CVS Flashcards
1
Q
Where is apex beat
A
5th left intercostal space and mid-clavicular line
2
Q
Stroke Volume
A
Volume of blood ejected from each ventricle during systole
3
Q
Cardiac output
A
Volume of blood each ventricle pumps as a function of time (litres per minute)
Stroke Volume (L) x Heart rate (BPM)
4
Q
Total Peripheral Resistance
A
The total resistance to flow in systemic blood vessels from beginning of aorta to vena cava - arterioles provide the most resistance
5
Q
Preload
A
Volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction
6
Q
What is effect on preload when veins dilate?
A
Decreased preload since venous return decreases (decrease in P in right atrium)
7
Q
End-Diastolic Volume
A
How much blood is in the ventricles before it pumps
8
Q
Afterload
A
The pressure the left ventricle must overcome to eject blood during contraction
9
Q
What is effect on after load from a dilation of arteries
A
Decreased afterload
10
Q
Contractility
A
Force of contraction and the change in fibre length (how hard the heart pumps).
11
Q
When cardiac muscle contracts what is effect on length of:
Myofibrils
Sarcomere
A
When muscle contracts myofibrils stay the same length but the sarcomere shortens - force of heart contraction that is independent of sarcomere length
12
Q
Elasticity
A
Myocardial ability to recover normal shape after systolic stress
13
Q
Diastolic dispensability
A
The pressure required to fill the ventricle to the same diastolic volume
14
Q
Compliance
A
How easily the heart chamber expands when filled with blood volume
15
Q
Starlings law
A
Force of contrition is proportional to the end diastolic length of cardiac muscle fibre (the more ventricle fills the harder it contracts).
↑ venous return = ↑ end diastolic volume = ↑ preload = ↑ sarcomere stretch = ↑ force of contraction thus = ↑ stroke volume and force of contractions
16
Q
What is effect of standing on cardiac output?
A
Standing decreases venous return due to gravity, thus cardiac output decreases.
Causes a drop in blood pressure, stimulating baroreceptors to increase BP
17
Q
What is effect on force of contraction if cardiac muscle is below optimal length (e.g. at rest)
A
Decreased force of contraction
18
Q
Heart sounds: What is S1 (Lub)
A
mitral and tricuspid valve closure
19
Q
Heart sounds: What is S2 (dub)
A
aortic and pulmonary valve closure
20
Q
Heart sounds: What is S3 and when would you hear it
A
In early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure
21
Q
Heart sounds: What is S4
A
‘Gallop’, in late diastole, produced by blood being forced into a stiff hypertrophic ventricle - associated with left ventricular hypertrophy
22
Q
Name risk factors for atherosclerosis
A
- Age - increases with age
- Tobacco smoking - leads to endothelium erosion
- High serum cholesterol
- Obesity - since more pericardial fat and thus increase in inflammation - Diabetes - hyperglycaemia damages endothelium
- Hypertension
- Family history
23
Q
Describe structure of an atherosclerotic plaque
A
A complex lesion consisting of: • Lipid • Necrotic core • Connective tissue • Fibrous “cap”
24
Q
Eventually a plaque can occlude the vessel lumen - what can result from this?
A
Restriction of blood flow (angina) May rupture (thrombus formation and subsequent death)
25
What initiates atherosclerosis formation
Endothelial dysfunction as a result of injury to endothelial cells
26
What is released from damaged endothelial cells to attract leukocytes
chemoattractants
| concentration gradient of this also produced
27
Give examples of inflammatory cytokines found in plaques/promote atherogenesis
```
IL-1(B)
IL-6
IL-8, IL-4, IL-12
IFN-gamma
TNF-alpha
MCP-1
```
28
Give examples of cytokines that suppress atherosclerosis production
IL-5
IL-10
TGF-beta
29
What 2 coagulation factors help convert prothrombin to thrombin
Xa
| Va
30
Macrophages engulf fat cells to form what cells in atherogenesis
(Lipid-laden) foam cells
31
What are fatty streaks
Earliest lesion of atherosclerosis
| Consist of aggregations of foam cells and T-lymphocytes in the intimal layer of the vessel wall
32
What makes up intermediate lesions?
```
Composed of layers of:
-Foam cells
-Vascular smooth muscle cells
-T lymphocytes
Also adhesion of platelets to vessel wall
```
33
What drug can inhibit platelet aggregation?
Aspirin (anti-coagulant)
34
In fibrous.advanced plaques, what makes up the dense fibrous caps
Extracellular matrix proteins including collagen (strength) and elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris
35
What two ways can a thrombus form?
