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SchuMedTest > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the valves within the heart called & their location?

A

Tricuspid Valve (Right Side), and Mitral (Left Side), Aortic and Pulmonic

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2
Q

What prevents the mitral valve from prolapsing?

A

Papillary muscles, connected to the inside of the left ventricle via Chordae Tendineae

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3
Q

what does necrosis of the papillary muscles cause?

A

Mitral regurgitation. Backflow of blood into the right atrium

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4
Q

What is the pressure within the right ventricle?

A

25/10 mmHg (mean pressure is <10 mmHg - If higher considered pulmonary hypertension)

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5
Q

What is the pressure of the left side of the heart?

A

120/80 mmHg (if over ~130 or 140 mmHg or diastolic is over 90 mmHg - considered systemic hypertension)

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6
Q

Equation for Oxygen Delivery?

A

Delivery = Cardiac Output x Oxygen Content

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7
Q

What do Atrial OR Ventricular Septal Defects cause?

A

Allow blood to be shunted from one side to the other (Usually left to right flow - due to pressure; but may cause pulmonary hypertension and shunt reversal)

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8
Q

Name one mechanism in which a septal defect can form?

A

Post-septal heart attack - when there is a hole in the necrotic muscle separating the ventricles or atria.

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9
Q

What is the equation for Blood Pressure?

A

Pressure = Cardiac Output x Resistance (Low blood pressure may therefore be due to low resistance (vasodilation, ex: sepsis) or low flow state (heart failure or hypovolemia)

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10
Q

What is Shock?

A

Inadequate Tissue Perfusion

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11
Q

What is HYPOVOLEMIC Shock?

A

Decrease in circulating volume causing poor perfusion

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12
Q

What is Haemorrhagic Shock?

A

Hypovolemic shock caused by severe blood loss

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13
Q

What is Cardiogenic Shock?

A

Failure of the heart to pump enough blood to organs for perfusion

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14
Q

What is Vasodilation’s effect on Capacitance?

A

Increases capacitance, which results in hypovolemia

VasoCONSTRICTION decreases capacitance (which is used as a compensatory mechanism in the event of hemorrhage or low flow state)

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15
Q

What are the Clinical findings of someone with vasoconstriction?

A

Decreased capillary refill with peripheral cyanosis and hypothermia.

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16
Q

What are the Cardiac Cycle Steps?

A 
Step 1: Atrial Systole (P Wave)
Step 2: Isovolumetric Contraction (QRS Wave)
Step 3: Rapid Ejection
Step 4: Reduced Ejection (T Wave)
Step 5: Isovolumetric Relaxation
Step 6: Rapid Filling
Step 7: Reduced Filling
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17
Q

What is Atrial Fibrillation?

A

Heart Rhythm where atria do not have organized contraction (Irregularly Irregular)

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18
Q

What is The ‘A Wave’ for Central Venous Pressure?

A

Atrial Contraction; Correlates with P wave on ECG

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19
Q

What is the ‘C Wave’ for Central Venous Pressure?

A

Early Ventricular/Isometric contraction - caused by bulging of the tricuspid valve into the right atrium (Correlates with QRS complex)

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20
Q

What is the ‘V Wave’ for Central Venous Pressure?

A

Atrial pressure before the AV valve opens - during atrial filling (correlates with T wave on ECG)

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21
Q

What does the Jugular Venous Pressure clinically show?

A

Right Atrial Pressure

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22
Q

What are the Normal Heart Sounds?

A

S1: Closure of the Mitral and Tricuspid Valves
S2: Closure of the aortic and pulmonary Valves

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23
Q

What are the Extra Heart Sounds?

A

S3: Rapid filling of ventricular diastole
S4: Atrial filling phase of diastole

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24
Q

What is Systolic Heart Failure?

A

Dilated Ventricle - causing increased end-diastolic volume and end-diastolic pressure
Decreased stroke volume and ejection fraction

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25
Q

What are the symptoms of Systolic Heart Failure?

A

Dyspnea (Shortness of breath) on exertion or lying down
Fatigue and weakness
Edema (Swelling) in legs, ankles, and feet
Rapid or irregular heartbeat
Reduced ability to exercise
Persistent cough or wheezing with white or pink blood-tinged phlegm

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26
Q

What is Pulmonary Edema?

A

Increased interstitial and alveolar fluid in the lungs - causing stiffer lungs with hypoxia (decreased oxygen perfusion) and chest infiltrates on X-ray

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27
Q

What is Diastolic Failure?

A

The ventricle is stiff or non-compliant - causing increased end-diastolic pressure for the same end-diastolic volumes

The defect in filling causes stroke volume to decreased (regardless of maintained ejection fraction)

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28
Q

Where are the pacemaker cells found and what do they do?

