Na+ and water excretion

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30
Q

What is the percentage of hypertension that is essential?

A

90% (unknown cause, potentially multifactorial)

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31
Q

How does BP change with age?

A

systolic increases and diastolic decreases (therefore pulse pressure increases); in youth, CO is most important for BP; as you age, TPR becomes more significant (likely due to stiffening)

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32
Q

What are the best drugs for congestive heart failure?

A

Diuretics, Vasoactive Drugs, Beta-blockers, Drugs that affect the RAAS (renin angiotensin-aldosterone system)

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33
Q

What are the best drugs for hypertension?

A

diuretics, adrenergic inhibitors, direct vasodilators (usually used in combination therapy), calcium channel blockers, RAAS blockers

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34
Q

What are types of drugs that affect the vasculature?

A

direct-acting vasodilators, nitrates and phosphodiesterase-5 inhibitors, calcium channel blockers, and adrenergic inhibitors

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35
Q

What are the Direct-Acting Vasodilators?

A

Hydralazine, Sodium nitroprusside; Minoxidil and Fenoldopam used less

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36
Q

What is Hydralazine?

A

Potent and direct arteriolar dilator –Acts at the level of the precapillary arterioles, has no effect on systemic veins; Cellular mechanism unknown; Arteriolar dilation results in fall in blood pressure, which leads to baroreceptor-mediated increase in sympathetic outflow (e.g. reflex tachycardia); used less often now

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37
Q

What are the contraindications for Hydralazine?

A

use with caution in patients with underlying CAD because could precipitate myocardial ischemia - Often combined with beta-blocker to blunt the reflex tachycardia response

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38
Q

When is Hydralazine particularly helpful?

A

Remains helpful in hypertensive patients with increasing creatinine (where want to avoid ACEi or ARB in the acute setting); Also used in combination with venodilator isosorbide dinitrate to treat systolic heart failure

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39
Q

What are the drawbacks of Hydralazine?

A

Low bioavailability - Extensive first pass hepatic metabolism and great variety of metabolizers; Short half-life (2-4 hours), although effect persists up to 12 hours since it binds avidly to vascular tissues

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40
Q

What are the side effects of Hydralazine?

A

Headache (increased cerebral vasodilation), Palpitations (secondary to reflex tachycardia), Flushing (increased systemic vasodilation), Nausea, Anorexia; NOTE: rare, but can cause Lupus like syndrome (especially in slow acetylators)

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41
Q

What is Minoxidil?

A

Arteriolar vasodilator – No significant venodilation; Mechanism of Action: Increase in potassium channel permeability leading to smooth muscle cell hyperpolarization and relaxation; used in Severe or refractory hypertension; Good, reliable GI absorption

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42
Q

What are the drawbacks of Minoxidil?

A

Can lead to reflex adrenergic stimulation and subsequent increased heart rate (like Hydralazine); Also can decrease renal perfusion, resulting in fluid retention – Attenuated with co-administration of a diuretic; Short half-life – Longer pharmacologic effects (binds avidly to vascular tissues); usually dosed once or twice per day

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43
Q

What are the side effects of Minoxidil?

A

Reflex tachycardia, Fluid retention, Hypertrichosis (excessive hair growth) - it’s the topical formulation in Rogaine; Pericardial effusion (rare)

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44
Q

What is Sodium Nitroprusside?

A

Potent “balanced” vasodilator – Acts on both arterioles and veins; Hemodynamic effect: Decrease arterial/systemic resistance, Increase venous capacitance; Sum of these effects depends on LV function –Normal LV function: decrease in cardiac output due to reduction in venous return –Reduced LV function: decreased systemic resistance (afterload) results in improved forward flow (cardiac output)

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45
Q

When should Sodium Nitroprusside be used?

A

Hypertensive emergency (Very potent, rapid action; often used with concurrent beta-blocker); Severe congestive heart failure

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46
Q

How is Sodium Nitroprusside used?

A

Administered by continuous IV infusion; Onset of action begins within 30 seconds and peak affect is achieved in 2 minutes; Effect wanes within minutes of discontinuation

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47
Q

What are the side effects/toxicities of Sodium Nitroprusside?