1 - Superficial endothelial injury. Involved denudation of the endothelial covering over the plaque. Sub-endocardial connective tissue matrix then exposed and platelet adhesion occurs due to reaction with collagen.
Thrombus adherent to surface of the plaque.
2 - Deep endothelial fissuring, which involves an advanced plaque with a lipid core.
Plaque cap tears, allowing blood from lumen to enter inside of plaque. Core is highly thromogenic and thrombus can form in plaque, expanding its volume and distorting its shape. Thrombus can extend into the lumen.
36
Why is plaque core highly thrombogenic?
Contains lipid-lamellar surfaces and tissue factor (which triggers platelet adhesion and activation) that is produced by macrophages and exposed collagen
37
What cells release cytokines in atherosclerosis and what is result of this?
Monocytes
Macrophages
Damaged endothelium
Promotes further accumulation of macrophages as well as smooth muscle migration/proliferation.
38
What is released by proliferating smooth muscle in atherogenesis
Collagen
39
*Give examples of cytokines released in atherosclerosis
Platelet-derived growth factor
Interleukin-1
Transforming Growth Factor-1
40
What is angina
Chest pain, often also spreading to the shoulders, arms, and neck, owing to an inadequate blood supply to the heart.
41
Describe different types of angina
Stable angina - induced by effort and relieved by rest.
Unstable angina - recent onset (<24 hours) or deterioration in previously stable angina, with symptoms frequently occurring at rest. Angina of increasing frequency/severity, occurring on minimal exertion or at rest. Form of acute coronary syndrome.
Crescendo pattern.
42
Myocardial ischaemia resulting in angina occurs when there is a mismatch between blood supply and metabolic demand. What can cause this?
* Atheroma/stenosis of coronary arteries thereby impairing blood flow - most common cause
* Valvular disease
* Aortic stenosis
* Arrhythmia
* Anaemia - thus less O2 can be transported
43
Give example of an ischaemic metabolite and what do they do?
Adenosine
Stimulate nerve endings and produce pain
44
Give examples of angina risk factors
- Smoking
- Sedentary lifestyle
- Obesity
- Hypertension
- Diabetes mellitus
- Family history
- Genetics
- Age
- Hypercholesterolaemia
(also more common in men)
45
Describe initiation of atherosclerosis
* Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier
* Local cellular proliferation and incorporation of oxidise lipoproteins occurs
* Mural thrombi on surface and subsequent healing and repeat of cycle
46
Describe when is meant by adaptation in atherosclerosis
* As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed
* This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix
* May progress to unstable plaque
47
As plaque continues to encroach on the lumen, exposure of what? can stimulate T cell accumulation
Tissue HLA-DR antigens
48
Describe the clinical stage of atherosclerosis (follows adaption stage)
• The plaque continues to encroach upon the lumen and runs the risk of haemorrhage or exposure of tissue HLA-DR antigens which might stimulate T cell accumulation
• This drives an inflammatory reaction against part of the plaque contents
• Complications develop including ulceration, fissuring, calcification and
aneurysm change
49
What is a fatty streak?
Macrophages filled with abundant lipid (foam cells) and smooth muscle cells with fat
50
Describe the intimal cell mass of an atheroma
Collections of muscle cells and connective tissue
| without lipid - “cushions”
51
What can you do to see if someone has a local haemorrhage
Local haemorrhage may mean iron deposition and calcification
52
Why are complicated plaques prone to rupture
Show calcification and mural thrombus, making them vulnerable to rupture
53
Complications of Plaque rupture
- Acute occlusion due to thrombus
- Chronic narrowing of vessel lumen with healing of the local thrombus
- Aneurysm change
- Embolism of thrombus +/- plaque lipid content
54
*Describe clinical presentation of angina
- Central chest tightness or heaviness
- Provoked by exertion, especially after meal or in the cold windy weather or by
anger or excitement
- Relieved by rest or GTN spray
- Pain may radiate to one or both arms, the neck, jaw or teeth
- May be dyspnoea, nausea, sweatiness and faintness
55
*Describe scoring of angina (stable)
* 1. Have, central, tight, radiation to arms, jaw & neck
* 2. Precipitated by exertion
* 3. Relieved by rest or spray GTN
* 3/3 = Typical angina
* 2/3 = Atypical pain
* 1/3 = Non-anginal pain
56
Differential diagnosis of angina
- Pericarditis/myocarditis
- Pulmonary embolism
- Chest infection
- Dissection of the aorta
- GORD
57
Diagnosis of angina
```
12 lead ECG
Treadmill test/exercise ECG
CT scan Calcium scoring
SPECT/myoview
Cardiac catheterisation
```
58
*Describe 12 lead ECG of angina patient
* Often normal
* May show ST depression
* Flat or inverted T waves
* Look for signs of past MI
59
Describe exercise ECG/treadmill test
* Put ECG on patient, then make them run on treadmill uphill - trying to induce ischaemia
* Monitor how long patient is able to exercise for
60
Describe exercise ECG/treadmill test result on an angina patient
* If you see ST segment depression then this is a sign of late-stage ischaemia
* Many patients unsuitable e.g. can’t walk, very unfit, young females and bundle branch block
61
Describe CT scan calcium scoring for angina diagnosis
CT the heart and if there is atherosclerosis in the arteries then the calcium will light up white - if there is significant calcium then this would indicate angina
62
Describe SPECT/myoview and what it can show
Radio-labelled tracer injected into patient.
