Cardiology Flashcards
How does blood flow through the Heart.
What is the anatomy of the myocardium and what parts of the heart are supplied by what arteries,
Myocardium -
Right Atrium: sinus node artery (which is a branch of the RCA in 55% of cases & LCx in 45%
Left Atrium: is supplied by the LCx
Right Ventricle (posterior portion): RCA and posterior descending branch (PDA) & LAD Right Ventricle (anterior portion):
RCA and LAD: Left Ventricle (posterior) is supplied by LCx, PDA & LAD, Anterior Left main, LAD & LCx Apex is supplied by LAD
Septum is supplied by septal branches of LAD, PDA and AV nodal branch of RCA.
What Acute Coronary Syndrome Pathophysiology
A term that is used for a group of 3 clinical presentations that are indicative of myocardial ischeamia:
1) Unstable angina (UA)
2) NSTEMI & STEMI
What is the Pathophysiology of Angina
What is Angina
Angina is an episodic, clinical syndrome that results from transient myocardial ischemia, causing pain in any of the cardiac sites. Due to a narrowing in the coronary arteries the body is not able to adapt by increasing blood flow to the myocardium, the cells that are distal to the narrowed artery are then forced to metabolise anaerobically. A bi-product of this metabolism is lactic acid, which causes pain. A supply to demand mismatch.
Define Stable Angina pectoris
Stable angina
- is transient, predictable, associated with an increase in myocardial O2 demand.
Define Unstable Angina
- Advanced angina with presence of transient thrombi formation over atherosclerotic lesions. There is impending infarction. new onset, Prolonged at rest or not relieved with rest
- chronic stable which develops in severity, frequency or is more easily triggered
- A change in a patient’s normal pattern of angina warrants investigation
What is a Myocardia Infarction
Define Acute Myocardial Infarction
Irreversible necrosis or death of myocardial tissue, usually due to prolonged ischemia resulting from an atherosclerotic plaque with superimposed thrombus.
STEMI
- A more severe form of MI. ST elevation indicates relatively large amount of heart muscle damage as CA totally blocked (full thickness muscle damage) by red thrombus. Aim transport for PCI within a appriopriate timeframe and thrombolyise if aproppriate
NSTEMI
- Blood clot/white thrombus only partially occludes artery as a result only portion of the heart muscle supplied by affected artery dies (decreased blood flow to area). Unstable Angina is the same process as NSTEMI however the difference being that UA resolves prior to death of any myocardium and NSTEMI involves some myocardial death
Complete Occlusion
↓
No O2 Supply→Irritation→CCP, Initial ECG changes, Changes in membrane permeability, Arrhythmia→PVCs, VF/VT
↓
Aerobic→Anaerobic metabolism ↓
No energy → Na+/K+ pump fails & pH ↑ → Increased intracellular sodium ↓
Increased intracellular water (water follows Na+)→Swelling→Burst
↓
Release of enzymes, K+,Ca+, Na+, H=→Irritation & altered resting membrane potential in injured cells→Infarction, ECG changes, Arrhythmias, reduced contractility and CO→LVF/Cardiogenic shock, pathological Q waves
↓
Cell death→Necrosis
↓
5-10 Days 3-4 Weeks
Cell repair→Soft myocardium→Ventricular aneurysm, ventricular/papillary rupture
↓
Scar tissue→Fibrous tissue→Loss of function
What is the Pathophysiology of Cardigenic Shock
Cardiogenic shock is a serious condition that occurs when your heart cannot pump enough blood and oxygen to the brain, kidneys, and other vital organs. Cardiogenic shock is considered a medical emergency and should be treated immediately. The most common cause of cardiogenic shock is a heart attack
Cardiogenic Shock - associated with Right Ventricular Infarct
Approx. 19-51% of patients with inferior AMI have right ventricular involvement. The most serious complication of right ventricular infarction is SHOCK - decrease in preload, less in right ventricular ejection therefore less returning to left side of heart - causing decrease in stroke volume.
What is the definition of
- Stoke Volume (SV)
- Cardiac Output (CO)
- Systemic Vacular Resistence (SVR)
- Mean aterial Pressure (MAP)
- Preload / Afterload
- Sytolic BP & Diastolic BP,
Stroke Volume
- Stroke volume: is the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction Not all of the blood that fills the heart by the end of diastole (end-diastolic volume - EDV) can be ejected from the heart during systole. Thus the volume left in the heart at the end of systole is the end-systolic volume (ESV). The SV volume may be calculated as the difference between the left ventricular end-diastolic volume and the left ventricular end-systolic volume (ESV).