A

Risk of thiocyanate accumulation/toxicity (Clinically: blurred vision, tinnitus, disorientation, and/or nausea followed; Routine to monitor serum levels of thiocyanate if sodium nitroprusside is used for more than 24 hours; Higher risk of toxicity in the setting of renal impairment)

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48
Q

What is Fenoldopam?

A

Rapid acting potent arteriolar vasodilator; Maintains or enhances renal perfusion (unlike other IV antihypertensives) –Facilitates natriuresis via activation of renal tubular D1 receptors; Does not stimulate alpha- or beta-adrenergic receptors like Dopamine does

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49
Q

What is the mechanism of Fenoldopam?

A

Selective agonist of peripheral dopamine 1 (D1) receptors; Activation of D1 receptors results in arteriolar vasodilation via a cAMP-dependent pathway

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50
Q

How is Fenoldopam administered?

A

Continuous intravenous infusion –Rapid onset of action
(Achieves 50% of maximal effect within 15 minutes, reaches steady state in 30 to 60 minutes) AND Rapid offset of action (Elimination half-life less than 10 minutes)

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51
Q

What are the side effects of Fenoldopam?

A

Headache, Dizziness, tachycardia; Increased intraocular pressure by slowing aqueous humor drainage (therefore avoid in patients with history of glaucoma); NOTE: Does not cause thiocyanate toxicity

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52
Q

When are nitrates used?

A

–Angina pectoris
–Acute coronary syndromes
–Heart Failure

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53
Q

What is the nitrate mechanism of action?

A

Result in vascular smooth muscle relaxation

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54
Q

What are the hemodynamic effects of nitrates?

A

–Venodilation (Venous pooling, Diminished venous return, Decreased right sided filling, Decreased left sided filling)
–Systemic arterial resistance generally unaffected
–Cardiac output may fall secondary to decreased preload (especially in intravascular deplete or “preload sensitive” patients)
–At higher doses, arteriolar dilation (Coronary artery dilation)
Venodilation ultimately leads to decreased LV preload, lowers LV wall stress, causing decreased myocardial oxygen demand

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55
Q

What are the different kinds of nitrates?

A 
Many formulations are available, and which one to use depends on clinical objective; In Acute Angina: sublingual nitroglycerin tablets or sprays (Peak action within 3 minutes (rapid absorption into blood stream via oral mucosa) and effect diminished after 15-30 minutes (deactivated in the liver), Can also be used prophylactically before situations that are known to precipitate angina; Chronic management of CAD: long-acting nitrates (sustained release formulations)
include Oral (duration of action up to 14 hours), Isosorbide dinitrate, Isosorbide mononitrate, Transdermal patch or topical paste
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56
Q

What is unique about nitrate use?

A

Drug tolerance develops with continued use – Need for a “drug holiday” in order to avoid tachyphylaxis (some docs say take during the day but not overnight)

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57
Q

When is IV nitroglycerin used?

A

Most useful in the acute treatment of the hospitalized patient with unstable angina, pulmonary edema, or heart failure; Can be given with continuous administration

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58
Q

What are the side effects of nitroglycerin?

A

Hypotension, Reflex tachycardia, Headache, Flushing

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59
Q

What is Sildenafil?

A

Phosphodiesterase-5 Inhibitor; Decreases pulmonary vascular resistance in patients with pulmonary arterial hypertension, inhibits the breakdown of cGMP in the pulmonary vasculature, leads to enhancement of vasodilation (and oxygenation); also known as Viagra!

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60
Q

What are the contrandications for Sildenafil?

A

Cannot be used with nitrates (Can result in severe systemic hypotension)

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61
Q

What are calcium channel blockers?

A

Common property is ability to impede the influx of Ca++ through membrane channels in cardiac and smooth muscle cells

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62
Q

What are the 2 types of calcium channels in cardiac tissue?

A
  1. L-type channel (target of currently available CCBs) - Responsible for Ca++ entry that maintains phase 2 (“plateau”) of the action potential; 2. T-type channel - Plays a role in the initial depolarization of nodal tissues
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63
Q

How do calcium channel blockers work?

A

Decreases the concentration of intracellular Ca++ available to contractile proteins; In vascular smooth muscle cells: leads to vasodilation; in cardiac cells: leads to a negative inotropic effect

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64
Q

What are the 2 main groups of calcium channel blockers and what are their names?