It's taken up by the coronary arteries where there is good blood supply - this will light up.
Where there is little blood supply these areas will not light up.
If there is no light after exercise then this is indicative of myocardial ischaemia.
63
Describe treatment of angina
Modify risk factors - stop smoking, encourage exercise, weight loss
Treat underlying conditions
Pharmacological - Aspirin, Statins, Betablockers, GTN spray, Ca2+ channel blocker
Revascularisation
64
*What is purpose of revascularistion and when would it be used?
To restore patent coronary artery and increase flow reserve
Done when medication fails (most) or when high risk disease is identified
65
*What are the 2 types of revascularisation?
Percutaneuos Coronary Intervention (PCI)
| Coronary Artery Bypass Graft (CABG)
66
Describe Percutaneous Coronary Intervention (PCI - revascularisation)
- Dilating coronary atheromatous obstructions by inflating balloon within it
- Insert balloon and stent, inflate balloon and remove it, stent persists and keeps artery patent
- Expanding plaque = make artery bigger
67
Pros of Percutaneous Coronary Intervention
less invasive
convenient
short recovery
repeatable
68
Cons of Percutaneous Coronary Intervention
risk of stent thrombosis, not good for complex disease
69
Describe example of Coronary Artery Bypass Graft (CABG)
Left Internal Mammary Artery (LIMA) used to bypass proximal stenosis (narrowing) in Left Anterior Descending (LAD) coronary artery
70
Pros of Coronary Artery Bypass Graft (CABG)
good prognosis, deals with complex disease, one time treatment
71
Cons of Coronary Artery Bypass Graft (CABG)
invasive
risk of stroke or bleeding
one time treatment, but
need to stay in hospital - long recovery
72
Give example of aspirin
salicylate
73
Describe how aspirin works
Antiplatelet effect (inhibits platelet aggregation) in coronary arteries thereby avoiding platelet thrombosis.
COX inhibitor - reduces prostaglandin synthesis including thromboxane A2 resulting in reduced platelet aggregation
74
*Side effect of aspirin
Gastric ulceration
75
Example of statin
Simvastatin
76
*How do statins work
- HMG-CoA reductase inhibitors - Reduces cholesterol produced by liver
- Reduce events and LDL-cholesterol
- Anti-atherosclerotic
77
*How do beta blockers work?
Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway.
B1activation→Gs→cAMP to ATP→contraction
Reduce force of contraction
78
What is the effect on the heart by beta blockers
Reduces HR (-vely chronotropic)
Reduces left ventricle contractility (-vely inotropic)
Reduces cardiac output
79
Side effects of beta blockers
```
Tiredness
Nightmares
Bradycardia
Erectile dysfunction
Cold hands and feet
```
80
*When should you not give beta blockers?
Asthma
Heart failure/heart block
Hypotension
Bradyarrhythmias
81
What are 1st line antianginal drugs
Glyceryl Trinitrate spray
| Beta blockers
82
Effects of Glyceryl Trinitrate spray
- Nitrate that is a venodilator
- Dilates systemic veins thereby reducing venous return to right heart
- Reduces preload
- Thus reduces work of heart and O2 demand
- Also dilates coronary arteries
83
Side effects of Glyceryl Trinitrate spray
Profuse headache immediately after use
84
Example of a calcium channel blocker
Verapamil
85
How do calcium channel blockers work?
