Cardiology Flashcards
(136 cards)
1
Q
How does prolonged sympathetic and RAAS activation lead to deleterious remodeling in chronic heart failure
A
Initially, sympathetic drive and RAAS activation increase perfusion by:
* ↑ Heart rate and contractility
* Vasoconstriction (to maintain perfusion pressure)
* Fluid retention (↑ circulating volume)
Over time, these compensatory responses:
* ↑ Hemodynamic stress (↑ preload/afterload)
* Cause cardiac fibrosis, hypertrophy, and dilation
* Lead to progressive cardiac deterioration and symptomatic decompensation
2
Q
What is the most common site of origin for atrial fibrillation (AF) triggers?
A
- Aberrant electrical foci in the pulmonary veins, near their ostia entering the left atrium
- These foci are often targeted in catheter ablation procedures (pulmonary vein isolation) for symptomatic, paroxysmal A
3
Q
What are the cardiac changes associated with normal aging?
A
- Sigmoid-shaped interventricular septum
- Decreased left ventricular cavity size
- Shortened base-to-apex (long-axis) dimension
- Dilated aortic root
- Enlarged left atrium
4
Q
which valve closes first: pulmonic or aortic?
A
aortic
5
Q
What does late diastolic collapse of the right atrium on echocardiogram indicate?
A
- Cardiac tamponade, due to elevated pericardial pressure
- Occurs because the right atrium has low pressure during late diastole, making it susceptible to external compression by pericardial fluid
6
Q
What is Beck’s triad
A
Indicative of cardiac tamponnade: hypotension, JVD, muffled heart sounds
7
Q
What is the pathophysiology of pulsus paradoxus, especially in cardiac tamponade?
A
- During inspiration, venous return to the right heart increases.
- In cardiac tamponade, the stiff pericardial sac prevents the right ventricle from expanding outward.
- Instead, the RV bulges into the LV, displacing the interventricular septum.
- This reduces LV filling, causing a drop in stroke volume and systolic BP.
- If the inspiratory drop in systolic BP is >10 mmHg, it’s called pulsus paradoxus.
8
Q
Heart sounds heard with hypertrophic cardiomyopathy
A
S4
Mid-systolic murmur due to left ventricular outflow obstruction
9
Q
What are the key compensatory mechanisms triggered in hypovolemic shock?
A
- ↓ Blood volume → ↓ central venous pressure (CVP) → ↓ preload → ↓ cardiac output (CO)
- Baroreceptor activation → ↑ sympathetic tone → ↑ systemic vascular resistance (SVR) to maintain perfusion
- ↓ Tissue perfusion → tissue hypoxia → anaerobic metabolism → lactic acidosis
- Metabolic acidosis → triggers increased ventilation (hyperventilation) → ↓ CO₂ → compensatory respiratory alkalosis
10
Q
What are the threshold values for normal ejection fraction and how are they used to classify heart failure?
A
11
Q
What is a patent ductus arteriosus (PDA) and how does it affect oxygen levels in the pulmonary artery?
A
- PDA is a left-to-right shunt: oxygenated blood flows from the aorta into the pulmonary artery.
- This mixes oxygenated blood with deoxygenated blood from the right ventricle.
- Result: ↑ PaO₂ (partial pressure of oxygen) in the pulmonary artery — higher than normal.
12
Q
Blood flow to which part of the body is reduced during systole?
A
Coronary arteries (especially left coronary artery) experience reduced blood flow during systole.
* During systole, the left ventricle contracts, generating high intraventricular pressure. * This compresses the coronary vessels, especially on the left side, reducing perfusion. * Most left coronary artery perfusion occurs during diastole, when the heart relaxes.
13
Q
Do baroreceptors increase or decrease firing when blood pressure drops?
A
Baroreceptors decrease their firing when blood pressure is low.
* Baroreceptors are stretch-sensitive mechanoreceptors in the carotid sinus and aortic arch. * When BP drops, there is less stretch → ↓ baroreceptor firing. * This signals the brainstem (nucleus tractus solitarius) to: * Increase sympathetic outflow → ↑ heart rate, ↑ contractility, ↑ vasoconstriction * Decrease parasympathetic activity
14
Q
Under what conditions is atrial natriuretic peptide (ANP) released?