A

Within the Sinoatrial (SA) Node - they set the baseline heart rate

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29
Q

What happens when the Parasympathetic Nervous System Impact is stopped to the Heart (+ What Nerve)?

A

Vagus nerve. In absence of the PSNS stimulation (i.e., Heart Transplant) the HR is closer to the inherent automaticity of the SA node (~100 BPM)

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30
Q

How does the Sympathetic Nervous System affect Heart Rate?

A

Increases HR from resting levels - i.e., through the use of Catecholamines (from the Adrenal gland)

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31
Q

What is the impact of Heart Rate on Cardiac Perfusion?

A

Increased heart rate decreases perfusion to the left ventricle

Perfusion to the left ventricle through the coronary artery only occurs during diastole as pressure is too high during systol - causes Demand Ischemia (When Heart Rate is too High and Blood Pressure is too low)

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32
Q

What is Demand Ischemia?

A

When Heart Rate is too high and blood pressure is too low - causing poor perfusion to the tissue

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33
Q

Impact of Age on Heart Rate?

A

Decreased maximal heart rate
Aorta becomes stiffer
The ventricles are less compliant
Decreased maximal oxygen consumption

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34
Q

What is Starling’s Law?

A

Contractile energy is related to the length of a muscle fibre

There is an optimal length - beyond the optimal length, there is no increase in tension produced and the heart may enter decompensated (deterioration) heart failure

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35
Q

Frank-Starling Curve (Normal heart vs. Failing Heart)?

A

Normal: Stroke volume can reach normal levels with a response to increasing preload

Failing Heart: Stroke volume is diminished and does not respond well to an increasing preload

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36
Q

What is Law of Laplace?

A

Tension = (Pressure x Radius)/(Wall Thickness x 2)

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37
Q

What is Contractility (Inotropy)?

A

Ability to shorten in response to stimulus (intrinsic property of muscle cells)

Independent of preload and afterload

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38
Q

How does the Sympathetic Nervous System affect Contractility?

A

increases with SNS activiation

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39
Q

What is The Compensatory Responses to Blood Loss? (Decreased Pre-load)

A
  • Maximizing Cardiac Output
  • Increases Contractility
  • Vasoconstriction (reduced capacitance)
  • Redistributing Cardiac output to perfuse essential organs (Brains, Heart, Lungs)
  • Respiratory rate increases
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40
Q

What are the Acute Compensatory Responses to Increased Afterload?

A
  • Ventricular dilation (increase in preload (EDV) can increase contractility
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41
Q

What are the Chronic Compensatory Responses to Increased Afterload?

A
  • Heart undergoes hypertrophy (concentric hypertrophy)
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42
Q

Types of Hypertrophy?

A
  • Physiological (Athlete’s heart) - Tend to have lower HR, reversible and not pathological
  • Concentric - Pressure overload
  • Eccentric - Volume overload
  • Hypertrophic cardiomyopathy
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43
Q

Is Potassium safe for the heart?

A

No, potassium makes membrane potential less negative, increasing excitability (Arrhythmias can occur)

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44
Q

Cardiac vs. Skeletal Cell Action Potential?

A

Cardiac - Plateau that is secondary to slow voltage-gated channels (which carry calcium)

Both have fast voltage-gated channels

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45
Q

What is the resting membrane potential?

A

-55 to 60 mV

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46
Q

When does membrane potential cause voltage-gated sodium channels to open (action potential)?

A

When threshold of -40 mV is hit

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47
Q

What is the path of the Cardiac Conduction System?

A
  • Generated by SA node
  • Atrioventricular (AV) Node via atrial internodal pathway fibres (Should be within one direction)
  • Delayed before entering Purkinje conductive system
  • Left and Right bundle branches
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48
Q

What is the RAAS System stand for?

A

Renin-Angiotensin-Aldosterone System

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49
Q

What is the role of Renin? and What causes it to be released?

A

From juxtaglomerular cells - converts angiotensinogen to angiotensin I

Causes of Release:

  • Increased sympathetic activity (Beta 1 Receptor)
  • Low blood pressure
  • Decreased Blood Volume
  • Decreased sodium reabsorption in the Kidney
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50
Q

What is the function of ACE?

A

Converts angiotensin I to angiotensin II

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51
Q

What is the function of Angiotensin II?

A
  • Aldosterone secretion
  • Vasoconstriction
  • Hypertrophy
  • Vasoconstriction of arterioles in the kidney
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52
Q

RAAS and Heart Failure?

A

RAAS is activated in heart failure

  • initially for compensatory (vasoconstriction maintains blood pressure and salt/water retention maintains ventricular preload)
  • Eventually becomes decompensatory
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53
Q

What are Angiotensin Converting Enzyme (ACE) Inhibitors?