- Primary arterodilators
- Dilates systemic arteries resulting in BP drop
- Thus reduces afterload on the heart
- Thus less energy required to produce same cardiac output
- Thus less work on heart and O2 demand
86
Acute coronary syndrome is an umbrella term that includes what?
ST-elevation myocardial infarction
Unstable angina
Non-STEMI
87
Describe what causes a STEMI
• Develop a complete occlusion of a MAJOR coronary artery
previously affected by atherosclerosis
• This causes full thickness damage of heart muscle
• aka a Q-wave infarction - see a pathological Q wave
88
How can you diagnose a STEMI
Can be diagnosed on ECG at presentation
Tall T waves
ST-elevation and subsequent pathological Q wave
May present as new Left bundle branch block (LBBB)
89
What causes a NSTEMI
Developing a complete occlusion of a minor or partial occlusion of a major coronary artery previously affected by atherosclerosis.
Leads to partial thickness damage of heart muscle
90
What can be seen on an ECG of a NSTEMI
Non-Q wave infarction
| ST depression and/or T wave inversion
91
*What is the difference between a NSTEMI and unstable angina
In a NSTEMI there is occluding thrombus which leads to myocardial necrosis and a rise in serum troponin (T) or creatine kinase-MB (CK-MB)
92
Describe Type 1 MI
Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection
93
Describe type 2 MI
MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension
94
Describe type 3/4/5 MI
MI due to sudden cardiac death, related to PCI and related to CABG respectively
95
Epidemiology in UK of STEMI
5/1000 per annum in UK
96
Risk factors of acute coronary syndrome
- Age
- Male
- Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55
- Smoking
- Hypertension, diabetes mellitus, hyperlipidaemia
- Obesity & sedentary lifestyle
97
Give brief overview of pathophysiology of acute coronary syndrome
- Rupture or erosion of the fibrous cap of a coronary artery plaque
- Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation
- The presence of a rich lipid pool within the plaque and a thin, fibrous cap is associated with an increased risk of rupture
- Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow
- Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/ fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia or Sudden CVS death
98
Describe features of plaque causing unstable angina
plaque has a necrotic centre and ulcerated cap and the thrombus results in PARTIAL OCCLUSION
99
Describe features of plaque causing myocardial infarction
plaque also has a necrotic centre but the thrombus results in TOTAL OCCLUSION
100
Clinical presentation of unstable angina
* Chest pain; new onset, at rest with crescendo pattern
* Breathlessness
* Pleuritic pain
* Indigestion
101
Clinical presentation of acute coronary syndrome
```
Recent destabilisation of pre-existing angina with moderate or severe limitations of daily activities.
Acute central chest pain, lasting more than 20 minutes, associated with:
• Sweating
• Nausea and vomiting
• Dyspnoea
• Fatigue
• Shortness of breath
• Palpitations
```
- Distress and anxiety
- Pallor
- Increased pulse and reduced BP
- Reduced 4th heart sound
- May be signs of heart failure (increase in jugular venous pressure)
- Tachy/bradycardia
- Peripheral oedema
102
*When would acute coronary syndrome present without chest pain
Diabetics
| Elderly
103
*Give example of signs of heart failure (state 3)
```
Increase in jugular venous pressure
Swelling in ankles, legs and feet
Dyspnoea (when exert or lie down)
Rapid or irregular heart beat
Reduced ability to exercise
Persistent cough or wheezing with white or pink blood-tinged phlegm
Fatigue and weakness
```
104
Differential diagnosis of acute coronary syndrome
- Angina
- Pericarditis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
- Oesophageal reflux/spasm
105
Diagnosis of Acute Coronary syndrome
12 lead ECG
Biochemical markers: Troponin (T and I), CK-MB, Myoglobin
CXR
106
What would 12 lead ECG of acute coronary syndrome look like?
Can be normal
ST depression and T-wave inversion (this tends to occur hours/days after) (NSTEMI) are highly suggestive of an ACS, particularly if associated with anginal chest pain
Can get hyperacute (tall) T waves
107
What is the most sensitive and specific biochemical marker of myocardial necrosis
Troponin - T and I
108
Decrease how concentration of Troponin T and I changes from the onset of chest pain
Serum levels increase within 3-12 hours from the onset of chest pain and peak at 24-48 hours
They then fall back to normal over 5-14 days
109
What can Troponin T and I levels be used to determine
Can act as prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation
110
Describe levels of myoglobin after an MI
Becomes elevated very early in MI but the test has poor specificity since myoglobin is present in skeletal muscle
111
What can Chest X-ray show
Cardiomegaly
Pulmonary Oedema
Widened mediastinum (aortic rupture)
112
Describe treatment of acute coronary syndrome
```
Pain relief (GTN spray or IV opioid)
Anti-emetic
Oxygen
Antiplatelets
Beta-blockers
Statins
ACE inhibitors
Coronary revascularisation
Risk factor modification
```
113
What can be used as pain relief in acute coronary syndrome
GTN spray
| Iv opioid
114
What oxygen levels would you aim for in acute coronary syndrome?