A
ANP is increased in response to atrial stretch, which occurs when there is:
* Increased blood volume
* Increased venous return
* Increased atrial pressure
* Volume overload states (e.g., heart failure)
15
Q
Fill out the gaps in this diagram
A
16
Q
Which cardiac tissues have fastest to slowest excitability?
A
17
Q
What are the effects of ANP and BNP and where are both peptide hormones released from?
A
18
Q
Where is the most deoxygenated blood in the human body found?
A
- In the coronary sinus, which drains cardiac venous blood.
- This is because the myocardium extracts 60–75% of oxygen from arterial blood — the highest oxygen extraction of any tissue.
19
Q
Explain the action potential cycles of pacemaker and non-pacemaker cells
A
20
Q
What causes visible systolic pulsations in aortic regurgitation, and what do they indicate?
A
In aortic regurgitation (AR), the left ventricle ejects a massive stroke volume to compensate for regurgitated blood. This results in high systolic pressure, producing visible systolic pulsations in:
* Head and neck (e.g., carotid pulsations, de Musset sign)
* Fingertips
* Retina
* Liver, spleen, and other vascular beds
These findings are signs of a hyperdynamic circulation.
21
Q
classify the heartbeats in order of end-diastolic volume
A
Z > X > Y
22
Q
What does this situation represent
A
Increase in cardiac contractility (e.g. inotrope administration)
23
Q
What does this situation represent
A
Increase in VR (e.g. NS infusion)
24
Q
What does this situation represent
A
Exercise
25
How does age-related aortic stiffening affect systolic, diastolic, and pulse pressure?
Related to decreased aortic compliance due to eastin replacement with collagen.
26
Afferent vs efferent limbs of carotid sinus
Afferent = glossopharyngeal nerve
Efferent = vagus nerve
27
Why do children with tetralogy of Fallot squat down?
To increase SVR such that the shunt through the VSD is now L --> R
28
Why does atrial septal defect (ASD) cause a widely split, fixed S2?
* Normally: S2 splits only during inspiration, when ↑ venous return to the right heart delays pulmonic valve closure (P2).
* With ASD: Constant left-to-right shunt → chronically increased right ventricular volume.
* This causes persistently delayed P2 throughout the respiratory cycle.
* Result: Wide and fixed S2 splitting (no variation with respiration)
29
Changes in sBP, dBP and pulse pressure during exercise
sBP increases
dBP unchanged
pulse pressure increased
30
Pressure changes in atria and ventricles in large VSDs
31
What are the roles of natriuretic peptides?
32
Where does atrial flutter usually arise?
Cavotricuspid isthmus of the RA
33
What kind of hypertension is related to normal aging?
Isolated systolic hypertension (high pulse pressure)
34
What is this change from baseline (full line) in the volume-pressure curve associated with?
Exercise: increased stroke volume, increased preload and afterload
35
When would you expect this change in the volume pressure curve?
Increased contractility = increased afterload
E.g. when giving an inotropic agent
36
When would you expect this change in the volume pressure curve?
Increased afterload + decreased stroke volume. For instance, aortic stenosis.
37
When would you expect this change in the volume pressure curve?
Increased preload with increased in SV and slight increase in afterload. E.g., normal saline infusion
38
When would you expect this change in the volume pressure curve?
Decreased preload with slight decrease in afterload. E.g. selective vasodilators like nitroglycerin
39
When would you expect this change in the volume pressure curve?
Increased preload
Decreased afterload
E.g. arteriovenous fistula
40
What kind of cardiomyocyte hypertrophy does endurance training vs weight training lead to?
41
What are the key cardiac adaptations to long-term endurance training?
Increased preload due to increased blood volume and decreased SVR (increased capillary density for better tissue O2 delivery) = eccentric hypertrophy of the heart.
This leads to increased EDV and the stroke volume is also increased, so overall there is **no change in ejection fraction**.
Maximum cardiac output is increased due to increased contractility and blood volume
42
What diseases processes lead to eccentric vs concentric hypertrophy of the heart?