- SV = EDV - EDV
Cardiac Output:
- Cardiac output (CO) is the blood volume the heart pumps through the systemic circulation over a period measured in liters per minute.
- CO= SV x HR
Systemic Vascular Resistence
- Systemic vascular resistance (SVR) refers to the resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature
Mean Aterial Pressure
- Mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole. MAP is influenced by cardiac output and systemic vascular resistance.
Preload
- Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling
Afterload
- Is the force or load against which the heart has to contract to eject the blood.
Systolic Blood Pressure
- Pressure in your arteries during the contraction of your heart muscle.
Diastolic Blood Pressure
The bottom number refers to your blood pressure when your heart muscle is between beats.
What is the Pathophysiology of Left Venticular Failure and Acute Pulmonary Oedema.
LVF
Left ventricular failure occurs when there is dysfunction of the left ventricle causing insufficient delivery of blood to vital body organs. Chronic or poorly controlled hypertension causes increased afterload and therefore increased cardiac workload, which can lead to hypertrophy of the left ventricle.
Acute Pulmonary Oedema (APO)
Leakage of fluid from the pulmonary circuit and interstitium into the alveolar spaces. Whether Cardiogenic or non-Cardiogenic in origin, regulation and balance between capillary hydrostatic and oncotic (Hyrdostatic overcome Oncotic) pressure, lymphatic drainage and alveolar permeability is compromised.
This results in the shift and thus accumulation of fluid in the alveoli, causing respiratory compromise
What is the Pathophysiology of Tachycardia Narrow Complex.
A narrow complex tachycardia or atrial tachycardia which originates in the ‘atria’ but is not under direct control from the SA node (but instead are coming from a collection of tissue around and involving the atrioventricular (AV) node). SVT can occur in all age groups. Results in ↓ CO & ↓ ventricular filling time
Indepth:
The electrical conduction through the heart starts at the sinoatrial (SA), which then travels to the surrounding atrial tissue to the atrioventricular (AV) node. At the AV node, the electrical signal is delayed for approximately 100 milliseconds. Once through the AV node, the electrical signal travels through the His-Purkinje system, which distributes the electrical signal to the left and right bundles, and ultimately to the myocardium of the ventricles. The pause at the AV node allows the atria to contract and empty before ventricular contraction.
There are 4 differntials with narrow complex tachycardia.
- SVT (Regular QRS Complexes)
- Sinus Tachy (NSR with HR > 100)
- Atrial Fibrilation (Regulary Irregular QRS Complexes)
- Atrial Flutter (High Atrial rate with a SAW TOOTH like apperance).
The most common cause of SVT is an orthodromic reentry phenomenon, which occurs when the tachycardia is secondary to normal anterograde electrical conduction from the atria to the AV node to the ventricles, with retrograde conduction via an accessory pathway from the ventricles back to the atrial.
A narrow QRS complex (< 120 milliseconds) indicates the ventricles are being activated superior to the His bundle via the usual pathway through the His-Purkinje system. This implies that the arrhythmia originates from the sinoatrial (SA) node, the atrial myometrium, the AV node, or within the His bundle.
Types of SVT
Atrioventicular Nodal Re-entrant Tachycardia (AVNRT)
- AVNRT is caused by a reentry circuit in or around the AV node. The circuit is formed by the creation of two pathways forming the re-entrant circuit, namely the slow and fast pathways. The fast pathway is usually anteriorly situated along septal portion of tricuspid annulus with the slow pathway situated posteriorly, close to the coronary sinus ostium.Sustained reentry occurs over a circuit comprising the AV node, His Bundle, ventricle, accessory pathway and atrium.
Atrioventicular Re-entrant Tachycardia (AVRT).
- Atrioventricular reentrant tachycardia occurs when a reentrant circuit is present outside of the AV node through an abnormal conduction pathway that connects the atrium to the ventricles. This pathway is termed an “accessory pathway” or a “bypass tract.” The presence of this congenitally abnormal accessory pathway is seen in W_olff-Parkinson-White (WPW) syndrome._
What is the Pathophysiology of Atrialfibrilation and Atrialflutter.
Atrial Flutter
Atrial flutter is a type of supraventricular tachycardia caused by a re-entry circuit within the right atrium. The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a fairly predictable atrial rate of around 300 bpm (range 200-400).
Ventricular rate is determined by the AV conduction ratio (“degree of AV block”). The commonest AV ratio is 2:1, resulting in a ventricular rate of ~150 bpm.
Higher-degree AV blocks can occur — usually due to medications or underlying heart disease — resulting in lower rates of ventricular conduction, e.g. 3:1 or 4:1 block.