94-98% oxygen saturation
| 88-92% in those with COPD
115
What is an antiemetic
drug that prevents nausea and vomiting
116
What risk factors need to be modified in patient with acute coronary syndrome
* Stop smoking
* Lose weight and exercise daily
* Healthy diet
* Treat hypertension & diabetes
* Low fat diet with statins
117
What method of revascularisation would you use in patient with high risk of mortality/in high risk group e.g. recent MI
CABG
118
In an atheromatous plaque rupture, what allows platelet aggregation (and thus activation)
IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other)
119
What converts fibrinogen to fibrin?
| What happens to fibrin in thrombosis
Thrombin
fibrin is insoluble and in atherosclerotic ruptures can result in the formation of a fibrin mesh over platelet plug and thus formation of a thrombotic clot
120
Give examples of orally administered antiplatelets
Aspirin
| P2Y12 inhibitors
121
*How do P2Y12 inhibitors work?
Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation
122
Give examples of P2Y12 inhibitors
Clopidogrel
Prasugrel
Ticagrelor
123
When can you use P2Y12 inhibitors
if allergic to aspirin
| can also be used alongside aspirin as a dual anti-platelet therapy
124
Side effects of P2Y12 inhibitors
neutropenia (low neutrophils), thrombocytopenia (low platelets) and INCREASED RISK OF BLEEDING
also avoid if CABG planned
125
Give example of only IV administered antiplatelet
Glycoprotein IIb/IIIa antagonists
126
When could you give Glycoprotein IIb/IIIa antagonists
In patients with ACS undergoing Percutaneous Coronary Intervention in combination with aspirin and oral P2Y12 inhibitors
127
*Main side effect of Glycoprotein IIb/IIIa antagonists
INCREASES RISK OF MAJOR BLEEDING
128
Examples of Glycoprotein IIb/IIIa antagonists
Abciximab
Tirofiban
Eptifbatide
129
Example of Beta blockers (in ACS)
Atenolol (IV then oral)
| Metoprolol (IV then oral)
130
Side effects of Beta blockers
Avoid with asthma, heart failure, hypotension and
| bradyarrhythmias
131
What enzyme is inhibited by statins
HMG-CoA reductase
132
Examples of statins (oral)
Simvastatin
Pravastatin
Atorvastin
133
Examples of ACE inhibitors (oral)
Ramipril
| Lisonopril
134
Define acute myocardial infarction
Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial
ischaemia due to COMPLETE occlusion of artery by thrombus
135
True or False:
| STEMI is the most common medical emergency
True
136
Risk Factors of acute MI
- Age
- Male
- History of premature coronary heart disease
- Premature menopause
- Diabetes mellitus
- Smoking
- Hypertension
- Hyperlipidaemia
- Obesity and sedentary lifestyle
- Diabetes mellitus
- Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55
137
Why is early reperfusion important in STEMI
May salvage regions of the myocardium - reducing future mortality and morbidity
138
Describe pathophysiology of a STEMI
- Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque
- This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial necrosis within 15-30 minutes in a STEMI (since major artery occluded fully)
139
How is a transmural Q wave produced in STEMI
Ischaemia of the sub-endocardial myocardium
| transmural means occurring across the entire wall of an organ or blood vessel
140
Describe clinical presentation of an acute MI
* Severe, ongoing chest pain for more than 20 mins
* Pain may radiate to the left arm, jaw or neck
* Pain DOES NOT usually respond to sublingual GTN spray - opiate analgesia is required
* Pain described as substernal pressure, squeezing, aching, burning or even sharp pain
* Associated with; sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations
* Breathlessness
* Fatigue
* Distress and anxiety
* Pale, clammy and marked sweating
* Significant hypotension (low BP)
* Bradycardia or tachycardia
141
Differential diagnosis of acute MI
Stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis and MSK chest pain
142
*Diagnosis of STEMI
* Diagnosed on presentation
* ST elevation
* Tall T waves
* L bundle branch block (LBBB)
* T wave inversion and pathological Q waves follow
143
*Diagnosis of a NSTEMI
* Diagnosis is retrospective made after troponin results
| * ST depression and T wave inversion
144
Why is continuous monitoring required when in A and E and have MI