Concentric = pressure overload (e.g. chronic HTN, aortic stenosis)
Eccentric = volume overload (e.g. aortic and mitral regurgitation), ischemic heart disease and hypetrophic cardiomyopathy
43
Which coronary artery is affected when there is STEMI in leads II, III, aVF?
Inferior leads: Right coronary artery
44
Which coronary artery is affected when there is STEMI in leads V1, V2?
Anteroseptal leads: left anterior descending artery
45
Which coronary artery is affected when there is STEMI in leads V3-V4?
Anterioapical: left anterior descending artery
46
Which coronary artery is affected when there is STEMI in leads V5-V6?
Anterolateral: circumflex artery
47
Which coronary artery is affected when there is STEMI in leads I and aVL ?
Lateral: circumflex artery
48
EKG changes in STEMI in first 1-2 hours
ST elevation
49
At which point does the T wave become hyperacute in a STEMI?
Minutes to hours
50
When does the Q wave form in STEMI
1-12 hours post-infarction
51
How long does T wave inversion last on STEMI
Appears within 2-5 days, lasts weeks to months
52
What is a sign on an EKG that there has been a STEMI long time ago
Q-wave with baseline EKG
53
What is the role of prostacyclin (PGI₂) in preventing thrombus formation, and how does atherosclerosis interfere with this?
Prostacyclin is secreted by endothelial cells and synthesized from prostaglandin H₂ via prostacyclin synthase. It inhibits platelet aggregation, reduces platelet adhesion to the endothelium, induces vasodilation
Nitric oxide supports these effects. Atherosclerosis impairs endothelial synthesis of prostacyclin and nitric oxide, promoting localized thrombosis.
54
What is the normal physiological response to myocardial ischemia?
Normal response: Ischemic myocardium releases vasodilators (e.g., adenosine, NO), causing dilation of coronary arterioles to recruit more blood flow.
55
Are patients with a ventricular septal defect (VSD) typically symptomatic?
No. Many patients, especially those with small VSDs, are asymptomatic.
They may have no shortness of breath, cyanosis, or clubbing.
The left-to-right shunt delivers oxygenated blood to the right ventricle, increasing its oxygen saturation (SaO₂), but systemic circulation remains unaffected.
56
How can vasodilators exacerbate myocardial ischemia?
▸ In non-ischemic areas, vasodilation ↑ blood flow.
▸ In ischemic areas, arterioles are already maximally dilated, so no increase in flow.
▸ This may steal blood from ischemic zones → coronary steal → worsened ischemia.
57
Pregnancy changes in afterload
Decrease:
58
What is coronary sinus dilation most commonly a sign of?
Pulmonary hypertension
59
Other name for R --> L heart shunts and vice versa
R -> L = cyanotic heart defects
L -> R = acyanotic heard defects
60
In which portion of the septum do VSDs typically occur
Membranous
61
What pathological process is a mid-diastolic rumble a sign of, and whatp physiological process can accentuate it?
Turbulent flow through a stenotic atrioventricular valve, most commonly mitral stenosis.
Increased venous return can accentuate this sound
62
Most common CHD associated with Down Syndrome?
Complete atrioventricular defect
63
Why is there a murmur in mild coarctation of the aorta, and how is it best described?
In mild coarctation, collateral vessels (e.g., internal thoracic arteries to intercostals) develop to bypass the obstruction.
This retrograde flow through intercostal arteries causes a continuous murmur, best heard over the interscapular area (posterior chest).
There may also be a systolic murmur at the coarctation site.
Chronic pressure overload can lead to concentric LVH and an S4 heart sound.
64
describe the formation of the interatrial septum during embryogenesis
65
What is a cryptogenic stroke and what are potential underlying causes?
A cryptogenic stroke is an ischemic stroke of unknown origin, even after thorough evaluation (including imaging, cardiac workup, and labs).
It often suggests an unrecognized embolic source, such as:
* Patent foramen ovale (PFO)
* Paroxysmal atrial fibrillation (not caught on short-term monitoring)
* Occult malignancy
* Hypercoagulable state
* Atrial septal aneurysm
66
What is the biggest determinant of severity of tetralogy of fallot?
Degree of right ventricular outflow tract obstruction
67
What auscultation sound is characteristic of an ASD?