A

Non-dihydropyridines (Verapamil, Diltiazem); Dihydropyridines (Amlodipine, Felodipine, Isradipine, Nicardipine, Nifedipine, Nisoldipine)

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65
Q

What do calcium channel blockers affect clinically?

A
  1. Angina pectoris - Decrease myocardial oxygen consumption: decrease BP (decrease afterload); decrease contractility; decrease HR (verapamil and diltiazem); 2. Coronary artery spasm - Coronary artery vasodilation; 3. Hypertension - Arteriolar smooth muscle cell relaxation; 4. Supraventricular arrhythmias - (Verapamil and Diltiazem): decrease conduction velocity and increase refractoriness of atrioventricular node
66
Q

What are side effects of calcium channel blockers?

A

Verapamil: Hypotension, Bradycardia, AV block, Constipation; Diltiazem: Hypotension, Peripheral edema, Bradycardia; Dihydropyridines: Hypotension, Headache, Flushing, Peripheral edema

67
Q

How are calcium channel blockers given?

A

Usually administered orally – Many long-acting once a day formulations are available

68
Q

What do alpha 2 agonists do?

A

Lead to diminished sympathetic outflow from the medulla, Reduce peripheral vascular resistance and diminished cardiac stimulation, Result in a fall in blood pressure and heart rate

69
Q

What are some alpha 2 agonists?

A
  • Clonidine
  • Alpha-methyldopa
  • Guanabenz
  • Guanfacine
70
Q

What is Reserpine? What does it do?

A

–It inhibits uptake of norepinephrine into storage vesicles in postganglionic and central neurons
–Leading to norepinephrine degradation
–Results in a depletion of catecholamines
–Decreases total peripheral resistance

71
Q

What are the toxicities associated with Reserpine?

A

CNS toxicity: Sedation, Impaired concentration, Psychotic depression; For these reasons, it is rarely prescribed

72
Q

What are some alpha 1 antagonists?

A

Prazosin, Terazosin, Doxazosin

73
Q

What are non-selective alpha 1 and alpha 2 antagonists?

A

Phentolamine, Phenoxybenzamine

74
Q

What do alpha 1 antagonists do?

A

Historically, used for hypertension, However, in the ALLHAT trial, patients treated with doxazosin experienced more adverse cardiac outcomes than those treated with a thiazide diuretic

75
Q

When are non-selective alpha 1 and alpha 2 antagonists used?

A

Used in the treatment of pheochromocytoma, Otherwise, rarely used; Blocking the presynpatic alpha 2 receptor interferes with the normal feedback inhibition of norepinephrine release (leading to pronounced reflex sympathetic side effects)

76
Q

What is perfusion pressure?

A

pressure gradient across a vascular bed

77
Q

What are the differences between pulmonary and systemic circulation?

A

When compared with the systemic circulation, the pulmonary circulation is characterized by much lower pressures and resistances, although the blood flow is the same.

78
Q

How is blood flow the same in pulmonary and systemic circulation?

A

The reason that pulmonary blood flow can be equal to systemic blood flow is that pulmonary pressures and resistances are proportionately lower than systemic pressures and resistances.

79
Q

How is blood flow distributed in the lungs?

A

The distribution of blood flow within the lungs is uneven and the distribution can be explained by the effects of gravity; In the upright position, Zone 1 has the lowest blood flow and zone 3 has the greatest blood flow. In the supine position, blood flow is uniform. Blood flow is greater to the lower lobes than to the upper lobes. The lower lobe vessels are 2-3x larger in diameter than the upper lobe vessels (gravity and alveolar pressure differences)

80
Q

What is the blood flow in Zone 1? The pressures driving blood flow?

A

Lowest blood flow; pressure of alveoli is more than arterial pressure is more than venous pressure

81
Q

What is the blood flow in Zone 2? The pressures driving blood flow?

A

Medium blood flow; arterial pressure is more than pressure of alveoli is more than venous blood pressure

82
Q

What is the blood flow in Zone 3? The pressures driving blood flow?

A

Highest blood flow; arterial pressure is more than venous pressure is more than pressure of alveoli

83
Q

How do left-sided heart disease affect pulmonary blood flow?