Atrial flutter with 1:1 conduction can occur due to sympathetic stimulation or in the presence of an accessory pathway — especially if AV-nodal blocking agents are administered to a patient with WPW.
Atrial flutter with 1:1 conduction is associated with severe haemodynamic instability and progression to ventricular fibrillation.
Atrial Fibrilation.
Atrial Fibrilation is characterized by high frequency excitation of the atrium that results in both dyssynchronous atrial contraction and irregularity of ventricular excitation. Whereas AF may occur in the absence of known structural or electrophysiological abnormalities, epidemiological association studies are increasingly identifying comorbid conditions, many of which have been shown to cause structural and histopathological changes that form a unique AF substrate or atrial cardiomyopathy.5
What is the Pathophysiology of AV Heart Blocks
Overview
Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart’s conduction system. This disruption in normal electrical activity can be transient or permanent, and then further characterized as delayed, intermittent, or absent. In general, there are three degrees of AV blocks.
First Degree
In first-degree AV block, the P waves always precede the QRS complexes, but there is a prolongation of the PR interval. That is, the PR interval will be greater than 200 milliseconds in duration without any dropped beats. There is a delay, without interruption, in conduction from the atrium to the ventricle. In other words, while the impulse is slowed, it is still able to get through to the ventricles. The delay is typically due to a minor AV conduction defect occurring at or below the AV node.
Second Degree (Type 1: Mobitz: Wenckebach)
In second-degree Mobitz type 1 AV block, there is a progressive prolongation of the PR interval, which eventually culminates in a non-conducted P wave meaning the QRS complex is dropped.
Second degree, Mobitz type 2
In second-degree type II AV nodal block (a.k.a. Mobitz Type II AV block), the AV node becomes completely refractory to conduction on an intermittent basis. For example, three consecutive P waves may be followed by a QRS complex, giving the ECG a normal appearance, then the fourth P wave may suddenly not be followed by a QRS complex since it does not conduct through the AV node to the ventricles.
Third Degree (Complete Block)
In third-degree, or complete, heart block there is an absence of AV nodal conduction, and the P waves are never related to the QRS complexes. In other words, the supraventricular impulses generated do not conduct to the ventricles. Instead, if ventricular conduction occurs, it is maintained by a junctional or ventricular escape rhythm. There is a complete dissociation between the atria and ventricles.
What is the Pathophysiology of RBBB
RBBB
When the right bundle branch is interrupted, electrical stimuli from the atrioventricular (AV) node conducts to the bundle of His and down the left bundle branch. The left ventricle depolarizes first while the right ventricle polarized later, causing the characteristic ECG findings.
In normal cardiac conduction, impulses travel equally down the left and right bundles, with the septum activated from left to right and the formation of small Q waves in lateral leads
In RBBB, the left ventricle is activated normally, thus the early part of the QRS complex correlating to septal depolarisation is unchanged
There is delayed activation of the right ventricle as depolarisation originates from the left ventricle across the septum. This produces a secondary R wave (R’) in the precordial leads, and a wide, slurred S wave in lateral leads
Normal activation of the left ventricle means that cardiac axis remains normal in isolated RBBB
Clinical Findings include
QRS duration > 120ms
RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)
What is the Pathophysiology of LBBB
In normal cardiac conduction, impulses travel equally down the left and right bundles, with the septum activated from left to right and the formation of small Q waves in lateral leads
In LBBB, conduction delay means that impulses travel first via the right bundle branch to the RV, and then to the LV via the septum
Septal activation is thus reversed eliminating lateral Q waves
The overall depolarisation vector from the right to left ventricle produces tall R waves in lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3). The delay between activation of the RV and LV produces the characteristic “M-shaped” R wave seen in lateral leads
Delayed overall conduction time to the LV extends the QRS duration to > 120 ms
What is the pathophysiology of Rate related chest Pain
Rate related chest pain occurs when the HR is to high and is unable to prefuse the heart Adequtley.
During Systole the heart ejects oxygenated blood out of the heart to organs in the rest of the body in order to deliver oxygen to them. During this process the Aortic Valve opens and the subendocardial coronary vessels are closed. During Diastole the Aortic Valve is closed allowing for venticular filling, The Subendocardial vessles open allowing perfusion to the intrvascular spectum and the heart.
When someones heart rate is high, the heart doesn’t have as much time to relax, reducing the time a person is in diastole therefore the Aortic Valve stays open and the Subendocardial vessles won’t open as often or for as long as normal. This leads to ishcemia and results in pain.
