Cardiology Flashcards
What are the valves within the heart called & their location?
Tricuspid Valve (Right Side), and Mitral (Left Side), Aortic and Pulmonic
What prevents the mitral valve from prolapsing?
Papillary muscles, connected to the inside of the left ventricle via Chordae Tendineae
what does necrosis of the papillary muscles cause?
Mitral regurgitation. Backflow of blood into the right atrium
What is the pressure within the right ventricle?
25/10 mmHg (mean pressure is <10 mmHg - If higher considered pulmonary hypertension)
What is the pressure of the left side of the heart?
120/80 mmHg (if over ~130 or 140 mmHg or diastolic is over 90 mmHg - considered systemic hypertension)
Equation for Oxygen Delivery?
Delivery = Cardiac Output x Oxygen Content
What do Atrial OR Ventricular Septal Defects cause?
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)
Name one mechanism in which a septal defect can form?
Post-septal heart attack - when there is a hole in the necrotic muscle separating the ventricles or atria.
What is the equation for Blood Pressure?
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)
What is Shock?
Inadequate Tissue Perfusion
What is HYPOVOLEMIC Shock?
Decrease in circulating volume causing poor perfusion
What is Haemorrhagic Shock?
Hypovolemic shock caused by severe blood loss
What is Cardiogenic Shock?
Failure of the heart to pump enough blood to organs for perfusion
What is Vasodilation’s effect on Capacitance?
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)
What are the Clinical findings of someone with vasoconstriction?
Decreased capillary refill with peripheral cyanosis and hypothermia.
What are the Cardiac Cycle Steps?
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
What is Atrial Fibrillation?
Heart Rhythm where atria do not have organized contraction (Irregularly Irregular)
What is The ‘A Wave’ for Central Venous Pressure?
Atrial Contraction; Correlates with P wave on ECG
What is the ‘C Wave’ for Central Venous Pressure?
Early Ventricular/Isometric contraction - caused by bulging of the tricuspid valve into the right atrium (Correlates with QRS complex)
What is the ‘V Wave’ for Central Venous Pressure?
Atrial pressure before the AV valve opens - during atrial filling (correlates with T wave on ECG)
What does the Jugular Venous Pressure clinically show?
Right Atrial Pressure
What are the Normal Heart Sounds?
S1: Closure of the Mitral and Tricuspid Valves
S2: Closure of the aortic and pulmonary Valves
What are the Extra Heart Sounds?
S3: Rapid filling of ventricular diastole
S4: Atrial filling phase of diastole
What is Systolic Heart Failure?
Dilated Ventricle - causing increased end-diastolic volume and end-diastolic pressure
Decreased stroke volume and ejection fraction
What are the symptoms of Systolic Heart Failure?
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
What is Pulmonary Edema?
Increased interstitial and alveolar fluid in the lungs - causing stiffer lungs with hypoxia (decreased oxygen perfusion) and chest infiltrates on X-ray
What is Diastolic Failure?
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)
Where are the pacemaker cells found and what do they do?
Within the Sinoatrial (SA) Node - they set the baseline heart rate
What happens when the Parasympathetic Nervous System Impact is stopped to the Heart (+ What Nerve)?
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)
How does the Sympathetic Nervous System affect Heart Rate?
Increases HR from resting levels - i.e., through the use of Catecholamines (from the Adrenal gland)
What is the impact of Heart Rate on Cardiac Perfusion?
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)
What is Demand Ischemia?
When Heart Rate is too high and blood pressure is too low - causing poor perfusion to the tissue
Impact of Age on Heart Rate?
Decreased maximal heart rate
Aorta becomes stiffer
The ventricles are less compliant
Decreased maximal oxygen consumption
What is Starling’s Law?
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
Frank-Starling Curve (Normal heart vs. Failing Heart)?
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
What is Law of Laplace?
Tension = (Pressure x Radius)/(Wall Thickness x 2)
What is Contractility (Inotropy)?
Ability to shorten in response to stimulus (intrinsic property of muscle cells)
Independent of preload and afterload
How does the Sympathetic Nervous System affect Contractility?
increases with SNS activiation
What is The Compensatory Responses to Blood Loss? (Decreased Pre-load)
- Maximizing Cardiac Output
- Increases Contractility
- Vasoconstriction (reduced capacitance)
- Redistributing Cardiac output to perfuse essential organs (Brains, Heart, Lungs)
- Respiratory rate increases
What are the Acute Compensatory Responses to Increased Afterload?
- Ventricular dilation (increase in preload (EDV) can increase contractility
What are the Chronic Compensatory Responses to Increased Afterload?
- Heart undergoes hypertrophy (concentric hypertrophy)
Types of Hypertrophy?
- Physiological (Athlete’s heart) - Tend to have lower HR, reversible and not pathological
- Concentric - Pressure overload
- Eccentric - Volume overload
- Hypertrophic cardiomyopathy
Is Potassium safe for the heart?
No, potassium makes membrane potential less negative, increasing excitability (Arrhythmias can occur)
Cardiac vs. Skeletal Cell Action Potential?