A

The normal distribution of blood flow becomes disturbed in disease states affecting the left side of the heart. These changes include increased vascular markings, redistribution of blood flow, pulmonary edema, and pleural effusions and will be reviewed later in the lecture.

84
Q

What is unique about pulmonary blood flow?

A

Low resistance, high compliance vascular bed; Changes in cardiac output as well as pleural/alveolar pressure affect pulmonary blood flow; The pulmonary circulation reacts differently to stimuli such as hypoxia than the systemic circulation; The pulmonary circulation is normally in a state of mild vasodilatation

85
Q

How does exercise affect pulmonary blood flow?

A

With exercise, cardiac output will increase; Pulmonary blood flow can increase up to 4-5x baseline levels; Increased blood flow is accommodated by both recruitment and vasodilatation (this prevents development of pulmonary edema); Net effect is a decrease in pulmonary vascular resistance

86
Q

How does exercise affect pulmonary pressure? CO? PVR?

A

PA pressure increases (so mean pressure increases), CO increases, PVR decreases

87
Q

How does altitude affect pulmonary pressure? CO? PVR?

A

PA pressure increases (so mean pressure increases), CO stays relatively constant, PVR increases

88
Q

What is high-altitude pulmonary edema?

A

A form of non-cardiogenic pulmonary edema related to an abnormal rise in pulmonary artery pressure and pulmonary vascular resistance in response to hypoxia; Related to altitude, exertion, speed of ascent, and individual susceptibility; Reversal is rapid by going to lower altitude or oxygen administration.

89
Q

What are the classifications of pulmonary hypertension?

A
  1. PAH; 2. pulmonary hypertension with left-sided heart disease; 3. pulmonary hypertension with lung diseases and/or hypoxia; 4. pulmonary hypertension due to chronic thrombotic and/or embolic disease; 5. miscellaneous
90
Q

What is pulmonary venous hypertension?

A

PAP mean of 25mmHg or greater at rest or 30mmHg or greater with exercise
AND
PCWP or LVED more than 15mmHg

91
Q

What is pulmonary arterial hypertension?

A 
PAP mean 25mmHg or greater at rest or 30mmHg or greater with exercise
AND
PCWP or LVEDP 15mmHg or less
PVRI 3 Wood units/m2 or greater
No left-sided heart disease
92
Q

What are some common left heart etiologies?

A

valvular heart disease, cardiomyopathies, ischemic heart disease, pericardial disease, tumors (myxoma), congenital

93
Q

How does left atrial pressure affect fluid exchange in the lung?

A

In the normal lung, fluid moves continuously outward from the vascular to the interstitial space. When left atrial pressure increases, hydrostatic pressure increases in the microcirculation and the rate of transvascular fluid filtration rises. When lung interstitial pressure exceeds pleural pressure, fluid moves across the visceral pleura, creating pleural effusions.

94
Q

What is adult respiratory distress syndrome?

A

Non-cardiogenic pulmonary edema can occur in critically ill patients when there is injury to the microvascular membrane resulting in a marked increase in the amount of fluid and protein leaving the vascular space

95
Q

What is Pulmonary Vascular Redistribution?

A

pulmonary blood flow is redirected into the upper lobes - Patient may be asymptomatic; PCW 12-18mmHg

96
Q

What is Pulmonary Interstitial Edema?

A

Get pulmonary interstitial edema, causing haziness of the vessels and Kerley B lines (linear markings at the periphery of the lower lung fields indicate interlobular edema); Patient will be short of breath; PCW more than 18mmHg

97
Q

What is Pulmonary Edema?

A

Get alveolar edema, patient in marked distress, with opacification of the air spaces, a butterfly pattern around the hila, and pleural effusions; The patient is cyanotic (blue), rales and wheezing, frothy pink sputum; PCW more than 25 mmHg

98
Q

How do the lungs handle acute vs chronic changes?

A

If elevation of pulmonary venous pressure is slowly progressive and chronic, higher pulmonary capillary wedge pressures can be accommodated with fewer clinical and radiological signs due to enhanced lymphatic drainage and the chronic changes to the vasculature previously described.

99
Q

What are symptoms of pulmonary congestion?

A

dyspnea, orthopnea, paroxysmal noctural dyspnea, hemoptysis, cough, fatigue

100
Q

What are symptoms of systemic congestion?