A

(-pril) Drugs
Mechanism of Action:
- Inhibition of ACE & blocking the synthesis of angiotensin II

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54
Q

What are the effects of ACE inhibitors?

A
  • Dilates arteries and veins (decreased blood pressure)
  • Increases bradykinin formation (contributes to vasodilation)
  • Inhibition of myocardial remodelling
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55
Q

What are the indications for ACE Inhibitors?

A
  • Hypertension (especially with diabetes)
  • Heart failure with a decreased ejection fraction
  • Kidney protection (nephropathy, from diabetes)
    - note: Angiotensin II contributes to proteinuria
  • Post-myocardial infarct (acute and chronic)
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56
Q

What are some adverse effects of ACE Inhibitors?

A
  • Cough (Common)
    • it may be due to bradykinin; maybe an indication to
      change to ARB
  • Hypotension
  • Worsening Renal Function (usually reversible)
  • Hyperkalemia
  • Angioedema (Swelling of tongue and airway - RARE)
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57
Q

What are the Contraindications of ACE inhibitors?

A
  • Pregnancy
  • Hyperkalemia
  • Severe renal dysfunction
  • Hypotension
  • Allergy to ACEi
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58
Q

What are Angiotensin Receptor Blockers (ARBs)?

A

(-Sartan)
Mechanism of Action: Block AT-II receptors (specifically on the heart and blood vessels)

  • Does not increase bradykinin
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59
Q

What are the effects of ARBs?

A
  • Vasodilation
  • Downregulation of SNS
  • Renal excretion of Salt and water
  • Inhibit myocardial remodeling and fibrosis
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60
Q

What are the indications of ARBs?

A

(Similar to ACEi - but ACEi are usually first-line and ARBs are reserved for those who can not tolerate ACEi)

  • Hypertension (especially with diabetes)
  • Heart Failure with a decreased ejection fraction
  • Kidney protection (nephropathy, from diabetes)
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61
Q

What are the Adverse Effects of ARBs?

A

Similar to ACEi (But no cough and Angioedema is more rare)

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62
Q

What are the Contraindications of ARBs?

A
  • Pregnancy

- Concomitant use of ACEi (no additional benefit)

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63
Q

What are Aldosterone Antagonists (Spironolactone)?

A

Mechanism of Action: Antagonist of Aldosterone

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64
Q

What are the effects of Aldosterone Antagonists?

A
  • Myocardial fibrosis
  • Vasoconstriction
  • Release of NE
  • Increase of Na+ and water retention
  • Potassium excretion
    - NOTE: Considered a K+ sparing diuretic (but the
    actual diuretic effect is weak.
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65
Q

What are the indications for Aldosterone Antagonists?

A
  • Heart Failure
  • Post-myocardial infarction with ejection fraction <40%
  • Patients with hypokalemia due to diuretic effect
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66
Q

What are the adverse effects of Aldosterone Antagonists?

A
  • Hyperkalemia (More frequent with Renal Dysfunction, ACEi use, NSAID use)
  • Gynecomastia (due to off-target antiandrogenic effect)
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67
Q

What are the contraindications of Aldosterone Antagonists?

A
  • Pre-existing hyperkalemia

- Renal Dysfunction/renal failure (relative contraindication/not absolute)

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68
Q

What are Digitalis (Digoxin)?

A

Mechanism of Action:
1. Inhibition of Na+ K+ ATPase (Heart Failure Indication)
- Increased Ca2+ in the cell - causing an increase
myocardial contractility
2. Indirect Vagal Effect (Atrial Fibrillation Indication)
- Increased relative parasympathetic effect on the heart
decreased intrinsic rate of SA node and the conduction
velocity through the AV node.

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69
Q

What are the indication of Digoxin?

A
  • Systolic heart failure (low dose chronic medication for morbidity benefit - NO mortality benefit)
  • Chronic Atrial Fibrillation (with heart failure)
    - Not useful for paroxysmal atrial fibrillation
    - Not effective in patients with high sympathetic drive
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70
Q

What are the adverse effects of Digoxin?

A
  • Proarrhytmic (Supraventricular Tachycardia, ventricular tachycardia, bradycardia)
  • Yellow-green visual changes
  • Nausea.Vomiting
  • Confusion
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71
Q

What are the contraindications of Digoxin?

A
  • Hypokalemia/hypercalcemia (predispose to toxicity)
  • Caution with decreased renal function
  • AV-block (will worsen)
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72
Q

What are the two types of Nitrodilators?

A
  • Organic Nitrates (work by generating nitric oxide - causing vasodilation)
  • Sodium Nitroprusside (releases nitric oxide)
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73
Q

What is the Mechanism of Action of Nitrodilators?