Cardiac - Plateau that is secondary to slow voltage-gated channels (which carry calcium)
Both have fast voltage-gated channels
What is the resting membrane potential?
-55 to 60 mV
When does membrane potential cause voltage-gated sodium channels to open (action potential)?
When threshold of -40 mV is hit
What is the path of the Cardiac Conduction System?
- 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
What is the RAAS System stand for?
Renin-Angiotensin-Aldosterone System
What is the role of Renin? and What causes it to be released?
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
What is the function of ACE?
Converts angiotensin I to angiotensin II
What is the function of Angiotensin II?
- Aldosterone secretion
- Vasoconstriction
- Hypertrophy
- Vasoconstriction of arterioles in the kidney
RAAS and Heart Failure?
RAAS is activated in heart failure
- initially for compensatory (vasoconstriction maintains blood pressure and salt/water retention maintains ventricular preload)
- Eventually becomes decompensatory
What are Angiotensin Converting Enzyme (ACE) Inhibitors?
(-pril) Drugs
Mechanism of Action:
- Inhibition of ACE & blocking the synthesis of angiotensin II
What are the effects of ACE inhibitors?
- Dilates arteries and veins (decreased blood pressure)
- Increases bradykinin formation (contributes to vasodilation)
- Inhibition of myocardial remodelling
What are the indications for ACE Inhibitors?
- 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)
What are some adverse effects of ACE Inhibitors?
- Cough (Common)
- it may be due to bradykinin; maybe an indication to
change to ARB
- it may be due to bradykinin; maybe an indication to
- Hypotension
- Worsening Renal Function (usually reversible)
- Hyperkalemia
- Angioedema (Swelling of tongue and airway - RARE)
What are the Contraindications of ACE inhibitors?
- Pregnancy
- Hyperkalemia
- Severe renal dysfunction
- Hypotension
- Allergy to ACEi
What are Angiotensin Receptor Blockers (ARBs)?
(-Sartan)
Mechanism of Action: Block AT-II receptors (specifically on the heart and blood vessels)
- Does not increase bradykinin
What are the effects of ARBs?
- Vasodilation
- Downregulation of SNS
- Renal excretion of Salt and water
- Inhibit myocardial remodeling and fibrosis
What are the indications of ARBs?
(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)
What are the Adverse Effects of ARBs?
Similar to ACEi (But no cough and Angioedema is more rare)
What are the Contraindications of ARBs?
- Pregnancy
- Concomitant use of ACEi (no additional benefit)
What are Aldosterone Antagonists (Spironolactone)?
Mechanism of Action: Antagonist of Aldosterone
What are the effects of Aldosterone Antagonists?
- 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.
What are the indications for Aldosterone Antagonists?
- Heart Failure
- Post-myocardial infarction with ejection fraction <40%
- Patients with hypokalemia due to diuretic effect
What are the adverse effects of Aldosterone Antagonists?
- Hyperkalemia (More frequent with Renal Dysfunction, ACEi use, NSAID use)
- Gynecomastia (due to off-target antiandrogenic effect)
What are the contraindications of Aldosterone Antagonists?
- Pre-existing hyperkalemia
- Renal Dysfunction/renal failure (relative contraindication/not absolute)
What are Digitalis (Digoxin)?
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.
What are the indication of Digoxin?
- 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
What are the adverse effects of Digoxin?
- Proarrhytmic (Supraventricular Tachycardia, ventricular tachycardia, bradycardia)
- Yellow-green visual changes
- Nausea.Vomiting
- Confusion
What are the contraindications of Digoxin?
- Hypokalemia/hypercalcemia (predispose to toxicity)
- Caution with decreased renal function
- AV-block (will worsen)
What are the two types of Nitrodilators?
- Organic Nitrates (work by generating nitric oxide - causing vasodilation)
- Sodium Nitroprusside (releases nitric oxide)
What is the Mechanism of Action of Nitrodilators?
- Converted to nitric oxide, which activates G-cyclase
- cGMP: produces vasodilation by lowering intracellular
calcium
What is the effect of Phosphodiesterase-5 (PDE-5) inhibitors?
- used to treat erectile dysfunction
- blocks the metabolism of cGMP - thereby causing vasodilation
- Combination of PDE-5 and Nitrodilators causes rapid, profound hypotension
What are the effects of Nitrodilators?
- Vasodilators
- Myocardial Oxygen Demand Decreased
What are the indications of Nitrodilators?
- Angina
- (Including prinzmetal’s Angina - due to coronary
spasm) - (Myocardial infarction with ongoing ischemic pain)
- (Acute pulmonary edema precipitated by myocardial
ischemia)
- (Including prinzmetal’s Angina - due to coronary
How can nitrodilators be administered?
- Nitroglycerin (IV, Sublingual, Transdermal)
- Isosorbide Dinitrate (Oral or Sublingual)
What are the adverse effects of Nitrodilators?
- Headache
- Decreased blood pressure
- Withdrawal syndromes: rebound angina or coronary spasms