A

Edema, ascites, RUQ pain (liver congestion), central and peripheral cyanosis

101
Q

What is dyspnea?

A

One of the principle symptoms of cardiac and pulmonary disease; Described as an abnormally uncomfortable awareness of breathing; Cardiac dyspnea is most commonly associated with and caused by pulmonary congestion. The interstitial and alveolar edema stiffens the lung and stimulates respiration by activating “J” receptors in the lung; Cardiac dyspnea can also occur in the setting of a reduced cardiac output.

102
Q

What can sudden onset dyspnea be a symptom of?

A

pulmonary edema, pulmonary embolism, pneumothorax, asthma

103
Q

What can dyspnea on exertion mean?

A

heart failure, pregnancy (normal), pleural effusion from cancer

104
Q

What is BNP?

A

A vasoactive peptide that is released by myocardial stress. It is released from atrial cells when they are stretched. The actions of BNP oppose the physiologic abnormalities of heart failure. A useful test in the emergency room for patients presenting with dyspnea. BNP normal in patients with lung disease. Levels of BNP are correlated with severity of congestive heart failure and predict prognosis/mortality.

105
Q

What is orthopnea?

A

Dyspnea that develops in the recumbent position that is relieved by elevation of the head by pillows. In advanced heart failure, patients often sleep sitting up in a chair.

106
Q

What is the mechanism of orthopnea?

A

in the recumbent position, there is reduced pooling of blood in the lower extremities and abdomen and blood is displaced from the extrathoracic to the thoracic compartment (increased venous return). There is a further rise in baseline pulmonary venous and capillary pressures

107
Q

What is the differential diagnosis for orthopnea?

A

lung disease, ascites (any condition in which the vital capacity is low)

108
Q

What is Paroxysmal Nocturnal Dyspnea?

A

Usually occurs at night; Patient awakens suddenly, with a feeling of severe anxiety and suffocation, sits bolt upright, and gasps for breath; May be associated with wheezing (cardiac asthma); Distress may persist for 30 minutes even when patient sits up; patient may be afraid to go back to sleep

109
Q

What is the mechanism of Paroxysmal Nocturnal Dyspnea?

A

redistribution of blood flow from dependent portion of the body, reduced adrenergic support of left ventricular function during sleep, normal nocturnal depression of the respiratory center

110
Q

What can cough represent?

A

pulmonary venous hypertension; pulmonary edema; compression of the tracheobronchial tree by an aortic
aneurysm; When associated with pulmonary/cardiovascular disorders, ough is dry, irritating, spasmodic, and nocturnal; pulmonary edema may be associated with frothy, pink-tinged sputum

111
Q

What is hemoptysis?

A

Expectoration of blood; Due to escape of red cells into the alveoli from congested vessels; In cardiac disease, usually seen with chronic valve disease such as mitral stenosis

112
Q

What is the differential diagnosis for hemoptysis?

A

Differential diagnosis: lung disease, cancer, tuberculosis, pulmonary embolism, pulmonary AV fistula

113
Q

What are the consequences of Pulmonary Hypertension?

A

Whether the pulmonary hypertension is post-capillary or pre-capillary, the right ventricle which is used to working under low pressure is unable to work under higher pressures and the right ventricle will fail. The right ventricle
demonstrates a heightened sensitivity to afterload change

114
Q

What is cardiac edema?

A

associated with dyspnea; generally symmetrical; lower extremities to the abdominal wall; anasarca (total body edema)

115
Q

What is cyanosis?

A

Cyanosis is a bluish discoloration of the skin and mucous membranes due to an increased quantity of reduced hemoglobin

116
Q

What is central cyanosis?

A

due to decreased arterial oxygen saturation (right-to-left shunting or impaired pulmonary function)

117
Q

What is peripheral cyanosis?

A

cutaneous vasoconstriction due to low cardiac output or exposure to cold air

118
Q

What is clubbing?

A

Clubbing results from arterial hypoxemia and results from increased capillaries with increased blood flow through extensive arteriovenous aneurysms and an increase of connective tissue in the terminal phalanges of the fingers and toes. Seen in congenital heart disease and pulmonary disease.

119
Q

What is the most common cause of right heart failure?

A

Left heart failure

120
Q

What is heart failure?