Widely split S2 with no variation on inspiration
68
What is Eisenmenger syndrome?
69
Most common complication of bicuspid aortic valve
Early onset aortic stenosis
70
Findings during a tet episode of tetralogy of Fallot in terms of pressure in the RV, RA and pulmonary artery
RV increased pressure
RA normal pressure
PA normal pressure
This is because increased straining = R -> L shunting through the VSD
71
What change in cardiac parameters does inspiration cause
Increase RV preload, decreased LV preload
72
What change in cardiac parameters does Valsalva cause
Decreased preload:
Intrathoracic pressure rises significantly. This pressure **compresses the vena cava and other thoracic veins**.
As a result, less blood returns to the right atrium → ↓ right ventricular preload. With less blood entering the lungs, left ventricular preload also drops shortly after.
73
What change in cardiac parameters does hand grip cause
Increased LV afterload
74
Effect of PDA ligation on afterload
Increased.
In a patent ductus arteriosus (PDA), blood from the aorta (high pressure) flows into the pulmonary artery (lower pressure), which reduces the resistance the left ventricle must pump against—in other words, afterload is decreased while the PDA is open.
75
Pharmacological treatment of PDA
NSAIDs = COX inhibitors = PGE-2 synthesis inhibition
76
Why is VSD murmur sometimes not heard at birth?
77
Describe the evolution of the murmur heard with normal PDA
78
Name 4 mechanical complications of MI and describe their time course and clinical findings
79
How does tamponnade resulting from MI present?
Distended JVP, obstructive shock, hypotension
80
At which point of the cardiac cycle are the LV vs the RV perfused
81
Condition mimicking angina but in a smoking female <50y with no other risk factors for angina
Symptoms triggered by excessive vagal tone and endothelial dysfunction.
82
Concerns about which condition should be raised when a patient develops neurological dysfunction following administration of fibrinolytics?
Intracerebral hemorrhage
83
What is the cause of sudden cardiac death in myocardial infarction
Malignant ventricular arrhythmia: VFib or VTach triggered by electrical instability in the ischemic myocardium
84
Pharmacological management of acute MI in a patient with COPD
Cardioselective beta blockers (B1) - e.g. metoprolol
85
Describe the histological changes in an MI within the first 24 hours
86
Describe the histological changes in an MI within 1-7 days post-MI
87
Describe the histological changes in an MI within 7 days-8 weeks post-MI
88
Mechanism through which nitroglycerin reduces angina symptoms
Peripheral vasodilation = decreased preload
89
What is hibernating myocardium
90
Statins MoA
Increased LDL receptor expression on hepatocytes
91
% of coronary blood flow that must be obstructed for symptoms of angina to appear
>70%
92
molecule promoting replacement of myocardium with fibroblasts days-weeks post-MI
transforming growth factor beta
93
Tell me about cardio effects of cocaine intoxication and management
94
Most common complication of statin use
Myopathy
95
Cardiovascular effects of hyperthyroidism
Decreased SVR due to vasodilation
96
Lab and exam findings in pulmonary embolism
acute onset chest pain and dyspnea, may be accompanied by syncope/near-syncope
tachycardia, tachypnea, jugular venous distension and clear lungs
respiratory alkalosis due to hyperventilation, low O2 saturation
97
What are the 2 extra heart sounds and when are they heard? What pathologies are associated with each?
98
Best diuretic for HFrEF patients
Mineralocorticoid receptor antagonists (e.g. spironolactone) = potassium-sparing diuresis
99
What kind of diuretics act at the distal convoluted tubule
Thiazide diuretics
100
Effects of dobutamine on BP and HR
101
Effects of dopamine (low-dose vs high-dose) on HR and BP
Low dose: D1>B1>a1 so decreased BP and increased HR
High dose: a1>B1>D1 so increased BP and decreased HR
102
Effects of epinephrine (low-dose vs high-dose) on HR and BP
Low dose: B1>B2>a1 = decreased BP and increased HR
High dose: A1>B1>B2 so increased BP and decreased HR
103
What histological finding in the lungs is associated with left-sided heart failure, and how is it detected?