A
  • Converted to nitric oxide, which activates G-cyclase
    - cGMP: produces vasodilation by lowering intracellular
    calcium
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74
Q

What is the effect of Phosphodiesterase-5 (PDE-5) inhibitors?

A
  • used to treat erectile dysfunction
  • blocks the metabolism of cGMP - thereby causing vasodilation
  • Combination of PDE-5 and Nitrodilators causes rapid, profound hypotension
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75
Q

What are the effects of Nitrodilators?

A
  • Vasodilators

- Myocardial Oxygen Demand Decreased

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76
Q

What are the indications of Nitrodilators?

A
  • Angina
    • (Including prinzmetal’s Angina - due to coronary
      spasm)
    • (Myocardial infarction with ongoing ischemic pain)
    • (Acute pulmonary edema precipitated by myocardial
      ischemia)
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77
Q

How can nitrodilators be administered?

A
  • Nitroglycerin (IV, Sublingual, Transdermal)

- Isosorbide Dinitrate (Oral or Sublingual)

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78
Q

What are the adverse effects of Nitrodilators?

A
  • Headache
  • Decreased blood pressure
  • Withdrawal syndromes: rebound angina or coronary spasms
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79
Q

What are the contraindications of Nitrodilators?

A
  • Hypotension

- Recent ingestion of PDE-5 inhibitor (for erectile dysfunction)

80
Q

What are the two classifications of Calcium Channel Blockers (CCBs)?

A
  • Dihydropyridines (-pine): Vascular Selectivity
    - i.e., Nifedipine, Amlodipine
  • Non-dihydropyridines: Cardiac selectivity with minor vascular effect
    - i.e., Verapamil, Diltiazem
81
Q

What do Non-dihydropyridines act on?

A
  • They act on the SA and AV node to decrease automaticity and delay conduction
  • They also have vasodilator effect
  • Decrease myocardial contractility
82
Q

What is the mechanism of Action for CCBs?

A

Inhibition of L-type voltage-sensitive calcium channels (preventing calcium entry into the cell)

83
Q

What are the indications of Calcium Channel Blockers (CCBs)?

A
  • Hypertension (Mostly DHPs)
  • Angina (Second-line therapy, following beta-blockers)
    • Unless Prinzmetal’s angina (due to coronary spasms -
      first line)
  • Arrhythmias (Non-DHPs, because of decreased AV node conduction)
84
Q

What are the Contraindications of Calcium Channel Blockers (CCBs)?

A
  • Hypotension
  • Flushing, headache (vasodilator effect, especially with DHPs)
  • Bradycardia
  • Heart block
  • Decreased myocardial contractility
  • worsening heart failure with non-DHPs (Verapamil/Diltiazem)
85
Q

What is Prinzmetal’s Angina?

A
  • Caused by spasm in the hearts arteries that temporarily reduces blood flow
86
Q

What is the mechanism of action of Hydralazine?

A
  • Arterial Vasodilator
    • Results in increased cardiac output due to a decrease
      in systemic pressure
87
Q

What are the Clinical Indications of Hydralazine?

A
  • Hypertension (Oral or IV)
    • More effective antihypertensive agents are now
      available
    • For patients with heart failure who can’t take ACEi or
      ARBs
88
Q

What is the Mechanism of Action for beta-Adrenergic Receptor Blocking Agents (‘Beta-Blockers’)?

A

(-lol)

  • Blockage of Adrenergic Beta-1 Receptor
    • Causes:
      - Decreased heart rate (negative chronotropy)
      - Decreased contractility (negative inotropism)
      - Slowed conduction (negative dromotropy)
  • Blockage of Beta-2 Receptor
    • Causes:
      - Bronchospasm
89
Q

What are the classifications of Beta-Blockers? (-lol)

A
  • Non-selective (Both beta-1 and beta-2 receptors)
    - i.e., Propranolol
  • Cardioselective (Blocks beta-1 and beta-2 receptors)
    - i.e., Metoprolol
    - Used as anti-hypertensive, post-MI, and heart failure
  • Third Generation (Mixed blockade of alpha-receptors and non-selective beta-receptor blockade)
    - i.e., Carvedilol
    - Vasodilator actions in addition to beta-blocker effects
90
Q

What are the clinical indications of Beta-Blockers?

A
  • Hypertension (not first-line therapy)
  • Post-myocardial Infarction (once clinically stable)
    - Beta-blockers are contraindicated in acute MI
  • Angina (Improves oxygen supply/demand)
  • Heart Failure (Improves mortality; although counterintuitive)
91
Q

What are the Adverse Effects of Beta-Blockers?