A

Not a disease - a syndrome! An inability of the heart to pump blood at a sufficient rate to meet the metabolic demands of the body (e.g. oxygen and cell nutrients) at rest and during effort or to do so only if the cardiac filling pressures are abnormally high; A complex clinical syndrome characterized by abnormalities in cardiac function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention and a reduced longevity; A complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

121
Q

What is the prevalence of heart failure?

A

Prevalence: 1% ages 50–59, more than 10% over age 80; More deaths from HF than from all forms of cancer combined; Most common cause for hospitalization in age 65+

122
Q

What have been the models of heart failure?

A
  1. cardiorenal model (the 50s), 2. the hemodynamic model, 3. the neurohormonal model, 4. the genetic model
123
Q

How is heart failure classified?

A

right sided vs. left sided; acute vs. chronic; dilated vs. hypertrophic vs. restrictive; cardiac vs. non-cardiac; systolic vs. diastolic; compensated vs. decompensated; high vs. low output; forward vs. backward

124
Q

How does changing the preload affect the tension?

A

Increase preload, increase tension (Frank Starling effect)

125
Q

What is isotonic contraction?

A

same tension
shortening = stroke volume

126
Q

What is Pes?

A

Pressure at the end of systole - usually about 90% of systolic blood pressure

127
Q

How do you calculate arterial elastance?

A

Ea = Pes/Sv

Can be rewritten as Ea = HR*TPR

128
Q

What determines arterial elastance?

A

total peripheral resistance, heart rate

129
Q

What can occur during remodeling?

A

fibrosis, hypertrophy, apoptosis

130
Q

What are the steps of heart failure?

A
  1. myocardial injury; 2. fall in LV performance, increase in wall stress; 3. activation of RAS and SNS; 4. fibrosis, apoptosis, hypertrophy, myotoxicity, cellular changes; 5. remodeling of LV; 6. morbidity and mortality, arrhythmia, pump failure; NOTE: can also cause heart failure symptoms, peripheral vasoconstriction, sodium retention, hemodynamic alterations
131
Q

What are the symptoms of heart failure?

A

FACES - fatigue, activity alteration, chest congestion, edema, shortness of breath; may also present with difficulty sleeping and weight loss

132
Q

How does adrenergic pathway affect heart failure progression?

A

For alpha 1: 1. Increased CNS outflow; 2. increased vascular sympathetic activity; 3. alpha 1; 4. vasoconstricion; 5. disease progression; For a1, b2, and b1: 2. increased cardiac sympathetic activity; 3. adregnergics; 4. myocyte injury, myocyte hypertrophy, increased arrhythmias; can also cause sodium retention through a1/b1 and increased renal sympathetic activity

133
Q

What are the vasoconstricting neurohormones?

A

endothelin, aldosterone, angiotensin II, epinephrine

134
Q

What are the naturetic neurohormones?

A

ANP, BNP

135
Q

How does salt and water retention affect heart failure?

A

Initially augments preload, but ultimately leads to pulmonary congestion and anasarca

136
Q

How does vasoconstriction affect heart failure?

A

Initially maintains pressure for perfusion of vital organs (brain, heart), but ultimately exacerbates pump dysfunction, increases cardiac energy expenditure

137
Q

How does sympathetic stimulation affect heart failure?

A

Initially increases heart rate and ejection, but ultimately increases energy expenditure

138
Q

How does cytokine activation affect heart failure?

A

Initially causes vasodilatation, but ultimately causes skeletal muscle catabolism, deterioration of endothelial function, impaired contraction, LV remodeling, cachexia.

139
Q

How does hypertrophy affect heart failure?

A

Initially unloads individual muscle fibers, but ultimately leads to deterioration and death of cardiac cells: cardiomyopathy of overload

140
Q

How does increased collagen affect heart failure?

A

Initially may reduce dilatation, but ultimately impairs relaxation

141
Q

What is concentric vs eccentric remodeling?

A

Concentric: wall thickening, typically causes pressure overload, due to increase in afterload; eccentric: chamber enlargement, causes volume overload, due to increase in preload

142
Q

What are the 4 basic mechanisms of heart failure?

A
  1. Increased Blood Volume (Excessive Preload)
  2. Increased Resistant to Blood Flow (Excessive Afterload)
  3. Decreased contractility
  4. Decreased Filling
143
Q

What are the etiologies of increased blood volume?

