CV system patho Flashcards
What are the different causes of cardiac disease
The histology of cardiac muscle
Histology of cardiac muscle: Cardiac tunics and their relationship to the pericardium. The three tunics are homologous to those of blood vessels: endocardium = tunica intima; myocardium = tunica media; and epicardium = tunica adventitia. The pericardium is composed of two layers: the outer parietal pericardium and the epicardium, or visceral pericardium, which is in contact with the heart and roots of the great vessels. The parietal pericardium has two regions: a serosa facing the pericardial cavity and, peripheral to that, a fibrosa.
Chest radiographs with borders of the heart
Where are heart sounds best heared?
- Not alwya sinc orrespondence with their anatomical lcoation
- Mitral valve - apex
- Tricuspid valve - left parasternal border
- Pulmonary valave - L 2/3rd intercostal spaces,
- Aortic valve - left sternal border for regurgitation murmurs and right second intercostal space for ejection murmurs.
Cardiac cycle relationships with heart sounds
The P wave represents atrial depolarization; the PR interval, atrioventricular conduction time; the QRS, ventricular depolarization; and, the T wave, ventricular repolarization, or recovery. The S1 heart sound co-occurs with the QRS complex and marks the beginning of systole, and the S2 heart sound occurs after the T wave and marks the beginning of diastole.
ECG basic structure
Activation of cardiac contraction
- An aciton potential starts at the sinoatrial node and travels through atrial muscle cells to Atrioventriuclar node.
- After a short delay at the AV node, the AP spreads throught the interventricular septum in modified cardiac muscle cells called purkinje fibres and then through muscle cells to the whole ventricle.
- The action potential follows the same path each tine, giving rise to electrical signals that can be detected on the body surface by electrocardiogram (ECG)
- Damage during Myocardia cinfarctiosn chnges the ECG pattern and may cause arrhythmias.
Coronary arterial vasculatur.
The right and left coronary arteries can be seen coming off the aortic valve cusps
The right coronary artery supplies the sinoatrial node and most often the posterior aspect of the heart; the left coronary artery divides into the left anterior descending and the circumflex arteries
Factors affecting the cardiac output
Ventricular ypertorphy and the pathogenesis
Ventricular hypetrophy = compensatory change related to alterations in pressure and/or vilume imposed on the wall of the ventricle.
Patho LVH/RVH:
- Sustained pressur ein the ventricles increases wall stress
- Changes in wall stress alter gene expression in the muscle
- Changes in gene expression lead to duplication of sarcomeres (contractile elements of muscles)
- Changes occur in wall stress when there is an increase in afterload:
- Afterload is the reisstance the ventricle contracts against to eject blood in systole
- Increased afterload produces concentric hypertorphy of the ventricular wall - Sarcomeres duplicate parallel to the long axis of the cells,c ausing individual muscle fibres to be thicker
- Causes of concentric LVH due to increased afterload include primary hypertension (HTN; most common), aortic valve stenosis, and hypertrophic cardiomyopathy (HCM)
- Causes of conceteric RVH due to increased afterload include pulmonary HTN (PH) and pulmonary valve stenosis.
- CHnage soccur in wall stress when there is an increase in preload:
- Preload = volume of bloo din ventricle that must be expelled during systole
- Preload correltes with left and right ventricle end-diastolic volumes
- Increased preload increases SV via frank Starling pressure relationship
- Increased preload causes dilation and hypertrophy (eccentric hypertrophy) of the ventricular walls. Sarcomeres duplicate in series (on top of each other) causing individual muscle fibres to increase in length and width
- Causes of eccentric hypertropy of the LV due to increased preload include:
- Mitral valve (MV) or AV regurgitation
- Left toright shunting of blood (eg in VSD). More blood returns to L side of heart as right side is receiving more blood than usual
- Causes of eccentric hypertrophy of RV due to increased preload include tricuspid valve and PV regurgitation.
Sides of the heart
- Normal heart. 4 chambers
- R side = pumps venous blood into the lungs
- Oxygenated blood returns from the lungs into the L atrium and is propelled by the left ventricule into the aorta
- Thw insets show closed valves, the tricuspid valve has 3 leaflets, and mitral has 2.
- The aorticx an dpulmonary artery valves have 3 leaflets and resemble one another except coronary arteries originate from behind the cusps in the aorta.
S3 heart sound - most clinically significant etxra heart sound
- May be normal in some children/young adults (more energeti expansion and illing of LV) but its pathological after 40.