A
  • Fatigue
  • Limited exercise capacity
  • Weight gain
  • Erectile dysfunction
  • Bronchospasm
  • Bradycardia
  • Worsening of Heart Failure
  • Masking of the symptoms of hypoglycemia
  • Nightmares/Depression
  • Rebound tachycardia/hypertension/ischemia (with abrupt discontinuation)
92
Q

What are the Contraindications of Beta-Blockers?

A
  • Severe bradycardia
  • Cardiogenic shock
  • Untreated heart failure
  • Severe asthma/bronchospasm
  • Severe [eripheral vascular disease with worsening claudication/rest pain
93
Q

What causes the ‘P wave’ on an ECG?

A

Caused by atrial action potential (delay between P and Q is caused by AV node)

94
Q

What can cause an abnormal ‘P wave’?

A

Amplitude high or long in time if atria are enlarged

- Right atrium enlargement: Tall P wave in inferior leads
- Left atrium enlargement: Large negative component in V1
95
Q

What does a lack of ‘P wave’ Indicate?

A

indicates atrial fibrillation

96
Q

What does the P-R Interval indicate?

A

Reflects depolarization (but mostly conduction through the AV node)

97
Q

What does an elongated P-R interval indicate?

A

elongated due to increased delay in AV node (may not be pathologic)

98
Q

What does an absent or short PR interval (with rapid heart rate) indicate?

A

Wolff-Parkinson-White (WPW) Syndrome

99
Q

What is Wolff-Parkinson-White (WPW) Syndrome? (Rare)

A
  • An extra signaling pathway between the atria and ventricles (congenital) which causes a fast heart beat
100
Q

What creates the QRS Complex?

A

Caused by ventricular action potential through the Purkinje system.

101
Q

What causes an widened QRS complex?

A

Purkinje system conduction is slowed

- May indicate bundle branch block

102
Q

What causes a large QRS complex indicate?

A

Indicates that there is a problem but isn’t specific to a particular pathology

103
Q

What causes a small QRS complex?

A

Due to the dampening of signals by pericardial effusion

104
Q

What causes the ‘Q Wave’?

A

Caused by septal depolarization (should be a negative wave)

105
Q

What does an excessively large Q wave (~1/3 height of R wave) indicate?

A

Indicates prior damage to the muscle due to MI

106
Q

What does a large Q wave depression in lead I, II, and aVF indicate?

A

Right coronary artery supply is impacted

107
Q

What does a large Q wave depression in lead I, aVL, V5 and V6 indicate?

A

Circumflex and sometimes LAD artery supplies are impacted

108
Q

What does a large Q wave depression in lead V1, V2, +/- V3 and V4 indicate?

A

LAD artery supplies are effected

- V4 (indicates more septal involvement)

109
Q

What causes the ‘R Wave’?

A

Caused by ventricular depolarization (should be a positive wave)

110
Q

What does a too large or wrong axis R wave indicate?

A

May indicate hypertrophy

111
Q

What does a too small ‘R wave’ indicate?

A

May indicate ventricular damage

112
Q

What causes the ‘S Wave’?

A

caused by remaining ventricular depolarization (moving away from the leads)

113
Q

What causes the ST Segment of the ECG?

A

Caused by ventricular mechanical systole (no conduction)

- Flat wave that should be at baseline

114
Q

What does a ST depression indicate?

A

May indicate Ischemia

115
Q

What are the symptoms you could see with a ST depression?

A
  • Heaviness
  • Tightness
  • Pressure (angina)
116
Q

What may a ST elevation indicate?

A

May indicate:

  • myocardial infarction
  • pericarditis
117
Q

What does ST elevation related to Infarction look like?

A

leads in specific location of infarct are elevated

- Abnormalities are more likely to be irreversible

118
Q

What are the ECG findings for Pericarditis?

A

All ST segments are elevated

119
Q

What causes the ‘T Wave’?

A

Caused by repolarization of the ventricles (should be sloped but not spiked)

  • Due to repolarization conducting through muscle, not conducting system (no T-wave for atrium)
120
Q

What does an Inverted T wave indicate?

A

Seen in myocardial infarction and ischemia (can change over time)

121
Q

What does a late or prolonged T wave indicate?

A

caused by delayed repolarization

122
Q

What does the QT interval measure?

A

measures the complete repolarization phase

- varies slightly between males (<440 ms) and females (<460ms)

123
Q

What does a too long QT interval indicate?

A

if too long, depolarization may occur before repolarization is complete

124
Q

What are the signs of Infarction?

A

ST elevation
T wave inversion (may not actually be pathological)
Increased Q wave

125
Q

What are the signs of Ischemia?