Finding: Hemosiderin-laden macrophages (also called heart failure cells) in the alveolar spaces
Mechanism: Left ventricular dysfunction → ↑ pulmonary capillary pressure = Extravasation of RBCs into alveoli = RBCs phagocytosed by macrophages
Hemoglobin iron converted to hemosiderin, detected by Prussian blue stain, blue-black within golden-brown cytoplasmic granules of macrophages
104
Digoxin toxicity
105
Which medication classes reduce cardiovascular mortality in patients with heart failure with reduced ejection fraction (HFrEF)?
These medications reduce cardiac remodeling and neurohormonal activation, leading to lower mortality in HFrEF.
106
Where are the components of the RAAS (renin-angiotensin-aldosterone system) primarily found or secreted?
a) Renin – secreted by juxtaglomerular cells in the kidney, in response to ↓ renal perfusion
b) Angiotensin I – formed in the systemic circulation from angiotensinogen by renin
c) Angiotensinogen – produced by the liver
d) Aldosterone – secreted by the adrenal glands in response to angiotensin II
✅ Bonus: Angiotensin II is generated primarily in the small pulmonary vessels by ACE and is higher in the pulmonary vein than the pulmonary artery.
107
Which heart chamber is the most posterior?
The left atrium
108
What are structures that can be compressed when the LA is enlarged?
The esophagus = dysphagia
The left recurrent laryngeal nerve = hoarseness (Ortner syndrome)
109
Which heart chamber is the most anterior?
The right ventricle
Most commonly injuredin trauma
110
Most common locations of atherosclerosis
Abdominal aorta > coronary artery > popliteal artery > carotid artery > circle of Willis
111
Immune cell involved in pathogenesis of atherosclerosis
Macrophages (LDL-laden)
112
Name 5 cyanotic heart diseases
1. Truncus arteriosus
2. Transposition of the great arteries
3. Tricuspid atresia
4. Tetralogy of Fallot
5. TAPVR
113
Shunts required for survival in tricuspid atresia
ASD
VSD/PD
114
4 anomalies in tetralogy of Fallot
115
Frequency of acyanotic heart defects
VSD > ASD > PDA
116
Infection commonly associated with thoracic aortic aneurysm
Tertiary syphilis
117
Types of aortic dissections and their management
Type A: Ascending. Tx = surgery
Type B: Descending. Tx = beta blockers
118
Where is the infarction located (murally) in STEMI vs NSTEMI
119
Etiologies of sudden cardiac death
Usually due to lethal arrhythmia (e.g. Ventricular fibrillation)
120
Myocardial hibernation vs myocardial stunning
121
Most commonly occluded coronary vessels
LAD > RCA > LCX
122
Localize the MI for each coloured section
Dark blue: lateral section: LCX
Pink: inferior section: RCA
Pale blue: anteroseptal: LAD
Very pale blue: anteroapical: LAD
Intertwined: anterolateral: LAD or LCX
123
DDx of ST elevation on EKG that is not MI
Pericarditis
Early repolarization
124
Cause of progression from paroxysmal AFib (self-resolving) to persistent AFib
Atrial remodeling
125
Management of patient with acute RCA MI developing severe hypotension (+ pathophysiology)
Atropine (anticholinergic):
126
What does prolonged QT interval predispose to
Torsade de pointes
127
Iatrogenic causes of prolonged QT
128
What is this EKG typical of?
129
2 types of CCB and what are they used for?
- Nondihydripyrimidine = arrhythmias
-Dihydripyrimidine = peripheral vasodilator
130
Electrolyte driver of QT interval
Potassium
131
Compare and contrast rate and rhythm control (methods) and which is the first-line treatment for AFib?
132
Compare classes Ia, Ib and Ic antiarrhythmics in terms of binding to Na+ channels
133
Which class of antiarrhythmics binds to Na+ channels in the inactivated state?
Class Ib (e.g. lidocaine)
134
Blockade of which channel is responsible for widened QRS
Na+
135
Contrast and compare class I antiarrhythmics in terms of inhibition of phase 0, K+ channel blockade and effect on AP duration
136
How does ventricular aneurysm present post-MI on an EKG
Persistent ST elevation