Due to high likelihood of significant cardiac arrhythmias
145
What leads of an ECG show change in an acute MI of anterior heart
ST elevation in V1-3
146
What leads of an ECG show change in an acute MI of inferior heart
ST elevation in leads II, III, aVF
Also Q waves and T wave inversion may also be present
147
What leads of an ECG show change in an acute MI of lateral heart
Change in leads I, aVL, V5-V6
148
What leads of an ECG show change in an acute MI of posterior heart
ST depression V1-V3
Dominant R wave
ST elevation in V5-V6
149
What leads of an ECG show change in an acute MI of anterolateral heart
ST elevation in leads I, aVL and V3-V6 (pericardial leads)
Loss of general R wave progression in pericardial/V waves
May also be T wave inversion
150
Occlusion of what vessels cause an acute anterolateral MI
Left anterior descending (LAD)
or LAD with RCA or LCx artery
151
Occlusion of what vessels cause an acute inferior MI
Right coronary artery
152
Occlusion of what vessels cause an acute right ventricular MI
Proximal coronary artery
Frequently associated with RBBB
(inferior-posterior wall)
153
What leads of an ECG show change in an acute septal MI
ST elevation, Q wave formation and T wave inversion in the leads overlying the septal region of the heart (V2 and V3)
154
When is hyperkalemia frequently seen
Renal failure
| Those on K sparing diuretics
155
Describe ECG of hyperkalemia
Mild hyperkalemia: Leads II, V2 and V4 demonstrate tall, tented, symmetrical T waves with a narrow base.
Moderate K overdose: QRS complex broadens and the S wave is widened in leads V3 - V6.
ST segment disappears.
P wave duration is increased, but amplitude is decreased.
Large K overdose: P wave duration and PR interval duration both increase until P wave disappears. QRS complex is broadened.
156
ECG of hypokalemia
https://meds.queensu.ca/central/assets/modules/ECG/hypokalemia.html
157
Evolution of STEMI on ECG
- After the first few minutes, the T waves become tall, pointed and upright, and there is ST segment elevation
- After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop
- After a few days, the ST segment returns to normal
- After weeks or months, the T wave may return to upright but the Q WAVE REMAINS
158
Other diagnosis of acute MI
- Troponin I or T increased
- Myoglobin increased
- Transthoracic echocardiography (TTE) may be helpful to confirm MI, as wall-motion abnormalities are detected early in STEMI
159
Describe prehospital treatment of acute MI
* Aspirin 300mg chewable
* GTN (sublingual)
* Morphine
160
Describe hospital treatment of acute MI
* IV morphine
* Oxygen if their sats are below 95% or are breathless
* Beta-blocker - Atenolol
* P2Y12 inhibitor - Clopidogrel
161
Other treatment of acute MI (not usual/first prehospital or hospital)
Coronary revascularisation
Fibrinolysis
Risk factor modification
162
When would you give coronary revascularisation to STEMI patient
Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 MINUTES of first medical contact
- If not possible then give patient fibrinolysis and then transfer to PCI centre after infusion
163
What is fibrinolysis
Enhance the breakdown of occlusive thromboses by the
| activation of plasminogen to form plasmin
164
Describe risk factor modifications of STEMI treatment
* Stop smoking
* Lose weight and exercise daily
* Healthy diet
* Treat hypertension & diabetes
* Low fat diet with statins
165
Describe secondary prevention of STEMI
* Statins
* Aspirin long term
* Warfarin if large MI
* Beta blockers
* ACE inhibitors
166
Complications of MI
```
Sudden death - often within hours often due to ventricular fibrillation
Arrhythmias
Persistent pain
Heart failure
Mitral incompetence
Pericarditis
Cardiac rupture
Ventricular aneurysm
```
167
Why do you get arrhythmias as a complication of a MI
Get them in the first few days due to electrical instability following infarction, pump failure and excessive sympathetic stimulation
168
How long do you get persistent pain for after a MI and why
12 hours to a few days after due to progressive myocardial necrosis
169
Why do you get heart failure as a result of an MI
- When cardiac output is insufficient to meet the bodies metabolic demands
- Due to ventricular dysfunction following muscle necrosis also resulting in
arrhythmias
170
Why do you get mitral valve incompetence?