A
  • Mitral Regurgitation
  • Aortic Regurgitation
  • Volume Overload
  • Left to Right Shunts
  • Chronic Kidney Disease
144
Q

What are the etiologies of increased afterload?

A
  • Aortic Stenosis
  • Aortic Coarctation
  • Hypertension
145
Q

What are the etiologies of decreased contractility?

A 
•Ischemic Cardiomyopathy
–Myocardial Infarction
–Myocardial Ischemia
•Myocarditis
•Toxins
–Anthracycline
–Alcohol
–Cocaine
146
Q

What are the etiologies of decreased filling?

A
  • Mitral Stenosis
  • Constriction
  • Restrictive Cardiomypoathy
  • Cardiac Tamponade
  • Hypertrophic Cardiomyopathy
  • Infiltrative Cardiomyopathy
147
Q

What is the pathophysiology of systolic heart failure? Diastolic?

A

Systolic: impaired contraction likely due to coronary artery disease (dilated ventricle); diastolic: Impaired filling likely due to hypertension (concentric, hypertrophic ventricle)

148
Q

What are the demographics of patients with systolic heart failure? Diastolic?

A

Systolic: all ages; diastolic: 60+

149
Q

What does systolic heart failure cause? Diastolic?

A

Systolic: decreased contractility, ejection fraction; diastolic: decreased capacitance

150
Q

Are any gallop murmurs heard in systolic heart failure? Diastolic?

A

Systolic: S3; diastolic: S4

151
Q

What is dilated heart failure?

A

Dilated left/both ventricle(s) with impaired contraction; may be due to: Ischemic, idiopathic, familial, viral, alcoholic, toxic, valvular

152
Q

What is hypertrophic heart failure?

A

Left and/or right ventricular hypertrophy; may be due to: Familial with autosomal dominant inheritance

153
Q

What is restrictive heart failure?

A

Restrictive filling and reduced diastolic filling of one/both ventricles, Normal/near normal systolic function; may be due to: Idiopathic, amyloidosis, endomyocardial fibrosis

154
Q

How is heart failure diagnosed?

A

physical exam, chest x-ray, EKG, echocardiogram, blood tests (Na, BUN, creatinine, BNP), exercise test, MRI, cardiac catheterization

155
Q

What is the NYHA Classification?

A

Way to classify heart failure. I (Mild): No limitation of physical activity, No undue fatigue, palpitation or dyspnea; II (Mild): Slight limitation of physical activity, Comfortable at rest, Less than ordinary activity results in fatigue, palpitation, or dyspnea; III (Moderate): Marked limitation of physical activity, Comfortable at rest, Less than ordinary activity results in fatigue, palpitation, or dyspnea; IV (Severe): Unable to carry out any physical activity without discomfort, Symptoms of cardiac insufficiency at rest, physical activity causes increased discomfort

156
Q

What is different about NYHA Classification and ACC/AHA Staging?

A

With NYHA, you can move within the classification - can go from IV to I; with ACC/AHA, once you have symptoms you can never go below Stage C again

157
Q

What is ACC/AHA Staging?

A

Staging of heart failure. Stage A: High risk for developing HF (asymptomatic; may be obesity, chemo, family hx, etc); Stage B: Asymptomatic LV dysfunction (something is wrong structurally but no symptoms); Stage C: Past or current symptoms of HF; Stage D: End-stage HF
Hunt, et

158
Q

What are the goals of heart failure treatment?

A
  1. Identification and correction of underlying condition causing heart failure.
  2. Elimination of acute precipitating cause of symptoms.
  3. Modulation of neurohormonal response to prevent progression of disease.
  4. Improve long term survival.
159
Q

What are the standard pharmacological treatments for heart failure?

A
  • ACE inhibitors
  • Angiotensin Receptor Blockers
  • Beta Blcokers
  • Diuretics
  • Aldosterone Antagonists
  • Statins
  • Vasodilators
  • Inotropes
160
Q

How do diuretics affect heart failure?

A

reduce fluid volume

161
Q

How do vasodilators affect heart failure?

A

decrease preload and afterload

162
Q

How do inotropes affect heart failure?

A

augment contractility

Cardio (9 decks)

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