- Thought to be caused by sudden rush of blood entering volume overloaded LV/RV (stiff ventricle).
- Best heard at apex with patient in left lateral decbitus position.
- Commonly occurs with regurgitant types of murmurs involving any of the valves. It is the first cardiac sign of congestive HF where increased ventricular volume stretches MV or TV ring, causing vol overload from mitral or tricuspid regurgitation. An S3 heart sound produces a ventricular gallop. An S4 heart sound coincides with atrial contraction in late diastole and then wave in jugular venous pulse.
- S4 heart sound is less diagnostic value than S3 as disorders causin stiff ventricles are so diverse and S4 doesnt predict patients haemodynamic findings .
- S4 is never normal and caused by increased reisstance to filling (decreased compliance) in L/R heart after vigorous atrial contraction. It is heard best at apex. Causes of decreased ventricular compliuance include concentric ventiruclar hypertrophy (L/R) and a volume overload ventricle. In a volume overloaded L/R ventricle, it is commonly present along with S3.
- S4 heart sound and wave of JVP are absent in atrial fibrillation.
- Presence of S4 produces atrial gallop. S3&S4 is sumamtion gallop
Heart sounds - S1/S2
- S1 heart sounds = closure of MV + TV (MV before TV) in systole. Moving columns blood abruptly decelerte and this set sup vibrations of chordae tendinae, ventricles + blood. Bets heart at apex, corresponding with carotid or radial pulse.
- S2 heart sound = closure of AV and PV and marks beginning of diastole. Bets hearf at L2/3 intercostal space
- Aortic component (A2) normally preceds pulmonary componenet (P2) of S2 heart sound. Unlike S1 heart sound, S2 split on inspiration. As diaphragm descends it causes a further decreased in intrathoracic pressure which increases flow of blood out of VC into Right side of heart. This causes flattening of jugular neck veins. The excess amount of blood in right side of the heart delays closure of PV, causing P2 to separate more from a2. This split is best heard over PV area. A2 and P2 become single sound on expiration as intrathroacuc pressure becomes less negative. An accentuated A2 is heard in primary hypertension (increased pressure causes it to snap chit), and an accentuated P2 is heard in pulmonary hypertension (increased pressure causes it to snap shut).
HearT Murmurs
- May occur in systole/diastole
- May be caused by structural valve disease (eg, damage form rheumatic fever) or stretching of the valve ring (eg vol ovrload in L/R sided HF).Murmurs often caused by stretchign of valve rings are functional murmurs.
- Murmurs often radiate - eg av stenosis radiates into neck and MV regurg -> axilla
- Graded 1-6 in terms of intensity. 1&2 hard to hear, G3 easy to hear, 4-6 oftne accompanied by palpable precordial thrill. Grade 6 are audible without stethoscope.
- Murmur and abnormal heart osunds (eg, S3&4) change their intensity with repsirations.
Jugular Venous Pulses.
Consequences of Ventricular hypetrophy
- L/R sided heart failure. Excess work imposed on ventricles by either increase in afterload or increase in preload.
- Anginal pectoris with exercise (LVH complciation). Muscle is concentrically thickened, angina may occur with excercise as muscle wlal so thicken that subendocardium tissue receives dangerously low levels of 02 causing chest pain. HR increases whcih decreases tiem for diastole and filling of CAs so even less blood flow to subendocardium (normall subendocardium receives leats amoutn of blood from coronary arteries).
- Pathologic S4 heart sound is commonly present in LVH and/or RVH: Corrleates with atrial contraction in late diastole producing atrial gallop. Caused by blood entering non compliant ventricle (problem filling) which can be present in concentric hypetrophy or eccentric hyeretpphy (from overload and resist mor eblood in late diastole). Examples in pic.
- Pathologic S3 heart sound commonly in L.R sided eccentric hypertrophy. S3 heart sound cause dby blood entering vol overloaded chamber in early diastole. in voluem ovelroad in MV/TV regurgitation or AV/PV regurgitation.
heart fialure syndrome
Heart failru efindings/ images
clinical features of L/R HF
Chronic passive ocngestion of the lungs
Chronic passive congestion of the lungs. Increased venous pressure leads to extravasation of red blood cells (RBCs) into the alveoli and alveolar oedema. The hemosiderin formed from haemoglobin released from haemolysed RBCs is taken up by intra-alveolar macrophages (“heart failure cells”).