Due to myocardial scarring preventing valve closure.
| can happen in first few days or later
171
Why do you get pericarditis after MI
Due to transmural infarct resulting in inflammation of pericardium
(more common in STEMI)
172
Why do you get ventricular aneurysm after MI
Due to stretching of newly formed collagenous scar tissue
173
Why do you get cardiac rupture after an MI (early or late)
Early rupture - the result of shearing between mobile and immobile myocardium
Late rupture - due to weakening of wall following muscle necrosis and acute inflammation
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Define cardiac failure
The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body
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Is cardiac failure a sign, a symptom, a syndrome or a diagnosis on its own?
Syndrome
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What can result in cardiac failure
Can result from any structural or functional cardiac disorder that impairs the hearts ability to function and meet the demands of supplying sufficient oxygen and nutrients to the metabolising body
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Epidemiology of cardiac failure
25-50% of patients die within 5 years of diagnosis
1-3% of general population
around 10% in the elderly
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Main cause of cardiac failure
Ischaemic heart disease
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Causes of cardiac failure
IHD
Cardiomyopathy (disease of heart muscles, where the walls have
become thickened, stiff or stretched)
Valvular heart disease e.g. aortic stenosis, aortic and mitral
regurgitation
Cor pulmonale
Hypertension
Alcohol excess
Any factor that increases myocardial work e.g. anaemia, arrhythmias, hyperthyroidism, pregnancy and obesity
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Risk factors of cardiac failure
- 65 and older
- African descent
- Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men
- Obesity
- People who have had an MI
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What is it called when heart failure progresses and the mechanisms to reduce effects of heart failure become overwhelmed and become pathophysiological?
Decompensation
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What are methods by body that try to maintain cardiac output and peripheral perfusion after heart failure, by physiological compensatory changes
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Venous return change (preload)
Outflow resistance (after load)
Sympathetic system activation
Renin Angiotensin Aldosterone system
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Describe changes in venous return after heart failure
Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole
This increased diastolic volume/preload stretches the myocardial fibres and myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction. (starlings law)
However, in heart failure, the failing myocardium actually doesn't contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease.
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What is outflow resistance (after load)
Outflow resistance (afterload) is the load or resistance against which the ventricle contracts
Itismadeupof:
• Pulmonary and systemic resistance
• Physical characteristics of the vessel walls
• The volume of blood that is ejected
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Describe how outflow resistance/afterload changes following heart failure
When there is an increase in afterload, there is an increase in end- diastolic volume and a decrease in stroke volume and thus a DECREASE in cardiac output.
Increase of end-diastolic volume leads to dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload
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Where are baroreceptors located?
arterial wall of the aorta, carotid arteries and in the heart walls and major veins
187
Describe decompensation of sympathetic nervous system from heart failure
Baroreceptors detects a drop in arterial pressure or increased venous pressure (due to blood back flow) and stimulates SNS.
Increase force of contraction (inotropic) and thus Stroke volume and heart rate and thus CO.
In HF, chronic sympathetic activation down regulates receptors that cause this. Means diminished effect of sympathetic activation and CO stops increasing in response to SNS activation.
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Describe decompensation of renin-angiotensin system from heart failure
Reduced CO means a diminished renal perfusion, thereby activating the renin-angiotensin system:
(angiotensinogen is converted to angiotensin I under the action of renin, angiotensin I is then converted to angiotensin II under the act of angiotensin converting enzyme (ACE), angiotensin II then stimulates the release of aldosterone from the adrenal cortex above the kidneys and ADH which stimulates water retention.
Angiotensin II and Aldosterone increase Na+ reabsorption and thus water reabsorption.)
Results in increased volume of blood -> increased BP -> increase venous pressure ->
Increases pre-load -> increases stretch of heart and thus force of contraction, SV and CO.
*However, with increased force of contraction the cardiac myocytes require more energy and thus more blood however in heart failure there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output.
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*What is systolic heart failure
Inability of the ventricle to contract normally resulting in a decrease in cardiac output.
Caused by ischaemic heart disease, myocardial infarction and cardiomyopathy (disease of heart muscle thus impairing function).
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*What is diastolic heart failure
Inability of the ventricles to relax and fill fully thereby decreasing stroke volume and decreasing cardiac output
191
Causes of diastolic heart failure
Hypertrophy (due to chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this) of ventricles resulting in there being less space for blood to fill in and thus decreased cardiac output.