A

ST Depression
- If seen with ST elevation; elevation is more important
- ST depression may just be an artifact of ST
elevation
T Wave inversion (may not be pathological)

126
Q

What the ECG Changes of Right Atrial Hypertrophy?

A

Tall P wave in leads II, III, aVF

127
Q

What the ECG Changes of Left Atrium Hypertrophy?

A

Long notched or biphasic P wave in leads I, II, or V1

128
Q

What the ECG Changes of left ventricular Hypertrophy?

A

Large S wave in V1 and Large R wave in V6

129
Q

What the ECG Changes of Right Ventricular Hypertrophy?

A

Large R wave in V1, V2, and V3 (Usually, R wave is only larger than S wave in V4, V5, and V6)

130
Q

What happens to conduction when a bundle branch is blocked?

A

The conduction must go through the muscle instead

which is much slower - Widened QRS

131
Q

What is the equation for resistance in systemic circulation?

A

1/R (Total) = 1/R1 + 1/R2 + 1/R3

In parallel

132
Q

What is the resistance between heart and lungs?

A

In series

R(Total) = R1 + R2+ R3

133
Q

What are the types of control on the heart rate?

A

Neural control: autonomic nervous system

Local control: metabolites, hormones

134
Q

What is happens to blood pressure within Arterioles?

A

BP drops off in the arterioles

135
Q

What is the pressure within the Venous system?

A

The blood pressure is very low

136
Q

Where is the volume largest in the circulatory system?

A

Highest in systemic veins and venules

137
Q

What is the equation for blood flow?

A

(Pressure 1 - Pressure 2)/ Resistance

138
Q

What is Hematocrit?

A

RBC percentage of total blood volume
(RBCs are most of the cells while WBC and platelets make up a minority of the content)

Normal: 40-45% for women and men respectively

139
Q

What is the impact of hematocrit on blood velocity?

A

Directly proportional

If 60% hematocrit, the viscosity will cause flow and pressure disturbances

140
Q

What is the method for acute regulation of blood pressure?

A

Autonomic Nervous System

 - Baroreceptors
 - Effector Nerves
141
Q

What are Baroreceptors?

A

Cells that are sensitive to stretch

142
Q

What are the nerves involved in the autonomic control of Blood Pressure?

A
  • Glossopharyngeal Nerve (PNS): From the carotid body baroreceptors
  • Vagus Nerve (PNS): From the aortic baroreceptors
143
Q

What are the chronic methods to control blood pressure?

A
  • Autonomic nervous system still plays a role
  • RAAS
  • Anti-Diuretic Hormone (ADH; Vasopressin)
  • Atrial Natriuretic Peptide (ANP)
  • Local control of Vascular Resistance
144
Q

How does Anti-diuretic Peptide Hormone (ADH; Vasopressin) work?

A

Acts to:

  • Increase permeability of distal tubules and collecting ducts to water (increased water reabsorption in kidney)
  • Stimulates thirst in the hypothalamus
145
Q

What are the factors that affect Diffusion to Tissues?

A
  • Concentration gradient
  • Surface area of diffusion
  • Thickness of Membrane
  • Permeability of Vessel
146
Q

Does Blood Flow impact the Concentration Gradient?

A

Yes. Increased flow results in decreased efficiency of exchange

However,

because blood concentration is higher - diffusion rate is overall greater, and exchange is more powerful

147
Q

What is the Fick Principle?

A

Uptake = flow x ([arterial O2] - [Venous O2])

148
Q

What type of molecules are restricted from freely flowing into cells?

A 
Polar Molecules
Large Molecules (i.e., Ions, Glucose, and macromolecules, etc.)
149
Q

What are the factors affecting Blood Flow?

A
  • Perfusion Pressure
  • Geometry of blood vessels (Vessel length & Radius)
  • Blood Viscosity (hematocrit, RBC deformability)
150
Q

How does Red Blood Cell (RBC) deformity impact fluidity?

A

allows passage through capillaries

151
Q

What organ is responsable for the removal of RBCs?

A

Spleen

152
Q

How does the spleen repair older RBCs?

A

RBCs must squeeze through small holes to return to circulation

Bits of denatured proteins that form lumps can be removed in this process

153
Q

How does the spleen remove RBCs from circulation?

A

RBCs trapped in spleen can be removed by macrophages

154
Q

What is Hereditary Spherocytosis?

A

RBCs have lower membrane deformity than normal, and are readily trapped by the spleen - resulting in Anemia.

155
Q

What is Sickle Cell Disease?

A

Distorting of RBCs, causing them to become rigid.

The deformity occurs because Hemoglobin aggregates when O2 is decreased

156
Q

What is a Hydrostatic pressure gradient?

A

Pressure which promotes overall filtration

157
Q

What is Edema?