Also caused by Aortic Stenosis (the narrowing of the aortic valve) which also increases afterload and thus decreases CO
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What characterises acute heart failure (not chronic)
Pulmonary and/or peripheral oedema with or without signs of peripheral hypotension
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What classification system can be used for assessment of severity of symptoms of heart failure
New York Heart Association (NYHA) classification
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*Describe the New York Heart Association (NYHA) classification for severity of symptoms of heart failure
Class I: No limitation (asymptomatic) - exercise = no fatigue, dyspnoea or palpitation
Class II: Slight limitation (mild HF (heart failure)) - comfortable at rest, normal activity = fatigue, dyspnoea and palpitations
Class III: Marked limitation (moderate HF) - comfortable at rest, gentle activity = fatigue, dyspnoea & palpitations
Class IV: Inability to carry out any physical activity without discomfort
(severe HF) - symptoms occur at rest
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On NYHA classification of severity of heart failure, what is the main difference between Class II and Class III
Class II (mild) - slight limitation: comfortable at rest, normal activity gives fatigue, dyspnoea and palpitations
Class III (moderate) - marked limitation: comfortable at rest also, but GENTLE activity gives fatigue, dyspnoea and palpitations
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*What are 3 cardinal symptoms of cardiac failure? (main symptoms)
Shortness of breath
Fatigue
Ankle swelling
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Clinical presentation of heart failure - less common symptoms
a persistent cough, which may be worse at night
wheezing
a bloated tummy
loss of appetite
weight gain or weight loss
confusion
dizziness and fainting
a fast heart rate (tachycardia)
a pounding, fluttering or irregular heartbeat (palpitations)
some people with heart failure may also experience feelings of depression and anxiety
198
Signs of heart failure
- Dyspnoea especially when lying flat (orthopnoea)
- Cold peripheries
- Raised jugular venous pressure (JVP)
- Murmurs and displaced apex beat
- Cyanosis
- Hypotension
- Peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output
- Tachycardia
- Third & fourth heart sounds
- Ascites
- Bi-basal crackles
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Diagnosis of heart failure
Blood tests
Chest X-ray
ECG
Echocardiography
If BNP and ECG normal then heart failure is unlikely, but if both abnormal, go to an echocardiogram
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Diagnosis of heart failure: Describe blood tests that can be done
Brain natriuretic peptide (BNP)
- secreted by ventricles in response to increase mycocardial wall stress
- increased in patients with heart failure
- levels correlate with ventricular wall stress and severity of heart failure
also FBC, U and Es and liver biochem
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Diagnosis of heart failure: What would be looked for on a chest x-ray
* Alveolar oedema
* Cardiomegaly
* Dilated upper lobe vessels of lungs
* Effusions (pleural)
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Diagnosis of heart failure: What would be looked for on an Echocardiogram
* Assess cardiac chamber dimension
* Look for regional wall motion abnormalities, valvular disease and cardiomyopathies
* Look for sign of MI
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Treatment after HF
Lifestyle changes
Diuretics
ACE inhibitors
Beta-blockers (start at a low dose and titrate up)
Digoxin
Inotropes
Revascularisation
Surgery to repair (mitral valve repair, aortic or mitral valve replacement)
Heart transplant (young)
Cardiac resynchronisation - improve the coordination of atria and ventricles
204
Give examples of lifestyle changes to treat HF
avoid large meals, lose weight, stop smoking, exercise, vaccination
205
Why give diuretics as heart failure treatment
Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion.
Symptomatic relief
206
What are different diuretics that could be given
* Loop diuretic - furosemide
* Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in the distal convoluted tubule)
* Aldosterone antagonist (thereby inhibiting ADH release resulting in water loss) - spirolactone but beware of renal impairment and hyperkalaemia
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Example of a loop diuretic
Furosemide
208
Example of a thiazide diuretic
Bendroflumethiazide
209
Example of an aldosterone antagonist
Spirolactone
| Epelerone
210
Examples of ACE inhibitors
Ramipril
Enalipril
Captopril
211
ACE inhibitor side effects
Cough, hypotension, hyperkalaemia and renal dysfunction
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*Why does ACE inhibitor cause you to cough
since inhibit ACE and thus the breakdown of substance P and bradykinin which results in cough
213
*Alternative to ACE inhibitor if cough is a problem
Angiotensin Receptor Blocker e.g. Canderstan or Valsartan
214
Example of a beta-blocker
Bisoprolol
| Nebivolol
215
What patients can NOT be given beta-blockers
Asthmatics