A

Excessive accumulation of fluid in the tissue (as a result of lymphatic drainage being less than net fluid filtration)
- due to imbalance of starling forces (altered “K - Capillary Filtration Coefficient “ or insufficient lymphatic drainage)

158
Q

Causes of Aortic Stenosis?

A
  • Congenital Bicuspid Valve (Present around age 50 - 60)
  • Age-related calcific (aka degeneration AS - Most common)
  • Rheumatic heart disease
159
Q

How does aortic stenosis affect blood flow?

A

causes obstruction to the ejection of blood from the left ventricle (pressure gradient is increased)

160
Q

How does the Left Ventricle compensate to increased pressure from Aortic Stenosis?

A

concentric hypertrophy (minimizing wall tension and left ventricular work - Laplace Law for Afterload)

161
Q

What are the physical exam findings for Aortic Stenosis?

A
  • Murmur (systolic crescendo/decrescendo murmur - radiating to the neck; louder as it worsens)
  • Pulse with a long, slow upstroke (due to increased ejection time)
162
Q

What investigations will you order for Aortic Stenosis?

A
  • ECG (for left ventricular hypertrophy)
  • Echocardiogram - diagnostic (shows hypertrophy, the pressure gradient across the valve)
  • Cardiac Catheterization - investigate coronary arteries to decide if the patient needs coronary artery bypass.
163
Q

What are the clinical features of the Latent period of Aortic Stenosis?

A

Aortic (asymptomatic) period

AS is gradually progressive, may be asymptomatic for years

164
Q

what are the symptoms of Aortic Stenosis?

A
  • Angina Pectoris (when patients have co-existing coronary artery disease - contributes to myocardial ischemia)
  • Syncope or presyncope (At rest - due mostly t arrhythmias; Exercise - due to inability of cardiac output)
  • Congestive heart failure (Dyspnea with exertion - due (1) to limited ability to increase stroke volume; (2) pulmonary edema
  • Other:
    • Sudden death (due to arrhythmia or sudden vasodilation with hypotension)
    • Endocarditis
165
Q

What is the Management for Aortic Stenosis?

A
  • Surgical replacement of the valve
  • Other (when surgery not tolerated)
    • Valvotomy (stretch stenotic valve with ballons - HIGH
      rate of complications and recurrence)
    • Replace valve with a transvalvular approach
      (percutaneously)
166
Q

What indications for surgical replacement of Stenotic Aortic Valve?

A

when symptoms develop, can be either (1) bioprosthetic or (2) mechanical valve

167
Q

What is the cause of Mitral Stenosis?

A

Almost always due to rheumatic heart disease

168
Q

What does Mitral Stenosis cause?

A

Causes obstruction to flow across the mitral valve - with pressure increased in the left atrium.

169
Q

What happens to the heart with Mitral Stenosis?

A

Left atrium stretches and dilates, Pulmonary Hypertension, Pulmonary Edema, compensatory hypertrophy of the right ventricle

(Atrial Fibrillation is common - scarring and fibrosis of atria from Rheumatic inflammation)

(Thrombi can also develop and embolize - causing stroke)

170
Q

What happens to the Left Ventricle (LV) during mitral stenosis?

A

End diastolic volume may be low (therefore, cardiac output may be low)

171
Q

What are symptoms of Mitral Stenosis?

A 
Dyspnea
Pulmonary Edema
Hemoptysis
Exercise intolerance
Atrial fibrillation
Thromboembolism
Signs of right heart failure (diastolic/preserved ejection-fraction)
172
Q

What are some medical therapies for Mitral Stenosis?

A

Diuretics (for pulmonary edema)

Anticoagulation (for atrial fibrillation and risk of thrombus or previous embolic event)

Monitor for recurrent rheumatic fever - which leads to progression of rheumatic heart disease

173
Q

What are the surgical management options for Mitral Stenosis?

A

Valvuloplasty (Percutaneously opening stenotic valve with balloon)

Surgical Valve repair/replacement

(Should be considered when patients develop symptoms OR if there is moderate to severe (1) Mitral Stenosis and (2) pulmonary hypertension (even with minimal symptoms)

174
Q

At what point of the cardiac cycle does Aortic Regurgitation occur?

A

Occurs during diastole

175
Q

What causes Acute Aortic Regurgitation?

A

Infective Endocarditis

Aortic Dissection or Trauma

176
Q

What does Aortic Regurgitation Cause?

A

Sudden increase in LV preload

Increase in after load (due to distention with regurgitant blood volume)

Can lead to pulmonary edema

Note - Left ventricular size is normal and is non-compliant

Note - Forward stroke volume decreases; cardiac output is matained with compensatory tachycardia
(this is not well tolerated - results in cardiogenic shock and pulmonary edema)

177
Q

What determines the amount of regurgitant blood flow?

A

Size of regurgitant orifice

Diastolic pressure gradient across the aortic valve

Duration of Diastole

178
Q

What causes chronic Aortic regurgitation?

A

Rheumatic fever

Endocarditis

Congenital Abnormality of Valve

Connective tissue disorder

179
Q

What does Chronic Aortic Regurgitation Present with?

A

Volume and pressure overload to the left ventricle

No isovolumetric relaxation phase as the ventricle fills early from the aorta

Decreased Aortic diastolic pressure (= increase in pulse pressure) - CAUSES A DECREASE IN CORONARY PERFUSION

180
Q

What are the symptoms of Chronic Aortic Regurgitation?

A

Symptoms of Congestive Heart Failure will develop (as LV dilates and decompensates)

Pulse pressure is increased, resulting in the pulse feeling “bounding”

181
Q

What causes Mitral Regurgitation?

A

Mitral Valve Prolapse (Most common) - Myxomatous Degenration (Connective tissue disorder - resulting in thickening of mitral valve leaflets)

Rheumatic heart Disease (Acute Rheumatic Fever - hypersensitivitiy reaction following Group A strep Pharyngitis; self-antigens of heart & anti-M protein antibodies)
Note - Initial attack usually in childhood, results: Pancarditis (Myocarditis, pericarditis, endocarditis)

Infective Endocarditis

Ruptured Papillary Muscles

Functional or Secondary Mitral Regurgitation due to Left Ventricular Dilation (Ischemic)

182
Q

What are the Acute causes of Mitral Regurgitation?

A

Endocarditis

Ruptured Papillary Muscles

183
Q

What are the chronic (Either Ischemic or Non-ischemic) causes of Mitral Regurgitation?

A

Ischemic: Functional Mitral Regurgitation

Non-ischemic: Rheumatic, Degenerative, Endocarditis

184
Q

What are the changes to the heart seen with Acute Mitral Regurgitation?

A

Blood can be ejected either into systemic circulation or back into the left atrium = decreased afterload

Increased LV preload (from the added regurgitated blood in the Left Atrium re-entering the Left Ventricle)

Stroke volume is decreased (as a portion goes into the Left Atrium)

Pulmonary Hypertension

Severe Pulmonary Edema

185
Q

How does the Heart compensate for Mitral Regurgitation?

A

Eccentric Hypertrophy develops

They are prone to atrial fibrillation

186
Q

Why does Eccentric Hypertrophy develop in the setting of Mitral Regurgitation?

A

Increased End Diastolic Volume (causes wall thickening to return wall tension)

187
Q

What is Chronic Decompensated Mitral Regurgitation (Congestive Heart Failure)?

A

Forward flow and stroke volume are usually maintained (Via Frank-starling mechanism: Increased Preload = increased stretch and therefore contraction)

When the ventricle fails overtime - systolic dysfunction develops with decrease in cardiac output and symptoms of heart failure

188
Q

When is Mitral Regurgitation considered Decompensated?

A

When Ejection fraction is below 60%

Increasing ventricle size measured by echo

Estimation of effective regugitant orifice (ERO) and volume overload (regurgitant volume)

NOTE - Repair or replacement of the valve when the left ventricle has developed systolic failure will not be well tolerated (as this increases the afterload)

189
Q

What causes functional mitral regurgitation?

A

Normal mitral valve but left ventricular dilation results in stretching/distortion of the mitral valve annulus

OR

Left ventricular remodeling can displace papillary Muscles

190
Q

What are the symptoms for Mitral Regurgitation?

A

Fatigue

shortness of breath

Decreased exercise tolerance

Note - they develop after the left ventricle has dilated and Ejection fraction has decreased (optimal window for surgical management has passed)

191
Q

What are the medical therapies for Mitral Regurgitation?

A

There are no therapies for chronic Mitral Regurgitation to delay progression.

Anticoagulation for patients with atrial fibrillation should be considered

192
Q

What are the surgical treatment for Mitral Regurgitation?

A

Mitral Repair (to preserve Mitral Annulus & Papillary Muscles - which are important for LV systole)

Mitral Replacement (Bioprosthetic, Mechanical)

193
Q

What happens if you choose Bioprosthetic mitral valve?

A

Long-term anticoagulation is not required; however, valve will deteriorate overtime and require replacement after a number of years

194
Q

What happens if you choose a mechanical mitral valve?

A

Long-term anticoagulation is required to prevent thrombus formation/embolism (durable and will function for many years)

195
Q

What factors must you consider when determining the mitral valve replacement type?

A

Age, Thrombus Risk Factors, and Patient preferences

196
Q

Page 64

A

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SchuMedTest (9 decks)

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